This document provides information on paracetamol (acetaminophen) poisoning, including its introduction, mechanisms of action, toxicity, clinical features, investigations, management, and antidote. It discusses that paracetamol is metabolized to a toxic metabolite that can cause liver damage if glutathione levels are depleted. Patients presenting with elevated liver enzymes and international normalized ratio following ingestion should receive N-acetylcysteine to replenish glutathione levels based on standardized treatment protocols. Timely administration of N-acetylcysteine within 10 hours of ingestion can prevent liver injury from paracetamol poisoning.
this presentation is about the acetaminophen or paracetamol as its second name and its overdose reactions and activities. and its toxic effects that may be harmful and cause damages in the people.
this presentation is about the acetaminophen or paracetamol as its second name and its overdose reactions and activities. and its toxic effects that may be harmful and cause damages in the people.
Please find the power point on Paracetamol poisoning. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Rodenticide Poisoning + Rat Killer paste poisoning managementVasif Mayan
Rodenticide paste poisoning
Case Study
Clinical features
Management
Investigations
Treatment guidelines
pathogenesis
N acetyl cysteine
Coumarins
other rodenticides
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Please find the power point on Paracetamol poisoning. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Rodenticide Poisoning + Rat Killer paste poisoning managementVasif Mayan
Rodenticide paste poisoning
Case Study
Clinical features
Management
Investigations
Treatment guidelines
pathogenesis
N acetyl cysteine
Coumarins
other rodenticides
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
Sean Kelly is an Emergency Physician and Intensivist who's the director at Gosford ICU in New South Wales. He's also the medical director at ICCMU. He gave this great talk at Bedside Critical Care 2012 on Daydream Island. He'll be at SMACC. Check out the ICCMU website.
Lecture on some therapeutic poisons based on subject of Forensic Medicine. Aspirin , Salicylate, aconite and barbiturates poisoning is beutifully explaned with treatments
NAC, Physostigmine & Neostigmine: Their efficacy as antidote - By RxVichu!!! ...RxVichuZ
This powerpoint encompasses some details regarding the pharmacology, ADRs, interactions, dosage regimens and special points that need to be kept in mind, while using the antidotes "ACETYLCYSTEINE, PHYSOSTIGMINE & NEOSTIGMINE".
Do go through this, and let me know your reviews.
Regards,
Vishnu.
Non-steroidal anti-inflammatory drugs is a class of analgesic medication that reduces pain, fever and inflammation. Since most episodes of back pain involve inflammation, NSAIDs such as ibuprofen and naproxen are often an effective treatment option.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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2. INTRODUCTION
Paracetamol , also known as acetaminophen or
APAP (N- acetyl-p-aminophenol)
It is a deethylated active metabolite of phenacetin
discovered in 1877 , which was used as an
analgesic and antipyretic and is banned now
because of its analgesic abuse nephropathy.
In 1893, was first discovered in the urine of
individuals who had taken Phenacetin.
In 1950, Paracetamol tablets were in introduced
in UK.
By 1963, Paracetamol was available worldwide
3. ACTIONS
To date mechanism of action is not completely
understood.
The main mechanism proposed is the inhibition of
cyclooxygenase(COX) and recent findings suggest
that it is highly selective for COX-2.
By inhibition of COX it prevents generation of
prostaglandins from arachidonic acid, which are inturn
converted to numerous other proinflammatory
mediators.
Poor inhibitor of prostaglandin synthesis in the
peripheral tissues but a potent COX inhibitor in the
brain.
By Central subcortical action raising the pain
threshold it raises pain threshold – Acts as an
analgesic
Good and promptly acting anti pyretic by reducing
4. has negligible antiinflammatory action - inability
to inhibit COX in the presence of peroxides which
are generated at sites of inflammation, but are not
present in the brain.Good and promptly acting
anti pyretic
The ability of paracetamol to inhibit COX-3 could
also account for its analgesic-antipyretic action.
does not stimulate respiration or affect acid-base
balance;
does not increase cellular metabolism.
does not affect platelet function or clotting factors
and is not uricosuric.
Plasma t½ is 2–3 hours. Effects after an oral dose
last for 3–5 hours.
5. Paracetamol Combinations
Available as IR(immediate release) – 325mg and
500mg doses , ER(extended release) – 650mg
Formulations and preparations – Elixirs,
suspensions, tablets(meltable and chewable),
capsules, rectal suppositories
Combinations –
Opioids - codein, tramadol, etc..
NSAIDS – Mephanamic acid,
6.
7.
8. MECHANISM OF TOXICITY
A small proportion of acetaminophen is
metabolized by a phase I reaction to a
hepatotoxic metabolite formed from the parent
compound by the cytochrome P450 CYP2E1.
This metabolite, N-acetyl-p-benzoquinoneimine
(NAPQI), is detoxified by binding to
“hepatoprotective” glutathione to become
harmless, water-soluble mercapturic acid, which
undergoes renal excretion.
When excessive amounts of NAPQI are formed,
or when glutathione levels are low, glutathione
levels are depleted and overwhelmed, permitting
covalent binding to nucleophilic hepatocyte
macromolecules forming acetaminophen-protein
“adducts.”
9. The binding of acetaminophen to hepatocyte
macromolecules is believed to lead to
centrilobular hepatic necrosis
Even in the absence of hepatotoxicity, renal
failure can occur because of renal papillary
necrosis.
Large doses act on brain stem and cause rapid
death.
11. CLINICAL FEATURES
Phase I (0-24 h) Anorexia, nausea, vomiting
Phase II (24-72 h) Right upper quadrant pain,
elevated liver enzymes, PT and INR may be
elevated
Phase III (72-96 h) Vomiting, symptoms of liver
failure, renal failure and pancreatitis may occur
Phase IV (>4 days) Resolution of symptoms or
progression to fatality
12. Acetaminophen causes dose-related centrilobular
hepatic necrosis after single-time-point ingestions, as
intentional selfharm, or over extended periods, as
unintentional overdoses, when multiple drug
preparations or inappropriate drug amounts are used
daily for several days, e.g., for relief of pain or fever.
In these instances,8 g/d, twice the daily
recommended maximum dose, over several days can
readily lead to liver failure.
Use of opioid-acetaminophen combinations appears
to be particularly harmful, because habituation to the
opioid may occur with a gradual increase in opioid-
acetaminophen combination dosing over days or
weeks.
A single dose of 10–15 g, occasionally less, may
produce clinical evidence of liver injury.
Fatal fulminant disease is usually (although not
13. Minimum toxic doses for single ingestion
Adults – 7.5-10 g
Children – 150mg/kg:200mg/kg in healthy
children aged 1-6 years.
Fatal dose : 20-25 g
Fatal period : 2 to 4 days
14. INVESTIGATIONS
Serum acetaminophen concentration
Liver function tests – ALT, AST, Bilirubin(Direct and
indirect), alkaline phosphatase
Prothromin time with International normalised ratio
RBS
Renal function tests(electrolytes, BUN, creatinine)
Lipase and amylase(c/o abdominal pain)
Arterial blood gas analysis and ammonia
Urinanalysis( for hematuria and proteinuria)
ECG(to detect additional clues for co-ingestants)
CT brain(if altered mental status)
15.
16. Blood levels of acetaminophen correlate with
severityof hepatic injury (levels >300 μg/mL 4 h
after ingestion are predictive of the development
of severe damage; levels <150 μg/mL suggest
that hepatic injury is highly unlikely).
Whether or not a clear history of overdose can be
elicited, clinical suspicion of acetaminophen
hepatotoxicity should be raised by the presence
of the extremely high aminotransferase levels in
association with low bilirubin levels that are
characteristic of this hyperacute injury
17. FACTORS THAT ALTER RISK
Induced P450 : chronic alcohol,
barbiturates, phenobarbital, isoniazid,
Glutathione depletion: chronic
ingestion paracetamol, malnutrition,
starvation, alcohol
Hepatitis C virus(HCV) infection was
found to be associated with an
increased risk of acute liver injury in
patients hospitalized for acetaminophen
overdose
18. Therefore, in chronic alcoholics, the
toxic dose of acetaminophen may be as
low as 2 g, and alcoholic patients should
be warned specifically about the
dangers of even standard doses of this
commonly used drug.
19. Management
As there are no early symptoms that predict
acetaminophen toxicity, poisoning severity
following an acute ingestion is quantified by
plotting a timed serum acetaminophen
concentration on the modified Rumack-Matthew
nomogram, drawn no less than 4 hours after
ingestion, serves as a guide for management.
20. Rumack-Matthew nomogram
Rumack-Matthew nomogram (the acetaminophen
toxicity nomogram or acetaminophen nomogram), is
used to interpret serum acetaminophen
concentrations in relation to time since ingestion, in
order to assess potential hepatotoxicity.
The nomogram predicts the risk of hepatotoxicity on
a single acetaminophen concentraion, measured at
one time. It is not a prognostic tool and, hence, does
not predict fulminant hepatic failure or death.
The nomogram predicts potential toxicity beginning at
4 hours after ingestion up to 24 hours after ingestion.
Acetaminophen concentraions measured earlier than
4 hours post-ingestion may not be reliable.
Concentrations measured 4-18 hours post-ingestion
21. The upper line of the nomogram is the “probable”
line, also known as the Rumack-Matthew line. About
60% of patients with values above this line develop
hepatotoxicity. The lower line on the nomogram is the
“possible” line, which was subsequently added later
per request of the U.S. FDA. The possible line, also
known as the “treatment” line, incorporates a 25%
margin of error in measurement variations or
uncertainty regarding the time of ingestion.
The nomogram cannot be used if the patient
presents more than 24 hours after ingestion or has a
history of multiple acetaminophen ingestions. Its
reliability decreases for ingestions of extended-
release acetaminophen formulations or for co-
ingestions of acetaminophen with agents that delay
gastric emptying and acetaminophen absorption
(e.g.anticholinergics or opioids).
22.
23. Treatment includes gastric lavage, supportive
measures, and oral administration of activated
charcoal or cholestyramine to prevent absorption of
residual drug.
Treatment with activated charcoal (AC), 1 g/kg
(maximum dose 50 g) by mouth in all patients who
present within four hours of a known or suspected
acetaminophen ingestion, unless there are
contraindications to its administration like sedated
patients not on endotracheal tube and those
presenting after 4 hours of overdose.
Studies have shown that induced emesis and gastric
lavage limit the absorption of acetaminophen after
simulated overdose and in clinical trials However,
these therapies appear to be less effective than
activated charcoal, so they are not routinely
24. ANTIDOTE: N-
ACETYLCYSTEINE
N-acetylcysteine is the accepted antidote for
acetaminophen poisoning and is given to all patients
at significant risk for hepatotoxicity. Serious
hepatotoxicity is uncommon and death extremely rare
if N-acetylcysteine is administered within eight hours
following acetaminophen overdose.
The key to effective treatment is to start therapy
before the onset of liver injury, which can be defined
biochemically by an elevation of the alanine
aminotransferase (ALT).
In patients with high acetaminophen blood levels
(>200 μg/mL measured at 4 h or >100 μg/mL at 8 h
after ingestion), the administration of N-acetylcysteine
25. In addition, when N-acetylcysteine is
administered late following acetaminophen
ingestion to patients with evidence of hepatic
failure, it decreases mortality and improves
hepatic and cerebral function
This agent provides sulfhydryl donor groups to
replete glutathione,which is required to render
harmless toxic metabolites that would otherwise
bind covalently via sulfhydryl linkages to cell
proteins,resulting in the formation of drug
metabolite-protein adducts.
26. Indications for N-acetylcysteine
therapy
Serum acetaminophen concentration drawn at four hours
or more following acute ingestion of an immediate-release
preparation is above the "treatment" line of the treatment
nomogram for acetaminophen poisoning
A suspected single ingestion of greater than 150 mg/kg
(7.5 g total dose regardless of weight) in a patient for
whom the serum acetaminophen concentration will not be
available until more than eight hours from the time of the
ingestion.
Patient with an unknown time of ingestion and a serum
acetaminophen concentration >10 mcg/mL (66 µmol/L).
Patient with a history of ingestion and evidence of ANY
liver injury.
Patients with delayed presentation (>24 hours after
ingestion) consisting of laboratory evidence of liver injury
(ranging from mildly elevated aminotransferases to
27. Common protocols
20 hour IV protocol — The 20 hour intravenous
(IV) protocol for N-acetylcysteine treatment has
been used in the United Kingdom since the
1970s.
The approved 20 hour IV dosing regime is
complicated and is performed as follows:
150 mg/kg in 200 mL of D5W infused over 1 hour,
followed by 50 mg/kg in 500 mL of D5 W over 4
hours and then 100 mg/kg in 1000 mL of D5W
over 16 hours
This treatment protocol provides a total of 300
mg/kg over 20 to 21 hours
28. 72 hour oral protocol — The 72 hour oral (PO) dosing
protocol for N-acetylcysteine treatment has been used
successfully in the United States for more than 30
years, and consists of the following:
A loading dose of 140 mg/kg PO, followed by
A dose of 70 mg/kg PO every four hours for a total of
17 doses
The dose does not need to be adjusted if the patient
has been treated with activated charcoal.
The incidence of hepatotoxicity for patients treated
within eight hours of ingestion is less than 10 percent,
but increases to approximately 40 percent if treatment
is delayed beyond 16 hours.
29. Other protocols
A 12-hour protocol for N-acetylcysteine treatment -
involves the administration of 100 mg/kg of N-
acetylcysteine over two hours as a loading dose, and then
administration of 200 mg/kg over 10 hours
Intermittent IV infusion may be considered for late-
presenting or chronic ingestion. A loading dose of 140
mg/kg IV (diluted in 500 mL D5W) is infused over 1 h.
Maintenance doses of 70 mg/kg IV are given every 4 hours
for at least 12 doses (dilute each dose in 250 mL of D5W
and infuse over a minimum of 1 hour).
— Current dosing protocols for N-acetylcysteine in the
United States are calculated using patient bodyweight.
However, the maximum dose is based upon a weight of
100 kg for IV therapy and 110 kg for oral therapy
Clinicians often based dosing on actual weight with a low
rate of adverse events .
30. In most patients, either the oral or IV route is
acceptable. IV administration is favored for
patients with any of the following:
Vomiting
Contraindications to oral administration
(ie,pancreatitis,bowel ileus or obstruction, bowel
injury)
Hepatic failure
Patients who refuse oral administration
Patients with evidence of hepatic failure
31. NAC adverse effects
‘Non-IgE mediated anaphylaxis (previously called
anaphylactoid reactions) with intravenous
administration and vomiting with oral administration
are the most common adverse reactions associated
with N-acetylcysteine administration.
Like urticaria, flushing, angio oedema, wheezing ,
hypotension etc..
Patients receiving IV N-acetylcysteine warrant close
monitoring and all essential medications and tools
needed to treat anaphylaxis and airway emergencies
should be immediately available. These include
oxygen, antihistamine medication (eg,
diphenhydramine and ranitidine), albuterol,
epinephrine (1:1000 for intramuscular use),
32. with oral N-acetylcysteine develop nausea and
vomiting. Serotonin 5-HT3 receptor antagonists
(eg, ondansetron) are useful antiemetics. If the
patient vomits within 60 minutes of an oral dose
of N-acetylcysteine, the dose of N-acetylcysteine
should be repeated.
33. Methionine
An alternative antidote is methionine 2.5 g orally
(adult dose) every 4 hours to a total of 4 doses
upto a total of 10 grams orally, but this is less
effective, especially after delayed presentation.
Do not give activated charcoal as it will bind
methionine.
It acts by increasing glutathione synthesis.
34. DELAYED PRESENTATION
If patient presents 8-24 hours or later after an
acute ingestion, initiate therapy immediately and
evaluate for laboratory evidence of hepatatoxicity.
NAC administration in such cases has decreased
incidence of cerebral oedema and improved
survival.
Proposed mechanism in this setting include an
antioxidant effect, decreased neutrophil
accumulation and improved microcirculatory
blood flow supporting increased oxygen delivery
to hepatic tissue.
35. Chronic Ingestion
If a patient presents after multiple ingestions or
chronic ingestion of supratherapeutic doses of
acetaminophen over hours or days, evaluate for
the presence of a persistent serum APAP
concentration and laboratory indicators of
hepatotoxicity. Begin NAC therapy if the patient
has elevated aspartate aminotransferase (AST)
and alanine aminotransferase (ALT) levels or a
measurable serum APAP concentration.
36. Extended-Release Acetaminophen
Overdose
Extended-release acetaminophen consists of
acetaminophen 325 mg in immediate release (IR)
form surrounding a matrix of acetaminophen 325
mg formulated for slow release. Some alteration
of the elimination kinetics of this preparation may
affect the reliability of the Rumack-Matthew
nomogram to predict potential hepatotoxicity and
subsequent treatment based on serum APAP
concentrations.
Several studies show that the elimination of ER
and IR APAP preparations is nearly identical after
4 hours. However, some case reports have
documented APAP levels that are above the
37. Extended-Release Acetaminophen
Overdose
Given these findings, recommended
management for overdose of ER preparations
includes the measurement of 4-, 6-, and 8-hour
APAP concentrations. Begin NAC therapy if any
level crosses above the nomogram treatment
line. If the 6-hour level is greater than the 4-hour
level, begin NAC therapy.
More prolonged monitoring of APAP levels may
be necessary if the patient has food in his or her
stomach or has taken co-ingestants that delay
gastric emptying.
38. LIVER TRANSPLANTATION
If signs of hepatic failure (e.g., progressive jaundice,
coagulopathy, confusion) occur despite N-
acetylcysteine therapy for acetaminophen
hepatotoxicity, liver transplantation may be the only
option.
The United Kingdom King's College Hospital criteria
for the determination of the urgent need for
transplantation after acetaminophen-induced
fulminant hepatic failure include any one of the
following:
Arterial pH less than 7.3 after fluid
resuscitation(lactate levels >3.5 mmol/L)
Grade III or IV encephalopathy
Prothrombin time (PT) greater than 100 seconds
Serum creatinine level greater than 3.4 mg/dL
39. CONCLUSION
Because of the limited safety margin between
safe and toxic doses, the FDA has recommended
that the daily dose of acetaminophen be reduced
from 4 g to 3 g (even lower for persons with
chronic alcohol use), that all acetaminophen-
containing products be labeled prominently as
containing acetaminophen, and that the potential
for liver injury be prominent in the packaging of
acetaminophen and acetaminophen-containing
products.
Within opioid combination products, the limit for
the acetaminophen component has been lowered
to 325 mg per tablet
40. References
Harrison 19/e
Davidson 22/e
API 10/e
www.medscape.in
www.uptodate.in
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