Please find the power point on Benign Paroxysmal Positional Vertigo (BPPV). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Still's disease, sometimes referred to as Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disease characterized by the classic triad of persistent high spiking fevers, joint pain and a distinctive salmon-colored bumpy rash.
Please find the power point on Benign Paroxysmal Positional Vertigo (BPPV). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Still's disease, sometimes referred to as Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disease characterized by the classic triad of persistent high spiking fevers, joint pain and a distinctive salmon-colored bumpy rash.
Hemopneumothorax, or haemopneumothorax is the condition of having air in the chest cavity (pneumothorax) and blood in the chest cavity (hemothorax). A hemothorax, pneumothorax, or the combination of both can occur due to an injury to the lung or chest.
Hemopneumothorax, or haemopneumothorax is the condition of having air in the chest cavity (pneumothorax) and blood in the chest cavity (hemothorax). A hemothorax, pneumothorax, or the combination of both can occur due to an injury to the lung or chest.
Neonatal tetanus by Dr Afuye Olubunmi OlusolaAlade Olubunmi
Neonatal tetanus is an infectious disease caused by contamination of wounds from the bacteria Clostridium tetani, or the spores they produce that live in the soil, and animal faeces.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
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
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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!
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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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2.
A 60 yrs old houeswife ,uanabai thakur r/o katedhara M.P.
admitted on 24/9/13 in micu with c/o
1.difficulty in swallowing since 5 days
2. difficulty in opening mouth since 5 days
3.
H/o pain in both ears since 15 days
No h/o injury
No h/o fever / convulsion
No h/o consumption of any substance
Not taking any medication
No h/o similar complaints in past
No HT/DM/IHD in past
Non tobacco chewer
15. Historical perspective
The word tetanus comes from the Greek tetanos, which is derived from the
term teinein, meaning to stretch.
During World War I, tetanus occurred in 1.47 per 1000 British wounded and
in 12.5 per 1000 persons involved in the Peninsular campaign.
Nicolaier discovered Clostridium tetani in 1885 .
In 1889, Koch's pupil, Kitasato, obtained the bacillus of tetanus in pure
culture .
introduction of tetanus toxoid vaccination by Behring and Knorr in 1886.
16. Problem
Although it is an entirely preventable disease by immunization , the burden
of disease worldwide is great.
W.H.O considers reporting is inaccurate & incomplete, particularly in
devoleping countries,
In 2008 16628 cases 0f tetanus other than neonatal and 6658 cases reported
to who worldwide !
in 2009 Govt. of India reported (other than NT) 2051 cases and 160
death.there were 889 NT cases and 31 deaths!!
In 2009 maharastra reported 392 (other than NT) cases and 1 death.while 57
NT cases and 0 death !!! (park 21)
17. The Organism
Clostridium tetani is a gram positive, obligately anerobe, spore forming
bacillus, which give it a characteristic drumstick or a tennis racket
appearance.
distributed in soil and in intestine of
horses, sheep, cattle, dogs, cats, rats, chickens and nearly 10% of humans.
Hot and damp climate with soil rich in organic matter
Spores are especially resistant to heat, usual antiseptics and chemical agents
but are destroyed by autoclaving at 1200C for 15 minutes or boiling for
atleast 4 hours.
18.
19. Pathogenesis
Disease Occurs sporadically ,Affects unimmunized, partially immunized & fully
immunized who fail to maintain adequate immunity with booster doses of
vaccine
The incubation period ranges from 3-14 days, Although can as short as one day
to as long as several months have been reported
IP have prognostication and correlates with the severity of disease,
Tetanus usually follows a recognized injury.
It can complicate burns, ulcers, gangrene, necrotic snakebites, middle ear
infections, septic abortions, childbirth, intramuscular injections, and surgery.
Up to 50% of cases the injury not considered serious enough to seek medical
treatment.
In 15-25% of patients, there is no evidence of a recent wound
20. Pathogenesis
Contamination of wounds with spores of C.tetani.
Germination & toxin production – in wounds with low oxidation –
reduction potential ( devitalized tissues, F.B, active infection )
Tetanospasmin ( neurotoxin )
Tetanolysin ( hemolysin
Tetanospasmin ( exotoxin ) produced locally , released into bloodstream .
Binds to peripheral motor neuron terminals & nerve cells of ant.horn of
spinal cord
The toxin after entering axon , transported to nerve cell body in brain stem
& spinal cord – retrograde intraneuronal transport
Toxin – migrates across synapse – presynaptic terminals- blocks the release
of Glycine & GABA from vesicles.
21. Pathogenesis
The blocking of neurotransmitter
release
by
Tetanospasmin
involves
cleavage
of
Synaptobrevin – essential for
proper fn of synaptic vesicle
release apparatus
With diminished inhibition –
resting firing rate of alpha motor
neurons increases – rigidity
Lessened activity of reflexes
which limit polysynaptic spread
of
impulses,
agonists
&
antagonists recruited - spasms
22. Clinical presentation
Four clinical forms of this disease are recognized depending upon the extent
and location of neurons involved.
Generalized
Neonatal
Cephalic
local.
23. Clinical presentation
Generalized tetanus
Commonest form and is characterized by increased muscle tone and generalized spasms.
Usually, the first symptom is trismus or lock jaw. Dysphagia, stiffness and pain in
neck, shoulder and back muscles appears.
Rigidity of abdomen and facial grimacing, popularly known as
„Risus sardonicus‟ ,opsthotonus.
Appearance of generalized muscle spasms, occurring spontaneously or due to minor
stimuli
Spasms may lead to respiratory compromise necessitating respiratory support.
Spasms can cause compressive fractures of the spine, rupture of muscles, rhabdomyolysis
and renal failure.
These are maximum during the first two weeks of illness and decrease thereafter in
frequency and intensity.
24. Clinical presentation
Autonomic Disturbances Seen in Tetanus
Sustained or labile hypertension
Progressive and refractory hypotension
Peripheral vasoconstriction
Tachycardia (episodic commonly)
Bradycardia and asystole
Arrythmias
Fever
Profuse diaphoresis, salivation
Increased bronchial secretions
Gastric stasis and ileus
Urinary retention
25. Clinical presentation
Localised tetanus
This is a relatively uncommon and benign form of the
Disease process in which patients have persistent contraction of muscles in
same anatomic area as the injury preceding the tetanus.
Local tetanus might generalize over time but overall mortality is about 1%.
The most important indicator for poor prognosis was the progression to
secondary generalization (27%).
26. Clinical presentation
Cephalic tetanus :
This involves cranial nerves and has an overall incidence of 6%.
It commonly results from middle ear infections and head injuries.
Facial muscles are most commonly affected, followed by 6th, 3rd, 4th and
12th cranial nerves in the order of frequency.
Trismus may be present but usually follows other cranial nerve deficits in
42% of patients.
Although, overall mortality described is high (15-30%), many cases with a
milder disease have been reported from India.
27. Clinical presentation
Neonatal tetanus
This form of tetanus still has a high incidence and mortality in the
developing countries
The common age of onset is between 5 and 15 days following birth.
Common presenting complaints are rigidity, spasms, failure to
suck, trismus, fever and seizures.
Due to lack of inhibiting influences from higher centers in newborns, the
anterior horn cells react more violently, resulting in more spasms.
Overall mortality is around 70% and most patients with severe disease die.
30. Ablett Classification of the Severity of Tetanus
I Mild- Mild to moderate trismus; general spasticity; no respiratory
embarrass - ment; no spasms; little or no dysphagia
II Moderate -Moderate trismus; well-marked rigidity; mild to moderate but
short spasms; moderate respiratory embarrassment with an increased
respiratory rate greater than 30, mild dysphagia
III Severe -Severe trismus; generalized spasticity; reflex prolonged spasms;
respiratory rate greater than 40; apnoeic spells, severe dysphagia;
tachycardia > 120.
IV Very severe- Grade III and violent autonomic disturbances involving the
cardiovascular system. Severe hypertension and tachycardia alternating with
relative hypotension and bradycardia, either of which may be persistent
31. Diagnosis
Tetanus is diagnosed by clinical observation.
Electromyographic studies are occasionally useful in questionable cases.
Antitetanus antibodies are undetectable in most tetanus
patients, “protective” concentration of 0.01 IU/L.
Rare patients apparently develop antibodies that are not protective.
Attempts to culture C. tetani from wounds are not useful in diagnosis
„Spatula test‟ to aid in diagnosis with a sensitivity of 94% and specificity of
100%. (Apte and Karnad )`
32. Differential diagnosis
Strychnine poisoning,
Dystonic reactions to neuroleptic drugs or other central dopamine.
Treatment with anticholinergic agents (benztropine or diphenhydramine) is
rapidly effective against dystonic reactions.
Dental infections can produce trismus, and should be sought, but they do
not cause the other manifestations of tetanus.
33. Management
Management of tetanus patients involves a team approach.
The defined goals of treatment include the following :
a) halting production of toxin within the wound,
b) neutralization of unbound toxin,
c) control of muscle spasms,
d) management of autonomic instability,
e) supportive therapy,
f) management of complications,
g) prevention
34. Management
Halting the production of toxin
Wound management eradicate spores and change conditions for germination, thereby preventing
further elaboration and absorption of the neurotoxin.
Antibiotic therapy :
Penicillin still remains a standard therapy in many parts of the
world, although metronidazole seems to be replacing it and is being
considered as a drug of choice by.
The usual dose of penicillin is 100,000 – 200,000 IU/kg/day given
intravenously or intramuscularly. Metronidazole is used at a dose of 500 mg
every 6 hours intravenously or per orally and 400 mg rectally every 6
hours, for 7-10 days.
35. Management
Neutralization of the unbound toxin
This is achieved through passive immunization with either human or equine
tetanus immunoglobulin. should be undertaken as early as possible since the
toxin becomes inaccessible once it is bound to the nerve terminus.
The usual dose of equine preparation is 500- 1000 IU/kg given
intravenously or intramuscularly.
The dose of HTIG is 5000-8000 IU intramuscularly.
Usual dose for prophylaxis is1500-3000 IU of equine and 250-500 IU of
human preparation.
37. Supportive Management
Secure airway/tracheostomy/ventilatory support
Pts recovering from tetanus should be actively immunized
Hydration
Nutrition
Physiotherapy
Prophylactic anticoagulation
Bowel, bladder, back care
Treatment of intercurrent infection
38. Prevention – Active Immunization
For partially immunized, unimmunized and recovering from tetanus
It stimulates production of protective antitoxin
2 prep :
combined vaccine : DPT
monovalent vaccine : plain / formol toxoid tetanus vaccine , adsorbed
39. Combined vaccine
According to National Immunization, 3 doses of DPT – at intervals of 4-8
wks, starting at 6 wks age, followed by
booster at 18 months age
2nd booster (only DT) at 5-6 yrs
3rd booster ( only TT) after 10 yrs age
40. Monovalent vaccines
Purified tetanus toxoid ( adsorbed ) supplanted the palin toxoid – higher &
long lasting immunity response
Primary course of immunization – 2 doses
Each 0.5 ml , injected into arm given at intervals of 1-2 months
The longer the interval b/w two doses, better is the immune response
1st booster – 1 yr after the initial 2 doses
2nd Booster : 5 yrs after the 1st booster ( optional )
Freq boosters to be avoided
41. Passive immunization
•
•
•
•
•
•
•
Human Tetanus Hyperimmunoglobulin :
250-500 IU
Does not cause serum sickness
Longer passive protection compared to horse ATS( 30 days / 7 -10 days
ATS ( EQUINE )
1500 IU s/c after sensitivity testing
7 – 10 days
High risk of serum sickness
It stimulates formation of antibodies to it , hence a person who has once
received ATS tends to rapidly eliminate subsequent doses.
42. Active & Passive Immunization
In non immunized persons
1500 IU of ATS / 250-500 units of Human Ig in one arm & 0.5 ml of
adsorbed tetanus toxoid into other arm /gluteal region
6 wks later, 0.5 ml of tetanus toxoid
1 yr later , 0.5 ml of tetanus toxoid
43. Prevention of neonatal tetanus
Clean delivery practices
3 cleans : clean hands, clean delivery surface, clean cord care
Tetanus toxoid protects both mother & child
Unimmunized pregnant women : 2 doses tetanus toxoid
1st dose as early as possible during pregnancy
2nd dose – at least a month later / 3 wks before delivery
Immunized pregnant women : a booster is sufficient
No need of booster in every consecutive pregnancy
44. Prevention of tetanus after injury
All wounds should be thoroughly cleaned soon after injury
Remove all foreign bodies, soil, dust, necrotic tissue
A – completed course of toxoid/booster < 5 yrs ago
B- completed course of toxoid / booster >5 yrs ago & < 10 yrs ago
C- completed course of toxoid / booster >10 yrs ago
D- not completed course of toxoid / immunity status unknown
45. Wounds < 6hrs, clean, non penetrating & negligible tissue
damage
Immunity Category
Treatment
•
A
B
C
D
•
Nothing more required
Toxoid 1 dose
Toxoid 1 dose
Toxoid complete course
•
•
•
•
•
•