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Objectives
At the end of this presentation students will be able to :
Define the term Tetanus.
State the overview of Tetanus.
State the epidemiology of Tetanus.
Outline the incidence of Tetanus.
Explain the causative agents of Tetanus.
Describe the pathophysiogy of Tetanus
 State the risk factors of Tetanus.
State the classification of Tetanus.
Describe the clinical manifestation of Tetanus.
Objectives
 State diagnostic measures/or investigations used to confirm
Tetanus.
List differential diagnosis for Tetanus.
Outline the medical management of Tetanus.
Discuss the midwife’s role in the management of Tetanus.
State the prognosis of Tetanus.
Outline the preventative measures to be taken.
Outline Jamaica’s Immunization schedule
List the complications of tetanus.
• Tetanus is an acute, often
fatal, infectious neurological
disease that caused by
contamination of wounds from
the bacteria Clostridium tetani
that live in the soil, and animal
faeces.
• Tetanus is the only vaccine preventable disease that is infectious
but not contagious.
• It is a major international public health problem, as spores are
ubiquitous (omnipresent).
• Tetanus remains a problem in the developing and under
developed countries. It is most prevalent in industrial
establishment, where agricultural workers are employed.
• Tetanus occurs worldwide but is more common in hot, damp
climates with soil rich in organic matter especially during summer.
• The disease occurs almost exclusively in persons who are
unvaccinated or inadequately immunized.
• Maternal and neonatal tetanus are important causes of maternal
and neonatal mortality.
• Although easily prevented by maternal immunization with tetanus
toxoid vaccine, and aseptic obstetric and postnatal umbilical-cord
care practices
• Maternal and neonatal tetanus persist as public-health problems
in 48 countries, mainly in Asia and Africa.
• Tetanus was first described in Egypt over 3000 years ago (Edwin
Smith Papyrus). It was again described by Hippocrates
• There are between 800,000 and 1 million deaths due to Tetanus
each year; 80% of these deaths occur in Africa and South East
Asia. It remains endemic in 90 countries world wide.
• Neonatal tetanus was long recognised by clinicians in resource-
poor settings as an important cause of neonatal death.
• However, since babies affected by this disease usually are born at
home and die there without registration of either event, the true
burden was unknown.
• Maternal tetanus has the same risk factors and means of
prevention as neonatal tetanus,whether pregnancy ended with
birth, miscarriage, or abortion.
• Maternal and neonatal tetanus claim about 180,000 lives
worldwide every year, almost exclusively in developing countries.
• In 1999, the elimination of maternal tetanus was added to the
goals of the elimination programme for neonatal tetanus, and the
initiative was renamed the Maternal and Neonatal Tetanus
Elimination Program.
• Good progress has been made in the 22 years since the neonatal
tetanus elimination programme began.
• Worldwide mortality from neonatal tetanus was estimated at 180,
000 in 2002, which represents a 78% reduction since the late
1980s.
• In developed countries, tetanus is now little more than a medical
curiosity; maternal and neonatal tetanus are exceedingly rare.
• However, tetanus as a whole continues to cause about 213,000–
293,000 deaths worldwide each year, predominantly in low-
income and middle income countries.
• Despite widespread immunization of infants and children
in the United States since the 1940s, tetanus still occurs
in there.
• The majority of reported tetanus cases are birth-
associated, occurring in low income countries among
insufficiently vaccinated mothers and their newborn
infants, following unhygienic deliveries and abortions and
poor postnatal hygiene and cord care practices.
• Tetanus is caused by an exotoxin produced by the
bacterium Clostridium Tetani, found worldwide in soil, in
inanimate environment, in animal faeces & occasionally
human faeces.
• Clostridium Tetani is a slender, gram-positive, motite,
anaerobic rod that may develop a terminal spore, giving it
a drumstick appearance.
is in the intestine of animals, including
human in which the organism is a harmless normal
inhabitat.
• Clostridium Tetani entry into the body usually involves
implantation of spores into a wound
• The organism is sensitive to heat and cannot survive in
the presence of oxygen. After gaining entry, Clostridium
Tetani spores can persist in the body for months, waiting
for the proper oxygen-free environment where they can
germinate and develop.
• The bacteria then produce tetanus toxins, circulates in the
body blocking nerve impulses that allow muscles to relax.
Any break in the skin are potential entry ways for the
bacteria.The usual locations for the bacteria to enter the
body are:
• Puncture wounds such as those caused by rusty nails,
splinters, and human, animal or insect bites, parenteral
drug abuse
• In neonates usually via infected umbilical stumps
• Transmission by contaminated wounds- Gangrene,
Abscess, Burns, crush wounds or Open fractures,
• Tissue injury from surgery and IV drug access sites
• Otitis media, dental infection, abortion, and pregnancy.
• Neonates born to mothers who were not immunized
against tetanus
• Females during delivery or abortion that are unimmunized
or not fully immunized against tetanus
• Agricultural workers
• Environmental and social factors: unhygienic custom
habits,unhygienic delivery practices
• Underdeveloped countries with limited resources
• Poor maternal and child health care protocols
Tetanus may be categorized into the following clinical
types:
• Generalized tetanus
• Localized tetanus
• Cephalic tetanus
• Maternal tetanus
• Neonatal tetanus
• This is the most common form of tetanus and make up
roughly 80% of tetanus cases
• Approximately 50-75% of patients with generalized
tetanus present with trismus (“lockjaw”), which is the
inability to open the mouth secondary to masseter muscle
spasm.
• Nuchal rigidity (inability to flex the neck forward) and
dysphagia are also early complaints that cause risus
sardonicus, the scornful smile of tetanus, resulting from
facial muscle involvement.
• As the disease progresses, patients have generalized
muscle rigidity with intermittent reflex spasms in response
to stimuli (e.g., noise, touch).
• Tonic contractions cause opisthotonos (ie, flexion and
adduction of the arms, clenching of the fists, and
extension of the lower extremities).
• During these episodes, patients have an intact sensorium
and feel severe pain.
• The spasms can cause fractures, tendon ruptures, and
acute respiratory failure.
• Spasms continue for 3-4 weeks
• Recovery usually begins in 3 weeks and takes
approximately 4 weeks
• It occurs by sprouting new nerve terminals in the spinal
cord and leading to relaxation of contracted muscles.
• Incubation period is 8 days (2-14 days), dependent on site
of injury from CNS
• Faster onset of symptoms means poor the prognosis.
• Death occurs when spasms interfere with respiration.
• Descending pattern: lockjaw
→stiffness of neck →difficulty
swallowing→rigidity of
abdominal and back muscles.
• Patients with localized tetanus present with persistent
rigidity in the muscle group close to the injury site.
• The muscular rigidity is caused by a dysfunction in the
interneurons that inhibit the alpha motor neurons of the
affected muscles.
• No further central nervous system (CNS) involvement
occurs in this form, and mortality is very low.
• The contraction and the spasm is milder, usually last for
few days before subsiding
• Prognosis – excellent ( only 1% of cases being fatal)
• Cephalic tetanus is uncommon and usually occurs after
head trauma or otitis media.
• Patients with this form present with cranial nerve (CN)
palsy.
• Involvement of cranial nerves III, IV, VI and XII may also
occur either alone or in combination.
• The infection may be localized or may become
generalized.
• Incubation period: few days Mortality: high
•Tetanus occurring during pregnancy or within 6 weeks after
any type of pregnancy termination, is one of the most easily
preventable causes of maternal mortality.
It includes postpartum or puerperal tetanus
(i) postpartum or puerperal tetanus, usually resulting from
septic procedures during delivery,
(ii) postabortal tetanus, following septic maneuvers during
induced abortion
(iii) Tetanus during pregnancy, generally resulting from
inoculation through a nongenital portal of entry(via caerean
section)
• Neonatal tetanus (tetanus neonatorum) is a major cause
of infant mortality in underdeveloped countries.
• It is a form of generalized tetanus that occurs in newborn
infants born without protective of passive immunity
because the mother is not immune.
• Infection results from umbilical cord contamination during
unsanitary delivery, unaseptic cord care
• Symptoms usually appear by the 3rd day after birth but in
some case as early as 5 hours after infection.
• Initial SYMPTOMS: Excessive unexplained crying
followed by refusal of feeds and apathy
• The baby develops progressive feeding difficulty due to
reflex spasm of massetter makes feeding painful,
pharyngeal muscles goes into spasm and cause chocking
as a result of dysphagia
• At the end of the first week of life, infected infants may
develop rigidity with spasms.
• Neonatal tetanus has a very poor prognosis.
• Spasm of larynx and respiratory muscles are induced by
stimuli such as touch, noise, bright light, resulting in
episodes of apnoea and cyanosis.
• Constipation persists until spasms are relieved, becomes
rigid,develops paralysis, and may develop opisthotonic
posturing(in extension) and experience painful spasm.
• Inter-current infections (a disease that intervenes during
the course of another disease), dehydration and acidosis
complicate the condition.
• Baby has neonatal
tetanus with
complete rigidity
• Risus sardonicus: Contraction of the muscles at the angle
of mouth and frontalis
• Trismus (Lock Jaw): convulsive contraction and spasm of
Masseter muscles.
• Opisthotonus: Spasm of extensor of the neck, back and
legs to form a backward curvature.
• Muscle spasticity
• The affected individual is conscious throughout the
illness, but cannot stop contractions, making tetanus a
truly dreadful disease.
• Tetany - prolonged muscular action causes sudden,
powerful, and painful contractions of muscle groups.
These episodes can cause fractures and muscle tears.
• If respiratory muscle is involved – apnoea.
• Dysphagia occurs in moderately severe tetanus as a
consequence of pharyngeal muscle spasms, and onset is
usually insidious over several days.
• Reflex spasms develop in most patients and can be
triggered by minimal external stimuli such as noise, light,
or touch.
• The spasms last seconds to minutes; become more
intense; increase in frequency with disease progression;
and can cause apnoea, fractures, dislocations, and
rhabdomyolysis.
• Laryngeal spasms can occur at any time and can result in
asphyxia.
• Autonomic dysfunction-Tetanospasmin has a disinhibitory
effect on the autonomic nervous system (ANS) due to
increased release of catecholamines it causes : fever,
Sweating, Peripheral vasoconstriction, Labile/Sustained
Hypertension, Episodic tachycardia, dysrhythmias and
cardiac arrest
• Occasionally period of bradycardia & hypotension
Other symptoms include: Drooling, Hand or foot spasms,
Irritability, Uncontrolled urination or defecation
• In severe tetanus, sudden generalised tonic contractions
of all muscle groups, or tetanospasms/tetanic seizure,
result in opisthotonos, adduction of the shoulders, flexion
of the elbows and wrists, and extension of the legs,
usually accompanied by rise temperature.
• Onset and disease progression are more rapid in
neonatal tetanus than in non-neonatal tetanus, often
taking hours instead of days
:
• History and Clinical Manifestation
• There are currently no blood tests that can be used to
diagnose tetanus.
• Diagnosis is done clinically based on the presence of
trismus, dysphagia, generalized muscular rigidity, and/or
spasm.
• Laboratory studies may demonstrate a moderate
peripheral leukocytosis.
• The diagnosis is made strictly based on clinical
manifestations.
• Cultures of tetanus patients’ wounds frequently fail to detect
growth of C tetani
• Negligible serum tetanus antibody concentrations can
support but cannot prove the diagnosis.
• Tetanus antibody test.
• Blood studies such as CBC, PT, PPT, INR, U&Es and LFTs
and urine analysis: to detect complications of the disease
• The spatula test is one diagnostic bedside test.
• This test involves touching the oropharynx with a spatula
or tongue blade.This test typically elicits a gag reflex, and
the patient tries to expel the spatula (ie, a negative test
result). If tetanus is present, patients develop a reflex
spasm of the masseters and bite the spatula (ie, a
positive test result).
• Other tests may be used to rule out meningitis, rabies,
strychnine poisoning, or other diseases with similar
symptoms.
• Neuroleptic Malignant Syndrome,
• Acute abdominal emergencies, Encephalitis, Meningitis,
Hysteria, Rabies, Seizure disorder, Stroke, Subarachnoid
Hemorrhage.
• Strychnine poisoning /used as a pesticide- rat poison,
• Drug induced dystonic reactions e.g. Phenothiazines
toxicity, Stimulant use,
• In neonates tetanus must be differentiated from neonatal
seizures, meningitis, and metabolic disorders such as
hypoglycaemia and hypocalcaemia.
• The differential diagnosis of tetanus also includes other
causes of trismus such as dental infections, tonsillitis,
parotitis, temporomandibular joint disease, stiff man
syndrome,CNS infections, and psychogenic tetanus.
• If treatment is not sought early, the disease is often fatal.
The principles of management are:
1. Elimination of source of toxin.
2. Toxin neutralization
3. Control of muscular rigidity and spasms
4. Supportive care
MANAGEMENT OF TETANUS Cont’d
Elimination of the source of toxin
• Wound exploration, cleansing and debridement are
important to reduce bacterial load.
• Antibiotic therapy is given (IV Metronidazole 500mg,
q8hrly).
• Iv Penicillin is usually given but may worsen the spasm
because it has a central GABA antagonistic effect.
MANAGEMENT OF TETANUS Cont’d
Toxin Neutralization
• Neutralization of circulating toxin is done by giving
subcutaneous anti tetanus serum (ATS) at 10,000IU stat
after a negative test dose, an alternative is IM human
tetanus.
• Immunoglobin 500 IU stat where available.
MANAGEMENT OF TETANUS Cont’d
Control of spasm
• Benzodiazepines such as Diazepam,Lorazepam,
Midazolam.
• IV diazepam is given in infusion 5% Dextrose water in
0.9% normal saline.
• Diazepam dose is to be titrated in response to spasm
frequency and to be reduced in event of any drowsiness.
• IV diazepam 20mg every 2hrs via intravenous push can
be given for breakthrough spasms.
MANAGEMENT OF TETANUS Cont’d
Control of spasm cont’d
• Barbiturates such as IV Phenobarbital are second line
drugs.
• Neuromuscular blockade with Atracurium, Vecuronium or
Pancuroium is required in severe cases with violent
spasms and respiratory depression.
• Other alternatives are morphine, Fentanyl, Clonidine,
Atropine, continuous spinal anaesthesia.
MANAGEMENT OF TETANUS Cont’d
Supportive care
• Autonomic instability has been treated with combined
alpha and beta blockers, for example; Labetalol with
varying success.
• Patient is to be nursed in a dark quiet room
• NPO
• A spasm chart is to be kept.
• DVT prophylaxis with Sc Clexane or Heparin
MANAGEMENT OF TETANUS Cont’d
Supportive care Cont’d
• feeding can be recommended once patient is spasm free.
• Physiotherapy may assist in mobilization once patient is
spasm free.
• ICU admission, tracheostomy may required in severe
cases
•AIM1- AIRWAY MANAGEMENT
Intubation and mechanical ventilation
• In severe cases , if the infant gets frequent episodes of
laryngeal spasms, apneic attacks with cyanosis
or central respiratory failure.
AIM 2- PREVENTION OF FURTHER TOXIN ABSORPTION
Neutralization of free toxin is done by administrating human
tetanus immunoglobulin; however, the antitoxin cannot
dislodge toxins in the nerve root.
• The route of administration is intra muscular or intrathecal
Dose:500-1000 IU
• Oral feeding should be stopped and IV line should be
established for providing adequate fluids , calories ,
electrolytes and for administration of various drugs.
• After 3 – 4 days of treatment. milk feeding through
nasogastric tube may be started.
Aim 3- RELEIVING CLINICAL SYMPTOMS
• I.M injections should be avoided unless neccessary.
• Temperature should be maintained within normal limits.
• Relief of symptoms is by using benzodiapenes.
• Diazepam prevents spasms by causing GABA mediated
central inhibition, it promotes muscle relaxation.
• Obtain a detailed history to ascertain cause of illness and
other compliant such present symptoms of tetanus.
• Perform complete head to toe asssessment -to ascertain
clinical manifestations
• Nurse patients in a semirecumbent position to decrease
the risk for aspiration of gastric contents
• Maintenance of oxygen is essential as needed
• Oropharyngeal secretions should be gentle suctioned
periodically.
• Provide supportive care.
• Strict intake and output monitoring, maintain fluid balance
chart: for early detection of myoglobinuria, prevention of
renal shut down and dehydration.
• Assist with siting IV access for taking bloods samples and
IV fluids
• Administer IV fluids as ordered to maintain adequate
hydration.
• Assist in taking off bloods for investigations such
as:Complete blood count, urea and electrolytes, liver
function test, serology (HIV, VDRL).
• Provide comfort by changing soiled diaper promptly, bed
linen should be clean and free from offensive odors.
• Nurse patient in a dark quiet and isolated room; spasms
are precipitated by minimal stimuli therefore, efforts
should be made to avoid noxious stimuli including bright
lights, pain, loud noises. Blindfold neonates with a cloth
bandage.
• Reassure parents and relatives, if the patient is a neonate
• If the mother is the patient, provide words of comfort to
her and relatives that bring reassurrance
• Monitor vital signs (TPR, B/P and Spo2) every 2-4 hours
or more according to the severity of the case to detect
abnormalities and for prompt intervention.
• Group activities and avoid unnecessary procedures and
manipulations to prevent overstimulation.
• Administer antipyretic, analgesic, antibiotic and other
medications as ordered- Antibiotic therapy is needed to
abolish bacteria from wound site. Commonly used:
crystalline penicillin or metronidazole.
• ANS Instability treated by: alpha and beta blockers, i.v
magnesium.
• Maintain NPO status as ordered
• Insert a nasogastric tube for hydration, feeding and
administration of oral medications
• Meet nutritional needs- After 3-4 days of treatment, milk
feeding through nasogastric tube may be started, divided
feed over 24 hours. In neonates, give expressed breast
milk every 3 hours (risk of hypoglycaemia)
• Assist with meeting hygienic needs, mouth care is
essential.
• Provide safety- bed rails up at all time due to the risk of a
fall from seizure activities.
• Provide intensive nursing care, closely monitor patient for
complications such as hypertension or hypotension,
sepsis, renal or cardiac failure
• Catherize patient- for monitoring output
• Handle the patient carefully, while sedated and as little as
possible; change position every 3 to 4 hours to avoid
bedsores.
• Teach family the danger signs and instruct them to call the
nurse for the slightest respiratory symptom (cough,
difficulty breathing, apnoea, excessive secretions,
cyanosis, etc.).
• Perform daily urinanalysis- to ascertain the present of
proteinuria
• Administer enema and other stool softeners as ordered if
constipation noted-This provide comfort and aid with
elimination
• Complete a class 1 notification form and send it to Health
Department, the Public Health Nurse should be made
aware- Tetanus is a potentially fatal disease so
preventation of others cases is vital.
• Educate family members regarding the importance of
being vaccinate against Tetanus
• Monitor patient for symptoms such as muscle pains,
weakness,irregular heartbeat, vomiting, and confusion.
Due to risk of developing rapid skeletal muscle breaks
down.
• Observe output for tea-colored urine- this indicate muscle
breakdown products, such as the protein myoglobin, this
harmful to the kidneys and may lead to kidney failure.
• Document all finding and care given. Report all abnormal
findings promply
• Prognosis is dependent on incubation period, time from
spore inoculation to first symptom, and time from first
symptom to first tetanic spasm.
• In general, shorter intervals indicate more severe tetanus
and a poorer prognosis.
• Patients usually survive tetanus and return to their pre
disease state of health.
• Recovery is slow and usually occurs over 2-4 months.
The prognosis in neonatal tetanus is worse if:
1. Onset of symptoms occurs within 1st week of life
2. Interval between lockjaw and onset of spasms is less
than 48hours
3. High fever and tachycardia are present
4. Spasms, especially of larynx resulting in apnoea and are
very severe and frequent.
• Clinical tetanus does not produce a state of immunity;
therefore, patients who survive the disease require active
immunization with tetanus toxoid to prevent a recurrence.
• Vaccination and good wound care are important to help
prevent tetanus infection.
Vaccination
• Protection from vaccines, as well as a prior infection, do
not last a lifetime. This means that if you had tetanus or
got the vaccine before, you still need to get the vaccine
regularly to keep a high level of protection against this
serious disease.
• CDC recommends tetanus vaccines for people of all
ages, with booster shots throughout life
• Herd immunity is NOT acquired, immunity is only obtain
through vaccination.
• Immunization pregnant women or women of child bearing
age is an important strategy to reduce the incidence of the
disease, because IgG Abs are transferred across the
placenta to foetus and protect the newborn.
• The last dose of TT/DT should be received at least 2 weeks
prior to delivery; this causes passive immunization to child
• For previously immunized pregnant women: 1 Dose of
TT/DT is sufficient if the 2nd pregnancy is within the next 5
years.
• Tetanus is administered along with Diphtheria toxoid and
pertussis killed vaccine as combination called DPT.
• Since tetanus can occur at any age and in both sexes:
primary immunization is essential for which 3 doses of
DPT are given intramuscularly 1month apart.
• Boosters are given at 18th month, 5years,10years and 16
years of age.
• Tetanus can not survive autoclaving at 249.8°F (121°C)
for 20 minutes. Surgical and obstetric instructments
MUST property sterilized.
Good Wound Care
• Immediate and good wound care can also help prevent
infection.
• Don’t delay first aid of even minor, non-infected wounds
like blisters, scrapes, or any break in the skin.
• Wash hands often with soap and clean water or use an
alcohol-based hand rub if washing is not possible.
• Wash hands following gardening or dusting.
• 1st dose - 6th weeks (DPT)
• 2nd dose - 3 months (DPT)
• 3rd dose - 6 months (DPT)
• 1st booster - 18 months (DPT)
• 2nd booster - 4-6th year (DPT)
• 3rd booster - 10-11th year (DT)
• Pulmonary infections and cardiovascular instability are the
most common complications.
• Laryngospasm and/or spasms of muscles of respiration.
• Fractures of spine and/or long bones from sustained
contraction.
• Hypertension and/or abnormal heart rhythm due to
hyperactivity of autonomic nervous system.
• Nosocomial infections – sepsis from indwelling catheters,
decubitus ulcers, hospital acquired pneumonia.
• Pulmonary embolism especially in elderly and IV drug
users.
• Renal insufficiency.
• Aspiration pneumonia.
• Death in 11% of reported cases, more common in
persons older than 60yrs, unvaccinated persons. Causes
include laryngospasm, cardiac arrest.
• Hinfey, P. B. & Brusch, J. L., (2019) Infectious disease:
tetanus,https://emedicine.medscape.com/article/229594
• Ropera, M.H., Vandelaerb, J.H. & Gassec, F.L .,(2007)
Maternal and neonatal tetanus.Weybridge, VT, USA
• Blain, A.&Tiwari, T.S. P., (2018) Manual for the
surveillance of vaccine-preventable diseases,Centers for
Disease Control and Prevention

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Tetanus

  • 1.
  • 2. Objectives At the end of this presentation students will be able to : Define the term Tetanus. State the overview of Tetanus. State the epidemiology of Tetanus. Outline the incidence of Tetanus. Explain the causative agents of Tetanus. Describe the pathophysiogy of Tetanus  State the risk factors of Tetanus. State the classification of Tetanus. Describe the clinical manifestation of Tetanus.
  • 3. Objectives  State diagnostic measures/or investigations used to confirm Tetanus. List differential diagnosis for Tetanus. Outline the medical management of Tetanus. Discuss the midwife’s role in the management of Tetanus. State the prognosis of Tetanus. Outline the preventative measures to be taken. Outline Jamaica’s Immunization schedule List the complications of tetanus.
  • 4. • Tetanus is an acute, often fatal, infectious neurological disease that caused by contamination of wounds from the bacteria Clostridium tetani that live in the soil, and animal faeces.
  • 5. • Tetanus is the only vaccine preventable disease that is infectious but not contagious. • It is a major international public health problem, as spores are ubiquitous (omnipresent). • Tetanus remains a problem in the developing and under developed countries. It is most prevalent in industrial establishment, where agricultural workers are employed. • Tetanus occurs worldwide but is more common in hot, damp climates with soil rich in organic matter especially during summer.
  • 6. • The disease occurs almost exclusively in persons who are unvaccinated or inadequately immunized. • Maternal and neonatal tetanus are important causes of maternal and neonatal mortality. • Although easily prevented by maternal immunization with tetanus toxoid vaccine, and aseptic obstetric and postnatal umbilical-cord care practices • Maternal and neonatal tetanus persist as public-health problems in 48 countries, mainly in Asia and Africa.
  • 7. • Tetanus was first described in Egypt over 3000 years ago (Edwin Smith Papyrus). It was again described by Hippocrates • There are between 800,000 and 1 million deaths due to Tetanus each year; 80% of these deaths occur in Africa and South East Asia. It remains endemic in 90 countries world wide. • Neonatal tetanus was long recognised by clinicians in resource- poor settings as an important cause of neonatal death. • However, since babies affected by this disease usually are born at home and die there without registration of either event, the true burden was unknown.
  • 8. • Maternal tetanus has the same risk factors and means of prevention as neonatal tetanus,whether pregnancy ended with birth, miscarriage, or abortion. • Maternal and neonatal tetanus claim about 180,000 lives worldwide every year, almost exclusively in developing countries. • In 1999, the elimination of maternal tetanus was added to the goals of the elimination programme for neonatal tetanus, and the initiative was renamed the Maternal and Neonatal Tetanus Elimination Program. • Good progress has been made in the 22 years since the neonatal tetanus elimination programme began.
  • 9. • Worldwide mortality from neonatal tetanus was estimated at 180, 000 in 2002, which represents a 78% reduction since the late 1980s. • In developed countries, tetanus is now little more than a medical curiosity; maternal and neonatal tetanus are exceedingly rare. • However, tetanus as a whole continues to cause about 213,000– 293,000 deaths worldwide each year, predominantly in low- income and middle income countries.
  • 10. • Despite widespread immunization of infants and children in the United States since the 1940s, tetanus still occurs in there. • The majority of reported tetanus cases are birth- associated, occurring in low income countries among insufficiently vaccinated mothers and their newborn infants, following unhygienic deliveries and abortions and poor postnatal hygiene and cord care practices.
  • 11. • Tetanus is caused by an exotoxin produced by the bacterium Clostridium Tetani, found worldwide in soil, in inanimate environment, in animal faeces & occasionally human faeces. • Clostridium Tetani is a slender, gram-positive, motite, anaerobic rod that may develop a terminal spore, giving it a drumstick appearance. is in the intestine of animals, including human in which the organism is a harmless normal inhabitat.
  • 12.
  • 13. • Clostridium Tetani entry into the body usually involves implantation of spores into a wound • The organism is sensitive to heat and cannot survive in the presence of oxygen. After gaining entry, Clostridium Tetani spores can persist in the body for months, waiting for the proper oxygen-free environment where they can germinate and develop. • The bacteria then produce tetanus toxins, circulates in the body blocking nerve impulses that allow muscles to relax.
  • 14.
  • 15. Any break in the skin are potential entry ways for the bacteria.The usual locations for the bacteria to enter the body are: • Puncture wounds such as those caused by rusty nails, splinters, and human, animal or insect bites, parenteral drug abuse • In neonates usually via infected umbilical stumps • Transmission by contaminated wounds- Gangrene, Abscess, Burns, crush wounds or Open fractures, • Tissue injury from surgery and IV drug access sites • Otitis media, dental infection, abortion, and pregnancy.
  • 16.
  • 17. • Neonates born to mothers who were not immunized against tetanus • Females during delivery or abortion that are unimmunized or not fully immunized against tetanus • Agricultural workers • Environmental and social factors: unhygienic custom habits,unhygienic delivery practices • Underdeveloped countries with limited resources • Poor maternal and child health care protocols
  • 18. Tetanus may be categorized into the following clinical types: • Generalized tetanus • Localized tetanus • Cephalic tetanus • Maternal tetanus • Neonatal tetanus
  • 19. • This is the most common form of tetanus and make up roughly 80% of tetanus cases • Approximately 50-75% of patients with generalized tetanus present with trismus (“lockjaw”), which is the inability to open the mouth secondary to masseter muscle spasm. • Nuchal rigidity (inability to flex the neck forward) and dysphagia are also early complaints that cause risus sardonicus, the scornful smile of tetanus, resulting from facial muscle involvement.
  • 20. • As the disease progresses, patients have generalized muscle rigidity with intermittent reflex spasms in response to stimuli (e.g., noise, touch). • Tonic contractions cause opisthotonos (ie, flexion and adduction of the arms, clenching of the fists, and extension of the lower extremities). • During these episodes, patients have an intact sensorium and feel severe pain. • The spasms can cause fractures, tendon ruptures, and acute respiratory failure.
  • 21. • Spasms continue for 3-4 weeks • Recovery usually begins in 3 weeks and takes approximately 4 weeks • It occurs by sprouting new nerve terminals in the spinal cord and leading to relaxation of contracted muscles. • Incubation period is 8 days (2-14 days), dependent on site of injury from CNS • Faster onset of symptoms means poor the prognosis. • Death occurs when spasms interfere with respiration.
  • 22. • Descending pattern: lockjaw →stiffness of neck →difficulty swallowing→rigidity of abdominal and back muscles.
  • 23. • Patients with localized tetanus present with persistent rigidity in the muscle group close to the injury site. • The muscular rigidity is caused by a dysfunction in the interneurons that inhibit the alpha motor neurons of the affected muscles. • No further central nervous system (CNS) involvement occurs in this form, and mortality is very low. • The contraction and the spasm is milder, usually last for few days before subsiding • Prognosis – excellent ( only 1% of cases being fatal)
  • 24.
  • 25. • Cephalic tetanus is uncommon and usually occurs after head trauma or otitis media. • Patients with this form present with cranial nerve (CN) palsy. • Involvement of cranial nerves III, IV, VI and XII may also occur either alone or in combination. • The infection may be localized or may become generalized. • Incubation period: few days Mortality: high
  • 26.
  • 27. •Tetanus occurring during pregnancy or within 6 weeks after any type of pregnancy termination, is one of the most easily preventable causes of maternal mortality. It includes postpartum or puerperal tetanus (i) postpartum or puerperal tetanus, usually resulting from septic procedures during delivery, (ii) postabortal tetanus, following septic maneuvers during induced abortion (iii) Tetanus during pregnancy, generally resulting from inoculation through a nongenital portal of entry(via caerean section)
  • 28. • Neonatal tetanus (tetanus neonatorum) is a major cause of infant mortality in underdeveloped countries. • It is a form of generalized tetanus that occurs in newborn infants born without protective of passive immunity because the mother is not immune. • Infection results from umbilical cord contamination during unsanitary delivery, unaseptic cord care • Symptoms usually appear by the 3rd day after birth but in some case as early as 5 hours after infection.
  • 29. • Initial SYMPTOMS: Excessive unexplained crying followed by refusal of feeds and apathy • The baby develops progressive feeding difficulty due to reflex spasm of massetter makes feeding painful, pharyngeal muscles goes into spasm and cause chocking as a result of dysphagia • At the end of the first week of life, infected infants may develop rigidity with spasms. • Neonatal tetanus has a very poor prognosis.
  • 30. • Spasm of larynx and respiratory muscles are induced by stimuli such as touch, noise, bright light, resulting in episodes of apnoea and cyanosis. • Constipation persists until spasms are relieved, becomes rigid,develops paralysis, and may develop opisthotonic posturing(in extension) and experience painful spasm. • Inter-current infections (a disease that intervenes during the course of another disease), dehydration and acidosis complicate the condition.
  • 31. • Baby has neonatal tetanus with complete rigidity
  • 32. • Risus sardonicus: Contraction of the muscles at the angle of mouth and frontalis • Trismus (Lock Jaw): convulsive contraction and spasm of Masseter muscles. • Opisthotonus: Spasm of extensor of the neck, back and legs to form a backward curvature. • Muscle spasticity • The affected individual is conscious throughout the illness, but cannot stop contractions, making tetanus a truly dreadful disease.
  • 33. • Tetany - prolonged muscular action causes sudden, powerful, and painful contractions of muscle groups. These episodes can cause fractures and muscle tears. • If respiratory muscle is involved – apnoea. • Dysphagia occurs in moderately severe tetanus as a consequence of pharyngeal muscle spasms, and onset is usually insidious over several days.
  • 34. • Reflex spasms develop in most patients and can be triggered by minimal external stimuli such as noise, light, or touch. • The spasms last seconds to minutes; become more intense; increase in frequency with disease progression; and can cause apnoea, fractures, dislocations, and rhabdomyolysis. • Laryngeal spasms can occur at any time and can result in asphyxia.
  • 35. • Autonomic dysfunction-Tetanospasmin has a disinhibitory effect on the autonomic nervous system (ANS) due to increased release of catecholamines it causes : fever, Sweating, Peripheral vasoconstriction, Labile/Sustained Hypertension, Episodic tachycardia, dysrhythmias and cardiac arrest • Occasionally period of bradycardia & hypotension Other symptoms include: Drooling, Hand or foot spasms, Irritability, Uncontrolled urination or defecation
  • 36. • In severe tetanus, sudden generalised tonic contractions of all muscle groups, or tetanospasms/tetanic seizure, result in opisthotonos, adduction of the shoulders, flexion of the elbows and wrists, and extension of the legs, usually accompanied by rise temperature. • Onset and disease progression are more rapid in neonatal tetanus than in non-neonatal tetanus, often taking hours instead of days
  • 37. :
  • 38.
  • 39. • History and Clinical Manifestation • There are currently no blood tests that can be used to diagnose tetanus. • Diagnosis is done clinically based on the presence of trismus, dysphagia, generalized muscular rigidity, and/or spasm. • Laboratory studies may demonstrate a moderate peripheral leukocytosis.
  • 40. • The diagnosis is made strictly based on clinical manifestations. • Cultures of tetanus patients’ wounds frequently fail to detect growth of C tetani • Negligible serum tetanus antibody concentrations can support but cannot prove the diagnosis. • Tetanus antibody test. • Blood studies such as CBC, PT, PPT, INR, U&Es and LFTs and urine analysis: to detect complications of the disease
  • 41. • The spatula test is one diagnostic bedside test. • This test involves touching the oropharynx with a spatula or tongue blade.This test typically elicits a gag reflex, and the patient tries to expel the spatula (ie, a negative test result). If tetanus is present, patients develop a reflex spasm of the masseters and bite the spatula (ie, a positive test result). • Other tests may be used to rule out meningitis, rabies, strychnine poisoning, or other diseases with similar symptoms.
  • 42. • Neuroleptic Malignant Syndrome, • Acute abdominal emergencies, Encephalitis, Meningitis, Hysteria, Rabies, Seizure disorder, Stroke, Subarachnoid Hemorrhage. • Strychnine poisoning /used as a pesticide- rat poison, • Drug induced dystonic reactions e.g. Phenothiazines toxicity, Stimulant use, • In neonates tetanus must be differentiated from neonatal seizures, meningitis, and metabolic disorders such as hypoglycaemia and hypocalcaemia.
  • 43. • The differential diagnosis of tetanus also includes other causes of trismus such as dental infections, tonsillitis, parotitis, temporomandibular joint disease, stiff man syndrome,CNS infections, and psychogenic tetanus.
  • 44. • If treatment is not sought early, the disease is often fatal. The principles of management are: 1. Elimination of source of toxin. 2. Toxin neutralization 3. Control of muscular rigidity and spasms 4. Supportive care
  • 45. MANAGEMENT OF TETANUS Cont’d Elimination of the source of toxin • Wound exploration, cleansing and debridement are important to reduce bacterial load. • Antibiotic therapy is given (IV Metronidazole 500mg, q8hrly). • Iv Penicillin is usually given but may worsen the spasm because it has a central GABA antagonistic effect.
  • 46. MANAGEMENT OF TETANUS Cont’d Toxin Neutralization • Neutralization of circulating toxin is done by giving subcutaneous anti tetanus serum (ATS) at 10,000IU stat after a negative test dose, an alternative is IM human tetanus. • Immunoglobin 500 IU stat where available.
  • 47. MANAGEMENT OF TETANUS Cont’d Control of spasm • Benzodiazepines such as Diazepam,Lorazepam, Midazolam. • IV diazepam is given in infusion 5% Dextrose water in 0.9% normal saline. • Diazepam dose is to be titrated in response to spasm frequency and to be reduced in event of any drowsiness. • IV diazepam 20mg every 2hrs via intravenous push can be given for breakthrough spasms.
  • 48. MANAGEMENT OF TETANUS Cont’d Control of spasm cont’d • Barbiturates such as IV Phenobarbital are second line drugs. • Neuromuscular blockade with Atracurium, Vecuronium or Pancuroium is required in severe cases with violent spasms and respiratory depression. • Other alternatives are morphine, Fentanyl, Clonidine, Atropine, continuous spinal anaesthesia.
  • 49. MANAGEMENT OF TETANUS Cont’d Supportive care • Autonomic instability has been treated with combined alpha and beta blockers, for example; Labetalol with varying success. • Patient is to be nursed in a dark quiet room • NPO • A spasm chart is to be kept. • DVT prophylaxis with Sc Clexane or Heparin
  • 50. MANAGEMENT OF TETANUS Cont’d Supportive care Cont’d • feeding can be recommended once patient is spasm free. • Physiotherapy may assist in mobilization once patient is spasm free. • ICU admission, tracheostomy may required in severe cases
  • 51.
  • 52. •AIM1- AIRWAY MANAGEMENT Intubation and mechanical ventilation • In severe cases , if the infant gets frequent episodes of laryngeal spasms, apneic attacks with cyanosis or central respiratory failure. AIM 2- PREVENTION OF FURTHER TOXIN ABSORPTION Neutralization of free toxin is done by administrating human tetanus immunoglobulin; however, the antitoxin cannot dislodge toxins in the nerve root.
  • 53. • The route of administration is intra muscular or intrathecal Dose:500-1000 IU • Oral feeding should be stopped and IV line should be established for providing adequate fluids , calories , electrolytes and for administration of various drugs. • After 3 – 4 days of treatment. milk feeding through nasogastric tube may be started.
  • 54. Aim 3- RELEIVING CLINICAL SYMPTOMS • I.M injections should be avoided unless neccessary. • Temperature should be maintained within normal limits. • Relief of symptoms is by using benzodiapenes. • Diazepam prevents spasms by causing GABA mediated central inhibition, it promotes muscle relaxation.
  • 55. • Obtain a detailed history to ascertain cause of illness and other compliant such present symptoms of tetanus. • Perform complete head to toe asssessment -to ascertain clinical manifestations • Nurse patients in a semirecumbent position to decrease the risk for aspiration of gastric contents • Maintenance of oxygen is essential as needed • Oropharyngeal secretions should be gentle suctioned periodically. • Provide supportive care.
  • 56. • Strict intake and output monitoring, maintain fluid balance chart: for early detection of myoglobinuria, prevention of renal shut down and dehydration. • Assist with siting IV access for taking bloods samples and IV fluids • Administer IV fluids as ordered to maintain adequate hydration. • Assist in taking off bloods for investigations such as:Complete blood count, urea and electrolytes, liver function test, serology (HIV, VDRL).
  • 57. • Provide comfort by changing soiled diaper promptly, bed linen should be clean and free from offensive odors. • Nurse patient in a dark quiet and isolated room; spasms are precipitated by minimal stimuli therefore, efforts should be made to avoid noxious stimuli including bright lights, pain, loud noises. Blindfold neonates with a cloth bandage. • Reassure parents and relatives, if the patient is a neonate • If the mother is the patient, provide words of comfort to her and relatives that bring reassurrance
  • 58. • Monitor vital signs (TPR, B/P and Spo2) every 2-4 hours or more according to the severity of the case to detect abnormalities and for prompt intervention. • Group activities and avoid unnecessary procedures and manipulations to prevent overstimulation. • Administer antipyretic, analgesic, antibiotic and other medications as ordered- Antibiotic therapy is needed to abolish bacteria from wound site. Commonly used: crystalline penicillin or metronidazole. • ANS Instability treated by: alpha and beta blockers, i.v magnesium.
  • 59. • Maintain NPO status as ordered • Insert a nasogastric tube for hydration, feeding and administration of oral medications • Meet nutritional needs- After 3-4 days of treatment, milk feeding through nasogastric tube may be started, divided feed over 24 hours. In neonates, give expressed breast milk every 3 hours (risk of hypoglycaemia) • Assist with meeting hygienic needs, mouth care is essential. • Provide safety- bed rails up at all time due to the risk of a fall from seizure activities.
  • 60. • Provide intensive nursing care, closely monitor patient for complications such as hypertension or hypotension, sepsis, renal or cardiac failure • Catherize patient- for monitoring output • Handle the patient carefully, while sedated and as little as possible; change position every 3 to 4 hours to avoid bedsores. • Teach family the danger signs and instruct them to call the nurse for the slightest respiratory symptom (cough, difficulty breathing, apnoea, excessive secretions, cyanosis, etc.).
  • 61. • Perform daily urinanalysis- to ascertain the present of proteinuria • Administer enema and other stool softeners as ordered if constipation noted-This provide comfort and aid with elimination • Complete a class 1 notification form and send it to Health Department, the Public Health Nurse should be made aware- Tetanus is a potentially fatal disease so preventation of others cases is vital. • Educate family members regarding the importance of being vaccinate against Tetanus
  • 62. • Monitor patient for symptoms such as muscle pains, weakness,irregular heartbeat, vomiting, and confusion. Due to risk of developing rapid skeletal muscle breaks down. • Observe output for tea-colored urine- this indicate muscle breakdown products, such as the protein myoglobin, this harmful to the kidneys and may lead to kidney failure. • Document all finding and care given. Report all abnormal findings promply
  • 63. • Prognosis is dependent on incubation period, time from spore inoculation to first symptom, and time from first symptom to first tetanic spasm. • In general, shorter intervals indicate more severe tetanus and a poorer prognosis. • Patients usually survive tetanus and return to their pre disease state of health. • Recovery is slow and usually occurs over 2-4 months.
  • 64. The prognosis in neonatal tetanus is worse if: 1. Onset of symptoms occurs within 1st week of life 2. Interval between lockjaw and onset of spasms is less than 48hours 3. High fever and tachycardia are present 4. Spasms, especially of larynx resulting in apnoea and are very severe and frequent. • Clinical tetanus does not produce a state of immunity; therefore, patients who survive the disease require active immunization with tetanus toxoid to prevent a recurrence.
  • 65. • Vaccination and good wound care are important to help prevent tetanus infection. Vaccination • Protection from vaccines, as well as a prior infection, do not last a lifetime. This means that if you had tetanus or got the vaccine before, you still need to get the vaccine regularly to keep a high level of protection against this serious disease. • CDC recommends tetanus vaccines for people of all ages, with booster shots throughout life
  • 66. • Herd immunity is NOT acquired, immunity is only obtain through vaccination. • Immunization pregnant women or women of child bearing age is an important strategy to reduce the incidence of the disease, because IgG Abs are transferred across the placenta to foetus and protect the newborn. • The last dose of TT/DT should be received at least 2 weeks prior to delivery; this causes passive immunization to child • For previously immunized pregnant women: 1 Dose of TT/DT is sufficient if the 2nd pregnancy is within the next 5 years.
  • 67. • Tetanus is administered along with Diphtheria toxoid and pertussis killed vaccine as combination called DPT. • Since tetanus can occur at any age and in both sexes: primary immunization is essential for which 3 doses of DPT are given intramuscularly 1month apart. • Boosters are given at 18th month, 5years,10years and 16 years of age. • Tetanus can not survive autoclaving at 249.8°F (121°C) for 20 minutes. Surgical and obstetric instructments MUST property sterilized.
  • 68. Good Wound Care • Immediate and good wound care can also help prevent infection. • Don’t delay first aid of even minor, non-infected wounds like blisters, scrapes, or any break in the skin. • Wash hands often with soap and clean water or use an alcohol-based hand rub if washing is not possible. • Wash hands following gardening or dusting.
  • 69. • 1st dose - 6th weeks (DPT) • 2nd dose - 3 months (DPT) • 3rd dose - 6 months (DPT) • 1st booster - 18 months (DPT) • 2nd booster - 4-6th year (DPT) • 3rd booster - 10-11th year (DT)
  • 70. • Pulmonary infections and cardiovascular instability are the most common complications. • Laryngospasm and/or spasms of muscles of respiration. • Fractures of spine and/or long bones from sustained contraction. • Hypertension and/or abnormal heart rhythm due to hyperactivity of autonomic nervous system. • Nosocomial infections – sepsis from indwelling catheters, decubitus ulcers, hospital acquired pneumonia.
  • 71. • Pulmonary embolism especially in elderly and IV drug users. • Renal insufficiency. • Aspiration pneumonia. • Death in 11% of reported cases, more common in persons older than 60yrs, unvaccinated persons. Causes include laryngospasm, cardiac arrest.
  • 72.
  • 73. • Hinfey, P. B. & Brusch, J. L., (2019) Infectious disease: tetanus,https://emedicine.medscape.com/article/229594 • Ropera, M.H., Vandelaerb, J.H. & Gassec, F.L .,(2007) Maternal and neonatal tetanus.Weybridge, VT, USA • Blain, A.&Tiwari, T.S. P., (2018) Manual for the surveillance of vaccine-preventable diseases,Centers for Disease Control and Prevention

Editor's Notes

  1. An exotoxin is a toxin secreted by bacteria. An exotoxin can cause damage to the host by destroying cells or disrupting normal cellular metabolism. They are highly potent and can cause major damage to the host
  2. Opisthotonus or opisthotonos is a state of severe hyperextension and spasticity in which an individual's head, neck and spinal column enter into a complete "bridging" or "arching" position ntercurrent. See Intercur.] Intercurrent(adj). said of diseases occurring in the course of another disease.
  3. Difficulty swallowing (dysphagia) means it takes more time and effort to move food or liquid from your mouth to your stomach.
  4. Rhabdomyolysis is a breakdown of muscle fibers that occurs due to muscle injury
  5. Catecholamines are hormones made by your adrenal glands like dopamine, norepinephrine, and epinephrine Labile definition is - readily or continually undergoing chemical, physical, or biological change or breakdown : unstable
  6. Tetanic spasms can occur in a distinctive form called opisthotonos and be sufficiently severe to fracture long bones.
  7. Intrathecal administration is a route of administration for drugs via an injection into the spinal canal, or into the subarachnoid space so that it reaches the cerebrospinal fluid and is useful in spinal anesthesia