TETANUS

GULU COLLEGE OF HEALTH SCIENCES

DR.BEINE
INTRODUCTION

 Tetanos – a greek word – to strech

 First described by Hippocrates & Susruta
 A Neurological disease characterized by
increased muscle tone & spasms.
 DEFINITION

 Tetanus is acute poisoning from a neurotoxin

produced by Clostridium tetani.

 It’s the ONLY vaccine-preventable disease that

is infectious but not contagious from person to
person
Epidemiology
 Occurs sporadically
 Affects unimmunized, partially immunized & fully
immunized who fail to maintain adequate
immunity with booster doses of vaccine.
 Although it is an entirely preventable disease by
immunization , the burden of disease worldwide
is great.
 Estimated one million cases a year worldwide
 Mortality rates reported vary from 40% to 78%
 More common in areas where soil is cultivated, in rural areas,
in warm climates, during summer, among males.
 ETIOLOGICAL AGENT

 Clostridium tetani
 Gram positive bacillus
 Non capsulated
 Obligate anaerobe
 Drumstick appearance
 Motile but not tissue invasive
CLOSTRIDIUM TETANI
 Habitat - soil, dust, alimentary canal (intestinal tracts) and
feces various of animals
 Vegetative and spore forms
 Spores resistant to harsh conditions Heat (boiling),
radiation, chemicals, drying but killed by autoclaving at
1atm, 120°C for 15 min
 Vegetative form killed by antibiotics
 PREDISPOSING FACTORS

 Lack of immunization  burns,

 Trauma esp. if punctate or  ulcers,
contaminated  gangrene,
 Chronic wounds- necrotic  snakebites,
tissue  septic abortion,
 Non sterile invasive  childbirth,
procedures e.g. IDUs,
unhygienic deliveries
 intramuscular/intravenous
injections and
 Unhygienic cord practices
 surgery
 Foreign bodies
 Entry of C. tetani involves implantation of spore into a wound

 Spores can persist in the body for months,waiting for the

proper low O2 growth conditions to dvlp

 As soon as spores enters the human body and the conditions

are anaerobic, they germinate and release toxins
 PATHOPHYSIOLOGY

 Under the anaerobic conditions found in infected or necrotic

tissue, the bacillus secretes two toxins:
 Tetanospasmin and Tetanolysin.

 Tetanolysin damages the surrounding viable tissue and

optimizes conditions for bacterial multiplication.

 Tetanospasmin causes the clinical syndrome of tetanus,

 Tetanospasmin produced locally is released into
bloodstream,
 Binds to peripheral motor neuron terminals & nerve
cells of anterior horn of spinal cord

 The toxin after entering axon, is transported to nerve

cell body in spinal cord & brain stem(CNS) via axonal
retrograde intraneuronal transport

 Toxin – migrates across synapse – presynaptic terminals

– blocks the release of inhibitory neurotransmitters
from presynaptic vesicles (particularly the GABA and
Glycine), which is required to check the nervous impulse.
Patho. Ctd…

 The result is disinhibition of motor and autonomic neurons,

causing rigidity, muscle spasms and autonomic dysfunction.

 A relative deficiency of synaptic acetylcholine (similar to that

caused botulinum toxin) causes flaccid paralysis that is
clinically mild in humans.

 High toxin load results in diffusion of toxin via the blood to

nerves throughout the body

 Estimated lethal human dose of Tetanospasmin = 2.5ng/kg body

PATHOGENESIS cont’d
 Retrograde axonal transmission along motor nerve to CNS is
at 75-250 mm/day

 Exit of motor nerve & entry into inhibitory inter neurone

 Inhibition of GABA in interneurone results in unopposed

muscle contraction

 Inhibition of autonomic discharge results in excessive

sympathetic discharge and catecholamine release

 Recovery by sprouting of new axon terminals (receptors)

 CLINICAL FEATURES

 Tetanus usually follows a recognized injury, which

may be trivial or occur indoors.

 Other routes of entry include: burns, ulcers,

gangrene, snakebites, septic abortion, childbirth,
intramuscular/intravenous injections and surgery.
Shorter the incubation period, More severe the attack,

Worse the prognosis

…
 The incubation period (time from first injury to first
symptom) averages 5 -10 days (range 1-60 days),

 The clinical onset time (time from first symptom to

first spasm) varies between 1-7 days.

 Shorter incubation and onset times are associated

with more severe disease.
 MOTOR EFFECTS

 Conscious patient with spasms

- Elicited by light, sound, touch
- Characterized by fist clenching, flexion and adduction
of upper limbs, hyperextension of legs
- Spasms are painful
- May last 3-4 wks
 Tonic seizures
MOTOR EFFECTS cont’d…

 Lock jaw (Trismus) - masseter muscle involvement

 Risus sardonicus- facial and buccal muscle involvement
 Difficulty chewing, swallowing, talking and even breathing
 Muscle rigidity or spasm - Stiff neck, back muscles, board-like
abdomen and sometimes Opisthotonos.
 Hyperpyrexia
 Sphincter spasm causes urinary retention and dysuria or
constipation (Forced defecation)
OPISTHOTONUS POSTURE
The back muscles are more
powerful, thus creating the arc
backward

“Oposthotonus” by Sir
Charles Bell, 1809.

Baby has neonatal tetanus

with complete rigidity
Risus Sardonicus in Tetanus Patient
 AUTONOMIC DYSFUNCTION

 Increased RR and PR (Tachycardia)

 Labile B.P – HT due to ↑ systemic vascular resistance
 Myocardial irritability
 Arrythmias
 Increased protein catabolism
 Diaphoresis
 Cutaneous vasoconstriction
 Cause of death
 Respiratory failure (most common cause of death) due to
Hypoxemia, as a result of:
 Asphyxiation caused by:

 Laryngeal spasm and rigidity and

 Spasms of the abdominal wall, diaphragm, and chest

wall muscles
 Pharyngeal spasm → aspiration of oral secretions →

pneumonia, contributing to a hypoxemic death.

 Cardiac arrest ← Hypoxemia
 Pulmonary embolism is also possible.
CLINICAL PATTERNS

Localized- Precedes generalized tetanus

Generalized- Commonest presentation

Cephalic- Rare form of localized tetanus involving

bulbar muscles

Neonatal- Infantile form of generalized tetanus

 Types of tetanus:
local, cephalic, generalized, neonatal
 Incubation period: 3-21 days, average 8 days.

Uncommon types:
 Local tetanus: persistent muscle contractions in the same
anatomic area as the injury, which will however subside after
many weeks; very rarely fatal; milder than generalized tetanus,
although it could precede it. Excellent prognosis

 Cephalic tetanus: occurs with ear infections or following

injuries of the head; facial muscles contractions. High
mortality
 Most common types:
Generalized tetanus
- descending pattern: lockjaw  stiffness of neck  difficulty
swallowing  rigidity of abdominal and back muscles.
- Spasms continue for 3-4 weeks, and recovery can last for
months
- Death occurs when spasms interfere with respiration.

Neonatal tetanus:
- Form of generalized tetanus that occurs in newborn infants
born without protective passive immunity because the mother
is not immune.
- Usually occurs through infection of the unhealed umbilical
stump, particularly when the stump is cut with an unsterile
instrument.
NEONATAL TETANUS
Atypical presentation

Progressive development of feeding difficulties, ↓ movement,

stiffness, spasms, opisthotonos, dirty umbilicus.
Excellent prognosis

Turkey study,Dicle Med Sch, 1999

Risk factors, Clinical features and Prognostic factors in 55
neonates: Spasticity(76%), Lack of sucking(71%),
Trismus(60%), Fever(49%), Omphalitis(49%),
Irritability(24%), Risus sardonicus(22%),
Opishtononos(15%)
 DIFFERENTIAL DIAGNOSIS
 Peritonsillar, Parapharnygeal,  Epileptic seizures
retropharyngeal or dental  Narcotic withdrawal
abscesses
 Drug withdrawal
 Acute encephalitis with
brainstem involvement
 Meningoencephalitis of
bacterial or viral origin, but
 Rabies the combination suggesting
 Strychnine poisoning tetanus include:
 Hypocalcaemia  An intact sensorium

 Phenothiazines can →  Normal cerebrospinal

tetanus-like rigidity (eg, fluid
dystonic reaction, neuroleptic  Muscle spasms
malignant syndrome)
cntd

 Marked increased tone in central muscles ,

with superimposed generalized spasms &
relative sparing of hands & feet – suggest
tetanus
Investigations
 No specific lab tests exist for determining the diagnosis of
tetanus.
 Diagnosis is clinical - trismus, dysphagia, generalized muscular
rigidity, &/or spasm…
 Note: Diagnostic difficulty-localized, mild, very early d’se;

 Abd pain & rigidity may be mistaken for surgical pathology

 Isolated trismus- exclusion of other oropharyngeal pathology

 CBC- moderate leukocytosis

 Assay for antitoxin levels:
 Not readily available

 Serum level of ≥0.01IU/ml is considered protective, making

diagnosis of tetanus less likely

Investigation…
 CSF- findings usually within normal limits
 The spatula test-diagnostic bedside test
 Touching oropharynx (posterior pharyngeal wall) with a

spatula ( or a sterile, soft-tipped instrument0

 Negative test result: would normally be a Gag reflex

attempting to expel the spatula

 Positive test result: Involuntary contraction (a reflex

spasm) of the masseters, biting down on the spatula

 Sensitivity-94%, specificity-100%

 Neither the EEG nor EMG shows characteristic pattern

Investigations…
 Gram stain: C. tetani is not always visible on Gram stain
of wound material

 Its isolated in only about one third of cases.

 CXR

 RFT & electrolytes

 MANAGEMENT

 Third world d’se the Rx of which requires first world

technology (Delport, RSA)

 Sedation & ventilatory support (muscle relaxants) are

mainstay of mgt

 These are not always available for tetanus pts in dev’ping

countries in which the d’se is prevalent.
Goals of Treatment

 Neutralization of unbound toxin

 Eradication of the source of toxin

 Symptomatic Rx of the effects of the toxin;

- Control of muscle spasms and rigidity
- Control of autonomic dysfunction
 Minimize stimulation(from noise,light, touch etc)
Goals…
 Supportive intensive care and prevention of complications

 Prevention

 Investigations

 Managed in ICU
  Rx: Neutralization of unbound toxin
 Should be undertaken as soon as diag is made
 Tetanospasmin becomes inaccessible to antitoxin after it enters
the CNS -binds irreversibly to tissues

 Human tetanus immune globulin (HTIG)

 For Adults: Dose 500-6000 units, IM

 IT adm of HTIG is of unproven benefit in neonatal tetanus

 Local instillation is of no benefit.
 Anitetanus horse serum (ATS): usual dose is 50,000 units IM
or IV (risk of serum sickness is considerable)
 IV immune globulin (IVIG), which contains tetanus
antitoxin, may be used if HTIG is not available.
 Eradication of source of infection

 Thorough WOUND DEBRIDEMENT (esp of deep puncture

wounds)- to eradicate spores & necrotic tissue
(Because dirt and dead tissue promote C. tetani growth)

 Wide excision of at least 2cm of normal viable-appearing

tissue around the wounds margin

 Incision & drainage of abscesses

 Any wound manipulation should be delayed until several hrs
after adm of antitoxin
Eradication…

 ANTIBIOTICS: To eradicate C.tetani

 IV Metronidazole 500 mg every 6 to 8 hours for 7-14 days is

the drug of choice OR

 IV Doxycycline 100 mg 2 times a day

 Penicillin G (6 million units IV 6 hrly), which until recently

has been the traditional drug of choice acts synergistically
with tetanospasmin, being an antagonist of GABA
 Control of spasms & rigidity
 Traditionally, Heavy sedation + Artificial ventilation (+/-
muscle relaxants) are the mainstay of mgt
 This is usually achieved using benzodiazepines (GABA

agonists), such as
 Diazepam 0.1mg/kg IV or IM 1 - 4 hourly

 For most severe cases: 10 to 30 mg IV every 1 to 4

hours
 For Less severe cases: 5 to 10 mg orally every 2 to 4
hours. or
 Midazolam (adults, 0.1 to 0.3 mg/kg/hour IV infusion;

children, 0.06 to 0.15 mg/kg/hour IV infusion)

 Midazolam can be given as an intravenous infusion (2

-10 mg/hr).
…..
 Usually alternated with chlorpromazine
100mg (child: 12.5mg-25mg)
Dosage of Diazepam varies by age:
o Children > 30 days and < 5 years: 1 to 2 mg IV given

slowly or IM, repeated every 3 to 4 hrs as necessary

o Children ≥ 5 years: 5 to 10 mg IV or IM every 3 to 4

hrs
o Adolescents: 5 mg IV, repeated every 2 to 6 hrs as

needed (high doses may be required)

o Adults: 5 to 10 mg IV every 4 to 6 hrs, increased as

needed up to 40 mg/hour IV drip

 Vecuronium 0.1 mg/kg IV or other paralytic drugs (+
Mechanical ventilation)
 Cause Neuromuscular blockade, prevent reflex spasms

 For effective respiration

 Alternative: Pipecuronium, Rocuronium (Long-

acting)
 Current trend in mgt of spasms &
autonomic dysfunction
 Magnesium sulfate
 Magnesium sulphate is being advocated for as the drug
of choice in the control of spasms and autonomic
dysfunction

 An infusion of MgSO4 can be utilized to treat muscle

spasms and severe rigidity without the need for deep
sedation, mechanical ventilation, or neuromuscular
blockade.
Mg…
 Dosage: I.V Magnesium sulfate infusion dose is 50 -
100mg/kg/day
 Maintain serum levels between 4 to 8 mEq/L (eg, 4 g bolus
followed by 2 to 3 g/hour by IV continuous infusion)

 Has a stabilizing effect, eliminating catecholamine stimulation.

 The infusion rate should be titrated to control spasms while

retaining the patella tendon reflex, which is an effective guide
to magnesium overdose.
Mg…
 Precautions:
 The following vital signs should be closely
monitored for all patients receiving MgSO4:

 Patella reflex - Attenuation of the patella reflex is

the most important clinical marker of magnesium
toxicity, and clinically it is one of the earliest
effects of magnesium toxicity.
Mg…
• Magnesium is a physiological calcium antagonist and
there is a significant correlation between the depression
of the neuromuscular transmission and serum
magnesium concentrations.

• Preservation of the patella reflex has been shown to

correlate with the safety of the therapeutic range (2-
4mmols/l).
Mg…
 Respiration - Respiratory depression may
indicate magnesium overdose

 Heart rate – For bradycardia or tachycardia

 ECG - Prolonged PR interval is a sign of

magnesium toxicity
Mg…
NB:
1) If signs of magnesium overdose occurs (muscle
flaccidity with loss of patella reflex, respiratory
depression or prolonged PR interval on the ECG);

magnesium therapy should be temporarily

discontinued, diuresis enforced, and Ca gluconate
given if necessary.
Mg…

Once the sign of overdose disappears, the infusion

is to be recommenced at a lower dosage.

2) 10% calcium gluconate should be given if

clinical signs of hypocalcaemia are evident.

Anaesthesia 1997 Oct;52(10):956-62

Ped intensive & critical care societies Oct 2003; 4(4):480-484
 Mgt of autonomic dysfunction
 Due to uninhibited overproduction of CA
 α & β-blockers: Labetalol 0.25-1.0mg/min ( or

esmolol),
 to control episodes of hypertension and

tachycardia,

 Morphine sulfate: 0.5-1.0mg/kg/hr infusion,

 Every 4 to 6 hours,

 Total daily dose is 20 to 180 mg.

…
 MgSO4

 Other drugs:
 High dose Atropine (blockade of the
parasympathetic nervous system markedly
reduces excessive sweating and secretions),
 Clonidine (Lower mortality in clonidine-treated

patients than in those treated with conventional

therapy).
 Supportive care & prevention of
complications
 VENTILATION:
 Prophylactic intubation considered in all pts with mod-
severe manifestations

 In severe cases, neuromuscular blockade necessitates

mechanical ventilation

 Pancuronium-long acting, worsens ANS instability

(inhibitor of CA reuptake)
Supportive mgt…
 Vecuronium- short acting, less likely to cause ANS
dysfunction

 Baclofen -stimulates postsynaptic GABA beta

receptors

 SUPPORTIVE CARE:
 Dark & quiet env’t for the patient
Mgt…
 Avoid unnecessary procedures & manipulations - risk of
reflex spasms
 Chest physiotherapy, frequent turning, and forced coughing
are essential to prevent pneumonia

 Prophylactic Rx: sucralfate or acid blockers

 Good nursing care:

 Suction of secretions from the airway
 Maintenance of adequate hydration
Supportive care…
 Oral hygiene
 Avoidance of pressure sores & orthostatic pneumonia
 Early nutritional support- enteral feeding preferred.
 IV hyperalimentation avoids the hazard of aspiration
secondary to gastric tube feeding
 Constipation is usual, thus stools should be kept soft.
 A rectal tube may control distention.
 Bladder catheterization required if urinary retention occurs.
Supportive…
 Monitoring cardiac function by ECG to detect & prevent
toxin-induced arrhythmias & autonomic instability

 Analgesia +/- opioids is often needed: Pain mgt;

paracetamol 15mg/kg 4h
Note: It is imp’t to realize that the pt has unimpaired
consciousness & is often aware of what is taking place
unless heavily sedated

 Parental support
 Monitoring
 Blood glucose, urea & electrolytes

 Tetanus chart for frequency & intensity of spasms,

drugs, resp monitoring & other vital signs
 Core temperature

 BP, Pulse oximetry, cardiac monitoring

 Fluid input/output
 Caloric intake
 Prevention
 Primary prevention:
 Every child should receive tetanus vaccine
according to the EPI + Boosters

 TT to all women of childbearing age (15-45yrs)- 5

doses
 TT to pregnant mothers- 2 doses

 Sterile handling & care of umbilical cord

 Children < 7 years require 5 primary vaccinations, and
 Unimmunized patients > 7 years require 3.
 Children are given DTaP at
 2 months,

 4 months,

 6 months,

 15 to 18 months, and

 4 to 6 years;

 Then they should get a

o Tdap booster at age 11 to 12 years, and

o Td every 10 years thereafter

 Unimmunized adults are given
 Tdap initially, then
 Td 4 weeks later,
 Td 6 to 12 months later, and
 Td every 10 years thereafter.

 Adults who have not had a vaccine that contains

pertussis should be given a single dose of Tdap
instead of one of the Td boosters.
 Adults ≥ 65 who anticipate close contact with an infant <
12 months and who have not previously received Tdap
should be given a single dose of Tdap.

 Pregnant women should be given Tdap

during each pregnancy,
 Preferably at 27 to 36 weeks gestation,
 Regardless of when they were last vaccinated;
 Fetus can develop passive immunity from vaccines given at
this time.
 After injury, tetanus vaccination is given depending
on wound type and vaccination history;
tetanus immune globulin may also be indicated (see
table Tetanus Prophylaxis in Routine Wound
Management ).

 Patients not previously vaccinated are given a 2nd

and 3rd dose of toxoid at monthly intervals.
 Tetanus Prophylaxis in Routine Wound Management

History of Clean, Minor Wounds All Other Wounds*

Adsorbed TIG‡
Tetanus
Toxoid Td† TIG‡ Td†

Unknown
Yes No Yes Yes
or < 3 doses

Yes if > 10 Yes if > 5

≥ 3 doses years since No years since No
last dose last dose

* Such as (but not limited to) wounds contaminated with dirt, feces, soil, or
saliva; puncture wounds; crush injuries; avulsions; and wounds resulting from
missiles, burns, or frostbite.
† For patients ≥ 10 years who have not previously received a dose of Tdap, a single dose
of Tdap should be given instead of one Td booster. Children < 7 years should be given
DTaP or, if pertussis vaccine is contraindicated, DT. Children aged 7–9 years should be
given Td.
Prevention…
 Secondary:
 Wound cleansing & debridement

 Adm of Td & HTIG, when indicated

 Wounds to be considered prone to tetanus:

 Those longer than 6hrs
 PROGNOSIS
 Tetanus has a mortality rate of
 Worldwide: 50%

 In untreated adults: 15 to 60%

 In neonates, even if treated: 80 to 90%

 Mortality is highest at extremes of age and in drug abusers.

 Prognosis is poorer if
 the incubation period is short and symptoms progress

rapidly
 treatment is delayed.

 Course tends to be milder when there is no demonstrable focus

of infection.
 With use of modern supportive care, most patients recover.
Referenecs

 Uptodate 2022
 Harrisons 19th edition
 medscape
END