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.
4. History
Excessive cry was noticed 3days prior to presentation, consolable, no fever
Abnormal body movement involved both upper and lower limbs with the face.
Usually triggered by speech,noise, and touch.Several episodes since onset
lasting 1-2mins then resolving spontaneously with stiffening of the body and
no loss of sphincteric function.
Inability to feed was noticed a day to presentation as she couldn’t open her
mouth well and her cry were muffled.
Child presented here after being given medications with no improvement at
Centre Igboro Hospital
No hx of blood transfusion- Blood group and Genotype unknown. No hx of
surgery.
5. History Cont
Pregnancy was term.Mother received ANC at a ?Clinic. Did not receive T.T
Ddelivery was at the same centre via SVD and child did not cry immediately after
birth.Cried after suctioning of about 5mins.
Cord care is with hot charcoal and spirit.
Child is currently on breastmilk and water.
Yet to commence Immunisation as she was told to return a week after delivery.
She is the 4th of mother’s 4 children in a monogamous setting.Other siblings are
alive and well.Mother is a petty trader with no formal education married to a
catering shop worker with no formal education too.Family relocated 2months ago
from Sokoto and presently reside in a Family house of 8 rooms in Ilorin where they
occupy 3 of the rooms.Source of water is Tap and Rain.
6. Examination
Conscious with trismus and frequent spasms, pink in
room air, not pale, anicteric, hypothermic-35.5
degrees centigrade, well perfused, no significant
peripheral lymph node, no pedal oedema.
Anthropometry: Weight- 4kg, OFC- 37cm, Length-
47cm.
7. Systemic Examination
CNS: Conscious,Trismus +++, Spasms+++ to gentle touch.
No signs of meningeal irritation.Anterior Fontanelle is Patent
and Normotensive.Global hypertonia.
ABDOMEN: Full, moves with respiration, no scarification
marks, soft, no area of tenderness, no palpably enlarged
organ.Bowel sounds- hypoactive.
CVS: HR- 162bpm, HS- S1S2 only.
RESPIRATORY: RR- 60cpm, Equal Chest expansion,Resonant
Percussion note, Vesicular breath sounds.
11. Management
IVF 4.3% D/S => D10 at Maintenance i.e 400mls via Soluset over
24hours at 6dpm.
IV Diazepam 0.1mg/kg/dose 6hrly
IM Phenoobarbitone5mg/kg/dose 12hrly
IV Chlorpromazine 1mg/kg/dose 6hrly……This 3 in stagger doses.
IM ATS 1,000 i.u
IV Unasyn 150mg/kg/day in 2DD 12hrly
IM Genticin 5mg/kg/day in 2DD 12hrly
Clean umbilical cord with methylated spirit
Keep seizure chart
Nurse in quiet and dark environment
Monitor vital signs
12. Update
Child had repeated spasms and apneic
attack yesterday which necessitated
ambu bagging and assisted ventilation.
Anticonvulsants were discontinued and
diazepam dose was increased to ……….
15. INTRRODUCTION
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.
Greek words -“tetanosand teinein”, meaning
rigid and stretched, which describes the
condition of the muscles affected by the toxin,
tetanospasmin, produced by Clostridium
tetani
16. Tetanus spores are found throughout the
environment, usually in soil, dust, and animal waste.
Tetanus is acquired through contact with the
environment; it is not transmitted from person to
person.
17. BRIEF HISTORY
Tetanus is also known as “Lockjaw” was 1st described by
Hippocrates
Aetiology however remained shrouded in mystery until
1884 when Rattone & Carle discovered Clostridium tetani
18. EPIDEMIOLOGY
Worldwide distribution with endemicity in about 90
developing countries.
500 000—800 000 deaths from Neonatal Tetanus, 80%
in 12 SE Asian, African and Eastern Mediterranean
countries.
19. AETIOLOGY
Aetiologic agent is Clostridium tetani, a motile Gram +ve non-
capsulated spore-forming obligate anaerobe.
natural habitats include soil, dust as well as intestinal tract and
faeces of man and animals.
C. tetani, is not tissue invasive.
Clostridium tetani produces two exotoxins, tetanolysin and
tetanospasmin. The function of tetanolysin is not known with
certainty in man. Tetanospasmin is a neurotoxin and causes
the clinical manifestations of tetanus.
Tetanospamin is the 2nd most poisonous substance known.
20. PATHOGENESIS
C. tetani usually enters the body through a wound. Toxins
are produced and disseminated via blood and lymphatics.
Sometimes, the vegetative forms of the microbe are
destroyed but the spores are left behind in the wound.
In the presence of anaerobic (low oxygen) conditions, the
spores germinate into the vegetative forms which in turn
produce the toxins.
Tetanospasmin, a zinc metalloprotease, is released in the
wound and binds to the peripheral motor neuron terminal,
enters the axon, and via retrograde intraneuronal
transport, reaches the nerve cell body in the brainstem and
spinal cord.
21. PATHOGENESIS CONT
The toxin migrates across the synapse to
presynaptic terminals where it blocks the release
of the inhibitory neurotransmitters glycine and
gamma-aminobutyric acid (GABA). This
diminished inhibition results in an increase in the
resting firing rate of the motor neuron, and this is
responsible for the observed muscle rigidity and
unopposed muscle contraction and spasm.
21
22. PATHOGENESIS CONT
Localized tetanus occurs when only the nerves
supplying the affected muscle are involved.
Generalized tetanus occurs when the toxin
released at the wound spreads through the
lymphatics and blood to multiple nerve terminals.
The blood-brain barrier prevents direct entry of
toxin to the central nervous system (CNS).
23. 1. C. tetani enters
body from through
wound.
3. Germinates under anaerobic
conditions and begins to multiply
and produce tetanospasmin.
2. Stays in sporulated
form until anaerobic
conditions are presented.
4. Tetnospasmin spreads
using blood and lymphatic
system, and binds to motor
neurons.
5. Travels along the axons
to the spinal cord.
6. Binds to sites responsible
for inhibiting skeletal muscle
contraction.
24.
25. ROUTES OF ENTRY
- Contaminated wounds
- Intravenous drugs
-Umbilical stumps
-Traumatic injury from unsterilized objects
-Animal bite and frostbite
-Abscesses and chronic ulceration
-Gangrenes
-Intestinal surgery
-Female circumcision
26. RISK FACTORS
The triad of Ignorance, Poverty and Disease
Poor wound care, especially contaminated wounds and deep wounds
Use of unsterilised instruments
Circumcision,uvulectomy, IM injections, jigger extraction, etc.
Bad cultural practices
Lackadaisical attitude to immunisation
Climatic factors
Occupational factors
Pet—keeping
Presence of infection.
27. CLINICAL FEATURES
Incubation period varies between 2-14 days.
Age, onset time and frequency are important in the clinical
features.
Onset time is defined as interval between the first symptoms
and appearance of first sign.
Clinical Variants include:
-Generalized tetanus
-localized tetanus
-cephalic tetanus and
-neonatal tetanus.
28. GENERALIZED TETANUS
Most commonly encountered form of Tetanus
It is characterized by headache ,trismus or lockjaw, restlessness,
irritability, dysphagia and neck muscle spasm.
Risus sardonicus resulting from intractable spasm of facial
muscles.
Early symptoms characterized by sudden inability to suck (due to
spasm of buccal muscles), stiffness of the body followed by
generalized spasm.
Difficulty in swallowing . Spasm of the respiratory muscle can
lead to episodes of apnoea asphyxia and cyanosis.
29. LOCALIZED TETANUS
It is a milder form of the disease characterized by pain
and stiffness confined to the site of the wound.
CEPHALIC TETANUS
It is uncommon but invariably fatal .It involves bulbar
musculature .It occurs when portal of entry is at the
craniofacial region .features are retracted eyelid
,deviated gaze ,and spastic paralysis of the tongue
and pharyngeal musculature.
30. CLINICAL FEATURES
Neonatal Tetanus: referred to as ‘’disease of d
seventh day’’ in some parlance is a prototype of
generalized tetanus.
Occurs within 3-12 days of birth as progressive
difficulty in feeding with associated hunger and
crying ,failure to thrive ,poor sucking, grimacing and
irritability with subsequent tensed rigidity and spasm
.Stiffness to touch.
31. Others:
Opisthotonus and board- like rigidity.
Features of autonomic dysfunctions:
Tachycardia
Arrhythmia
Labile hypertension
Diaphoresis
Cutaneous vasoconstriction
32. INVESTIGATIONS
The diagnosis of tetanus is basically clinical.
There are no specific confirmatory tests.
The routine blood and CSF investigations are normal.
However , some baseline investigations could be
carried out on admission. These include :
I FBC : May show leucocytosis due to
a. Secondary bacteria infection
b. Stressed induced from sustained tetanic spasm
33. II Urea and Electrolyte
III Blood Sugar
IV Blood Culture
V Lumbar Puncture
Few diseases resemble tetanus in its fully developed form.
These can be differentiated on clinical grounds.
34. MICROBIOLOGY:
C. tetani is identifiable only in about 1/3 of cases.
Microscopy : it appears as a long thin motile G +ve rod.
It may show a terminal spore giving a
drumstick appearance.
Culture : C. tetani is an obligate anaerobe.
Proof of isolation of C.tetani rests on the
production of toxin and its neutralization by specific
antitoxin.
NB : neither preventive nor therapeutic use of antitoxin
should ever be withheld pending all these
demonstrations.
35. MANAGEMENT
Management of tetanus patients involves a
team approach. The approach depends upon
resources, personnel, and expertise at one’s
command.
36. MANAGEMENT
PRINCIPLES
1. Neutralisation of circulating toxins;
2. Control of spasm and rigidity;
3. Continued sedation;
4. Eradication of residual clostridial infection;
5. Adequate fluid and caloric intake;
6. Optimal nursing and supportive care
7. Prevention of recurrences.
8. Management of complications
9. Immunising survivors prior to discharge
37. 1.NEUTRALISATION OF CIRCULATING TOXIN
Preventing the action of circulating unbound neurotoxins.
Use of Antitetanus serum (ATS)
i. Human tetanus immunoglobulin (HTIG)—
500I.U. IM
ii. Immune equine (or bovine) tetanus
immunoglobulin-10 000—20 000 I.U. IM {SE :Serum
sickness (15% of cases)}
38. 2. CONTROL OF SPASMS
Judicious use of sedatives and muscle relaxants
i. Diazepam—0.1–0.2mg/kg 4hrly, then titrated to pt
response.
ii. Phenobarbitone (1mg/kg) + Diazepam (0.5mg/kg)
alt. 6hrly
iii. Paraldehyde—0.3ml/kg (1—2mg/kg)
+ Diazepam for breakthrough spasms
iv. NM blocking agents eg Pancuronium, Vecuronium,
+ mechanical ventilation.
3. CONTINUED SEDATION
Diazepam—0.5—1mg/kg/dose
Phenobarbitone—5mg/kg + Chlorpromazine—2mg/kg
39. 4. ERADICATION OF RESIDUAL CLOSTRIDIAL INFECTION
Thorough debridement
Antibiotics
i. Penicillin—100 000 I.U. /kg/day in divided doses x
10/
7 –14/
7.
ii. Metronidazole
iii. Erythromycin + Tetracycline
5. ADEQUATE FLUID AND CALORIC INTAKE
NG Tube for neonates; express breast milk
Correction of electrolyte and fluid deficiency IV
40. 6. OPTIMAL NURSING AND GENERAL SUPPORTIVE CARE
Dark, quiet and secluded setting
Prevention of pressure sores
Suction of the nasopharynx
Cardiorespiratory monitoring, etc.
7. PREVENTION OF RECURRENCES
Active immunization of survivors prior to discharge
Use of TT—0.5ml IM
ADDITIONAL MEASURES IN SEVERE CASES
Anticoagulation to prevent DVT
Administration of alpha & beta blockers
Control of arrhythmias.
41. COMPLICATIONS
Laryngospasm and spasm of respiratory muscles
leads to difficulty with breathing.
Hyperpyrexia.
Fractures of the spine or long bones may result
from sustained contractions.
Hyperactivity of the autonomic nervous system may
lead to hypertension and cardiac arrhythmia.
Nosocomial infections particularly septicaemia.
Aspiration pneumonia.
42. Rhabdomyolysis with the risk of acute tubular
necrosis.
Pulmonary emboli.
Gastric dilatation and paralytic ileus.
Hypoglycaemia
Laceration of mouth and tongue
Aspiration Pneumonitis
Pneumothorax
DVT
44. PROGNOSIS
Poor prognostic indices
Extremes of age
Short incubation period
Short time of onset
Non provocative spasms
Metabolic acidosis
Nearness to the CNS
Abnormal posturing
hyperpyrexia
Autonomic involvement
Inadequate nursing care
45. Severe cases- death from respiratory complication,
asphyxia and cardiac failure
Favourable cases- spasms become less frequent,
fever subsides, generalises muscle spasms diminish,
child able to feed.
Finally spasms disappears.
May remain stiff- stiffman syndrome
46. Prognosis Cont.
In patients who survive, recovery is complete—
without sequelae if supportive measures have
provided adequate ventilation.
Many prognostic grading systems (Phillips,
Hendrickse, Ablett, Dakar, and Udwadia) have been
developed.
The system reported by Ablett is simple, useful and
most widely used.
In Nigeria, the Hendrickse scoring system for
neonatal tetanus is commonly used.
47. Ablett Classification of the Severity of Tetanus
Grade Clinical features
I Mild Mild to moderate trismus; general spasticity; no respiratory
embarrassment; no spasms; little or no dysphagia
II Moderate Moderate trismus; well-marked rigidity; mild to moderate but short
spasms; moderate respiratory embarrassment with tachypnoea, mild
dysphagia
III Severe Severe trismus; generalized spasticity; reflex prolonged spasms;
tachypnoea; 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.
48. Hendrickse Scoring system for neonatal tetanus
Parameter 0 1 2 3
Age in days 1-4 5-8 9-12 >12
Time of onset <24hrs 24-48hrs >48hrs No
spontaneous
spasms
Spasm duration
(minutes)
Persistent Prolonged ,>2 Transient, <2 On stimulation
Temp variation
from normal
>30C 2-30C 1-20C <10C
Pneumonia
and/or
atelectasis
Definite and
widespread
Definite but
limited
Suspected Nil
49. PREVENTION
Tetanus is completely preventable and the preventive measures
are cheap and effective. The adopted preventive measures are:
(A) Retraining of traditional birth attendants and other
alternative care providers.
The package for retraining programmes should include
the following :
- Observing simple cleanliness at childbirth
- Hygienic handling of umbilical cord
- Cutting of umbilical stump with sterile instrument.
- Avoidance of harmful dressing
50. (B) Immunization with tetanus toxoid.
This can be achieved by the
following recommended measure: -
(1) Introduction of a school-based
immunization programmes
(2) Supplementary immunization of women
of child bearing age.
(3) Increasing community awareness about
Tetanus and immunization.
51. Immunization of women with tetanus toxoid
Dose When to give TT Level of
protection
Duration of
protection(yrs)
TT1 As early as possible during
pregnancy or at first
contact
None None
TT2 At least 4 weeks after TT1 80% 3
TT3 6-12 months after TT2
or during the next
pregnancy
95% 5
TT4 At least 1 year after TT3, or
during next pregnancy
99% 10
TT5 At least 1 year after TT4, or
during the next pregnancy.
99% Life
Usually a puncture wound or laceration, nails
Dead tissue
Extremely potent neurotoxin
Only creates small immune response so not enough antibodies for immunity and not usually any inflamation of the wound