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NEONATAL TETANUS
By
Dr. Afuye Olubunmi Olusola
10.08.15
Case Presentation
Name: A.M
Age: 7days
Sex: Female
Address: Ilorin
Tribe: Yoruba
Informant: Mother
Presenting Complaint
Excessive Crying - 3days
Abnormal Body Movement – 2days
Inability to feed – 1day
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.
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.
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.
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,ResonantPercussion note, Vesicular breath sounds.
Problems
7days old
Excessive crying
Abnormal body movement
Inability to feed
Poor ANC
Poor Cord care
Mixed feeding
Hypothermia
Assessment
7day old female with neonatal tetanus
Investigations
Urgent RBS- 5.1mmol/L
PCV -41%
FBC
E/U/Cr
Blood Culture
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
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 ……….
TOPIC PRESENTAION
OUTLINE Introduction
Brief history
Epidemiology
Aetiology
Pathophysiology
Route of Entry
Risk Factors
Clinical Features
Investigations
Management
Complications
Differential Diagnosis
Prognosis
Prevention
Conclusion
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
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.
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
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.
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.
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 intraneuronaltransport, reaches the nerve cell body in the brainstem and spinal cord.
PATHOGENESIS CONTThe 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
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).
1. C. tetani enters body from through
wound.
3. Germinates under anaerobic conditions and begins to multiply
and produce tetanospasmin.
2. Stays in sporulatedform 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.
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
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.
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.
GENERALIZED TETANUS
Most commonly encountered form of TetanusIt 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.
LOCALIZED TETANUSIt is a milder form of the disease characterized by pain and stiffness confined to the site of the wound.CEPHALIC TETANUSIt 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.
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.
Others:Opisthotonus and board- like rigidity.Features of autonomic dysfunctions:TachycardiaArrhythmia Labile hypertension Diaphoresis Cutaneous vasoconstriction
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 infectionb. Stressed induced from sustained tetanic spasm
II Urea and Electrolyte
III Blood Sugar
IV Blood Culture
V Lumbar PunctureFew diseases resemble tetanus in its fully developed form. These can be differentiated on clinical grounds.
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.
MANAGEMENT
Management of tetanus patients involves a team approach. The approach depends upon resources, personnel, and expertise at one’s command.
MANAGEMENTPRINCIPLES 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 care7. Prevention of recurrences.8. Management of complications9. Immunising survivors prior to discharge
1.NEUTRALISATION OF CIRCULATING TOXINPreventing the action of circulating unbound neurotoxins.Use of Antitetanus serum (ATS)
i. Human tetanus immunoglobulin (HTIG)—500I.U. IMii. Immune equine (or bovine) tetanus immunoglobulin-10 000—20 000 I.U. IM {SE :Serum sickness (15% of cases)}
2. CONTROL OF SPASMSJudicious use of sedatives and muscle relaxants
i. Diazepam—0.1–0.2mg/kg 4hrly, then titrated to ptresponse.ii. Phenobarbitone (1mg/kg) + Diazepam (0.5mg/kg) alt. 6hrlyiii. Paraldehyde—0.3ml/kg (1—2mg/kg) + Diazepam for breakthrough spasmsiv. NM blocking agents eg Pancuronium, Vecuronium, + mechanical ventilation.3. CONTINUED SEDATION
Diazepam—0.5—1mg/kg/dosePhenobarbitone—5mg/kg + Chlorpromazine—2mg/kg
4. ERADICATION OF RESIDUAL CLOSTRIDIAL INFECTIONThorough debridementAntibiotics
i. Penicillin—100 000 I.U. /kg/day in divided doses x10/
7 –14/7.
ii. Metronidazole
iii. Erythromycin + Tetracycline
5. ADEQUATE FLUID AND CALORIC INTAKENG Tube for neonates; express breast milkCorrection of electrolyte and fluid deficiency IV
6. OPTIMAL NURSING AND GENERAL SUPPORTIVE CAREDark, quiet and secluded setting Prevention of pressure soresSuction of the nasopharynxCardiorespiratory monitoring, etc.
7. PREVENTION OF RECURRENCESActive immunization of survivors prior to dischargeUse of TT—0.5ml IM
ADDITIONAL MEASURES IN SEVERE CASESAnticoagulation to prevent DVTAdministration of alpha & beta blockers Control of arrhythmias.
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.
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
DIFFERENTIAL DIAGNOSIS
Rabies.
Pharyngitis.
Encephalitis.
Meningitis.
Dystonic drug reactions.
Strychnine poisoning.
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
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
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.
Ablett Classification of the Severity of TetanusGrade 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 thecardiovascular system. Severe hypertension and tachycardiaalternating with relative hypotension and bradycardia, either of which may be persistent.
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
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
(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.
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
Situation on tetanus elimination
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