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

THANK YOU