2. PRESENTING COMPLAINTS
• 24 YEAR OLD FEMALE PRESSENTED TO ER WITH H/O LEFT SIDED
CHEST PAIN, DRY COUGH FOR 5 DAYS
• FEVER FOR 3 -4 DAYS
• H/O CLENCHING OF TEETH, ABNORMAL BENDING POSTURE WITH
NEXT EXTENSON 1 DAY BACK
3. H/O PRESENTING COMPLAINTS
• PATIENT WAS APPARENTLY NORMAL 5 DAYS BACK. THEN SHE
DEVELOPED LEFT SIDED CHEST PAIN WITH DRY COUGH
• FEVER FOR 3 – 4 DAYS
• H/O FALL FROM BED ON WOODEN SURFACE 3 DAYS BACK
• CLENCHING OF TEETH, ABNORMAL BENDING POSTURE WITH NECK
EXTENSION 1 DAY BACK – DURING THESE EPISODES PATIENT WAS
CONSCIOUS WITHOUT ANYTONGUE BITE OR URINARY INCONTINENCE
• PATIENT WAS INITIALLY TAKEN TO A LOCAL HOSPITAL FROM WHERE SHE
WAS TREATED BUT DID NOT RESPONDED TO TREATMENT AND WAS
REFERREDTO MOH
4. • NO H/OTRAUMA
• NO H/O MISSED ABORTION
• NO H/O DOG OR ANIMAL BITE
• NO H/O HYDROPHOBIA
• H/O IMMUNIZATION WAS NOT AVAILABLE
• NO H/O INTAKE OF ANY POISON OR DRUG
• NO H/O HEADACHE/VOMITING
H/O PRESENTING COMPLAINTS
5. • PAST HISTORY – NOT A KNOWN CASE OF DM/HTN/TB/COPD/STROKE/
ASTHMA/ CHRONIC BRONCHITIS
• PERSONAL HISTORY – no significant h/o
• MENSTRUAL HISTORY – LMP 21/03/22 FLOW FOR ONLY 1 DAY
• TREATMENT HISTORY – NOT AVAILABLE
6. GENERAL EXAMINATION
• PATIENT WAS NOT CONSCIOUS, DYSPNEIC
• NO PALLOR
• NO ICTERUS
• NO CYANOSIS
• NO CLUBBING
• NO PEDAL EDEMA
• NO LYMPHADENOPATHY
VITALS
• BP – 120/80 MM OF HG
• HR – 183 BPM
• TEMP – 102.4 OF
• RR – 36/MIN
• RBS – 103MG/DL
7. SYSTEMIC EXAMINATION
• CVS– S1 S2 HEARD, NO MURMUR/TACHYCARDIA
• RS – B/LVESICULAR BREATHING, NO ADDED SOUNDS
• P/A – SOFT, NONTENDER, NO ORGANOMEGALY/ ASCITES
• SKIN – NORMAL, NO SIGN OF ANY CUT /PUNCTURE WOUND
8. CNS – CRANIAL NERVES – NORMAL
VOR - PRESENT
NECK EXTENSION WITH OPISTHOTONUS +
MOTOR –TONE AND BULK NORMAL, POWER ATLEAST 3/5
DEEPTENDON REFLEXES – 2+
PUPILS – B/L EQUAL, REACTING TO LIGHT
KERNIG’S SIGN – ABSENT
SYSTEMIC EXAMINATION
9.
10. COURSE IN HOSPITAL
PATIENT ON ARRIVAL WAS IN COMATOSE STATE. HER GCS WAS LOW
E2V2M2
ANDWAS INTUBATED AND SHIFTEDTO ICU . WITH ABOVE MENTIONED
COMPLAINTS AND HISTORY AND BY DOING SYNDROMIC APPROACH
PROVSISONAL DIAGNOSIS OFTETANUS WAS MADE . MGSO4
INFUSION WAS STARTED TOTREAT MUSCLE SPASM/ RIGIDITY AND
NEUROMUSCULAR BLOCKING AGENT WAS GIVEN SOS .HUMANTETANS
IMMUNOGLOBULIN AND INJTETANUSTOXOID WAS GIVEN . PATIENT
TLC WAS HIGH ON ARRIVAL SO CULTURESWERE SENT . TETANUS IS
DIAGNOSIS OF EXCULSION . OTHER INVESTIGATION WERE DONETO
RULE OUT OTHER D/DX.TRACHEOSTOMY WAS DONE I/V/O PROLONGED
INTUBATION.
20. OPISTHOTONUS
• OPISTHOTONUS IS DEFINED AS A DRAMATIC ABNORMAL POSTURE
DUE TO SPASTIC CONTRACTION OF THE EXTENSOR MUSCLES OF THE
NECK, TRUNK, AND LOWER EXTREMITIES THAT PRODUCES A SEVERE
BACKWARD ARCHING FROM NECKTO HEEL.
22. PATHOPHYSIOLOGY
• THE TYPICAL POSTURE OCCURS DUE TO THE SIMULTANEOUS MASS
CONTRACTION OF AGONIST AND ANTAGONIST MUSCLE GROUPS ALONG
WITH INCREASEDTONE.
• THERE IS AN IMBALANCE BETWEEN FACILITATORY AND INHIBITORY
NEUROLOGIC PATHWAYS INNERVATING THE MUSCLE GROUPS INVOLVED.
• IN TETANUS, THE TOXIN BLOCKS THE PRESYNAPTIC SPINAL INHIBITORY
NEURONS.
23. CAUSES
• Infectious-- Meningitis, Encephalitis, Tetanus, Rabies, Cerebral malaria,
Neurosyphilis
• Poisoning -- Strychnine, phencyclidine, phenothiazines, lignocaine,
methoxyphenidine
• Developmental and Metabolic -- Cerebral palsy, Krabbe disease,
hyperbilirubinemia, and kernicterus, Gaucher disease, adenylosuccinate
lyase deficiency, infant alcohol withdrawal syndrome, which is more
commonly seen in neonates
• Increased Intracranial Pressure --Intracranial hemorrhage, subarachnoid
hemorrhage, hydrocephalus, or a space-occupying lesion
• Neurodegenerative Syndromes -- This includes neurodegeneration with
brain iron accumulation, Wilson disease, cerebral palsy, and Parkinson
disease. It has been described in neurometabolic disorders like maple
syrup urine disease, glutaric aciduria, Lesch Nehan syndrome.
24. TETANUS
TETANUS IS A NERVOUS SYSTEM DISORDER CHARACTERIZED
BY MUSCLE SPASMS THAT IS CAUSED BY THE TOXIN-
PRODUCING ANAEROBE CLOSTRIDIUM TETANI, WHICH IS
FOUND IN THE SOIL.
POTENT NEUROTOXIN PRODUCED BY THE ORGANISM IS
RESPONSIBLE FOR THE CLINICAL FEATURES.
INCUBATION PERIOD — 8 DAYS but ranges from 3 to 21 days
usually rod-shaped and up to
2.5 μm long, but they become
enlarged and tennis racket- or
drumstick-shaped when
forming spores
25. TETANUS CAN PRESENT IN ONE OF FOUR CLINICAL PATTERNS:
●GENERALIZED ●LOCAL ●CEPHALIC ●NEONATAL
• Generalized tetanus — most common and severe clinical form Tonic and periodic spastic
muscular contractions , classic clinical findings of tetanus such as:
●Stiff neck
●Opisthotonus
●Risus sardonicus (sardonic smile)
●A board-like rigid abdomen
●Periods of apnea and/or upper airway obstruction due to vise-like contraction of the thoracic
muscles and/or glottal or pharyngeal muscle contraction
●Dysphagia
26. • Local tetanus — Rarely, tetanus presents with tonic and spastic muscle
contractions in one extremity or body region
• Cephalic tetanus — Patients with injuries to the head or neck may
present with cephalic tetanus, involving initially only cranial nerves
• Neonatal tetanus — failure to use aseptic techniques in managing the
umbilical stump in offspring of mothers who are poorly immunized.
infants 5 to 7 days following birth Neonatal tetanus presents with
refusal to feed and difficulty opening the mouth due to trismus.
Sucking then stops and facial muscles spasm, which may result in risus
sardonicus (sardonic smile). hands are often clenched
27. PATHOPHYSIOLOGY
• PRODUCES THE METALLOPROTEASE TETANUS TOXIN (ALSO KNOWN AS TETANOSPASMIN).
• AFTER REACHING THE SPINAL CORD AND BRAINSTEM VIA RETROGRADE AXONAL TRANSPORT
WITHIN THE MOTOR NEURON, TETANUS TOXIN IS SECRETED AND ENTERS ADJACENT INHIBITORY
INTERNEURONS, WHERE IT BLOCKS NEUROTRANSMISSION BY ITS CLEAVING ACTION ON THE
MEMBRANE PROTEINS INVOLVED IN NEUROEXOCYTOSIS
• THE NET EFFECT IS INACTIVATION OF INHIBITORY NEUROTRANSMISSION THAT NORMALLY
MODULATES ANTERIOR HORN CELLS AND MUSCLE CONTRACTION. THIS LOSS OF INHIBITION (IE,
DISINHIBITION) OF ANTERIOR HORN CELLS AND AUTONOMIC NEURONS RESULTS IN INCREASED
MUSCLE TONE, PAINFUL SPASMS, AND WIDESPREAD AUTONOMIC INSTABILITY.
28. • TETANOLYSIN IS ANOTHER TOXIN PRODUCED BY C. TETANI DURING ITS EARLY
GROWTH PHASE. IT HAS HEMOLYTIC PROPERTIES AND CAUSES MEMBRANE
IN OTHER CELLS, BUT ITS ROLE IN CLINICAL TETANUS IS UNCERTAIN
• DURATION OF ILLNESS — TETANUS TOXIN-INDUCED EFFECTS ARE LONG LASTING
BECAUSE RECOVERY IS BELIEVED TO REQUIRE THE GROWTH OF NEW AXONAL NERVE
TERMINALS. THE USUAL DURATION OF CLINICAL TETANUS IS FOUR TO SIX WEEKS
29. PRESENTING FEATURES ON ADMISSION TO HOSPITAL FOR TETANUS
• TRISMUS (93–98%)
• GENERALISED MUSCLE TENSION (94–95%)
• MUSCLE STIFFNESS (96%)
• DYSPHAGIA (83%)
• DYSPNOEA (7%)
• MUSCLE SPASMS (46–80%)
• BODY TEMPERATURE >38·4°C (76%)
• PULSE ≥120 BEATS PER MIN (34%)
Hypertension and tachycardia are the most common features of autonomic nervous system
disturbance
31. ABLETT CLASSIFICATION OF TETANUS SEVERITY
• GRADE 1: MILD • MILD TO MODERATE TRISMUS • GENERALISED SPASTICITY • NO RESPIRATORY
COMPROMISE • NO SPASMS • LITTLE OR NO DYSPHAGIA
• GRADE 2: MODERATE • MODERATE TRISMUS • MARKED RIGIDITY • MILD TO MODERATE BUT SHORT
SPASMS • MODERATE RESPIRATORY COMPROMISE WITH AN INCREASED RESPIRATORY RATE (>30
BREATHS PER MIN) • MILD DYSPHAGIA
• GRADE 3: SEVERE • SEVERE TRISMUS • GENERALISED SPASTICITY • REFLEX PROLONGED SPASMS •
INCREASED RESPIRATORY RATE (>40 BREATHS PER MIN) • APNOEIC SPELLS • SEVERE DYSPHAGIA •
TACHYCARDIA (>120 BEATS PER MIN)
• GRADE 4: VERY SEVERE • CLINICAL FEATURES OF GRADE 3 TETANUS • VIOLENT AUTONOMIC
DISTURBANCES INVOLVING THE CARDIOVASCULAR SYSTEM • SEVERE HYPERTENSION AND TACHYCARDIA
ALTERNATING WITH RELATIVE HYPOTENSION AND BRADYCARDIA (EITHER OF WHICH MIGHT BE
PERSISTENT
32. TREATMENT
• WOUND MANAGEMENT
• ANTIMICROBIALTHERAPY -Metronidazole (500 mg intravenously [IV] every 8 hourly
• NEUTRALIZATION OF UNBOUND TOXIN — Human tetanus immune globulin (HTIG) is
the preparation of choice. single dose of 500 units intramuscularly.
• ACTIVE IMMUNIZATION — all patients with tetanus should receive active immunization
with a full series (eg, three doses in adults and children >7 years old) of tetanus and
diphtheria toxoid-containing vaccines, commencing immediately upon diagnosis
• CONTROL OF MUSCLE SPASMS — Generalized muscle spasms are life threatening since
they can cause respiratory failure, lead to aspiration, and induce generalized exhaustion in
the patient. Eg BENZODIAZEPINES AND OTHER SEDATIVES — effective in controlling the
rigidity and spasms associated with tetanus. diazepam for an adult is 10 to 30 mg IV and
repeated as needed every 1 to 4 hours
33. • NEUROMUSCULAR BLOCKING AGENTS — Neuromuscular blocking
agents are used when sedation alone is inadequate
• MANAGEMENT OF AUTONOMIC DYSFUNCTION --magnesium
sulfate for the management of autonomic dysfunction and as
adjunctive treatment for controlling spasms. Magnesium sulfate acts
as a presynaptic neuromuscular blocker, blocks catecholamine release
from nerves, and reduces receptor responsiveness to catecholamines
• AIRWAY MANAGEMENT AND OTHER SUPPORTIVE
MEASURES Airway management and other supportive
measures Endotracheal intubation, nutritional support, Prophylaxis of
thromboembolism
36. DIFFERENTIAL DIAGNOSIS OFTETANUS
• Drug-induced dystonias such as those due to phenothiazines
• Trismus due to dental infection
• Strychnine poisoning due to ingestion of rat poison
• Malignant neuroleptic syndrome
• Stiff-person syndrome
37. SSPE
• SUBACUTE SCLEROSING PANENCEPHALITIS (SSPE) IS A SLOWLY
PROGRESSIVE DEGENERATIVE DISORDER CAUSED BY MEASLES
VIRUS.
• IT IS CHARACTERIZED BY TYPICAL CLINICAL AND
ELECTROPHYSIOLOGICAL FEATURES IN THE FORM OF SLOW
MYOCLONIC JERKS, WITH PROGRESSIVE COGNITIVE
IMPAIRMENT, VISUAL SYMPTOMS, AND PERIODIC COMPLEXES ON
EEG, WITH RAISED TITERS OF ANTI-MEASLES ANTIBODIES IN CSF
AND SERUM.
39. REFERENCES
• Harrison's Principles of Internal Medicine 21e
• https://www.uptodate.com/contents/tetanus
• https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)33131-
3/fulltext
• https://www.health.state.mn.us/diseases/tetanus/hcp/tetwdmgmt.html
40. QUESTIONNAIRE
• ?What is the average duration of ventilatory stay in tetanus patients
• A) 1-2 weeks
• B) 2-4 weeks
• C) 3-5 weeks
• D) 4 – 6 weeks
41. QUESTIONNAIRE
• ?What is the average duration of ventilatory stay in tetanus patients
• A) 1-2 weeks
• B) 2-4 weeks
• C) 3-5 weeks
• D) 4 – 6 weeks
42. • ?What is the dose of the HumanTetanus Immunoglobulin administered in
management of tetanus
• A) 150 IU
• B) 250 IU
• C) 500 IU
• D) 1000 IU
QUESTIONNAIRE
43. • ?What is the dose of the HumanTetanus Immunoglobulin administered in
management of tetanus
• A) 150 IU
• B) 250 IU
• C) 500 IU
• D) 1000 IU
QUESTIONNAIRE
44. • What is the of neonatal tetanus?
QUESTIONNAIRE
45. • What is the of neonatal tetanus?
QUESTIONNAIRE
46. • Maternal tetanus
• Tetanus during pregnancy or within 6 weeks of the end of pregnancy (birth,
miscarriage, or abortion)
• Neonatal tetanus: suspectedAny neonatal death between 3 days and 28 days of age
in which the cause of death is unknown; or any neonate reported as having neonatal
tetanus between 3 days and 28 days of age, but for whom the disease is not
investigated
• Neonatal tetanus: confirmed Any neonate with a normal ability to suck and cry
during the first 2 days of life and who, between 3 days and 28 days of age, cannot suck
normally, and becomes stiff or has spasms (ie, jerking of the muscles)
