26. TETANUS Flashcards
Definition
Tetanus in general is defined as an acute disease manifested by (+) hypertonia (+) painful muscular contractions (+) generalized muscle spasms (+) ANS disturbance WITHOUT other apparent medical cause.
With the advent of widespread vaccinations, the incidence of tetanus has drastically decreased especially in developed countries.
Other forms of tetanus depending on the population include:
- Neonatal tetanus
- Maternal tetanus defined as tetanus occuring during pregnancy or within 6 weeks
ETIOLOGY
Tetanus is caused by a powerful neurotoxin; TETANOSPASMIN, produced by the bacterium Clostridium tetani.
Clostridium tetani is a motile, non-encapsulated, anaerobic, gram (+) rod which exists in either a vegetative or spore-forming state.
Spores are HIGHLY RESILIENT, can resist boiling and many disinfectants and can survive readily in the environment including soil and animal feces.
Once they enter into the body through abrasions, wounds or in the umbilical stump, they grow, multiply and release tetanospasmin, an exotoxin that enters the nervous system and cause the disease. Only those bacteria producing tetanospasmin can cause tetanus.
In 20-30% of cases, no puncture entry wound is found
Superficial abrasions to the limbs are the most common infection sites.
Deeper infections such as in fractures, abortions, or drug injections are associated with more severe disease.
In neonates, infection of the umbilical stump usually result form improper cord care. For example, in some culture, the cord is cut using grass. Or in others, animal manure is applied to the stump. Early circumcision and ear piercing can also result to neonatal tetanus.
Other risk factors for tetanus include:
- Age >60 yo (antibody levels decrease over time)
- Injection drug users (injecting heroin subcutaneously “skin-popping”
- Incomplete or absent vaccination
Pathogenesis
Mouthful to sizzz
Toxin production by C. Tetani are ENHANCED by the presence of:
1. Necrosis in the area of devitalized tissue
2. Calcium salts
3. Associated pyogenic infections
All of which aid establishment fo low oxidation-reduction potential
Once tetanus toxin is produced, it is secreted as a single 150 kDa protein that is cleaved to produce heavy (100 kda) and light (50 kda) chains linked by a disulfide bond.
The carboxy terminal of the heavy chain binds to specific membrane components in presynaptic motor neuron terminal
This binding results in toxin internalization and uptake into the nerves.
The toxin then migrates via retrograde axonal transport towards the inhibitory interneuron terminals on the brainstem and spinal cord including both interneurons producing glycine and y-aminobutyric acid (GABA) which are inhibitory neurotransmitters
Toxin degrades (Synaptobrevin), a protein required for docking neurotransmitter vesicles on the presynaptic membrane
ultimately, the release of these inhibitory neurotransmitters is blocked, leading to DISINHIBITION of the motor neurons
This results to the signs and syptoms seen in tetanus
Generally, the incubation period ranges from <24 hours to >1 month and shorter incubation periods are associated with a more severe disease and poorer prognosis
Clinical Manifestations
Tetanus produces a wide spectrum of clinical features that are broadly divided into
- Generalized tetanus
- Localized tetanus
- Cephalic tetanus
***In all forms of tetanus, mental status is normal which is an important consideration in differentiating tetanus from other diseases (exception: alterned sensorium due to respiratory failure)
GENERALIZED TETANUS
Generalized tetanus is the Most common. Presenting as generalized spastic disease.
In the typical progression of generalized tetanus, muscles of the face and jaw are often affected first.
Spasms of these muscles are knows TRISMUS or LOCKJAW when the jaw is affected and RISUS SARDONUS when the face is the one affected.
This is followed by spasms of the back muscles leading to backward arching of the head, neck and spine called OPISTHOTONOS.
In severe cases, spasms of the laryngeal muscles will cause complete AIRWAY OBSTRUCTION leading to sudden death
In the same way, spasms of the respiratory musckes result in respiratory failure
without ventilatory support, it is the most common causes of DEATH in tetanus
Spasms may be strong enough to produce Tendon Avulsions as well as CRUSH FRACTURES
During the 2nd week, autonomic disturbance becomes maximal. Death due to CV events become the major risk.
Blood pressure is usually labile, with rapid fluctuations form high to low accompanied by tachycardia.
Episodes of bradycardia and heart block can also occur.
Other autonomic manifestations include GI stasis, sweating, increased tracheal secretions and acute high-output renal failure
LOCALIZED TETANUS
Localized tetanus is uncommon and is characterized by sustained contractions of the muscles in the same area as the injury site
CEPHALIC TETANUS
cephalic tetanus is a rare form of disease associated with ear infections, otitis media or head and neck lesions
It presents as cranial nerve palsies most often affecting CN VIII with facial asymmetry
The pharyngeal and larngeal muscles may also be affected leading to airway obstruction
After 4 to 6 weeks, toxins are degraded and recovery from spasms depend on the regrowth of the axon nerve terminals
Diagnosis
Diagnosis of tetanus is CLINICAL
There are no laboratory tests to diagnose tetanus
Culture of clostridium tetani from a wound only provides supportive evidence because not all strains exhibit the toxin.**
Also, C. Tetani may be present in the wound in the absence of clinical disease
Serum measurement of anti-tetanus IgG before antitoxin administration may rule out suspected tetanus because serum levels >0.1 IV/mL are deemed protective and do not support the diagnosis of tetanus
However, the most important thing to remember is that treatment should not be deayed while these laboratory tests are being conducted.
Diff Dx
- Strychnine poisoning (rat poison)
- Drug-induced dystonia (phenothiazines, metoclopramide)
- Hypocalcemic tetany
- Malignant neuroleptic syndrome - autonomic instability, muscle rigidity, fever, altered sensorium
- Stiff-person syndrome - centrally mediated motor hyperexcitability presenting with persistent & intense spasms usually precipitated by voluntary movements, auditory, tactile or emotional stimuli, absence of trismus and risus sardonicus, rapid response to dizepam (+) autoabs to glutamic acid decarboxylase
Management
Patients with tetanus should be ADMITTED to the ICU
Ideally, patients should be placed in a calm, quiet environemnt because light and noise can trigger spasms
- Respiratory Management
It is important to establish SECURE AIRWAY early in tetanus
Patients must be SEDATED and given Neuromuscular blockers such as SUCCINYLCHOLINE for INTUBATION and MECH VENT
Occassionally, increased tracheal secretions and spasm of laryngeal muscles make endotracheal intubation difficult
Thus, tracheostomy should be done in these cases (Better tracheal suctioning and pulmonary toilette)
- TETANUS IMMUNOGLOBULIN and TOXOID (Neutralization of Unbound Toxin)
Ig should be given to neutralize the circulating tetanospasmin in the wound to prevent its uptake in the nerve terminals.** It does not neutralize toxins that are fixed in the nervous system already. Although, tetanus Ig does not ameliorate clinical symptos of tetanus** early reports, however, do suggest that it reduces mortality
recommended therapy is 3000 to 5000 IV of Human tetanus Ig (TIG) as a single IM dose, a portion of which should be injected around the wound. Repeat doses are unnecessary - long t1/2 28 days.
Tetanus toxoid must also be given opposite the site of teh TIG.
It is important that TIG be given before wound debridement because exotoxin may be released during wound manipulation.
- WOUND DEBRIDEMENT and ANTIBIOTICS (halting toxin production)
The entry would should be identified, cleaned and debrided of necrotic tissue in order to remove anaerobic foci of infection and prevent further toxin production.
METRONIDAZOLE 500 mg/IV q6 or 400 mg rectally q6 for 7 days is the preferred antibiotic.
An alternative is Penicillin, however, theoretically it may potentiate the effects of tetanospasmin through its GABAlytic effect
- Control of muscle spasms
BENZODIAZEPINES are frequently used and are generally effective in controlling rigidity and spasms in tetanus.
They also provide a sedative effect.
Diazepam has been used most frequently with the usual starting dose of 10-30 mg IV q1-4 PRN, as high as 500 mg may be required for adults
Ventilatory assistance is imperative at these higher doses.
Also when higher doses of IV Diazepam are used, its vehicle, Propylene glycol may produce hyperosmolarity and a high anion gap metabolic acidosis.
To avoid this problem, continuous infusion with IV Midazolam may be given as it does not require propylene glycol as vehicle d/t its water solubility.
Nondepolarizig neuromuscular blockers such as Vecuronium may also be used.
pancuronium should be avoided because it inhibits catecholamine uptake and may worsen autonomi instability.
- Management of Autonomic Dysfunction
For autonomic instability such as labile BP, Labetalol 0.25-1.9 mg/min has been frequently administered because of its dual a and B-blocking properties
IV Nicardipine may also be given as 5 mg/hr infusion and may be titrated by decrements or increments of 2.5 mg/hr every 15 minutes
- Other supportive measures
Energy demands in tetanus may be extremely high so early nutritional support is mandatory
Enteral feeding is preferred if enough calories can be administered using this route
Prophylactic treatment with PPI may be used to prevent GI hemorrhage from stress ulcers
Prophylaxis for thromboembolism with anticogulants should be given early
Physical Therapy should be started as soon as spasms have ceased since patients are often left with disability from prolonged drug-induced paralyisi and immobilization
- Immunization 0 patients who recover from tetanus should receive active immunization since tetanus toxin is weakly immunogenic, thus, previous infection does not confer immunity
Prognosis
Rapid development of tetanus is assoc. Iwth more severe disease and poorer outcome
It is important to note time of onset and length of incubation period.
Recovery may be complete unless periods of hypoventilation have been prolonged or other complications have ensued.
Nosocomial infections, decubitus ulcers, tracheal stenosis, GI hemorrhage and thromboembolic disease.
Neonates may be at increased risk of learning disabilities, behavioral problems, cerebral palsy and deafness
Prevention
Tetanus is prevented by GOOD WOUND CARE and IMMUNIZATION
In neonates, use of safe, clean delivery and cord-care practices as well as maternal vaccination are essential.
WHO guidelines for tetanus vaccination consist of:
- Primary course of 3 doses in infancy (DTaP x3)
- Booster at 4 to 7 years old
- Booster at 12 to 15 years old (Tdap x1)
- Booster in adulthood
Standard recommendation by WHO for prevention of maternal and neonatal tetanus requires administration of two doses of tetanus toxoid at least 4 weeks apart.
Individuals sustaining tetanus-prone wounds should be actively immunized if the vaccination status is: incomplete, unknown/unrecalled/last booster was given >10 years ago
Tetanus prone wounds include:
- Wounds >6 hrs old
- Contaminated with soil, saliva, feces or dirt
- Puncture or crush wounds
- Avulsions
- Wounds from missiles
- Burns
- Frostbite
Lastly, immunization programs should be sustained as there is NO TETANUS HERD IMMUNITY effect and tetanus contamination of soil and feces is widespread.
