Tetanus is an acute disease affecting the CNS and is now a rare disease in the western world, but not so in developing countries. Each year, approximately 2.8 million people sustain head injuries in the United States alone, resulting in approximately 2.5 million emergency evaluations, 300,000 hospital admissions and 60,000 deaths. There are several factor in our society that play role in high incidence of tetanus, there is still some religious tenets, cultural belief, and traditional healer that act as barrier to immunization and good wound care barrier, as to mention although in this case these factors did not contribute, and the barriers to immunization in this case were midwives uncertainty for conducting vaccination to low-birth-body-weight baby, and mother in this case is passively acccept with resignation that her children didnt received immunization due to midwives uncertainty. This is the first reported case tetanus complicating an untreated mild open head injury in Indonesia that underwent craniotomy debridement for source control .3
Tetanus primary manifestation is prolonged muscular spasm (without altered mental status) caused a neurotoxin produced by C. tetani that potentially given fatal complication. C. tetani, a Gram-positive anaerobic bacterium, exists as sporulated form in environment (usually in soil) throughout the world and found in gastrointestinal tract of animals and human. C. tetani spores enter the body through a wound or damage skin; in the presence of anaerobic conditions, the spores germinate. The bacteria produce two very potent toxins (tetanolysin and tetanospasmin), both toxins enter the blood stream and lymphatic system to disseminate through the body. Tetanolysin is thought to optimize conditions for bacterial proliferation. The clinical features of tetanus are caused by tetanospasmin, enters the peripheral nervous system directly from the contaminated wound, and is capable of affecting motor, sensory, and autonomic neurons. In approximately 20% of cases, no entry wound is noted. The primary pathological effect of tetanospasmin is the cleavage of synaptobrevin, which is a presynaptic protein. Synaptobrevin facilitates neurotransmitter fusion of vesicles to nerve membranes and release of their contents into the synapse. By cleaving synaptobrevin, neurotransmission is effectively blocked. Radiolabelled assays have shown tetanospasmin has a preference for inhibitory motor neurons, which explains the clinical picture of muscle rigidity. Toxins act at several sites within CNS, including peripheral motor end plates, spinal cord, and brain, as well as in the sympathetic nervous system. Toxin causes tetanus typical clinical manifestations by interfering with the release of neurotransmitters and block inhibitor impulses; leads to unopposed muscle contraction and spasm. Seizures may occur and the autonomic nervous system also is affected.1,4,5
After innoculation the incubation period ranges from 3 to 21 days, averaging about 10 days. In general, the further the injury site is from the central nervous system, the longer the incubation period. A shorter incubation period is associated with more severe disease complications and a higher mortality. In neonatal tetanus, symptoms usually appear from 4 to 14 days after birth, averaging about 7 days. The characteristic symptoms of tetanus are painful muscular contractions, primarily of the masseter and neck muscles and secondarily of trunk muscles. Trismus or “lockjaw”, is a common sign of tetanus. A common first sign suggestive of tetanus in older children and adults is abdominal rigidity, although rigidity is sometimes confined to the region of injury. Generalized spasms occur frequently induced by sensory stimuli. History of an injury or apparent port of entry may be lacking. Clinicians rarely recover the organism from the site of infection.1,4,5
There are four clinical features of tetanus: neonatal, generalized, localized, and cephalic; four Grade of tetanus as propose in Ablett Classification of tetanus severity: I (mild), II (moderate), III (severe), and IV (very severe) as we can see in Table 1. Neonatal tetanus occurs 3–7 days postdelivery. Difficulty feeding, poor suck/swallow, excessive crying often precede overt spasms. Generalized tetanus is the most common feature, accounting for > 80% of cases. The most common initial sign is spasm of the muscles of the jaw or “lockjaw”. Other signs may follow “lockjaw” from such painful spasms in other muscle groups in the neck, trunk, extremities, and generalized, seizure-like activity or convulsions in severe cases. Even with modern intensive care, generalized tetanus is associated with death rates of 10–20%. Localized tetanus is an unusual feature with consisting of muscle spasms in a confined area close to the site of the injury. Although localized tetanus often occurs in people with partial immunity and is usually mild, progression to generalized tetanus can occur. Cephalic tetanus is the rarest feature associated with lesions of the head or face and may also be associated with otitis media. The incubation period is short, 1–2 days. Unlike other, cephalic tetanus results in flaccid cranial nerve palsies rather than spasm, but spasm of the jaw muscles may also be present. Like localized tetanus, cephalic tetanus can progress to the generalized form. most cases of cephalic tetanus involve only the facial region below the eyebrows in CN V (trigeminal nerve) territory, in the periorbital region. Few cases attributable to the head injury usually were secondary to small scalp lacerations of the frontal temporal regions as a result of minor trauma. Cases secondary to open depressed skull fracture, such as our case, are almost unknown.5–17 Study from ethiopia showed us that trauma is the most common portal of entry in children as much as 79.2%. This can be explained by the high chance of ignoring pediatric trauma and lack of provision of tetanus prophylaxis. The most common cause of death was the respitatory failure secondary to uncontrolled spasm (laryngo- and diaphragm spasm); could be due to muscle relaxant poor escalation and lack of pediatric intensive care unit (ICU) care.1,18−20
Tetanus disease never is completely eradicated because the bacteria maintain natural reservoirs in soil, humans, and other animals. Furthermore, there is no naturally acquired immunity; the very small amount of toxin necessary to cause disease does not stimulate antibody production in the host. Tetanus is almost entirely vaccine preventable since the vaccine efficacy is virtually 100%. A 6-dose series of tetanus toxoid-containing vaccine (TTCV)-which includes 3-dose in the first year after birth, followed by booster dose in the 2nd year, in early childhood, and in adolescence has been shown to provide immunity and protect women through their childbearing years, though some countries still endorse a 5-dose series (shown in Fig. 4). Indonesia national immunization programs include 5-dose TT vaccination. Three-dose given before the first year after birth, boostered at 4–7 and 15 years old. Vaccination and good wound care are the main feature to prevent tetanus.4,21
The treatment of tetanus involves providing supportive care for symptoms of muscle spasms and potential respiratory compromise, neutralizing the remaining tetanus toxin, and good wound care for eradicating bacteria at the wound site. The defining factor that contribute to therapeutic success was time for immunoglobulin administration to neutralize the toxin and/or tetanus toxoid vaccination as we can se in table 2. Without treatment, the case fatality rate remains ~ 100%; with treatment, case fatality rates drop to 10–20%. For generalized tetanus case, intensive care, including endotracheal intubation, mechanical ventilation, deep sedation and/or paralysis is the mainstay of supportive care. Patients should have minimal environmental stimulation to avoid the reflex spasms. Benzodiazepines, particularly diazepam, are treatments of choice, since provide sedation, control muscle spasm, and provide anxiolysis. Intravenous magnesium sulfate can be used as an adjunct anti spasmodic agent that also decreases autonomic instability. Intrathecal baclofen has shown promise for severe spasms, but may not be feasible in resource-poor areas where intrathecal catheter insertion isn’t practical and mechanical ventilator support is unavailable; higher dose cause respiratory depression and cardiovascular instability. Autonomic instability can be treated with clonidine, b-blockers, and morphine.4,22−23
Rapid sequence intubation is mandated due to significant aspiration risk because of increased abdominal pressure, gastric stasis, and involvement of laryngeal muscles in tetanus patient. Preparation for a potentially difficult airway was in place and spontaneous ventilation was maintained by the induction of anaesthesia with sevoflurane in 100% O2. When general anaesthesia is performed, a deep level of anaesthesia is suggested to avoid triggering hypertensive crises and spasms during the procedure. Various intravenous and inhalation anaesthetic agents have been used without incidence in tetanus patients.24 In our case, there are several risk factor related to tetanus complications. Firstly, she never received any vaccination and the wound is not properly taken care of, moreover she did not get immunoglobulin to neutralize the toxin after the accident. All the factors above contribute to tetanus; the patient underwent craniectomy, debridement for source control under neuroanasthesia and post-operative care in pediatric ICU.
The pediatric intensive care of such cases requires halting further toxin production, neutralisation of circulating toxin, and control of the clinical manifestation induced by the toxin that has already gained access to the CNS. The basic tents of anaesthetic care in a patient with tetanus include consideration of the implication of a full stomach, prevention of the paroxysm of muscle spasm by maintaining a deep plane of anaesthesia or the use of regional anaesthesia and control of the autonomic instability. As the autonomic instability may be life-threatening, invasive arterial blood pressure monitoring may be indicated. Although uncommon, with prolonged tetanus, associated cardiomyopathy repeated exposure to catecholamines may be present. A perioperative assessment of renal and electrolyte balance required the presence of myoglobinuria and renal dysfunction. In our case, three weeks postoperative course was uneventful and the patient showed an excellent clinical recovery and discharged on 16th postoperative day.