| disease | Tetanus |
| alias | Severvday Convulsion (Neonatal Tetanus) |
Tetanus is an acute specific infection caused by the invasion of tetanus bacilli into body wounds, where they grow, reproduce, and produce toxins.
bubble_chart Etiology
Tetanus bacilli are widely present in soil and human and animal feces, and are a type of Gram-positive, anaerobic spore-forming bacilli. Neither tetanus bacilli nor their toxins can invade normal skin and mucous membranes, so tetanus always occurs after an injury. Any open injury, such as a weapon wound, open fracture, burn, or even small wounds like a thorn prick or a rusty nail puncture, can potentially lead to tetanus. Tetanus can also occur in newborns with unsterilized umbilical cord stumps and in cases of improperly sterilized artificial late abortions; it may occasionally occur after gastrointestinal surgery or the removal of foreign bodies that have been left in the body for many years. The presence of tetanus bacilli in a wound does not necessarily lead to illness; the occurrence of tetanus is related not only to the virulence and quantity of the bacteria or the lack of immunity but also to local hypoxia in the wound, which is a favorable factor for the disease. Therefore, tetanus is more likely to occur when the wound is narrow and deep, ischemic, has a lot of necrotic tissue, poor drainage, and is contaminated. Calcium chloride in the soil can cause tissue necrosis by promoting local hypoxia in the wound due to other pyogenic infections that require oxygen, which is conducive to the proliferation of anaerobic bacteria. Hence, puncture wounds from rusty nails or thorns contaminated with soil are more likely to cause tetanus.
The tetanus bacterium only needs to grow and reproduce locally in the wound, and the exotoxin it produces is the cause of tetanus. The exotoxins include tetanospasmin and tetanolysin. The former is the main toxin causing symptoms, with a special affinity for nerves, leading to muscle spasms; the latter can cause local tissue necrosis and myocardial damage. The tetanospasmin toxin reaches the anterior horn gray matter of the spinal cord or the motor nuclei of the brainstem through the bloodstream and lymphatic system, attaching to serum globulins. Once in the central nervous system, the toxin primarily binds to gangliosides on the synaptic vesicle membranes in the gray matter, preventing the release of inhibitory neurotransmitters (glycine or GABA), resulting in the loss of normal inhibitory function in the α-motor system, causing characteristic tonic contractions or paroxysmal spasms of the skeletal muscles. The toxin can also affect the sympathetic nervous system, leading to profuse sweating, unstable blood pressure, and increased heart rate. Therefore, tetanus is a form of toxemia.
bubble_chart Clinical Manifestations
The incubation period of tetanus averages 6 to 10 days, but it can be as short as less than 24 hours or as long as 20 to 30 days, or even several months. In some cases, tetanus may only occur after the removal of foreign objects that have been retained in the body for many years, such as bullet heads or shrapnel. Neonatal tetanus usually occurs about 7 days after the umbilical cord is cut, hence it is commonly referred to as "seven-day convulsion (neonatal tetanus)." Generally, the shorter the incubation period or the duration of prodromal symptoms, the more severe the symptoms and the higher the mortality rate.
Patients initially experience prodromal symptoms such as lack of strength, dizziness, headache, tension and soreness in the masseter muscles, dysphoria, restlessness, and yawning. These prodromal symptoms typically last 12 to 24 hours, followed by the onset of typical intense muscle contractions, starting with the masseter muscles, then sequentially affecting the facial muscles, neck muscles, back and abdominal muscles, limb muscles, diaphragm, and intercostal muscles. Patients begin to experience difficulty chewing and opening their mouths, followed by lockjaw; the facial muscles undergo paroxysmal spasms, giving the patient a distinctive "sardonic smile" expression. When the neck muscles spasm, neck stiffness occurs, with the head slightly tilted backward, making nodding impossible. The back and abdominal muscles contract simultaneously, but the back muscles are stronger, causing the lower back to arch, the head and feet to bend backward, forming a "opisthotonos" posture. When the limb muscles contract, due to the stronger flexor muscles compared to the extensor muscles, the limbs may exhibit flexion of the knees, elbows, and semi-clenched fists. On the basis of sustained tension and contraction, any slight stimulus, such as light, sound, vibration, or touching the patient's body, can induce spasms and convulsions in the entire muscle group. Each episode lasts from a few seconds to several minutes, during which the patient's complexion turns cyanotic, breathing becomes rapid, frothing at the mouth, drooling, teeth grinding, frequent backward tilting of the head, continuous limb spasms, and profuse sweating, causing extreme suffering. During the intervals between episodes, the pain slightly subsides, but the muscles still cannot fully relax. Intense muscle spasms can sometimes cause muscle rupture or even fractures. Spasms of the bladder sphincter can also cause urinary retention. Persistent spasms of the respiratory muscles and diaphragm can lead to respiratory arrest, resulting in the patient's death. Throughout the disease, the patient remains conscious and generally does not have a high fever. The appearance of a high fever often indicates the onset of pneumonia. The course of the disease generally lasts 3 to 4 weeks. After the second week, as the disease progresses, the symptoms gradually lessen. However, for a considerable period after recovery, some muscle groups may still exhibit tension and hyperreflexia.
Based on the injury history and clinical manifestations, a diagnosis can generally be made promptly. However, for patients with only certain prodromal symptoms, the diagnosis becomes more challenging, requiring heightened vigilance and close observation of the condition to avoid delayed diagnosis.
bubble_chart Treatment Measures
Tetanus is an extremely serious disease, and active comprehensive treatment measures should be taken, including eliminating the source of toxins, neutralizing free toxins, controlling and relieving spasms, maintaining airway patency, and preventing complications. The disability rate of tetanus is about 10%.
(1) Eliminating the source of toxins (wound management) For those with wounds, thorough debridement should be performed under the control of spasms. After removing necrotic tissue and foreign bodies, the wound should be left open to facilitate drainage, and washed with 3% hydrogen peroxide or 1:1000 potassium permanganate solution, and frequently wet-dressed. If the original wound has healed at the onset of the disease, debridement is generally not required.
(2) Using tetanus antitoxin to neutralize free toxins Since neither tetanus antitoxin nor human tetanus immunoglobulin can neutralize toxins already bound to nerve tissue, they should be used as early as possible to neutralize free toxins. Generally, 20,000 to 50,000 IU of antitoxin is added to 500 to 1000 ml of 5% glucose solution and slowly dripped intravenously: the dose should not be too large to avoid causing serum reactions. For patients with insufficient debridement and severe patients, an additional 10,000 to 20,000 IU of antitoxin is administered daily by intramuscular injection or intravenous drip for 3 to 5 days. Neonatal tetanus can be treated with 20,000 IU of antitoxin by intravenous drip, and umbilical injection can also be performed. There is also a treatment method of injecting 5000 to 1000 IU of antitoxin into the subarachnoid space, which is believed to allow the antitoxin to directly enter the brain tissue, with better effects, and systemic application of antitoxin can be avoided. If prednisolone 12.5 mg is added at the same time, it can reduce the inflammation and edema reactions caused by this injection.
(3) Controlling and relieving spasms Patients should be housed in single rooms, and the environment should be as quiet as possible to prevent light and sound stimulation. Attention should be paid to preventing bedsores. Controlling and relieving spasms is a very important part of the treatment process. If done well, it can largely prevent asphyxia and lung infections, reducing mortality.
1. For patients with milder conditions, sedatives and hypnotics can be used to reduce the patient's sensitivity to external stimuli. However, large doses should be avoided to prevent deep unconsciousness. Diazepam (5 mg orally, 10 mg intravenously, 3 to 4 times daily) is effective in controlling and relieving spasms. Sodium barbital (0.1 to 0.2 g, intramuscular injection) or 10% chloral hydrate (15 ml orally or 20 to 40 ml rectal infusion, 3 times daily) can also be used.
2. For patients with more severe conditions, chlorpromazine 50 to 100 mg can be added to 250 ml of 5% glucose solution and slowly dripped intravenously, 4 times daily.
3. For patients with severe spasms, even unable to undergo treatment and nursing, thiopental sodium 0.5 g can be used for intramuscular injection (be alert for laryngeal spasm, safer for patients who have undergone tracheotomy), paraldehyde 2 to 4 ml, intramuscular injection (paraldehyde has the side effect of stimulating the respiratory tract, not suitable for patients with lung infections), or muscle relaxants, such as amber chloride, tubocurarine chloride, triiodothyronine phenol, and aminocarbachol (used under the condition of tracheotomy and controlled respiration). If complicated by high fever and unconsciousness, corticosteroids can be added: prednisone 30 mg orally or hydrocortisone 200 to 400 mg, intravenous drip, once daily.
(4) Prevention and Treatment of Complications: Replenish water and electrolytes to correct the metabolic disturbances of water and electrolytes caused by severe muscle spasms, sweating, and inability to eat, such as dehydration and acidosis. For patients with milder symptoms, efforts should be made to encourage them to eat during the intervals between spasms. For patients with severe symptoms who cannot or refuse to eat, a gastric tube should be placed for tube feeding under the control of antispasmodic drugs or after a tracheotomy. Total parenteral nutrition can also be administered.
Penicillin (800,000 to 1,000,000 units, intramuscular injection, every 4 to 6 hours) can inhibit tetanus bacilli and help prevent other infections, and should be used early. Metronidazole 500 mg orally every 6 hours or 1 g rectally every 8 hours for 7 to 10 days can also be administered. According to literature reports, metronidazole is more effective than penicillin for tetanus. In addition, the airway should be kept clear, and for patients with frequent spasms that are difficult to control with medication, early tracheostomy should be performed; a suction device, ventilator, and oxygen should be available at the bedside for emergency use.
Tetanus is preventable, and the most reliable method of prevention is the injection of tetanus toxoid. Through the injection of toxoid, antibodies are produced in the human body and maintained at a certain concentration for a long period of time, which can neutralize the tetanus toxin entering the body and prevent the disease. Strengthening labor protection in industrial and agricultural production, avoiding trauma, popularizing new methods of childbirth, and correctly and timely handling wounds are also important preventive measures.
Even if the wound is severe, only 0.5ml of toxoid needs to be injected; if the wound is heavily contaminated, then 0.5ml of toxoid is injected, and 3 to 4 hours later, 250 to 500U of human tetanus immunoglobulin is injected intramuscularly at another site, allowing the antitoxin to neutralize the toxin first. The active immunity stimulated by the toxoid can exert its preventive effect before and after the antitoxin effect disappears.
2. Correctly handle wounds, timely and thorough debridement All wounds should be debrided. For heavily contaminated wounds, especially war wounds, all necrotic and non-viable tissues should be excised, foreign bodies removed, dead spaces incised, wounds opened, and fully drained without suturing. If it is found that the disinfection during childbirth is not strict, the umbilical area should be washed with 3% hydrogen peroxide solution, and then disinfected with iodine tincture.
3. Passive immunization Generally applicable to those who have not been injected with toxoid before and have one of the following conditions: ① obviously contaminated wounds; ② deep puncture wounds; ③ severe open injuries, such as open craniocerebral injury, open fracture, burns; ④ wounds that have not been debrided or improperly treated in time; ⑤ before surgery for some old wounds (such as foreign body removal).
The currently used passive immunization method is the injection of tetanus antitoxin (TAT) refined from animal (bovine or equine) serum. It is a heterologous protein, has antigenicity, can cause allergic reactions, and does not stay in the human body for a long time, being removed by the human body after 6 days. Therefore, this tetanus antitoxin is not ideal. The ideal product is human tetanus immunoglobulin, which has no allergic reactions, can stay in the human body for 4 to 5 weeks after a single injection, and has an immune effect more than 10 times that of tetanus toxin. Its preventive dose is 250 to 500U, intramuscular injection. Human tetanus immunoglobulin is less available, complex to prepare, and under the current circumstances where it cannot be widely used, the injection of tetanus antitoxin is still a major passive immunization method.
As soon as possible after injury, inject 1,500IU (1ml) of tetanus antibiotic intramuscularly. For heavily contaminated wounds or injuries that have been more than 12 hours, the dose can be doubled. The dose is the same for adults and children. If necessary, another injection can be given after 2 to 3 days.
Before each injection of antitoxin, inquire about any history of allergies and perform an intradermal allergy test: use 0.1ml of antitoxin, dilute with isotonic saline to 1ml. Inject 0.1ml of the diluted solution intradermally on the flexor surface of the forearm; on the same site of the contralateral forearm, use isotonic saline to observe for erythema, slight swelling, and induration, which indicates a positive reaction, and desensitization injection should be performed. However, this method cannot completely avoid the occurrence of allergic reactions, so it is best not to use this antitoxin for injection. Desensitization injection is to dilute 1ml of antitoxin with isotonic saline 10 times, divided into 1, 2, 3, 4ml, and injected subcutaneously in sequence every half hour. After each injection, observe for any reactions. If the patient develops pallor, weakness, urticaria or skin itching, sneezing, cough, joint pain, or even shock, immediately inject 50mg of Ephedrine or 1mg of adrenaline (adult dose) subcutaneously, and stop the antitoxin injection.
In addition to the aforementioned fractures, urinary retention, and respiratory arrest, the following complications may also occur: ① Asphyxia: Caused by persistent spasms of the larynx and respiratory muscles, as well as mucus blocking the trachea. ② Pulmonary infection: Laryngeal spasms, obstructed airways, accumulation of bronchial secretions, and inability to frequently change positions are all causes of pneumonia and atelectasis. ③ Acidosis: Respiratory acidosis due to poor breathing and insufficient gas exchange. Intense muscle contractions and incomplete fat breakdown after fasting increase acidic metabolic products, leading to metabolic acidosis. ④ Circulatory failure: Due to hypoxia and poisoning, tachycardia may occur, and prolonged conditions can lead to heart failure, even shock or cardiac arrest. These complications are often significant causes of patient mortality and should be actively prevented and treated.
1. Purulent meningitis, although presenting with symptoms such as "opisthotonos" and neck stiffness, does not exhibit paroxysmal spasms. The patient experiences severe headache, high fever, projectile vomiting, and sometimes altered consciousness. Cerebrospinal fluid examination shows increased pressure and elevated white blood cell count.
2. Rabies has a history of being bitten by a rabid dog or cat, primarily involving spasms of the swallowing muscles. The pharyngeal muscles have increased irritability; the patient immediately experiences spasms upon hearing or seeing water, severe pain, inability to swallow water, and excessive salivation.
3. Others such as temporomandibular arthritis, eclampsia, hysteria, etc. {|102|}
