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Препараты выбора при лечении столбняка








Столбняк (Tetanus) у новорожденного ребенка:
наблюдение из Лаоса

Автор Дата постинга
Oleg Blinnikov 15 май 2003 07:30

 Приветствую всех участников нового педиатрического форума.
Меня зовут Олег Игоревич Блинников.
Работаю я в отдаленной больнице в Лаосе земским врачом, выполняя работу хирурга, акушера, гинеколога, педиатра и так далее... Буду очень рад обсуждать трудные случаи в новом форуме… особенно рад получить ценный совет коллег. Для пробы коммуникаций посылаю фотографию новоржденного со столбняком… к сожалению ребенок погиб. Если у кого либо есть опыт лечения столбняка у новорожденных в условиях сельской больницы буду признателен за совет…

Victor S.Dovgan 15 май 2003 17:45

  Олег Игоревич — боюсь, что Вы единственный человек на форуме, способный рассказать об этой хвори. У интенсивистов проходила дискуссия по поводу лечения столбняка, но большого и живого отклика не получилось — болезнь в северных широтах редкая. http://www.medico.ru/discussion/intencive/int_001.htm
Поэтому у меня к Вам несколько вопросов:
Каковы пути заражения? (понятно, что, вероятнее, через пупочную ранку, но причина?..)
Где и как лечили?
И последнее: какое здравоохранение в Лаосе?
У меня, к сожалению, все знания об этой стране ограничиваются парой голливудских киношек, в которых бравые американские парни в погоне за вьетконговцами попадают в Лаос (джунгли и джунгли), а потому сильно нервничают. :-)

Oleg Fadeev 15 май 2003 19:50

  подвиг… натурально — подвиг. Ни разу не видел ребенка с клиникой столбняка.

Oleg Blinnikov 15 май 2003 20:10

 Уважаемый Виктор С. (извините. не знаю вашего отчества)
Я прочитал дискуссию… спасибо…
Добавлю из своего опыта… к нам поступил однажды 8 летний мальчишка с генерализованной формой столбняка. Входные ворота — небольшая старая рана на стопе… фотография пациента в приложении…
Лечение: противостолбнячная лошадиная сыворотка 1500 ед вм. Диазепам и Пенициллин… судороги удавалось купировать диазепамом и необходимости в экстренной интубации мы не видели. Тем не менее, нам известны рекомендации о ранней трахеостомии и продленной ИВЛ у таких больных… в связи с частым развитием пневмонии сильно отягощающей течение болезни… в этой связи мы перевели ребенка в центральную больницу… мне удалось проследить судьбу мальчика… в столичной больнице свободного аппарата для ИВЛ не оказалось и больного вели просто на Диазепаме и Пенициллине… видимо был обеспечен хороший сестринский уход… и удалось избежать осложнений, судорги стали реже и менее длительные, через месяц ребенок мог уже стоять и потихоньку ходить…
столбняк/tetanus

Первый день болезни.

столбняк/tetanus

Две недели спустя.

столбняк/tetanus

Через месяц от начала болезни.


У меня есть небольшая лекция на английском, которую я просто составил из наиболее интересных публикаций путем copy and paste, могу выслать при желании; насколько я понимаю, даже введение сыворотки играет относительную роль, так как связывает только еще циркулирующие токсины, но больной уже поступает с достаточно выраженной клиникой и эффект от сыворотки ограничен… человеческая сывооротка менее опасна в плане аллергии. Антибиотики играют так же условную роль… главная цель их применения — профилактика возможных осложнений… обработка раны имеет значение если она (рана) есть… у этого мальчика рана почти зажила, а у новорожденных пуповина так же выглядит не настолько измененной, чтобы проводить какие-либо хирургические манипуляции… столбняк у рожениц не есть противопоказание для гистеректомии. Главная задача — обеспечить хорошую релаксацию, адекватную вентиляцию… контроль вегетативных нарушений (Sympathetic overactivity) … тшательный сестринский уход (протокол у меня есть на английском)


>Поэтому у меня к Вам несколько вопросов:
>Каковы пути заражения? (понятно, что, вероятнее, через пупочную ранку,
>но причина?..)
================
Здесь в Лаосе в деревнях существует традиция, согласно которой роды должен принимать муж... естественно дома... при помощи родственников... повивальные бабки есть, но редко... я ездил по деревням и брал интервью у женщин и мужщин... пуповина пересекается остро заточенной бамбуковой палочкой...при этом пуповина, чтобы не скользила, кладется на древесный уголь.... никакие антисептики не используются...руки не моются... климат влажный .. дома на сваях..под домом живут домашние животные...свиньи коровы и так далее... пришлю как нибудь картинку... короче идеальная среда для столбняка... >Где и как лечили?
>И последнее: какое здравоохранение в Лаосе?

================
С удовольствием расскажу и об этом... что собственно будет видно по ходу обсуждения разных случаев которыми я хотел бы с вами поделиться

Смагин Александр 15 май 2003 20:00

  Олег Игоревич, здравствуйте! Я Смагин Александр, врач неонатолог-реаниматолог Омского перинатального центра. Меня очень затронуло ваше сообщение. Я работаю с новорожденными уже более 15 лет, но не то что у них, вообще столбняка живьем не видел.
Меня тоже заинтересовал путь заражения. Просто из любопытства - это же казуистика, такой случай описывать нужно в центральных журналах! Буду рад пообщаться, всегда преклонялся перед ЗЕМСКИМИ ВРАЧАМИ. Мечта с детства после Булгакова и Чехова, но увы...

Oleg Blinnikov 15 май 2003 20:15

 Коллеги...
в приложении небольшой обзор о котором я упоминал в предыдущем
письме... у меня есть коллекция полных текстов статей... некоторые
из них будут интересны интенсивистам...

 

 Tetanus.

 

1. The nature and magnitude of the problem Tetanus is an acute disease induced by an exotoxin of the tetanus bacillus, which grows anaerobically at the site of an injury. Occurrence is worldwide, but is most frequently encountered in densely populated regions in hot, damp climates with soil rich in organic matter. The true incidence of tetanus is not known, but is estimated to be between 500,000 to one million cases per year worldwide. The majority of cases occur in developing countries, with 50% of those cases occurring in neonates. The survey (November 2001) of National Statistical Center confirmed the assumption that neonatal tetanus is a major public health problem in the Lao People's Democratic Republic and showed an estimated neonatal tetanus mortality rate of between 8 and 10 per 1000 live births. This is partly because the coverage of antenatal care is very low and only 31% of pregnant women are immunized with tetanus toxoid, and partly because trained personnel assist fewer than 10% of deliveries. Based on these findings a national plan of action was developed towards maternal and neonatal tetanus elimination by 2005.
2. Infectious agent C. tetani is a slender, gram-positive, anaerobic rod that may develop a terminal spore, giving it a drumstick appearance. The organism is sensitive to heat and cannot survive in the presence of oxygen. The spores, in contrast, are very resistant to heat and the usual antiseptics. They can survive autoclaving at 121°C for 10-15 minutes. The spores are also relatively resistant to phenol and other chemical agents. The spores are widely distributed in soil and in the intestine and feces of horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. Manure-treated soil may contain large numbers of spores. In agricultural areas, a significant number of human adults may harbor the organism. The spores can also be found on skin surfaces and in contaminated heroin. There is no laboratory findings characteristic of tetanus. The diagnosis is entirely clinical and does not depend upon bacteriologic confirmation. C. tetani is recovered from the wound in only 30% of cases, and can be isolated from patients who do not have tetanus. Laboratory identification of the organism depends most importantly on the demonstration of toxin production in mice.
3. Reservoir Organisms are found primarily in the soil and intestinal tracts of animals and humans.
4. Mode of transmission
Transmission is primarily by contaminated wounds (apparent and inapparent). The wound may be major or minor. In recent years, however, a higher proportion of cases had minor wounds, probably because severe wounds are more likely to be properly managed. Tetanus may follow elective surgery, burns, deep puncture wounds, crush wounds, otitis media (ear infections), dental infection, animal bites, abortion, and pregnancy. In a few cases the portal of entry is either trivial e.g. rose thorn in the finger. Tetanus, however, does not occur only in classic "puncture" wounds. Between 1991 and 1994, no portal of entry was detected in 22% of the cases reported to the CDC (5). Therefore, relying on "proper wound management" alone will not effectively eliminate tetanus in adults. Patients of all ages must continue to be adequately immunized.
5. Incubation period
The incubation period, which is the time between the introduction of spores in the body and the first clinical symptoms, varies from 1 day to several months (usually 3-21 days). Most cases occur within 14 days. The duration of incubation, as well as the interval between first symptoms and generalized spasms (the period of onset), determine the severity of the disease and therefore the prognosis. In general, the shorter the period from injury to onset of symptoms and the shorter the time interval between symptoms and spasms, the more severe the tetanus will be.
6. Period of communicability
Tetanus is not contagious from person to person. It is the only vaccine-preventable disease that is infectious, but not contagious.
7. Susceptibility and resistance Susceptibility is general. Active immunity is induced by tetanus toxoid and persists at least 10 years after full immunization. Infants of actively immunized mothers acquire passive immunity that protects them from neonatal tetanus. Recovery from tetanus may not result in immunity; second attacks can occur. Primary immunization is indicated after recovery. The disease normally affects unimmunised or partially immunized people, and risk increases with age. Titres of antibodies to tetanus are inadequate to ensure protection in 50% of people older than 65 years. Whenever a previously-immunized individual sustains a potentially dangerous wound, a booster of toxoid should be injected.
8. Epidemics
In rare instances, outbreaks of tetanus among injecting drug users have occurred.
9. Pathogenesis
C. tetani usually enters the body through a wound. In the presence of anaerobic (low oxygen) conditions, the spores germinate. The toxin is produced during cell growth, sporulation and lysis. It migrates along neural paths from a local wound to sites of action in the central nervous system. Part of toxins, including tetanospasmin, is disseminated via blood and lymphatics. Toxins act at several sites within the central nervous system, including peripheral motor end plates, spinal cord, brain, and sympathetic nervous system. Tetanus toxin interferes with release of neurotransmitters, blocking inhibitor impulses. This leads to unopposed muscle contraction and spasm. Seizures may occur, and the autonomic nervous system may also be affected. Incubation may vary from as short as 24 h to as long as many months. This interval may be a reflection of the distance the toxin must travel within the nervous system and the quantity of toxin released. Tetanus toxin is one of the three most poisonous substances known, the other two being the toxins of botulism and diphtheria. Tetanus toxin is produced in vitro in amounts up to 5 to 10% of the bacterial weight. Because the toxin has a specific affinity for nervous tissue, it is referred to as a neurotoxin. The toxin has no known useful function to C. tetani. Why the toxin has a specific action on nervous tissue, to which the organism naturally has no access, may be an anomaly of nature.
10. Clinical features
Rapid case identification of tetanus is important clinically because hospitalization may be required.
Case definition: Acute onset of hypertonia and/or painful muscular contractions (usually of the muscles of the jaw and neck) and generalized muscle spasms without other apparent medical cause. Tetanus may be localized at the site of injury resulting in local pain and rigidity often with a low mortality. When local tetanus follows head, facial injuries or chronic otitis media, cephalic tetanus can occur which is a local variant (often involving cranial nerves particularly the seventh cranial nerve) but has a higher mortality. Both of these may progress to the more common generalized form, which may present with pain, stiffness, rigidity, trismus (rigidity of the masseter muscles), dysphagia, opisthotonus and spasms. The clinical pattern of generalized tetanus consists of severe painful spasms and rigidity of the voluntary muscles. The characteristic symptom of "lockjaw" involves spasms of the masseter muscle. It is an early symptom, which is followed by progressive rigidity and violent spasms of the trunk and limb muscles. Spasms of the pharyngeal muscles cause difficulty in swallowing. Death usually results from interference with the mechanics of respiration. On the basis of clinical findings, different forms of tetanus have been described. Generalized tetanus is the most common type (about 80%) of reported tetanus. The disease usually presents with a descending pattern. The first sign is trismus or lockjaw, followed by stiffness of the neck, difficulty in swallowing (spasms of the pharyngeal muscles), and rigidity of abdominal muscles. Other symptoms include a temperature rise of 2°-4°C above normal, sweating, elevated blood pressure, and episodic rapid heart rate. Spasms may occur frequently and last for several minutes. Spasms are usually worst during the first 2 weeks with autonomic instability following some days after the onset of spasms and often peaking during the second week of the disease. Rigidity may continue after the spasms and autonomic disturbances have started to improve. Spasms continue for 3-4 weeks. Complete recovery may take months. Local tetanus is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury. These contractions may persist for many weeks before gradually subsiding. Local tetanus may precede the onset of generalized tetanus, but is generally milder. Only about 1% of cases are fatal. Cephalic tetanus is a rare form of the disease, occasionally occurring with otitis media (ear infections) in which C. tetani is present in the flora of the middle ear, or following injuries to the head. There is involvement of the cranial nerves, especially in the facial area. Neonatal tetanus is a form of generalized tetanus that occurs in newborn infants. It develops in children born to inadequately immunized mothers, frequently after unsterile treatment of the umbilical cord or its stump. Neonatal tetanus is common in some developing countries (estimated >270,000 deaths worldwide per year). Maternal tetanus defined as tetanus occurring during pregnancy or within 6 weeks after any type of pregnancy termination. It includes postpartum or puerperal tetanus resulting from septic procedures during delivery, postabortal tetanus resulting from septic abortion and tetanus incidental to pregnancy, resulting from any type of wound during pregnancy.
12. Complications.5 Laryngospasm (spasm of the vocal cords) and/or spasm of the muscles of respiration leads to interference with breathing. Aspiration pneumonia is a common late complication of tetanus, found in 50%-70% of autopsied cases. Fractures of the spine or long bones may result from sustained contractions and convulsions. Hyperactivity of the autonomic nervous system may lead to hypertension and/or an abnormal heart rhythm. Nosocomial infections are common because of prolonged hospitalization. Secondary infections may include sepsis from indwelling catheters, hospital-acquired pneumonias, and decubitus ulcers. Pulmonary embolism is particularly a problem in drug users and elderly patients. Death. In recent years, tetanus has been fatal in approximately 11% of reported cases. Mortality of this condition is usually due to autonomic dysfunction or nosocomial infections especially pneumonias. Cases most likely to be fatal are those occurring in persons age >60 years (18%, and unvaccinated persons (22%). In about 20% of tetanus deaths, no obvious pathology is identified and death is attributed to the direct effects of tetanus toxin. The reduction in mortality over the last three decades is due largely to the use of exceptionally heavy sedation rather than to muscle paralysis to control the spasms and prevent lifethreatening effects of autonomic overactivity. The reduction in mortality has also been achieved by attention to detail and the improved care of long-term ITU patients. There is huge discrepancy between the incidence and related morbidity and mortality between the developed and developing world with over 400 000 neonatal deaths a year. 13. Differential diagnosis The differential diagnosis includes dystonic drug reactions, meningitis/encephalitis, rabies, tetany, strychnine poisoning, facial pathology (jaw stiffness, dental abscess). In neonates, one also has to exclude hypocalcaemia, hypoglycaemia, meningitis and meningoencephalitis, seizures due to other aetiologies. 5

14. Clinical assessment
Classification of grades of severity of tetanus
Mild The mild forms had long incubation periods and trismus (lockjaw), neck stiffness and risus sardonicus were the only symptoms. There were no convulsions and no general toxic disturbances such as hyperpyrexia. The prognosis was generally good with no case fatality Moderate Moderate forms are characterized by generalized spasmodic contractions with opisthotonos, but they are only provoked by external stimuli such as skin punctures, nasopharyngeal suction, loud noise or intense light. There is abdominal pain and backache, but no fever. The prognosis is less good. Severe In the severe forms, with short incubation periods, generalized convulsions are spontaneous and long-lasting, with frequent episodes of apnea, cyanosis and asphyxia. There are central nervous system disturbances such as hyperpyrexia, tachycardia or cardiac arrest. Even with specialized intensive care including respiratory assistance, the prognosis is extremely poor.
15. Case management
The goals of therapy are to eliminate the source of toxin, neutralize unbound toxin, prevent muscle spasm, and provide support, especially respiratory support until recovery. Prompt administration of TT and TIG may decrease the severity of the disease. Maintenance of the airway The critical factor in patients with tetanus is to maintain a patent airway. Laryngospasm occurs commonly as part of generalized spasms and can often be precipitated by oral secretions or manipulations. Due to the inability to swallow, secretions are a problem and patients are unable to clear them adequately. These can lead to laryngospasm. Fatal laryngospasm has been recorded before any generalized muscular spasm has occurred. When the patient develops spasms, which are not controlled by a small dose of diazepam and dysphagia is present, they should have the airway protected by intubation and early tracheostomy due to the predictable long course of these patients. It is important to intubate early rather than take the chance of the patient developing laryngospasm. Due to the tendency to laryngospasm on any stimulation these patients should never be intubated without sedation and a muscle relaxant (general anaesthesia). The trismus always relaxes with succinylcholine which is useable at this stage, but not later, once prolonged disuse has taken place. Sympathetic overactivity Sympathetic overactivity remains the major cause of death in patients with tetanus once the early deaths from airway obstruction and the deaths from respiratory failure have been eliminated. The syndrome of sympathetic overactivity results in a tachycardia (or occasionally a profound bradycardia), marked fluctuation in blood pressure (both hypotension and hypertension), excessive salivation and sweating. This fluid loss may result in large fluid losses and clinically significant dehydration. The effect on the heart can give rise to cardiomyopathy, ECG changes, dysrrythmias and myocardial infarction. Basal catecholamine concentrations may be increased 10-fold with greater increase in sympathetic neuronal activity compared with adrenal medullary activity (noradrenaline more marked than adrenaline). That is why treatment by paralysis alone is not logical as this treats only the somatic system and leaves sympathetic stimulation untreated. If one uses large doses of hypnotics sufficient to cause general anaesthesia, both the somatic and sympathetic nervous system will be inhibited centrally.
16. Treatment
I. Supportive Tracheostomy
A tracheostomy should be done under general anaesthesia in an operating theatre. Although percutaneous tracheostomy is now a routine technique in many intensive care units and may have certain advantages, it may not be available in developing countries. Deep venous thrombosis prophylaxis This is important as thromboembolic complications are an important cause of mortality due to prolonged immobility, dehydration and sympathetic overdrive. Subcutaneous heparin 5000 IU 8-hourly and graded stockings are recommended. intravenous injection of diazepam or might need to be paralysed to enable adequate physiotherapy. However, regular tracheal suctioning is essential to prevent atelectasis, lobar collapse and pneumonia. Immobility considerations are important and passive range-of motion exercises must be instituted to maintain muscle strength and prevent deformities and contractures. Splints may be required. Physiotherapy and occupational therapy would also be required during the rehabilitation phase. Ventilation Many patients with the generalized form of tetanus will require intubation and ventilation both for airway protection and respiratory support particularly if their forced vital capacity is less than 1200 ml (normal 4000 - 5000 ml) and their peak negative inspiratory pressure is less than 35 cm H2O (normal 75 to 100 cm H2O). Patients should all receive intermittent positive pressure ventilation (IPPV) with at least 5 cm H2O of positive end expiratory pressure (PEEP) provided there is no contraindication to PEEP. In the later stages of the disease other modes of ventilation may be introduced to allow an appropriate component of spontaneous ventilation (synchronized intermittent mandatory, continuous positive airway pressure or biphasic positive airway pressure ventilation). This allows reduction of sedation (if the primary pathology is improving), may minimize muscle wastage and may reduce the likelihood of critical illness neuropathies or myopathies. Physiotherapy and occupational therapy These patients need regular chest physiotherapy and often require a bronchodilator in the nebulizer. Due to the excessive secretions, both oral and bronchial, they are particularly prone to develop nosocomial pneumonias and areas of atelectasis. It is important to try and reduce the amount of secretions, which accumulate between the vocal cords and the tracheostomy cuff as this may predispose to lower respiratory infection due to microaspiration (continuous 'vocal aid' suctioning may help in this regard). Patients might require an additional intravenous injection of diazepam or might need to be paralysed to enable adequate physiotherapy. However, regular tracheal suctioning is essential to prevent atelectasis, lobar collapse and pneumonia. Immobility considerations are important and passive range-ofmotion exercises must be instituted to maintain muscle strength and prevent deformities and contractures. Splints may be required. Physiotherapy and occupational therapy would also be required during the rehabilitation phase. Intravenous lines A central line inserted under aseptic techniques must be used because of the intravenous penicillin (although there is a shift away from the use of penicillin to other antibiotics as will be mentioned later), which is usually given for the first 10 days. As soon as this line is no longer needed it should be removed, as it is just another source of infection. Try not to have any intravenous lines once the autonomic instability and spasms are well controlled on nasogastric tube medication. Fluid balance This is important due to increased losses from sweating, salivation and GIT losses. Being fluid replete may help to manage the autonomic instability. Acute renal failure is fairly common in generalized tetanus and may be due to the fluid shifts, cardiovascular instability and rhabdomyolysis. Feeding A nasogastric tube (NGT) should be passed on admission and can be used immediately for drugs provided there is no ileus and nasogastric feeds can be commenced as soon as possible. The regular tube feeds with additional supplementation with vitamins and trace elements must be given. The daily caloric requirements in well-controlled tetanus will be within 15% of the predicted requirements. Early enteral feed is recommended. If this is not possible then total parenteral nutrition should be commenced early. Some units would advocate prophylaxis for stress ulcers if the patient is not being fed enterally and this may be appropriate during the period of high sympathetic outflow. Expert nursing care A few points in the nursing care should be carefully verified:
(a) Meticulous tracheostomy care using low-pressure cuff tracheostomy tubes to try and prevent tracheal stenosis. These must be inflated correctly against a manometer.
(b) Tracheostomy securing tapes to be tied tightly with a 2-finger space only.
(c) The patient who is unable to breathe on his/her own, either because of heavy sedation or if he/she is paralysed, must have someone specialling him/her continuously.
(d) Use a constant-volume ventilator with all alarms correctly set.
(e) Meticulous care of pressure areas to prevent the development of bedsores.
(f) Routine oropharyngeal care (regular suctioning, dental suction, 'vocal-aid' suctioning).
(g) Routine ocular care (all heavily sedated patients).
(h) Pay particular attention to drip sites, tracheostome, urinary catheter and nasogastric tube to minimize the incidence of infection. The condition and the treatment may immunosuppress these patients making them more prone to infection. Strict aseptic technique and constant nursing surveillance to recognize life-threatening situations early are essential.
(i) Slight external stimuli such as noise or tactile stimulation can trigger muscle spasms and autonomic instability. The environment therefore needs to be kept as quiet and dark as possible. The nurses can co-ordinate care and contact activities by personnel from all disciplines in an effort to decrease incidence of stimulation and maintain a calm environment.
(j) Psychological care for both the patient and relatives is important and may best be co-ordinated and addressed by the nursing team who spend the most time with the patient and family. They may then bring it to the attention of the rest of the multidisciplinary team.
(k) The clinical course of tetanus is often unpredictable (particularly if there are associated complications of prolonged critical illness including ventilator associated pneumonias, generalized sepsis, gastrointestinal haemorrhage, thromboembolic complications). All these patients should therefore be closely monitored throughout their illness and for a period of recuperation thereafter. After the initial airway and autonomic problems it is often the level of nursing care of these long-term patients which dictates the morbidity and mortality.
II. Specific Surgical debridement
The patient should be carefully examined for a wound. Early surgical debridement is an essential part of the therapy as this obligate anaerobe requires devitalized tissue, which is potentiated by the production of Tetanolysin, a substance which disrupts cell membranes damaging viable tissue. It should include wide excision of the site of infection under general anaesthesia. It can be done under general anaesthesia at the same time as the tracheostomy. If the tetanus progresses (worsening autonomic instability and spasms) for more than 5-10 days following institution of adequate therapy, further exploration and debridement of the original wound should be undertaken as foreign bodies may frequently be missed on initial exploration.
III. Facilitative Heavy sedation Diazepam is the mainstay of the hypnotic drugs. It has a wide margin of safety, can be given orally (via a nasogastric tube), rectally or intravenously and is a sedative, anticonvulsant and a muscle relaxant. It is also cheap and available in most parts of the world. It does have a long cumulative half-life and has active metabolites. Initially, it can be given intravenously in 10 mg increments until the patient is stabilized. In patients with severe tetanus an infusion of thiopentone sodium may be necessary in addition to the diazepam to achieve adequate control. As soon as the patient can receive oral medications via a nasogastric tube diazepam should be given orally as should all the other drugs. Diazepam is then given as required and doses greater than 1 g/day may be necessary. It is initially started in a dosage schedule of approximately 20 mg 4}6-hourly and if this is insufficient the time interval between doses is reduced until the patient is receiving diazepam in doses that may exceed 100 mg 2-hourly. At this stage, if further sedation is still necessary, the dose of diazepam can be further increased but barbiturates and/or a phenothiazine should be added in addition. Chlorpromazine is a useful sedative with alphaadrenergic and anticholinergic effects. Morphine may be a useful addition for its sedation properties, which may not compromise cardiac performance. However, the opioids may contribute towards unwanted gastrointestinal effects (e.g. gastroparesis, prolonged ileus or constipation) which one should try to avoid or may need further management should they occur. When necessary, we have given 240 mg phenobarbitone 8-hourly orally (alternatively up to 600 mg of amylobarbitone over 24 h), 1 g diazepam over 24 h orally and 150 lg clonidine 8-hourly orally. In addition, occasional thiopentone infusions have been necessary. It is important, however, to space the doses of different drugs and try to give one drug at a time to avoid hypotension. Dosage of hypnotics is obviously far in excess of what a normal patient would tolerate and important signs to watch for overdosage are hypothermia and hypotension. This occurs particularly when the effects of the tetanus are wearing off. With the institution of therapy, the clinical severity of the disease should not progress and its severity may then be assessed by the amount of sedative drugs required. The tetanus usually runs its self-limiting, natural course within 3}4 weeks and the sedatives are usually reduced at this time after which it may take a week or more for the patient to wake sufficiently to be considered for extubation. If the spasms or autonomic instability recur then the patient is resedated for a further week and then weaning is attempted again. Even with the long-acting benzodiazepines (diazepam), one should look for signs of withdrawal (more of a problem with the shorter-acting benzodiazepines like midazolam) and the dose may need to be reduced slowly. Muscle relaxants Muscle relaxants are now used only intermittently to control severe spasms or to enable adequate physiotherapy. They have no beneficial effect towards the autonomic instability and make it difficult to assess the signs of anaesthesia when the patient is paralysed. Muscle relaxants that may be used include pancuronium, vecuronium, rocuronium and atracurium. Pancuronium and atracurium may, however, reduce haemodynamic stability due to catecholamine effects or histamine release. It must be remembered that problems have been reported with the extended use of non- depolarizing muscle relaxants. Agents like dantrolene and baclofen have been used with varying success. Heavy sedation alone may provide adequate neuromuscular relaxation. Sedation with propofol may allow control of spasms and rigidity without additional relaxant with appropriate effects noted on EMG. With our heavy sedation regimen described above, we have also found little need for neuromuscular blocking agents. Management of autonomic disturbance Sedation, which is useful for controlling spasms and rigidity, is also the first step in reducing autonomic instability and is essential in the management of tetanus. If the resting heart rate is more than 120 beats/min with adequate sedation, propranolol may be given in a starting dose of 10 mg twice daily by mouth. Concerns about beta-blockade and sudden death have, however, been raised. The use of of alpha-blockade should be avoided because it complicates the management without adding any positive contribution to the therapy. Alpha-blocking agents may have a small role if a patient has an unopposed vasoconstrictor response to beta-blockade. Labetalol (combined alpha- and beta-blockade) or the use of the short-acting agent esmolol may have a role although it is expensive and does not decrease catecholamine levels. Other components of autonomic instability may be treated with magnesium, which is cheap and reduces both catecholamine release and receptor responsiveness with few side-effects in the ventilated patient. Magnesium sulphate should be given as a 5 g loading dose over 20 min and then followed by an infusion of between 2 and 3.5 g/h for up to 4 weeks in ventilated patients. Appropriate monitoring of both Mg2` and Ca2` levels is required.
17. Medication Anti-tetanus serum About 1500 - 6000 units of human tetanus immunoglobulin (HTIG) should be given intravenously. A dose of 500 units may be as effective as the larger doses. Should this not be available the patient should receive 40 000 units of antitetanus serum (horse) intramuscularly and 40 000 units intravenously following a test dose as there is a 20% incidence of anaphylactic reactions. If the patient reacts to the test dose the anti-tetanus serum can be skipped. The true value of this therapy has not been validated and the rapidity with which the tetanospasmin fixes irreversibly to neural tissue may limit its value. The benefit of intrathecal HTIG is, as yet, not confirmed. Antibiotics Patients should be treated with intravenous benzylpenicillin in a dosage of 1megaunit 6-hourly. Metronidazole 500 mg intravenously 8-hourly (or rectal after a few days) is a safe and adequate alternative and in a prospective, open, non-randomized clinical trial those patients who received metronidazole had a lower mortality and a shorter hospital stay. Erythromycin, tetracycline, vancomycin, clindamycin, doxycycline and chloramphenicol would be alternatives to penicillin and metronidazole if those were unavailable or unusable in individual patients. Patients who have tetanus often have a pyrexia which might be as high as 40 C and this may be due to pyrogens, metabolic stimulation, muscular activity caused by the tetanus or due to toxin effects on the medullary centres of the brainstem. It can be expected and need not necessarily be indicative of an ongoing infection. Tetanus itself induces no immunity and these patients all require active immunization with tetanus toxoid. (Toxoid 0.5 ml by intramuscular injection on discharge with a follow-up booster at 2 months and again at 6 months.)
18. Prevention
Active immunization A booster should follow three intramuscular injections of tetanus toxoid every 7 years. Alum absorbed tetanus toxoid is very effective at preventing tetanus with a failure rate of 4 in 100 million immunocompetent individuals. If a wound has the possibility of being contaminated with dirt, faeces, soil or saliva or there is a lot of devitalized tissue then HTIG should be considered (250 units by intramuscular injection). Neonatal tetanus can be prevented by immunization of women during pregnancy. In most developing countries, routine immunization in infancy was not implemented until the mid 1980s. Therefore, many women of childbearing age from the developing countries may be susceptible to tetanus. For previously unimmunized women living in the developing countries, the World Health Organization (WHO) recommends five doses of tetanus toxoid in order to ensure long- term immunity. The first two doses given 1 month apart provide short-term immunity. These first two doses provide 80% protection to the newborn; the third dose increases the protection for the fetus to 95% (3). The third dose of tetanus (scheduled 6–12 months after the second and, therefore, not commonly given in pregnancy) induces a durable immunity for the woman lasting a minimum of 5 years, the fourth dose prolongs immunity for 10 years, and the fifth dose prolongs immunity for at least 20 years (4). In the United States, the ACIP recommends a three-dose primary series for unimmunized individuals or for those without documentation, followed with a booster dose every 10 years.

Oleg Blinnikov 15 май 2003 20:25

 Еще небольшое добавление... Я вскользь упомянул о столбняке у рожениц и случайно написал не то что хотел сказать... В одной статье мне встретилось упомнание о том... что при столбняке у рожениц гистеректомия не имеет преимуществ перед сохранением матки.... Ниже фотография столбняка у пациентки после родов.
Фотография из коллекции Вячеслава Дмитриевича Рындина, хирурга, работающего в ЮАР.
столбняк/tetanus

Oleg Blinnikov 15 май 2003 21:05

 Коллеги... спасибо за теплые слова...
Работа конечно здесь интересная... но всегда ощущается свой лимит... Нельзя объять необъятное и поэтому в каких то ситуациях нужно более глубокое знание предмета... с другой стороны есть моменты, когда знаешь что нужно сделать... но нет никаких к тому возможностей... любопытное положение складывается с появлением интернета, дигитальных камер... как видите возможен обмен опытом со взаимным интересом и все это надеюсь на благо наших пациентов.... Удалось мне здесь через ВОЗовский проект HINARI пробить свободный, бесплатный доступ через интернет к большинству биомедицинских журналов .... поток современной информации непосредственно на земской уровень... опять же что то новое...
Но самое главное это профессиональные онлайновые сообщества.... неформальные группы заинтересованных в своей работе врачей... это мне кажется прямой путь к более эффективному решению проблемных ситуаций при определении новых понятий, тактики лечения и так далее.. но эту культуру надо только создавать... и это не будет легко...
Всего доброго...
Критка и советы будут приняты с благодарностью и вниманием...

Victor S.Dovgan 15 май 2003 22:10

Олег Игоревич, если Вы согласны, то любую Вашу статью я опубликую на
Медико.ру в разделе ПУБЛИКАЦИИ.

Oleg Blinnikov 15 май 2003 23:15

 1. Спасибо...но обзор..лекция...как хотите.. который я сделал о столбняке не имеет моего авторства... это чистая компиляция из текстов уже имеющихся статей и книг... просто я собрал это для себя и своих докторов в форму удобную для обучения и ссылки при необходимости.... Боюсь что электронная публикация такого труда не будет правильна с точки зрения авторских прав.... если кому либо этот материал поможет в подготовке лекции - буду рад... если пригодятся фотографии - очень хорошо...пришлю еще... я понимаю что онлайновое сообщество и может существовать только по принципу "получил интересную информацию - поделись и своим опытом" тогда возникает интересный поток наблюдений, вопросов, фотографий, статей, переводов и так далее...

2. Благодаря тому что у меня есть доступ к полным текстам многих научных медицинских журналов сбор информации сильно облегчается. Мне известно что многие мои коллеги к сожалению имеют ограниченный доступ к полным текстам. Поэтому я и предложил поделиться этими статьями (не моими) в узком закрытом кругу профессионалов... что может быть не понравилось бы издателям...но опыт показывают, что авторы только рады если их труды больше читают коллеги... правда статьи в pdf и тяжеловаты...

3. Я горячо поддерживаю идеологию электронных публикаций по принципу giving away и считаю что пора сворачивать накопительство длинного листа печатных работ ради степеней, позиций и так далее...понимаю что в нашей российской жизни с этим надо считаться... но уже пора поворачиваться лицом к коллегам а не к аттестационным комиссиям...

4. Структура "Онлайновая конференция - Электронный журнал" идеальная среда для быстрых дискуссий и архивирования наиболее интересных идей, обзоров, фотографий и так далее... это и место для peer review...контроля качества.... но важна полная открытость и публикация отзывов, критики на статьи... возможность защиты материала автором так же должна быть обеспечена... возможно постепенно станет более достойно опубликоваться в таком "трудном", чисто электронном журнале, а не в бумажном, где отклик приходит через пару месяцев... эти преимущества системы online first уже быстро осваиваются многими ведущими издательствами.... но тем не менее... клубное интернет общение всегда будет иметь место в силу своей неформальности...большей свободы высказывания. быстроты реагирования и компетентности научного форума.... в среде хирургов мы экспериментируем в этом направлении.... адрес где можно познакомиться поближе с электронным сообществом Русская Хирургическая Сеть и журналом "Новый Хирургический Архив" www.surgeon.spb.ru

5. Сочту за честь быть опубликованным на Medico.Ru и постараюсь подготовиться к этому серьезно....

 
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