Page 1000 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 79: Tetanus 731

DIAGNOSIS AND LABORATORY TESTING TABLE 79-2 Drugs Used in Medical Management of Tetanus

The diagnosis of tetanus is based on clinical manifestations rather than Medication Indication Dose (Usual)
laboratory tests. In areas where tetanus is endemic diagnosis is relatively HTIG a Generalized tetanus 500-3000 IU intramuscular
easy, but in developed countries where the disease is less prevalent diag-
nosis can be delayed. The spatula test is a simple test that can be helpful Metronidazole Toxin production 500 mg IV/PO q6h
in diagnosis. In the presence of tetanus, the posterior pharyngeal wall (given in all cases)
will contract due to a reflex contraction of the masseters when touched Midazolam Spasms, sedation, and 0.3-30.0 mg/h IV (mean =9.0 mg/h), titrate
by a spatula. In a study by Apte and Kanad used the test on 400 patients cardiovascular instability to effect
with suspected tetanus and was found to have sensitivity of 94% and Magnesium Spasms and cardiovas- 40 mg/kg IV load over 30 minutes, then 1-3 g IV/h
a specificity of 100% for diagnosing tetanus. Although the clinical sulfate cular instability
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presentation for tetanus is usually characteristic, there is a differential Titrate to serum concentrations of 2-4 mmol/L
diagnosis that includes malignant hyperthermia, atropine poisoning or Cisatracurium Neuromuscular block- 1-2 μg/kg/min IV, titrate to effect
an adverse effect of metoclopramide, strychnine poisoning, and acute ade for severe muscle
hypercalcemia. In some cases, the diagnosis is difficult due to an atypi- spasms
cal presentation. For instance, dysphagia may be the major symptom. Dantrolene Rigidity and spasms 0.5-1.0 mg/kg IV q4-6h
The major clinical features on which the diagnosis of tetanus is based
are listed in Table 79-1 along with the features of other conditions with Clonidine Cardiovascular instability 300 μg q8h via nasogastric tube
which it can be confused. a Human tetanus immune globulin.
Tissue cultures are positive in less than 50% of patients. Since the
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organism is noninvasive, blood cultures are of little value except in diag- care often begins with an assessment of airway patency and the ability
nosing secondary infection. The severity of disease is inversely related of the patient to ventilate, later shifts focus to stabilizing the circulation
to the duration of the incubation period, which can be defined as the impacted by autonomic instability, and throughout requires vigilance to
time of injury to the first appearance of spasms. This can be useful to prevent complications of what is commonly a prolonged critical illness.
determine the timing and need for airway protection. For this reason, patients with a presumptive diagnosis of tetanus
A complete blood count will usually show a leukocytosis with a left should be admitted to the intensive care unit with consultation with a
shift, and less frequently, a lymphocytosis. Examination of urine may critical care specialist to help with management and complications of the
reveal proteinuria and leukocytes thought to result from accumulation disease. 14,15,27 Because the onset of the disease ranges from less than 1 to
of tetanus toxin in the kidneys. Other nonspecific laboratory abnor- 12 days, even patients with mild tetanus should be observed in a high
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malities include elevation of serum transaminases, increased catechol- acuity setting for at least 1 week, or 2 weeks if symptom resolution is
amine levels in serum and urine, and decreased serum cholinesterase slow. Patients with incubation periods of greater than 20 days who have
level. Creatinine phosphokinase (CPK) is usually normal initially but only localized rigidity can be safely discharged to a lower acuity setting
generally rises with the onset of muscular spasms. Idoko and colleagues after a few days of observation provided no progression of the disease
reported elevated cerebrospinal fluid (CSF) protein levels in 26 of 34 has occurred. As a general rule, the peak severity of tetanus can be
(76.5%) patients with tetanus. The elevation of CSF protein appeared roughly estimated by the time of injury to the first appearance of spasms;
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to correlate with disease severity. Nineteen patients with severe disease the earlier the spasms, the more severe the disease is likely to be. This
(10 ultimately fatal) had significantly higher CSF protein values (mean information can be useful to predict the timing and need for supportive
= 1582 mg/L) than mild cases (mean = 400 mg/L). 26 care. Medications commonly used in the management of tetanus are
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listed in Table 79-2 together with their indications and usual doses.
TREATMENT
WOUND MANAGEMENT
The goals of tetanus treatment are to reduce the production and depo-
sition of tetanospasmin, to prevent painful and potentially harmful Aggressive surgical treatment of tetanus-producing wounds is believed
muscle spasm, and to provide supportive care. 10,14,15 Limiting the reach to result in improved survival via the removal of spores and necrotic
of tetanospasmin is accomplished by successful management of the tissue necessary for toxin formation. Foreign bodies should be removed
responsible wound, antibiotic therapy, and administration of antitoxin. and wounds should be aggressively debrided and left open. The wound
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Muscle tetany is controlled by minimizing muscle stimulation and should be excised with a several centimeter margin of viable tissue, and
providing pharmacotherapy to prevent the muscle spasm. Supportive amputation should be considered if gangrene is present on an extrem-
ity wound. The decision to perform a hysterectomy on a patient who
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develops tetanus in the postpartum period should be based on the
presence of associated invasive bacterial sepsis, gangrene of the uterus,
TABLE 79-1 Differential Diagnosis of Tetanus: Clinical Features or uterine injury. Tetanus is not itself an indication for hysterectomy. 23
Tetanus Strychnine Neuroleptics SMS a Rabies Meningitis After debridement of necrotic tissue, the wound should be cared for as any
other wound that has not been complicated by clinical tetanus. This includes
Trismus + + + + − − vigilant observation of the wound for progression or secondary infection, as
Nuchal rigidity + + + + − + well as the application of a topical dressing. Local antibiotic therapy targeted
Risus sardonicus + + − − − − at Clostridium tetani or direct tetanus immunoglobulin instillation to the area
has not been well studied and its role has not been well established. 17
Opisthotonus + + + − + −
Muscle rigidity + + + − − − ANTITOXIN THERAPY
(continuous)
Muscle rigidity − − − + + − The administration of antitoxin to inactivate toxin already bound to the
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(intermittent) central nervous system has been shown to be of no benefit. Since only
unbound toxin can be neutralized, therapy is aimed at giving intramus-
Encephalopathy − − − − + +
cular human tetanus immune globulin (HTIG). In general, HTIG is
Rapid course − + + − − − given as soon as possible. 10,11,15 However, controversy persists regarding
a Stiff-man syndrome. the preferred route and dosage of antitoxin. The recommended dosage

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