Page 999 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

730 PART 5: Infectious Disorders

spinal neurons. The neurons that are affected secrete inhibitory neu- to exhaustion and hypoxia in patients. Laryngeal spasm may lead to
rotransmitters, that is, those that secrete GABA and glycine, are more asphyxia; early and aggressive airway management is indicated early in
sensitive to the toxin. Neurons that are involved become incapable the disease course because laryngeal spasm may occur at any time in the
of transmitter release and as a result there is no inhibition of motor disease course. In the Edmondson and Flowers series of 100 patients,
15
reflex responses. This leads to contractions of agonist and antagonist trismus and dysphagia (described as sore throat) were the presenting
muscles known as tetanic spasms. Once toxin is fixed to neurons, it symptoms in 75 cases and neck and back stiffness in 14 cases. However,
cannot be neutralized, even with administration of antitoxin antibod- in 88 cases, it was possible to demonstrate trismus on initial physical
ies. New nerve terminals and new synapses must form for resolution, examination. 14,18
on the order of 4 to 6 weeks. For this reason, therapy at the point of Spasms are initially tonic, followed first by high-frequency and
9
clinical tetanus is only supportive. then low-frequency clonic activity. In very severe tetanus, spasms may
The effect of tetanus toxin on the neuromuscular junction is presyn- occur so frequently that status epilepticus may be suspected, and may
aptic inhibition of acetylcholine release, which can result in paralysis of be forceful enough to cause fractures of long bones and of the spine.
muscles. Paralysis is less frequent and usually localized to areas of high Spasm-induced damage to muscles can also result in rhabdomyolysis
toxin concentration because the neuromuscular junction is not as sensi- complicated by acute renal failure. Spasms may be initiated by touch,
19
tive to tetanus toxin as the inhibitory neurons. Autonomic dysfunction noise, lights, and swallowing, even in the sleeping patient. Spasms severe
occurs later in the course of the disease because of the longer neuronal enough to require treatment may persist for up to 6 weeks.
path. Sympathetic and parasympathetic overactivity has been attributed In addition to being extremely painful, spasms can produce a variety
to impaired neuronal inhibition of the adrenal glands. 10 of significant secondary effects. Apnea occurs when spasms involve the
Because preformed circulating antibody to tetanospasmin can com- respiratory muscles or larynx. Paralysis of skeletal muscles may occur
pletely prevent development of the disease, tetanus occurs primarily in following periods of sustained spasms due to presynaptic inhibition of
nonimmunized or inadequately immunized patients, particularly the acetylcholine release at the neuromuscular junction. Similarly, paralysis
poor and elderly. 11,12 Although vaccination results in antitoxoid anti- of urinary bladder musculature together with spasm of perineal muscles
bodies that neutralize the toxin, disease is still possible in those who has been implicated in causing acute urinary retention. In pregnancy,
have been properly vaccinated and receive appropriate booster doses of spasms can cause abortion or miscarriage, although the fetus is not
vaccine. Many conditions may impair the immune response to vaccine, directly affected, since the toxin does not cross the placenta. Inadequately
including advanced HIV infection. The course in these may be atypical treated spasms can also produce fever, although secondary infection and
and milder. 13 direct and indirect actions of toxin on hypothalamic temperature regula-
tion are often implicated.
The autonomic nervous system dysfunction of severe tetanus usu-
CLINICAL MANIFESTATIONS ally occurs 1 to 2 weeks after the onset of the disease but may occur
20
The majority of cases of tetanus follow some type of trauma or injury; earlier. Manifestations of impaired sympathetic inhibition include
however, in 15% to 25% of cases a portal of entry cannot be determined tachycardia, labile hypertension alternating with hypotension, periph-
(cryptogenic tetanus). Portal of entry can range from minor trauma eral vasoconstriction, fever, and profuse sweating. Overactivity of
14
producing a break in the skin, burn injuries, infected umbilical stumps, the parasympathetic nervous system causes increased bronchial and
21
postoperative sites, ischemic ulcers, the uterus after septic abortions, salivary gland secretions, bradycardia, and sinus arrest. These hemo-
injection sites of narcotic addicts, and untreated otitis media. Cases of dynamic findings are similar to those seen in pheochromocytomas.
15
tetanus have been seen in intravenous drug users associated with skin Additional complications include pulmonary edema, myocardial
infections caused by use of inadequately sterilized needles. 14,16 The incu- dysfunction, acute respiratory distress syndrome, pneumonia, sepsis,
bation period can range from 3 days to 3 weeks, but cases have occurred pulmonary embolism, gastrointestinal bleeding, and poor nutritional
after several months. In general, the shorter the incubation period, the status. 1
a mild course. A prodrome of malaise, irritability, and headache has ■ LOCALIZED TETANUS
more severe the disease. However, a long incubation does not guarantee
been described but is usually not seen. 17 Localized tetanus is a less common presentation of tetanus and is char-
There are four basic forms of tetanus that can be distinguished clini- acterized by rigidity of the group of muscles in close proximity to the
cally: generalized, local, cephalic, and neonatal. Only generalized, local, site of injury without systemic signs. The presence of circulating anti-
and cephalic will be described in this chapter. In the adult intensive care toxin prevents the systemic spread of the toxin, but there is not enough
unit setting, generalized tetanus is the most likely to be encountered. antitoxin to stop local toxin uptake at a wound site. The toxin causes
■ GENERALIZED TETANUS painful muscle contractions that can last for weeks. The disease may be
mistaken for pain-induced muscle spasms. Local tetanus may develop
17
Generalized tetanus accounts for 80% of tetanus seen in clinical practice into generalized tetanus but is usually milder and less likely to be fatal,
and is characterized by diffuse muscle rigidity affecting any voluntary with mortality of approximately 1%. 4
involved. A majority of patients (75%) will present with rigidity of the ■ CEPHALIC TETANUS
muscle group. As the disease progresses, more muscle groups become
4
masseter muscle (trismus), which results in difficulty with opening the Cephalic tetanus is a rare form of the disease, occurring with otitis
mouth and chewing. It is not uncommon for these patients to present media, following head trauma or chronic infection or the head and neck.
to a dentist first. Other common manifestations include neck rigidity, Cephalic tetanus after scalp or facial injury tends to occur earlier with
stiffness, dysphagia, and reflex spasm. As the disease evolves the main an incubation period of 1 day to 2 weeks. It only involves the cranial
22
manifestations are muscle rigidity and reflex spasms. Muscle rigid- nerves and is defined as trismus plus paralysis of one or more cranial
ity in the facial muscles results in risus sardonicus (sardonic smile), nerves. Although the most common cranial nerve involved is VII, any
while opisthotonos is caused by rigidity of the vertebral muscles and cranial nerve can be affected. Patients can present with a confusing
antigravity muscles. Vertebral fractures are not uncommon when these clinical picture that may involve dysphagia, trismus, and focal cranial
muscle groups are involved. Abdominal muscle involvement may neuropathies. Isolated paralysis of the facial nerve may be due to Bell
17
17
mimic peritonitis, while nuchal rigidity can simulate meningitis. Reflex palsy or an early manifestation of cephalic tetanus. In cephalic tetanus,
23
spasms are present in 70% of patients and can be provoked by external cranial nerve palsies may precede trismus. 14,18 Progression to the gen-
stimuli such as noise or manipulation of the patient. These spasms eralized form can occur with cephalic tetanus and is associated with a
are tonic and clonic in nature and painful. Sustained spasms can lead poor prognosis. 4,22,24

section05_c74-81.indd 730 1/23/2015 12:37:40 PM