Journal of Veterinary Emergency and Critical Care 16(3) 2006, pp 199–207

Clinical Practice Review doi:10.1111/j.1476-4431.2006.00192.x

Tetanus: pathophysiology, clinical signs, diagnosis,

and update on new treatment modalities
Thomas Linnenbrink, DVM and Maureen McMichael, DVM, DACVECC

Abstract
Objective: To review the pathophysiology, clinical signs, diagnosis, and current treatment modalities used in
treating tetanus in small animals and humans.
Etiology: Tetanus is caused by the activity of a toxin released from the bacterial organism, Clostridium tetani.
The disease has an incubation period of 3 days to 3 weeks and usually follows a deep penetrating wound.
Diagnosis: The diagnosis of tetanus is usually based on history and clinical signs.
Therapy: Therapy of tetanus consists of direct and supportive care and includes toxin neutralization via
human or equine derived immunoglobulin, antimicrobial therapy to eliminate C. tetani, and central and
peripheral muscle relaxants to control hypertonicity. Adjunctive care may include positive pressure
ventilation, anticonvulsant medication, drugs to treat autonomic dysfunction, and nutritional support.
Prognosis: Prognosis varies based on severity of clinical signs at the time of diagnosis and the availability of
appropriate care.
(J Vet Emerg Crit Care 2006; 16(3): 199–207) doi: 10.1111/j.1476-4431.2006.00192.x

Keywords: antitoxin, Clostridium tetani, rigidity, tetanospasmin, tetanus toxoid

Introduction cases, misdiagnoses, or low number of tetanus cases

affecting dogs and cats. In humans, tetanus is primarily
The knowledge of tetanus extends back to the fifth-
found in underdeveloped countries with children and
century BC.1 In the late 1800s, several valuable discov-
neonates representing the majority of cases. There are
eries regarding tetanus were made including the toxin’s
an estimated 800,000 deaths from neonatal tetanus each
ability to infect multiple species. It was also discovered
year worldwide.5 Inadequate immunization and unhy-
that protection could be provided by passive transfer of
gienic medical practices, particularly during obstetric
antitoxin.1,2 In 1924, tetanus toxoid for immunization
procedures, are contributory.6–11
against tetanus was developed.1
The purpose of this article is to review the patho-
Tetanus is an acute toxigenic illness that affects mam-
physiology, clinical signs, diagnosis, and treatment of
mals and results in neurologic dysfunction. While sus-
tetanus in dogs and cats and to discuss the current
ceptibility and source of infection are generally
treatment strategies used in small animals and humans.
different between humans and animals, treatment goals
are similar. Tetanus in dogs and cats is most commonly
associated with a contaminated penetrating wound.
The low prevalence of the disease in dogs and cats can Pathophysiology
lead to delay in diagnosis allowing for progression of Tetanus generally occurs 5–10 days (range 3–18 days)
the disease prior to treatment.3,4 It is unclear if the low after inoculation of the organism. In humans a shorter
prevalence is due to incomplete reporting of tetanus incubation period correlates to a poorer prognosis.1,11
Tetanus is caused by the anaerobic, gram positive, non-
From the Animal Emergency Services of Rochester, Rochester, NY encapsulated spore-forming bacillus, Clostridium teta-
(Linnenbrink), and the Department of Small Animal Clinical Sciences,
College of Veterinary Medicine and Biomedical Sciences, Texas A&M ni.1,3 C. tetani forms resistant spores that can survive
University, College Station, TX (McMichael). high temperatures (i.e., boiling in water for several
Address correspondence and reprint requests to: minutes) and many common disinfectants. The spores
Dr. Maureen McMichael, Department of Small Animal Clinical Sciences, can be destroyed by autoclaving at 1 atm of pressure
Mail Stop 4474, College of Veterinary Medicine and Biomedical Sciences,
Texas A&M University, College Station, TX 77843-4474. and 120 1C for 15 minutes.3,12 The spores are commonly
E-mail: mmcmichael@cvm.tamu.edu found in soil and feces and are able to survive for

& Veterinary Emergency and Critical Care Society 2006 199

T. Linnenbrink and M. McMichael

months to years under optimal conditions in the envi-

ronment or within the body.1,3,6,7 While tetanus is typ-
ically nonpathogenic when ingested, provided the
organism remains within the gastrointestinal tract, it
is highly pathogenic when inoculated into an environ-
ment with low oxygen tension. Classically, this occurs
at the site of a penetrating wound contaminated with
soil or feces.1,3,4 Infections have occurred, however,
from surgical contamination (i.e., ingesta spillage dur-
ing intestinal resection), inadequate sterilization of in-
struments, and as a complication of improper
management of wounds.1,8,13–15 Tetanus may also oc-
cur with large burns, after intramuscular injections, and
following snakebite(s).16–19 The presence of necrotic tis-
sue or foreign material, coupled with a poor blood
supply, can result in an optimal environment for
sporulation.3,20 Vegetative spores produce 2 toxins,
tetanolysin and tetanospasmin. In vitro, tetanolysin is
capable of lysing erythrocytes and in vivo may result in
tissue damage resulting in an optimal local environ-
ment for bacterial growth.3,21 Tetanospasmin is an in-
active peptide that must be cleaved to its active form
via tissue or bacterial proteases. Tetanospasmin pro-
duces the classical neurological features associated with
tetanus. The DNA for tetanospasmin is packaged in a
plasmid that is not present in all strains of C. tetani, so
presence of the bacterium does not automatically indi-
cate toxicity.12 Dogs and cats are thought to be innately
resistant, 200 and 2400 times, respectively, to clinical
tetanus infection compared to humans.3 Tetanospasmin
is the target of tetanus antitoxin.3,8,22,23 Figure 1: Tetanus toxin uptake and transport. 1, wound with
The mechanism by which tetanus ultimately results vegetative spores producing tetanospasmin, which is cleaved to
in neurologic dysfunction is similar between humans produce disulfide linked light and heavy chains. Locally it at-
and animals in that it requires tetanospasmin to enter taches to peripheral nerves; 2, with heavy toxin burden hem-
atogenous spread to distant sites (other neuromuscular
the central nervous system (CNS) (Figure 1). The toxin
endplates or fourth ventricle); 3, attachment and internaliza-
undergoes cleavage into 2 disulfide-linked fragments,
tion of the toxin; 4, retrograde transport to the CNS at
the light chain and the heavy chain. A portion of the 75–250 mm/day; 5, toxin reaches and is internalized by inhib-
heavy chain of the toxin mediates attachment to pe- itory interneurons. Here the toxin inhibits the release of glycine
ripheral nerves followed by internalization. Once in- and g-aminobutyric acid (GABA).
ternalized, the toxin is incorporated into a vesicle and
transported retrograde to the CNS at 75–250 mm/day. infection is the irreversible blockade of neuronal inhi-
Retrograde transport is enhanced by neuronal stimula- bition of skeletal muscle with resultant generalized
tion.3,8,24 muscle spasm and alterations of autonomic control.
Additionally, if toxin load is high, tetanospasmin can Thus, recovery requires sprouting of new axon termi-
spread hematologically to other neuromuscular end- nals.24–28
plates and directly penetrate the CNS at the fourth
ventricle.2,3,21 The tetanus toxin, having traveled from
the neuromuscular endplate, eventually reaches the
Clinical Signs
motor nerve dendrites within the spinal cord and
brainstem. It is then internalized by inhibitory inter- In humans, there are 4 forms of tetanus recognized:
neurons. There, the toxin inhibits the release of 2 ne- cephalic, localized, generalized, and neonatal.1,8,12,20
urotransmitters: glycine and gamma-aminobutyric acid Cephalic tetanus is most often seen with otitis media
(GABA). The 2 function as inhibitor neurotransmitters and is rare.29,30 In animals, both the localized and gen-
in the brain and spinal cord. The end result of a tetanus eralized forms have been reported.24,31,32 Localized

200 & Veterinary Emergency and Critical Care Society 2006, doi: 10.1111/j.1476-4431.2006.00192.x
 Tetanus

tetanus is associated with a lower toxin load. Generally, On physical examination in affected animals, there is
it results in muscle rigidity at the site of infection that a significant increase in muscle tone along with epi-
may progress to the contralateral limb and eventually sodic muscle spasms affecting both agonist and antag-
spread throughout the CNS into the generalized form.3 onist muscle groups. The tonic contractions may be
The mortality rate is much lower with localized teta- triggered by stimuli that are auditory, tactile, or visual.
nus.3,20 Generalized tetanus is characterized by extreme Spasms may be so severe that bone fractures and ten-
muscle rigidity with the extensor muscle groups dom- don avulsions result.39 Additional problems reported in
inating. In animals, this rigidity results in an out- humans include hiatal hernias, dysuria, urine retention,
stretched tail, hypertonic myotactic reflexes, and constipation, and gaseous distension from increased
normal conscious proprioception. Cranial nerve in- sphincter tone.40 In humans, death is generally the re-
volvement and intracranial signs develop late in local- sult of respiratory failure in nonventilated patients and
ized tetanus and early in generalized tetanus. Cranial cardiac failure in ventilated patients.11,20,21,41,42
nerve involvement commonly manifests as cranial There are ancillary tests that may aide in the diag-
nerve motor nuclei hypertonicity such as risus sardon- nosis of tetanus. Changes seen on a complete blood
icus (facial muscle spasm), trismus (lockjaw), protru- count may include neutrophilic leukocytosis. The bio-
sion of the third eyelid, enophthalmos, laryngeal chemistry panel may show an elevated creatine kinase
spasm, and dysphagia.1,3,4 Neonatal tetanus is report- and aspartate aminotransferase.3 Cardiovascular ab-
ed mostly in developing countries in association with normalities that may be seen include arrhythmias, hy-
nonsterile umbilical cord techniques at birth. To the pertension, hypotension, and thrombosis. Arrhythmias
authors’ knowledge, this form of tetanus has not been that have been reported include sinus tachycardia,
reported in companion animals. bradycardia characterized by atrioventricular block, si-
Autonomic dysfunction is a significant complication nus arrest, and ventricular escape complexes.22,23,41
of tetanus infection in humans.7,8,33 Loss of inhibition of Electromyographic changes (prolonged electrical dis-
autonomic discharge leads to excess sympathetic activ- charges following needle insertion with normal nerve
ity and excess catecholamine levels. Findings reflecting conduction velocities) are present with tetanus, but
autonomic dysfunction include ptyalism, tachycardia testing, if necessary, should be delayed until after treat-
and tachypnea, hypertension (due to increased system- ment as it can result in progression of the disease.2,8,33
ic vascular resistance), and increased protein catabo- Isolation of C. tetani from the wound is difficult and
lism.1,33–35 Autonomic signs do not usually begin until is successful in only approximately 30% of the cases in
several days after the rigidity has set in and may persist humans.1,7,10 Identification of the toxin is also rarely
for 1–2 weeks.12,21,36 Basal catecholamine levels can be successful and is not used in humans. Gram stain may
up to 10 times the normal level during an autonomic be of questionable value given that the morphology of
storm.12,21,36,37 A dramatic illustration of this increase is the infecting organism is similar to other anaerobic
the rupture of an aneurysm secondary to hypertension bacteria and a positive gram stain is only seen in ap-
in a person with tetanus.34 Although reported in veter- proximately 33% of human patients with tetanus.1,10
inary medicine, autonomic dysfunction is not recognized Due to the critical nature of the disease, a suspected
as frequently in animals as it is in humans.23,36–38 It is case of tetanus warrants aggressive workup with rapid
unclear if this is related to inadequate monitoring, treatment based on history and clinical signs in the ab-
pathophysiological differences between humans and sence of a definitive diagnosis.
veterinary species, or a combination of the 2.

Vaccination
Diagnosis
As a result of their inherent resistance, dogs and cats
Diagnosis is based primarily on history and clinical are not vaccinated against tetanospasmin with tetanus
signs. Wounds may be present, healed, or hidden.3,15 toxoid. Interestingly, the clinical disease does not result
One example of a hidden wound is a hard palate splin- in protective antibody levels post-infection.3 Therefore,
ter in dogs from chewing on sticks. The ‘lock jaw’ pre- humans are still routinely vaccinated post infection.1 In
vents a thorough oral exam in most tetanus patients humans, tetanus anti-toxoid antibodies of 0.01 IU/mL
and these wounds often go unnoticed until ne- are thought to be protective.1,43 However, the original
cropsy.3,4,12,18 A history of gunshot, animal bite, or pen- study that established this antibody titer was per-
etrating injury should raise the index of suspicion of formed on guinea pigs in 1937. Tetanus cases have been
tetanus in an animal with appropriate clinical reported in humans with antibody concentrations high-
signs.3,4,12,18 er than this.16,44–46 For example, in 1 reported case, an

& Veterinary Emergency and Critical Care Society 2006, doi: 10.1111/j.1476-4431.2006.00192.x 201
T. Linnenbrink and M. McMichael

Table 1: Recommended medical therapy for tetanus3,7,8,22,40,58,59

Medication Species Dose Route Interval (hours) Duration

Immunotherapy
Human tetanus immunoglobulin C, F 500–1000 IU IM Once
Antitetanus equine serum C, F 500–1000 IU IVn,z, IM, SQ Once
Antimicrobial
Metronidazole C, F 30 mg/kg/day IV 8–12 7–14 days
Sedatives
Acepromazine C, F 0.02–0.06 mg/kgw IV 2–4 PRN
Chlorpromazine C, F 0.5–2 mg/kgw IV 6–8 PRN
Diazepam C 2–5 mg/kg/hrw IV CRI PRN
Diazepam F 2.5–5 mg/kgw IV 2–4 PRN§
Magnesiumz C 70 mg/kg IV Loading 30 minutes
100 mg/kg/dayw IV CRIk PRN
Methocarbamol C, F 330 mg/kg/daynn IV CRI PRN
Autonomic agents
Atropine C, F 0.05 mg/kgw IV PRN PRN
Glycopyrrolate C, F 0.005–0.011 mg/kgw IV PRN PRN

n
For products not containing Thimerosal.
wTitrate to lowest effective dose.
zRequires test dose.
§Oral route associated with hepatic toxicity.
zSuggested doses based on human protocols for treatment of tetanus with magnesium sulfate.p
k Titrate dose by 25% every 6 hours until muscle rigidity is at an acceptable level to allow swallowing of saliva, oral care, and physical therapy with a
clinical endpoint of respiratory depression.
nn
Maximum daily dose of 330 mg/kg.
C, canine; F, feline.

intravenous drug user with an antibody concentration ally).1,3,21 A novel delivery system has been developed
of 0.16 IU/mL developed clinical tetanus.16 that would allow the immunoglobulins to cross the BBB
and neutralize toxin that has penetrated the CNS.48,49
An in vitro study showed that this method did not alter
Therapy
the immunoglobulin’s affinity for tetanus in the pe-
Therapy encompasses both specific (antitoxin) and riphery.49 This new method is still in the development
generalized (supportive) care (Table 1). If left untreat- phase and has not been tested in vivo. Toxin that is
ed, the generalized form of the disease is often fatal.1,3 bound within the CNS cannot be successfully removed
The localized form, over time, can progress to the gen- nor is the duration of its effect altered by antitoxin ad-
eralized form.1,3,29 The focus of therapy is neutraliza- ministration. The recovery of neuronal function where
tion of circulating toxin, debridement of the wound, tetanospasmin is already bound requires the sprouting
administration of antibiotics effective against C. tetani of new receptors which takes approximately 3
organisms, sedatives for muscle spasms, and support- weeks.12,27 It is vital, therefore, to administer the anti-
ive and symptomatic care.1,3,7,8,20–22,47 toxin as early on in the disease process as possible.3,21,50
Currently, the recommended dose of antitoxin is
Tetanus immunoglobulin markedly different between animals and humans. In
Currently, 2 types of immunoglobulins directed against animals, wide dosage ranges varying from 100–1000 U/
tetanus toxin exist for the treatment of tetanus in an- kg with a maximal dosage of 20,000 U IV, IM, or SQ are
imals, equine anti-tetanus serum (ATS)a and human recommended.3 Other recommendations include
tetanus immune globulin (TIG).b ATS is licensed for 1000 U at the wound site or 1–10 U intrathecally.3 The
intramuscular (IM) and intravenous (IV) use and TIG is lack of a standard protocol makes appropriate admin-
licensed for IM use only.1,3,21 These immunoglobulins istration of antitoxin challenging in veterinary medi-
can neutralize toxin activity only when the toxin is cine.3,4,22 In humans, a single dose of antitoxin (500 IU
present in the blood, but are ineffective once the toxin is IM) proximal to the wound is recommended.20,21,41
transported into nerve cells. Neither ATS nor TIG can Adoption of this lower dosage given IM as the standard
cross the blood–brain barrier (BBB) and are ineffective of care has resulted in fewer untoward events.20,21,50,51
in neutralizing toxin already present in the CNS unless Previous dosing recommendations in humans were
they are administered directly into the CNS (intrathec- significantly higher (3000–5000 IU).41,52 The dose of

202 & Veterinary Emergency and Critical Care Society 2006, doi: 10.1111/j.1476-4431.2006.00192.x
 Tetanus

antitoxin is not based on the size of the patient, but already produced. Antibiotic therapy has been shown
rather on the amount of toxin to be neutralized. In fact, to reduce mortality and the need for muscle relaxants in
the dose of antitoxin is the same for adult and pediatric humans.52,58 The ideal antibiotic should have good
patients.20 In human medicine, intrathecal administra- penetration into anaerobic tissue. Current antibiotic
tion of immunoglobulin has not been approved, and recommendations in veterinary medicine include pen-
results of studies evaluating this treatment modality are icillin Gc (20,000–100,000 U/kg IV q 6–12 h), tetracy-
equivocal.53–55 The most recent study of this route of clined (22 mg/kg PO q 8 h), clindamycine (3–10 mg/kg
administration demonstrated a decrease in mortality, IV q 8–12 h), and metronidazolef (10 mg/kg IV q 8 h).3,4
hospitalization stay, and respiratory complications with The antibiotic of choice in human medicine is met-
intrathecal and IM administration versus IM adminis- ronidazole.7,21,58–60 A loading dose of 15 mg/kg may be
tration alone.55 administered followed by a maintenance dose of
There are 3 types of adverse reactions seen as a result 20–30 mg/kg IV daily for 7–14 days. Other recommen-
of administration of antitoxin: anaphylactic, an- dations include administering 500 mg IV q 8 h for 7–10
aphylactoid, and serum sickness.56 Anaphylactic reac- days or 600 mg PO q 6 h for 10 days7,21 (Table 1). Met-
tions are mediated by IgE (type I hypersensitivity ronidazole is superior to penicillin in its ability to pen-
reaction) and the chemical mediators histamine, se- etrate anaerobic tissue, reduce mortality, and shorten
rotonin, and the eicosanoids. The primary cell types the hospital stay in humans with tetanus compared
involved in this rapid reaction are mast cells and bas- with Penicillin G.58,60 Penicillin, like tetanus toxin, is a
ophils.56 Reactions typically occur in a matter of min- GABA antagonist that can result in increased risk of
utes and are not dose-dependent. Clinical signs include convulsions.61–63 Metronidazole toxicity, most frequent-
vomiting, weak pulses, tachycardia, hypotension, pul- ly manifesting itself as central vestibular disease, has
monary edema, neurologic dysfunction, urticaria, and been reported in both the veterinary and human liter-
angioedema. Treatment is directed at preventing fur- ature.64–66 Veterinary patients generally respond well to
ther release of the aforementioned mediators and at treatment with diazepam and withdrawal of metro-
depressing their response. Blocking the physiologic re- nidazole.64–66
sponse to mediator release should be attempted with Regardless of which antimicrobial agent is utilized,
antihistamines and epinephrine. Further histamine re- appropriate wound management is essential whenever
lease is prevented by epinephrine and glucocorti- possible. Wounds should be debrided to eliminate ne-
coids.56,57 crotic tissue and abolish the anaerobic environment,
Anaphylactoid reactions, which generally have mild- thus inhibiting further spore vegetation and toxin pro-
er clinical signs, are not immune mediated. Instead, duction.21 Although it has been suggested that the
they result from direct mast cell degranulation and are wound be flushed with hydrogen peroxide to increase
dose, rate, and concentration dependent. Clinical signs the oxygen tension, oxygen emboli have been reported
include urticaria, mild fever, and restlessness. An- from wound irrigation with hydrogen peroxide and
aphylactoid reactions generally respond to stopping caution is advised when utilizing this method.3,67
delivery of the antitoxin, administering diphenhydra-
mine, and restarting at a slower rate and/or at a more
dilute concentration.57 Environment, sedatives, and anticonvulsants
Serum sickness, a type III hypersensitivity reaction, One of the most important aspects of treatment is to
generally occurs within weeks of administration of an- provide patients with a dark, quiet, and well-padded
titoxin. Serum sickness is typically characterized by environment. Any stimulus (noise, light, touch) can
vasculitis, erythema, urticaria, neutropenia, lymph- trigger a violent spasm and this possible reaction
adenopathy, joint swelling, and proteinuria potentially should be taken into account when choosing an envi-
culminating in glomerulonephritis. This reaction is ronment (i.e., beeping fluid pumps, barking dogs). A
dose-dependent and is the result of antigen–antibody coordinated treatment schedule minimizes invasive
complexes becoming lodged in the endothelium incit- techniques and tactile sensation.3,20
ing an inflammatory cascade.56,57 The frequency of oc- In veterinary medicine, reflex spasms and convul-
currence of serum sickness in animals because of sions due to tetanus have typically been controlled with
tetanus antitoxin has not been reported. phenothiazines, benzodiazepines, and methocarbamolg
without the use of narcotics that can result in respira-
Antimicrobial therapy tory depression. Parasympatholytics (i.e., atropineh and
The goal of antibiotic therapy is to prevent further toxin glycopyrrolatei) are used to control bradycardia and
production by eliminating the clostridial spores. Anti- decrease airway secretions. The general goal is to
biotic administration does not have any effect on toxin control convulsions and muscle spasms without the

& Veterinary Emergency and Critical Care Society 2006, doi: 10.1111/j.1476-4431.2006.00192.x 203
T. Linnenbrink and M. McMichael

induction of profound respiratory depression that serum concentrations, there may be suppression of ace-
would require mechanical ventilation3,23 (Table 1). tylcholine release at the neuromuscular junction and
In human medicine, mechanical ventilation for teta- within the autonomic nervous system.75,76
nus is commonplace.21 Thus, heavy sedation, paralyt- Given the cost constraints that are often imposed on
ics, and narcotics are often included in the treatment veterinarians, avoidance of mechanical ventilation with
protocols.7,20,21 Additional muscle relaxants or paralyt- a very economical treatment is especially appealing.
ics are sometimes required based on the severity of the Magnesium use for control of muscle spasms and au-
muscle spasms.68–70 Dantrolene,j a direct skeletal mus- tonomic dysfunction appears to be safe as well as eco-
cle relaxant, is often combined with baclofen,k a GABA nomical in humans and clinical trials are needed to
agonist, to control muscle spasms.71 determine if this therapy is safe and efficacious in vet-
In humans with tetanus, autonomic dysfunction is a erinary medicine.21,40,74
potentially serious sequela that is characterized by pe-
riods of tachycardia and hypertension occasionally al- Other supportive measures
ternating with bradycardia and hypotension.35–37 Tetanus patients are best managed in an intensive care
Sympathetic overactivity, the most devastating aspect unit (ICU) or equivalent facility. One study in humans
of autonomic dysfunction, manifesting as extreme hy- demonstrated a 4-fold increase in mortality rate in pa-
pertension and tachycardia with increased systemic tients not managed in an ICU versus those managed in
vascular resistance, is very challenging to treat. There the ICU at the same hospital.7 One such reason for this
has been much interest in drugs that would control the higher mortality relates to the airway maintenance
autonomic dysfunction without overly sedating the pa- which is essential and may require a tracheostomy due
tient.33,40,72 to laryngospasm.20–22 In humans, the majority of pa-
In a limited number of human studies, magnesium, tients with generalized tetanus require prolonged pos-
when maintained at a supraphysiologic concentration, itive pressure ventilation. Changes in ventilatory
has shown promise both alone and in combination with techniques (positive end expiratory pressure [PEEP]
traditional agents in controlling autonomic dysfunction and low tidal volumes) and closer monitoring of pa-
and muscle spasm.72,73,74 Magnesium can function as a tients has resulted in decreased mortality.41 In veteri-
calcium antagonist and regulate muscle contraction, nary patients, mechanical ventilation is limited by
muscle relaxation, and neurotransmitter release. Mag- economic constraints and availability of ventilatory
nesium plays a crucial role in neuromuscular transmis- support.
sion and excitability. In one human study where Humans with generalized tetanus are consistently
magnesium concentrations in the majority (38 of 40) hypermetabolic resulting in a negative energy bal-
of patients were maintained between 2 and 4 mmol/L ance.8,12 This hypermetabolic state is the result of hype-
(normal reference range: 0.7–1.05 mmol/L), there were rthermia, increased muscle activity, and increased
decreased sedation requirements, decreased need for sympathetic discharge. Adequate nutritional support
ventilatory support, better tolerance of enteral feeding, is essential. Some debate exists over the appropriate
and reduced need for nursing care.40 While all patients nutritional route, enteral versus parenteral, or a com-
became hypocalcemic, none required calcium supple- bination of both.8,10,12 Several options exist for provid-
mentation and serum calcium levels returned to normal ing enteral nutrition. Placement of a nasoesophageal or
after magnesium therapy was discontinued.40 The loss nasogastric tube only allows for small volumes to be
of the patellar tendon reflex is an early sign of magne- delivered but does not require general anesthesia.
sium toxicity and was used as a method of monitoring These tubes can be a source of constant nasal and la-
in the aforementioned study.40,75 In several studies, ryngeal irritation (a significant problem in tetanus cases
magnesium dosages were titrated to reduce rigidity to where keeping stimuli to a minimum is essential) and
an acceptable level without causing respiratory depres- place debilitated patients at an increased risk of aspi-
sion.21 ration. Another option for nutritional support in pa-
Serum and total body magnesium is primarily regu- tients who cannot tolerate per os feedings is placement
lated by the kidneys via glomerular filtration and tu- of an esophagostomy tube, allowing delivery of enteral
bular reabsorption.73,75 Adequate renal function is nutrition without laryngeal or nasal irritation. The dis-
essential when instituting high-dose magnesium thera- advantage of this tube is the requirement of general
py.35,36,73 Hypermagnesemia, while rare in nonazotemic anesthesia for tube placement. It carries the same risk as
patients, can result in bradyarrhythmias, complete heart nasal tubes for esophagitis and aspiration. Percutane-
block, asystole, hypotension, coagulopathies, respirato- ous endoscopic gastrotomy tubes (PEG) may be a su-
ry depression, and decreased electrical transmission perior option to the aforementioned routes of enteral
across the neuromuscular junction.74–76 At very elevated nutrition. PEG tubes decrease the risk for gastroesopha-

204 & Veterinary Emergency and Critical Care Society 2006, doi: 10.1111/j.1476-4431.2006.00192.x
 Tetanus

geal reflux and aspiration pneumonia and allow the more effective alternative. Finally, magnesium appears
monitoring of gastric residuals. However, PEG tubes helpful in humans to control muscle spasms and auto-
have the disadvantages of requiring general anesthesia nomic dysfunction.
and a risk of peritonitis.24,76 In human medicine, supine It is clear that further studies are indicated in veter-
patients receiving enteral feeding have an increased inary medicine to evaluate appropriate therapy for
risk of gastroesophageal reflux and aspiration. Thus, it clinical tetanus infection in small animal patients. Stud-
has been recommended that these patient’s have the ies may focus on the use of magnesium, dose reduction
head of the bed elevated by 301.76 Providing partial or of tetanus immunoglobulin, and alternative antimicro-
total parenteral nutrition through a dedicated, sterilely bial therapy.
placed central venous catheter has the advantage of
minimal stimuli once the catheter is placed, but can
increase intracranial pressure when the jugular vein is
Footnotes
wrapped. Regardless of which type of nutritional de-
a
Tetanus Antitoxin (equine origin), Professional Biological Company,
livery system is utilized, it is clear that patients who are Denver, CO.
provided adequate nutritional support early in the dis- b
Tetanus Immune globulin (human), Bayer Corporation, Elkhart, IN.
c
ease process have a better prognosis.8 Finally, careful d
Penicillin G Potassium, Marsam Pharmaceuticals Inc., Cherry Hill, NJ.
Tetracycline, Mylan Pharmaceticals, Morgantown, WV.
monitoring of eliminations is important, as severe con- e
Clindamycin, Phoenix Scientific Inc., St. Joseph, MO.
f
stipation and urine retention can occur from increased g
Metronidazole, Abbott Laboratories, North Chicago, IL.
Methocarbamol, Fort Dodge Animal Health, Fort Dodge, IA.
sphincter tone.22 Once patients are in the convalescent h
Atropine, Neogen Corporation, Lexington, KY.
period, physical therapy should be instituted.8,21 i
Glycopyrrolate, Fort Dodge Animal Health.
j
Dantrolene, Procter and Gamble, Mason, OH.
k
Baclofen, Watson Laboratories Inc., Corona, CA.
Conclusion
Tetanus is the result of infection with C. tetani spores.
This bacteria is ubiquitous in the environment and is References
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2. Rossetto R, Rossetto O, Schiavo G, et al. Tetanus and botulinum
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