Critical Care and Resuscitation Volume 14 Number 4 December 2012316
Crit Care Resusc ISSN: 1441-2772 1 Decem-
ber 2012 14 4 316-323
The patients included in our review were all admitted to
the Royal Adelaide Hospital (RAH); initially, to the specific
tetanus ward, and later, to the intensive care unit. The two
series cover almost 30 years, preceding the emergence of
intensive care in Australia and New Zealand and extending
to the mid 1980s when it was well established. Some
procedures that were once used hesitantly have become
mainstream, while some treatments and clinical problems
are no longer seen.
The first series involves nine severe cases that presented
in 1957, published in 1959 by JRL,3 who was then the
Barker Research Fellow in Medicine at the RAH. His co-
worker was the late Maurice Sando OBE (hereafter “MS”),
who in 1957 was a senior registrar in anaesthesia, and later,
Director of the Department of Anaesthesia and Intensive
Care at RAH and Dean of the Faculty of Anaesthetists of the
Royal Australasian College of Surgeons. The second series
involves 56 unpublished cases, managed by JEG, RR and
DC between July 1967 and August 1985, of which 38 were
classified as severe.
Tetanus has a long history. Hippocrates wrote,1 “A convul-
sion after a wound is lethal ... In tetanus and opisthotonos
it is a fatal sign to sweat and for the body to be relaxed”;
and textbooks of the 1950s described devastating spasms,
often beginning with risus sardonicus and culminating with
opisthotonos — arching of the body between the heels and
the head.2 Death from asphyxia and exhaustion often
Materials and patient management
First case series
In the 1957 case series (Table 1), major spasms were
innovatively treated with neuromuscular blockade. The
authors instituted early tracheostomy, neuromuscular relax-
ants and intermittent positive pressure ventilation (IPPV) to
ensure effective ventilation. After intravenous (IV) rehydra-
tion, penicillin and equine antitetanic serum (ATS; 100000
units) were administered by IV and intramuscular (IM)
routes. To diminish light and sound stimuli that might
precipitate spasms, patients were customarily managed in a
darkened ward where staff wore tennis shoes. Sedation
was initiated with mephenesin (a centrally acting relaxant)
or chlorpromazine, with additional promethazine, pethi-
dine, chloral hydrate and oral and IM paraldehyde as
After debridement of necrotic tissue and suspected foci
of tetanus spores, tracheostomy was performed in patients
with impaired cough activity less than 24 hours after
admission, with one exception of 31 hours. A red rubber
cuffed tube sealed the respiratory tract, facilitating IPPV and
reducing regurgitation of gastric contents. This now funda-
mental measure was not universally accepted in the 1950s,
when metal tubes had been the norm. JRL and MS were
aware of tracheal ulceration from the cuffs and introduced
5 minutes of deflation 2-hourly to allow reperfusion of
When sedation did not control spasms, up to 90mg per
injection of tubocurarine was administered, intravenously at
• A review of two series of patients with tetanus from the
Royal Adelaide Hospital provides a historical perspective
on the evolution of intensive care in Australia. Nine
consecutive severe cases presenting in 1957 constituted
one of the first series published. Four patients died. The
second series of 38 severe cases, among a total of 56 cases
presenting between 1967 and 1985, included two deaths,
comparing favourably with survival in other contemporary
series. The specialty of intensive care evolved considerably
during this time.
• Neuromuscular blockade introduced in the first series
produced radical changes in management. Supportive
measures that were not then widely practised, involving
intermittent positive pressure ventilation, were used in the
second series for up to 46 days and evolved into standard
ICU practice. The option of using a tank respirator was
rejected. Older patients were susceptible to complications
commonly related to respiratory, cardiovascular and
diabetic comorbidities, but most returned to their previous
• Severe tetanus often resulted from mild injuries in patients
who were incompletely immunised. Four patients
developed tetanus following surgical procedures.
• The use of nitrous oxide in the first series was abandoned
owing to adverse effects on bone marrow function.
Complications reported in early literature, such as fractures
and myositis ossificans, presumably related to unrelieved
spasm, are no longer seen.
• Clinicians are now likely to see the condition only if working
with counter-disaster teams overseas.
Crit Care Resusc 2012; 14: 316–323
Tetanus and the evolution of intensive care in Australia
John E (Fred) Gilligan, AO, James R Lawrence, AO,
David Clayton and Robert Rowland
Critical Care and Resuscitation Volume 14 Number 4 December 2012317
first and subsequently by IM injection. IPPV was undertaken
with a Bear ventilator (Figure 1). When these measures did
not control cardiovascular hyperactivity, nitrous oxide was
introduced via an anaesthesia machine. The option of using
relaxants with a tank respirator was rejected, as IPPV
techniques allowed better access for patient management
(Marshall MG, Director of Anaesthesia, RAH, 1956–1962;
Paralysed patients required continual experienced medi-
cal supervision, including titration of medication. Ventila-
tion was assessed clinically and by venous carbon dioxide
combining power, assayed twice daily. Daily chest radiogra-
phy was performed. The FIO2 was 0.5. Biochemical and
other monitoring was limited at this time, unlike in the later
series, when early detection of trends by automated bio-
chemistry, bedside spirometry, frequent arterial blood gas
studies and advances in organ imaging enabled detection
of, for example, venous thromboses.
Nursing care included ventilator monitoring, tracheal and
pharyngeal suction, postural changes to help bronchial
drainage, and frequent passive movement of paralysed
limbs. Additional measures included detailed corneal, oral
and skin care and nasogastric nutrition. Expression of urine
from the bladder was effected into a penile sheath or by
suprapubic pressure into a pan.
Second case series
Earlier patients among the 56 in the second case series
were treated in the postoperative recovery ward, but from
1972 patients were treated in the new ICU. Their immunisa-
Table 1. Details of first case series*
Focus of infectionCurarization
1440 Tip of
15 43Infected ununited
of tibia and fibula;
8 30 Nail in sole
40% full thickness
burns of legs
4 143 6 (after onset
of disease)hours (after
14 days before
14 36 Hyster-
30 –3 24
5 36 Splinter in
M=male. F= female. *Table redrawn from Lawrence and Sando,3 page 114, used with permission. †Severe anaphylaxis after administration of equine
Critical Care and Resuscitation Volume 14 Number 4 December 2012 318
tion history was vague and their injury was frequently minor
(Table 2). The male:female ratio was 24:32, mean age was
62 years (range, 27–86 years; mode, 65 years), and most
patients were aged 60–79 years (Figure 2, A). Thirty-eight
patients were classified as having severe tetanus4 (Table 3).
The mean duration of ICU admission was 30.6 days (range,
1–64 days), and of neuromuscular blockade was 23.6 days
(maximum, 46 days). Treatment included 4000 units of
human tetanus immune globulin (except for five patients
given equine ATS), tetanus toxoid, and penicillin and other
antibiotics as required for intercurrent infections (eg, respi-
ratory). Eighteen patients classified as mild to moderate
cases all survived and are not discussed further here.
The severe cases (Grade III, as per Ablett’s classification4)
presented with a consistent pattern of dysphagia, trismus
and neck stiffness, followed by lumbar and abdominal
rigidity and generalised hyperreflexia. Progression to
opisthotonos and respiratory arrest occurred in three
patients presenting to the emergency department in
extremis. Emergency control of spasms was achieved by IV
thiopentone or diazepam with suxamethonium and rapid
sequence endotracheal intubation, followed by IPPV with
an ongoing regimen of sedation, neuromuscular blockade
and intensive supportive measures. Hypotension with
tubocurarine was not troublesome, perhaps modifying
autonomic effects; circulatory volume expansion was
required on occasion. Later in the series, pancuronium
replaced d-tubocurarine, with occasional tachycardia. A trial
suspension of neuromuscular blockade was performed,
usually weekly, to assess spasms. Weaning from ventilatory
support often extended several days beyond cessation of
Table 2. Apparent sites of Clostridium tetani
infection in 56 patients, 1967–1985, Royal Adelaide
Site of infection
Arm injury (usually minor)
Leg injury (usually minor)
Areas of chronic vascular insufficiency (leg)
Head and neck (carious teeth)
Gut: (a) Gangrenous bowel (b) Gut strangulation
Uterus: (a) Caesarean section (b) Illicit abortion
*One infection was from a below-knee amputation site.
Figure 2. Age distribution (A) and duration of
neuromuscular blockade by age group (B) among
38 patients with severe tetanus, July 1967 to
August 1985, Royal Adelaide Hospital
No. of days of neuromuscular blockade
No. of patients
Age group (years)
Age group (years)
Figure 1. Bear ventilator with anaesthesia machine
used in tetanus treatment, Royal Adelaide Hospital,
Photograph courtesy of Royal Adelaide Hospital intensive care unit.
Critical Care and Resuscitation Volume 14 Number 4 December 2012319
relaxants, because of the effects of sedation and residual
Because of the infrequent presentation of patients with
tetanus, initial misdiagnoses included hysteria, masseteric
spasm from dental sepsis, phenothiazine dystonic reactions
and the abdominal rigidity of peritonitis.
Five patients in the first case series survived. Four patients
died with major comorbidities (Table 1); one, with 40% full-
thickness burns, also suffered severe anaphylaxis associated
with equine ATS; another, with an abortion site infected
with Clostridium tetani, required a hysterectomy and appar-
ently also developed a septic syndrome; and a third was
dehydrated and in renal failure on admission when dialysis
and venous pressure assessment of rehydration were not
yet used at RAH.
In the second case series, 36 survivors of 38 severe cases
were discharged from hospital. Major problems encoun-
tered in their management are listed in Table 4. Episodes of
acute respiratory distress syndrome (ARDS)5,6 followed inha-
lation of gastric content from tracheostomy cuff leakage.
These resolved with continued IPPV, positive end-expiratory
pressure, antibiotics and mild dehydration measures. One
patient developed a residual restrictive ventilatory defect,
prompting lung function tests on a random selection of six
other patients, which were normal. One tracheostomy-
related stricture was associated with an older design of tube
(1969). A second was in a patient whose tracheostomy was
necessarily repeated at the site used previously during an
acute exacerbation of chronic respiratory failure. Both
strictures responded to tracheal dilation. Tracheal computed
tomography performed on six other asymptomatic patients
showed no significant narrowing. Skin tethering and stomal
granulations were relieved by minor surgery and silver
nitrate cautery, respectively.
Respiratory failure of central origin occurred in a woman
aged 30 years. After severe tetanus she developed uncoor-
dinated intercostal and diaphragmatic action, unrelated to
persistent drug effects. Her limb power was normal and
there was no Babinski response. This syndrome was not
consistent with polyneuropathy of the critically ill7 and was
possibly cephalic tetanus8 or a brainstem vascular accident.
Reinstituted ventilatory support was gradually withdrawn
over 5 weeks.
Of the two deaths, one 74-year-old male patient with
diabetes, transferred from ICU after 41 days of IPPV,
succumbed on a general ward. Autopsy revealed extensive
peripheral arterial disease and coronary atheroma. A large
recent myocardial infarction involved the anterior wall of
the left ventricle, confirmed histologically, but no evidence
of myocardial lesions ascribed to tetanus9 was found.
Raised small plaques adherent to the caecal, colonic and
rectal mucosa were shown histologically to be pseudomem-
branous colitis,10 either antibiotic related11 or ischaemic in
origin, which had not been suspected while the patient was
alive. The second death involved a woman aged 86 years,
who had been on IPPV for 20 days. She developed ARDS
and died before abdominal exploration could be performed
(this was the pre-laparoscopic era). Autopsy revealed a
perforated acute duodenal ulcer and peritonitis, confirming
the difficulty in diagnosing the acute abdomen in such
C. tetani was cultured from wounds in 21 of the 56
patients (37.5%), but the diagnosis is essentially clinical —
cultures from many of the patients with severe tetanus did
not grow the organism. Tetanus followed surgical condi-
Table 3. Severity of tetanus in 56 patients (based on
Ablett’s classification4), 1967–1985, Royal Adelaide
Mild, no dysphagia or respiratory difficulty
Moderate, dysphagia and increasing rigidity
Severe, requiring neuromuscular blockade,
relaxants and sedatives
As for Grade IIIa, plus autonomic disturbances
Figure 3: Effects of treatment with nitrous oxide on
haemoglobin and polymorph count in a patient
with severe tetanus
Figure reproduced from Lawrence and Sando,3 page 115,
Critical Care and Resuscitation Volume 14 Number 4 December 2012 320
tions in three patients: in one woman the organism was
cultured from the vagina following caesarean section. Two
patients developed peritonitis after strangulated ischaemic
gut — a reminder that C. tetani can be found in human
Comparison of the two case series produces several points
of interest. Neuromuscular blockade and IPPV had been
described in earlier case reports14,15 but Lawrence and
Sando’s series3 illustrating management of severe tetanic
spasms using muscle relaxants with IPPV confirmed a major
change in treatment, radically affecting the outcome of the
disease by preventing death from asphyxia during spasms.
They eschewed the option of using a tank respirator as too
They emphasised the advantages of relaxants over their
previous protocol of sedation in a quiet, darkened room:
[Neuromuscular blockade] eliminates the exhausting
painful spasms and rigidity, making the patient more
comfortable and less apprehensive. It allows nursing
procedures ... to be done more effectively by eliminat-
ing the strain of working as silently as possible in a
darkened room ... physiotherapy and adequate tracheal
aspiration can be performed without precipitating fur-
we feel that the technique of paralysis and mechanical
artificial ventilation has a real place in the management
of tetanus ... in the fulminating case or in the severe
case when sedation and other relaxant agents fail to
control reflex spasms and thoracic rigidity ... it should
not be left until ... the patient is in extremis.3
In the 1950s, the first steps towards the use of relaxants
in tetanus had been taken. However, the discussion in
major textbooks at the time on their use in combating
skeletal muscle spasm was hesitant and confused:
Curare and curare-like compounds ... probably repre-
sent the agents of choice if they are intelligently and
carefully administered ... D-tubocurarine chloride may
be used as a repository preparation in oil and wax ...
Succinylcholine ... [is] contraindicated in the treatment
of tetanus because of the possible dangers that attend
prolonged depolarisation of the motor endplate ... In
some cases a mechanical respirator will be necessary ...5
Lawrence and Sando3 emphasised continuous attendance
in such unstable patients along with early tracheostomy,
relaxants, IPPV plus meticulous airway care, including meas-
ures to limit the effect of cuff pressure on tracheal mucosa.
Damage from cuffs still remains a cause for concern,
although developments such as polyvinyl chloride construc-
Table 4. Principal adverse events during
management of 38 patients with severe (Grade III)
tetanus, 1967–1985, Royal Adelaide Hospital
Acute respiratory distress syndrome
Atelectasis, respiratory infection
(clinical and radiological)
Restrictive ventilatory defect1 No change.
Tracheal stricture2 Resolved with
Tracheostomy site skin tethering1
Tracheostomy site stomal
2 Resolved, silver
Central respiratory failure (cephalic
Right facial nerve weakness
1 No data
Hemiparesis from cerebrovascular
Sciatic nerve injury (intramuscular
1 Slow progress
Lateral popliteal nerve injury
2 Slow progress
Cardiac arrest (on presentation)3Recovered
Myocardial infarction2 1 recovered;
1 died (post ICU)
Atrial fibrillation, arterial embolism,
Deep venous thrombosis (leg)
Venous thromboses (arm)
Subclavian venous thrombosis,
carpal tunnel syndrome
Superficial major thrombophlebitis
at intravenous insertion site
Joint stiffness8 Resolved
Pseudomembranous colitis1 Autopsy
ICU=intensive care unit.
Critical Care and Resuscitation Volume 14 Number 4 December 2012321
tion and large-volume, low-pressure cuffs have reduced the
Lawrence and Sando16 found nitrous oxide useful as an
additional sedating agent for conscious and paralysed
patients, supplementing their regimen of basal sedation
and neuromuscular blockade. Administered via an anaes-
thesia machine, it reduced cardiovascular hyperactivity, but
they encountered dramatic falls in polymorph and reticulo-
cyte counts, which rapidly recovered upon its withdrawal
(Figure 3). Lassen and colleagues17 described similar find-
ings. Career pressures deflected Lawrence and Sando from
further exploration of these observations, which antedated
by many years what we now know as the limitations of this
agent in anaesthesia, considering current knowledge of its
role in human biology.18
By the time of the second case series, ICU educational
programs had enabled registered nurses to undertake
greater responsibilities with critically ill patients. Intravascu-
lar and electrocardiogram monitoring enabled early atten-
tion to be given to circulatory disturbances. The safe
management of paralysed ventilated patients for prolonged
periods, tentatively developed during the time of the 1957
series, became well established (Figure 2, B) — a key
development. While prolonged endotracheal intubation
was used in other conditions, early tracheostomy was
preferred for the commonly extended period of IPPV in
tetanus. The Bjork flap was used initially; later, a window
technique was used,19 usually performed at the time of
wound exploration. The Griggs dilational technique,20
developed at ICU RAH to obviate moving ventilated patients
over distances to operating theatres, was to come later.
Standard use of central venous lines markedly reduced
painful IM injections and multiple peripheral thrombophle-
bitides, which were problematic in the first case series. They
facilitated hydration, administration of medication, venous
pressure measurement and IV nutrition during periods of
gut stasis, although nasogastric intubation was preferred
for nutrition and for much medication. Enteral nutrition
may have accounted for the infrequency of significant
gastrointestinal bleeding21 in an era when prophylaxis was
Autonomic hyperactivity22,23 produced bouts of hyperten-
sion, hypotension, and ventricular and atrial tachyarrhyth-
mias in 13 of our patients. They responded to combinations
of alpha and beta blockade, antiarrhthymics, preload
adjustment and judicious infusion of inotropes. Chlorpro-
mazine, with combined alpha-adrenergic blockade and
anxiolytic effects, was especially useful. Thermodilution
studies during brief periods of autonomic hyperactivity in
sedated, paralysed patients typically returned a mildly ele-
vated cardiac output of around 9L/min with blood pressure
220/110mmHg. One patient required total alpha and beta
sympathetic blockade and titrated fluid and inotrope infu-
sion to achieve circulatory stability. With adequate sedation,
analgesia and control of tetanic spasms, asystole and
recurrent circulatory arrest24 described in patients receiving
beta-blockers and labetolol25 were not encountered, and it
is conceivable that vigorous beta blockade in the face of
high systemic vascular resistance may have produced left
ventricular failure in reported cases. There were reports of
epidural placement of local anaesthetic agents successfully
reducing circulatory hyperdynamic effects by sympathetic
blockade,26 but the duration of such techniques is necessar-
Interestingly, we encountered no overt polyneuropathy,
despite the use of repeated boluses of relaxants, considered
by some to be contributory.27,28 A sciatic nerve palsy was
thought to be the result of a misplaced intramuscular
injection. No obvious cause existed for the other neural
lesions (Table 4). Comorbidities common in the elderly,
particularly vascular and respiratory diseases, contributed
both to causation and some adverse events. For example, a
73-year-old man developed tetanus after below-knee
amputation, performed when atrial fibrillation produced
embolic dry gangrene of a digit; and an 81-year-old man
sustained an anterior myocardial infarction during IPPV,
requiring several days’ inotropic support before recovery.
Nonetheless, elderly patients commonly returned to accept-
able lifestyles: review of hospital records and questionnaires
sent to GPs regarding the 38 severe cases in our second
series indicated that 20 (53%) returned to a quality of life
similar to that enjoyed previously.
Earlier literature described kyphotic spinal deformities29
and vertebral crush fractures,30 presumably related to sus-
tained tetanic spasms. Myositis ossificans,31 a slow passive
deposition of calcium salts maturing into bone formation in
tendons,32 ligaments and joint capsules in tetanus, has been
noted in other central nervous conditions such as poliomye-
litis and musculoskeletal trauma.33 Gunn and Young34 noted
that physiotherapy in such conditions could involve joint
movements conducted against muscle spasm and con-
tended excessive force could produce local damage to
muscles and ligaments, resulting in the deposits. However,
such problems were not noted in the two series we
reviewed and are uncommon in recent publications. Con-
ceivably, the abolition of the effects of severe spasm on
tendons and ligaments by neuromuscular blockade and
maintenance of the normal range of joint movements with
relaxed muscles may have reduced these phenomena.
Two other Australian groups grappling with tetanus
produced significant reports during the period of the two
series discussed. Newton-John35 (1957–1980) described
106 cases with a fatality rate of 26% in an infectious
diseases hospital. In the severe group he progressed from
Critical Care and Resuscitation Volume 14 Number 4 December 2012322
using tank ventilators and uncuffed metal tracheostomy
tubes to IPPV using relaxants and cuffed tubes, though he
seemed cautious, awaiting “chest fixation” before using
such measures. Saady and Torda36 (1961–1972) managed
37 patients with conventional intensive care techniques.
Twenty-four severe cases treated with relaxants, tracheos-
tomy, cuffed tubes and IPPV returned a mortality of 23%.
These involved a death during tracheostomy, one from
sepsis, three from cardiomyopathy and three associated
with gastrointestinal bleeding. Two of the latter were given
steroids, advocated at the time for tetanus.37
Medication via the intrathecal route was an interesting
innovation. Miranda-Filho et al,38 in a Brazilian randomised
controlled trial, compared the outcomes of intrathecal
versus intramuscular antitetanus immunoglobulin in 120
patients, claiming “improved clinical progression”. It
appeared to reduce severity and fewer required mechanical
ventilation, although the difference was not significant.
Mortality, reduced from 35% to 18%, still exceeded other
recent ICU figures. Reports of paraplegia following the
technique encourage caution.39 The intrathecal route for
medication is worthy of consideration, but antispasmodic
agents such as baclofen used intrathecally40,41 seem best
confined to locations where conventional intensive care is
unavailable. Evidence suggests the only technique likely to
relieve life-threatening spasms involves the use of relaxants
Tetanus incidence and mortality in Australia following
World War II was high, especially in older adults with
incomplete immunity. Effective immunisation42 has cor-
rected this, with one death reported from 2003 to 2005.
Recently, from 2001–2008, the larger body of United
States data indicated a case fatality rate of 13.2% and, for
1998–2000, 31% among severe patients who required
mechanical ventilation,43 mainly among the incompletely
immunised,44 intravenous drug users, the elderly and those
with comorbidities such as diabetes. Similar figures are
quoted from Brazil.
However, as shown in our limited series, an overall death
rate of 3.6% (5.3% for severe cases) is achievable. Mortality
remains high in developing countries, and the current
generation of health professionals is likely to encounter the
disease only when working in medical teams attending less
developed nations in disasters such as floods, earthquakes
and civil disturbances (Cornish BL, Orthopaedic Surgeon,
Vung-Tau Field Hospital, Vietnam, 1978, personal commu-
The 53 years since the first series was published saw a
considerable improvement in tetanus outcomes, coinciding
with the evolution of intensive care. This disease, now
eminently treatable but requiring major resources, is fortu-
nately now rare. Its response to neuromuscular blockade
and effective supportive therapy can be considered a model
for intensive therapy. It may have prompted the more
widespread use of relaxants in various conditions requiring
IPPV, but the pros and cons of that debate are for another
Permission to publish this review was provided by the
Medical Staff Society, RAH.
John E (Fred) Gilligan, AO, Emeritus Director of Intensive Care
James R Lawrence, AO, Emeritus Professor of Medicine2
David Clayton, Intensive Care Physician1
Robert Rowland, Former Head of Tissue Pathology3
1 Royal Adelaide Hospital, Adelaide, SA.
2 University of Sydney, Sydney, NSW.
3 Institute of Medical and Veterinary Science, Adelaide, SA.
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