ACCCN's Critical Care Nursing

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3
S E C T I O N












Specialty Practice in Critical Care

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Emergency Presentations 22





David Johnson
Mark Wilson




additional common presentations to the Emergency
Learning objectives Department (ED): trauma and resuscitation emergencies,
respectively.
After reading this chapter, you should be able to: The chapter initially describes the organisational systems
l describe the uniqueness of the emergency care and processes of care in an ED environment, including
environment triage, extended practice nursing roles, multiple casualties/
l outline the development of Australasian triage models disaster management and transport/retrieval of critically
l discuss the process of initial patient assessment and triage ill patients. A select group of the most common emer-
nursing practice gency presentations and conditions related to critical care
l integrate emergency nursing principles and practice in practice are then described, particularly topics not dis-
initial patient care cussed in other chapters: acute abdominal pain, overdose
l describe the various roles of extended nursing practice in and poisoning, envenomation, near-drowning, hypother-
the emergency setting mia and heat illness. The initial clinical assessment and
l describe the principles and practice of patient preparation incidence of these common presentations is discussed,
for retrievals or transfers and the likely diagnoses associated with these presenta-
l discuss the principles for the management of disaster tions and their initial management in the ED are also
victims in the emergency department outlined. Ongoing management of these selected condi-
l discuss the initial nursing management of common tions are discussed in the relevant chapters in Section II
presentations to the ED, including chest pain, abdominal of this text.
pain, neurological, respiratory, poisoning, envenomation, Emergency nursing practice is the holistic care of indi-
submersion and heat illness. viduals of all ages who present with perceived or actual
physical and/or emotional alterations. These presenta-
tions are often undiagnosed and require a range of
prompt symptomatic and definitive interventions. Emer-
Key words gency clinical practice is usually unscheduled, episodic
and acute in its nature, and is therefore unlike any other
triage type of nursing in the demands it places on nursing
1,2
extended practice staff. In many instances the emergency nurse is the first
poisoning healthcare professional to be in contact with an acutely
ill or injured patient. Patient presentations include a full
retrieval range of acuity across the spectrum of possible illnesses,
disaster management injuries and ages.
envenomation
near-drowning BACKGROUND
heat illnesses
hypothermia Emergency nursing is unique, in that it involves the care
of patients with health problems that are often undiag-
nosed on presentation but are perceived as sufficiently
INTRODUCTION acute by the individual to warrant seeking emergency care
in the hospital setting. As patients present with signs and
Emergency nursing practice covers an enormous range of symptoms rather than medical diagnoses, refined assess-
clinical presentations. As the focus of this book is critical ment skills are paramount. Many skills required by
care, this chapter discusses conditions at the critical end emergency nurses are based on a broad foundation of
of the practice spectrum. Please read in conjunction with knowledge that serves as a guide in collecting informa-
Chapters 23 and 24, which describe the management of tion, making observations and evaluating data, and to 581

582 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

2-6
sort and analyse relevant information. This foundation
enables an emergency nurse to communicate appropri- TABLE 22.1 Australasian triage code
ately with other members of the healthcare team, and to
implement appropriate independent and collaborative Code Descriptor Treatment acuity
nursing interventions. Assessment is an important element
of emergency care; other chapters provide detailed infor- 1 Resuscitation Immediately
mation on the evaluation of critically ill patients. 2 Emergency Within 10 minutes
Emergency nurses are specialists in acute episodic nursing 3 Urgent Within 30 minutes
care, and their knowledge, skills and expertise encompass 4 Semiurgent Within 1 hour
almost all other nursing specialty areas. Emergency nurses
therefore possess a unique body of knowledge and skill- 5 Non-urgent Within 2 hours
sets to manage a wide variety of presentations across all
age groups; this includes familiarity with general physical
and emotional requirements of each age group as these included a time-based scale and different colours on the
1,7,8
relate to their presenting health needs. ED nurses work medical record to indicate priority. Subsequent modi-
2-4
cooperatively with prehospital emergency personnel, fication and refinement led to the Ipswich Scale in the
1,2,4,5,7
doctors and other healthcare personnel and agencies in 1970s–80s. These early triage systems reinforced the
the community to provide patient care. 2,3,5 Roles in the concepts developed by Larrey, and established a process
ED include triage, direct patient care, expediting patient for patients’ presentations to be seen in order of clinical
flow, implementing medical orders, providing emotional priority rather than time of attendance. In the 1990s the
support during crises, documenting care, and arranging impact of community expectations and national health
for ongoing care, admission to the hospital, transfer policy led to further enhancements of triage systems in
to another healthcare facility, or discharge into the Australia, and the Ipswich triage scale was adapted into
community. 5,6 the national triage scale (NTS). The NTS was subsequently
tested and demonstrated to have the essential character-
TRIAGE istics of utility, reliability and validity. 1,2,4,5,7,9-11 In 1993,
the NTS was adopted by the Australasian College for
7
Central to the unique functions of an ED nurse is the role Emergency Medicine (ACEM) in its triage policy, and
of triage; perhaps the one clinical skill that distinguishes subsequently renamed the Australasian triage scale (ATS)
an emergency nurse from other specialist nurses. Triage as it was implemented in most EDs in Australia and New
4
literally means ‘to sieve or sort’, and is the first step in Zealand (see Table 22.1).
any patient’s management on presentation to an ED. 1-3 The ATS is now a world-leading, reliable and valid triage
classification system for emergency patients, with demon-
HISTORY OF TRIAGE strated predictive properties for severity of illness, mortal-
Triage was first described in 1797 during the Napoleonic ity and the need for admission. 5,7,9-11 When properly
wars by Surgeon Marshall Larrey, Napoleon’s chief applied, presenting patients should receive the same
7
medical officer, who introduced a system of sorting casu- triage score no matter which ED they present to. 5,9,11
alties that presented to the field dressing stations. His
aims were military rather than medical, however, so the THE PROCESS OF TRIAGE
highest priority were given to soldiers who had minor All patients presenting to an ED are triaged on arrival by
wounds and could be returned quickly to the battle lines a suitably experienced and trained registered nurse. 2,10
with minimal treatment. 1,8 This assessment represents the first clinical contact and
The documented use of triage was limited until World the commencement of care in the department. The ideal
War I, when the term was used to describe a physical area features of a triage area are: a well-signposted location
where sorting of casualties was conducted, rather than a close to the patient entrance; ability to conduct examina-
description of the sorting or triage process itself. Triage tion and primary treatment of patients in privacy; a close
8
continued to develop into a formalised assessment physical relationship with acute treatment and resus-
process, with subsequent adoption for initial categorising citation areas; and appropriate resources including an
of patient urgency and acuity within most civilian EDs. 1,7,8 examination table, thermometer, a sphygmomanometer,
stethoscope, glucometer and pulse oximetry. 2,4,10
DEVELOPMENT OF TRIAGE PROCESSES IN As the first clinician in the ED to interview the patient,
AUSTRALIA AND NEW ZEALAND the triage nurse gathers and documents information from

Australia is a world leader in the development of emer- the patient, family and friends, or prehospital emergency
personnel. Professional maturity is required to manage
gency triage and patient classification systems. In the late the stress inherent in dealing with an acutely ill patient
1960s patients presenting to ‘casualty’ departments in and family members (under significant stress themselves),
Australia were not always triaged, 1,2,4,5 with many EDs while rapidly making informed judgement on priorities
using random models of care; ambulance presentations of care for a wide range of clinical problems. 10
were given priority and the ‘walking wounded’ seen in
order of arrival. In the mid-1970s, staff at Box Hill Hos- The triage nurse receives and records information about
pital in Melbourne developed a five-tiered system that the patient’s reason for presentation to the ED, beginning

Emergency Presentations 583

with a clear statement of the complaint in the patient’s TRIAGE ASSESSMENT
own words, followed by historical information and Patient assessment at triage has three major components:
related relevant details, such as time of onset, duration of quick, systematic and dynamic. Speed of assessment is
symptom/s, and what aggravates or relieves the symptom/s. required in life-threatening situations, with the focus on
A brief, focused physical assessment including vital signs airway, breathing, circulation and disability (A,B,C,D),
may be undertaken to identify the urgency and severity and a quick decision on what level of intervention is
of the condition, and may be collected as part of the required. A systematic approach to assessment is used for
triage process to inform decision making. 5,10,11 Triage all patients in all circumstances, to ensure reproducibility.
assessment generally should be no longer than 2–5 Finally, the triage assessment must be dynamic, in that
11
minutes, balancing between speed and thoroughness. several aspects can be undertaken at once, and acknowl-
From the information collected, the triage nurse deter- edging that a patient’s condition can change rapidly after
1-3
mines the need for immediate or delayed care, and initial assessment. Various assessment models are avail-
assigns the patient a 1–5 ATS category in response to the able, but fundamentally they all include components of
statement: This patient should wait for medical assessment observation, history-taking, primary survey and second-
and treatment no longer than … . 11 1-3,4,6,11,12
ary survey.
Patients with acute conditions that threaten life or limb
receive the highest priority while those with minor illness
or injury are assigned a lower priority. It may not be pos- Patient History/Interview
sible to categorise the patient correctly in all instances, The triage interview provides the basis for data gathering
but it is better to allocate priority on a conservative basis and clinical decision making regarding patient acuity.
and err on the side of a potentially more serious After an introduction, the triage nurse asks person-specific
problem. 3,8,10,11 Importantly, a triage allocation is dynamic open-ended questions. Use of close-ended questions or
and can be altered at any time. If a patient’s condition summative statements enables clarification and confir-
5-8
changes while waiting medical assessment/treatment, or mation of information received, and to check under-
if additional relevant information becomes available that standing by the patient. Privacy is important to ensure
12
impacts on the patient’s urgency the patient should be that the patient is comfortable in answering questions of
re-triaged to a category that reflects the determined a personal nature. Most EDs need to balance providing
urgency. 11,12 Frequent, ongoing observation and assess- an area that is private and accessible, yet safe for staff to
ment of patients is therefore routine practice following work in relative isolation.
the initial triage assessment.
A large component of the triage assessment may be based
on subjective data, which are then compared and com-
bined with the objective data obtained through the senses
Practice tip of smell, sight, hearing and touch to determine a triage
category: pulse, blood pressure, respiratory rate and char-
The aims of triage are to deliver the right patient to the right acteristics, oxygen saturation, capillary return, tempera-
treatment area at the right time. Triage decisions must be accu- ture, blood glucose level. One aspect of the history that
rate, ensure the patient’s safety and be reproducible across is difficult to quantify is intuition. This is that ‘sixth sense,
clinicians and departments. or gut feeling’ that tells us that something not yet detect-
able is wrong with the patient. This unexplained sense is
difficult to outline or apply scientific research models to,
but it has an important role to play in patient assessment
and should be acknowledged when something ‘doesn’t
The premise for a triage decision is that utilisation of feel right’. 6,11,12
valuable healthcare resources provide the greatest benefit
for the neediest, and that persons in need of urgent atten-
tion always receive that care. 1,2,4,5,11,12 Triage encompasses
the entire body of emergency nursing practice, and nurses Primary Survey
complete a comprehensive triage education program While taking a patient history, the triage nurse also
prior to commencing this role. A formal national triage simultaneously conducts a primary survey. As noted
training resource has been developed that provides the earlier, airway, breathing, circulation and neurological
essential education components to promote consistency function (deficit) is observed. If any major problem
in application of the ATS. 11,12 is observed, the interview is ceased and the patient
is transferred immediately to the acute treatment or
TRIAGE CATEGORIES resuscitation area. 8
After triage assessment is undertaken on arrival, patients
are allocated one of five triage categories using the
Australasian triage scale (ATS) (see Table 22.2). Prompt Secondary Survey and Physical Examination
assessment of airway, breathing, circulation and disability A secondary survey, involving a concise, systematic
remains the cornerstone of patient assessment in any physical examination, is conducted after the patient
clinical context, including triage. history and primary survey have been completed. The

584 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



TABLE 22.2 Australasian triage scale (ATS) category characteristics 5,11

ATS code Typical description
1 Immediately Life-Threatening (or imminent risk of deterioration)
Patients are critically ill, and require immediate transfer to a resuscitation area for initial resuscitation, with no delay at
triage. 3,5,11,12 The majority will arrive by ambulance, and will be suffering:
l multi-trauma
l shock
l unconsciousness
l convulsions
l extreme dyspnoea
l cardiorespiratory arrest.
2 Imminently Life-Threatening
Patients ‘at high risk’ of critical deterioration or have very severe pain from any cause. Assessment and treatment needs
to commence within 10 minutes for: 3,5,11,12
l chest pain or other symptoms suggestive of myocardial ischaemia, pulmonary embolism or aortic dissection
l important time-critical treatment (e.g. thrombolysis, antidote)
l severe abdominal pain or other symptoms suggestive of ruptured aortic aneurysm
l severe dyspnoea from any cause
l altered levels of consciousness
l acute hemiparesis / dysphasia
l fever, rash, headache, suggestive of sepsis or meningitis
l severe skeletal trauma such as femoral fractures or limb dislocations
l very severe pain from any cause (practice mandates the relief of pain or distress within 10 minutes)
3 Potentially Life-Threatening or Situational Urgency
Patients have significant illness or injury and should have assessment and treatment commenced within 30 minutes of
presentation. Typical patients include those with: 3,5,11,12
l moderately severe pain from any cause (e.g. abdominal pain, acute headache, renal colic), but not suggestive of critical
illness; practice mandates relief of severe discomfort or distress within 30 minutes
l symptoms of significant infections (e.g. lung, renal)
l moderate injury (e.g. Colles’ fracture, severe laceration without active haemorrhage)
l head injury, with transient loss of consciousness
l persistent vomiting / dehydration.
4 Potentially Serious
The patient’s condition may deteriorate, or adverse outcome may result, if assessment and treatment is not commenced
within 1 hour of arrival. Patients have moderate symptoms, symptoms of prolonged duration, or acute symptoms of
low-risk preexisting conditions, including: 3,5,11,12
l minor acute trauma (e.g. sprained ankle)
l minor head injury, no loss of consciousness
l mild haemorrhage
l earache or other mildly painful conditions
l practice mandates relief of discomfort or distress within one hour
l there is a potential for adverse outcome if time-critical treatment is not commenced within one hour
l likely to require complex work-up and consultation and/or inpatient management.
5 Less Urgent
The patient’s condition is minor or chronic; acute symptoms of minor illness, symptoms of chronic disease or with a
duration of greater than 1 week. Symptoms or clinical outcome will not be significantly affected if assessment and
treatment are delayed up to 2 hours from arrival. Examples include: 3,5,11,12
l chronic lower back pain with mild symptoms
l minor wounds: small abrasion/minor lacerations
l most skin conditions
l clinical administrative presentations (e.g. results review, medical certificates, repeat prescriptions).




equipment used includes a thermometer, stethoscope,
oxygen saturation monitor and sphygmomanometer, in Practice tip
combination with clinical skills. This examination is
not comprehensive but focuses on the presenting com- The triage physical assessment should be quick, accurate and
plaint while avoiding tunnel vision and wrong con- concise, focusing on the presenting complaint.
clusions. 3,12 Remember that the patient may not be able
to lie down or be exposed for an examination in
the triage area, and may be distressed. The triage process Approaches to Triage Assessment
should reflect a system of rapid assessment that A range of approaches to nursing assessment is applicable
8
is reproducible and adaptable to a variety of to triage assessments (see Table 22.3). Body systems
presentations. approach enables systematic examination of each body

Emergency Presentations 585

system to discover abnormalities (i.e. central nervous Mental Health Presentations
system, cardiovascular system, respiratory system, gastro- Patients with psychiatric problems presenting to an ED
intestinal system, etc.). 6,11,12 See also the relevant ‘system- should be triaged, assessed and treated as for other
based’ chapters.
presenting patients, with particular attention to appro-
priate initial medical assessment and management. 6,11,12
TRIAGE ASSESSMENT OF SPECIFIC Resources outlining specific mental health triage category
PATIENT GROUPS descriptors are readily available, and relate specific
While triage assessment is a complex process for a range aspects of mental health presentation with clinical
of patient presentations, some specific groups are more urgency and triage categories (see Table 22.4), including
demanding, such as mental health, paediatric and mass an outline of suggested responses, such as patient place-
casualty patients. ment requirements based on the level of risk and
urgency. 6,11-14


Practice tip Paediatric Presentations
Children presenting to the ED are assessed and assigned
If it is unclear what triage category should be assigned, the a triage category as for adults, although vital differences
patient should be allocated a higher category.
in paediatric anatomy, physiology and clinical presenta-
tions should be considered (see Chapter 25). The reli-
ance of information from parents or primary carers
and their capacity to identify deviations from normal
is important, particularly in supporting recognition of
TABLE 22.3 Aids to triage assessment often subtle indicators of serious illness in infants and
young children. Paediatric triage resources are available
Mnemonic Components to assist in identifying physiological alterations and
SOAPIE Subjective data applying the ATS based upon identified physiological
Objective data discriminators. Other important points to consider
12
Assessment (to enable formulation of a …) include:
Plan (that is …)
Implemented (and …) l children may suffer rapid decompensation due to
Evaluated (as to its success) limited physiological reserves; a short time is a
AMPLE Allergies long time in the life of a child, and may develop
Medications serious illness in a much shorter time than for an
Past medical history adult. 11,12,15
Last food and fluids ingested
Environmental factors and Events leading to l children are less able to tolerate pain in either physical
presentation or psychological terms. 11,12,15
l it is difficult to rationalise long waiting periods with
PQRST Provoking or Precipitating factors
Quality and Quantity (severity) of the symptom a child or parent of a sick child. The longer they wait,
Region/Radiation the more difficult an examination becomes. 11,12,15
Symptoms associated l parents are much less tolerant of waiting times
Time of onset and duration of episode, and for their sick child than they would be for
Treatment
themselves. 11,12,15





TABLE 22.4 Examples of a mental health triage tool 13
ATS Observation Action
1. Immediate Severe behavioural disorder with immediate l Provide continuous visual observation in safe environment
threat of dangerous violence to self or others l Ensure adequate personnel to provide restraint/detention
2. Emergency Severe behavioural disturbance with probable l Provide continuous visual observation in safe environment
risk of danger to self and others l Use defusing techniques
l Ensure adequate personnel to provide restraint/detention
3. Urgent Moderate behavioural disturbance or severe l Provide safe environment, frequent visual observations every
distress with possible danger to self and others 10 minutes
4. Semi-urgent Semi-urgent mental health problem with no l Regular visual observations at a maximum of every 30 minutes
immediate risk to self or others
5. Non-urgent No behavioural disturbance or acute distress l Regular visual sighting at a maximum of one hour intervals
with no danger to self or others

586 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

EXTENDED ROLES subsequent incremental doses in response to a reevalua-
tion of the patient’s pain score and vital signs (pulse,
Contemporary roles in many EDs have expanded to blood pressure and respiratory rate). Protocols directed
include clinical roles and functions that have emerged as towards moderate and minor pain may include either
a result of reengineering work practice processes in single or incremental IV analgesia or oral analgesia.
response to an increasing number of emergency presenta- Nurse-initiated analgesia protocols have also been found
tions, and to improve performance in patient flow, waiting to be safe and effective and to shorten the time ED
times, length of stay and patient satisfaction. 16-18 This patients wait for analgesia, 23,24 which should assist in
expanded scope of practice includes advanced clinical improving patient outcomes and satisfaction.
skills performed using agreed protocols and accreditation
supported by additional education and regular periods of CLINICAL INITIATIVE NURSE
performance review. The role has become known as an
advanced clinical nurse (ACN) or advanced practice nurse The clinical initiative nurse (CIN) is a specific advanced
17
(APN), involving, but not limited to, the following practice role introduced to primarily provide care for
advanced clinical skills: 16,18 waiting-room patients awaiting medical officer assess-
ment. The role was initially introduced into levels 5 and
l venipuncture and cannulation 6 metropolitan and several large rural EDs in New South
l arterial blood gas sampling Wales, to manage and reduce ED waiting times and asso-
l suturing ciated patient distress, improve ‘time seen’ rates, patient
l plaster application service satisfaction and patient outcomes (key perfor-
l ordering of radiology mance indicators). These and similar roles are now being
l ordering of pathology implemented nationally. The role includes initiation of
25
l administration of nurse-initiated narcotic analgesia treatment for lower-acuity waiting-room patients, follow-
and other medications. ing advanced practice protocols. The treatment provided
by the CIN includes ordering of radiology and/or patho-
NURSE-INITIATED X-RAYS logy investigations, administration of oral analgesia,
review and reassessment of waiting patients (particularly
Nurse-initiated radiology ordering enables investigations those who have waited longer than their triage bench-
of extremities, joints such as hips and shoulders, the chest mark time), and providing information and education to
and abdomen according to clinical protocols that list waiting patients and carers regarding waiting times, ED
19
inclusion and exclusion criteria based on findings from processes and patient education. The role acts as an
the ACN’s history-taking and clinical examination. The adjunct to the triage role, and maintains a close working
inclusion criteria reflect well-established clinical indica- relationship with the triage nurse. 25-27 The CIN role has
tors. While nurse-initiated radiology ordering is often contributed to timely access to interventions, investiga-
undertaken as an extended triage nurse function, it can tions and care for waiting patients, increases autonomous
be performed by any accredited nurse. The use of nurse- practice, independent decision making and enhances
initiated radiology, especially in association with extrem- patient advocacy. The role also provides opportunity for
ity injuries, is safe and accurate, reducing both waiting the clinical and professional development of emergency
time and department transit time and improving both nurses. 26
patient and staff satisfaction. 17,19-21

NURSE-INITIATED ANALGESIA NURSE PRACTITIONER
Although pain is a common complaint in the majority of The nurse practitioner (NP) level of health care is one of
the most important developments in contemporary
patients presenting to the ED, 22,23 management has previ- nursing and marks the opportunity for significant reform
ously been insufficient, especially in relation to the in Australian health care. Nurse practitioners, while
timeliness, adequacy and appropriateness of analgesia well established in North America, the UK and parts of
administered, 22,23 and resulting in poor patient satisfac- Europe, are a relatively recent development in Australia.
22
tion. To address these findings, many EDs developed Introduction of the NP level of service has been a
nurse-initiated analgesia protocols, standing orders or function of individual states rather than a national
pathways. Nurse-initiated analgesia protocols enable des- government process, and consequently implementation
ignated emergency nurses to implement analgesia regi- throughout Australia has been gradual, with title protec-
mens prior to assessment by a medical officer. These tion and practice privileges now legislated in five states
protocols are locally derived and note patient inclusion over a 15-year period.
and exclusion criteria for managing mild, moderate or
severe pain in both adult and paediatric patients, and Introduction of the NP has been complicated by existing
often include administration of an antiemetic. 22,23 A nomenclature relating to advanced practice roles in
numerical pain rating scale or a visual analogue scale is nursing, with titles such as advanced specialist, clinical
used to direct the type and route of analgesia administra- nurse consultant, clinical nurse specialist and advanced
tion. Severe pain protocols outline incremental intrave- practice nurse used interchangeably and at times prob-
nous narcotic administration, including incremental and lematically in the literature, 28,29 including internation-
30
total maximum administration dosages. After administra- ally. Consensus is gradually emerging that the NP
tion of the initial dose, the administering nurse gives role is evolving and developing globally as the most

Emergency Presentations 587

significant of the advanced practice roles in modern RETRIEVALS
health care. 29
Australasia has a variety of retrieval or transport models,
The NP scope of practice is determined by the clinical although most retrieval teams comprise doctors, nurses
setting of the authority to practise. There are three points and paramedics with specialised training in critical care.
in this central to the nature of the role: The skills of the escort personnel need to match the acuity
of the patient, so that they can respond to most clinical
1. Extended practice: The scope of practice of the NP problems. 47,48 Retrieval team staff therefore need to deliver
is subject to different practice privileges that are high-level critical care equal to the standard of the receiv-
protected by legislation, and occur outside the ing centre, but need to be familiar with the challenges
scope of practice for a registered nurse. These associated with working outside the hospital environ-
extended practice privileges mean that the NP ment. Standards for the transport of critically ill patients
functions in a grey area that incorporates some of have been established by the College of Critical Care
both medical and nursing activities. 28-31 Medicine (CICM) and the Australian College of Emer-
2. Autonomous practice: The NP engages in clinical gency Medicine (ACEM). 48
practice with significant clinical autonomy and
accountability, including responsibility for the When transporting an unstable patient it is essential that
complete episode of care. This autonomy means a minimum of two people focusing solely on the clinical
that the NP works in a multidisciplinary team in care aspects of the patient are present, in addition to
a clinical partnership role to optimise patient other staff transporting the patient and equipment. The
outcomes. 28-31 transport team leader is usually a medical officer with
3. Nursing model: Practice is firmly located in a advanced training in critical care medicine, or for the
nursing model, and an extensive, but evolving, transport of critical but stable patients, a registered nurse
body of literature relating to the NP role and with critical care experience. The skillset includes advanced
practice. 28-31 cardiac life support, arrhythmia interpretation and treat-
ment and emergency airway management. 48
National and international experience has demonstrated
a specific service that is highly regarded 32-35 and in PREPARING A PATIENT FOR
demand. 36,37 The NP service provides care to many under-
serviced groups such as the homeless, women and chil- INTERHOSPITAL TRANSPORT
38
dren, the elderly, rural and remote communities 36,40 and Adequate and considered preparation of the transport of
39
41
specialist services in acute care areas. Nurse practitioners a critically ill patient from one hospital area to another
are effective in managing common acute illnesses and should be appropriately planned and not compromised
39
injuries and stable chronic conditions, and provide an by undue haste. While strong evidence to support a ‘scoop
emphasis on health promotion and assessment and and run’ approach to patients in the field exists, this
disease prevention. 42 principle does not apply to interhospital or intrahospital
transport of a critically ill patient. Appropriate evaluation
The Australian experience has demonstrated that pressure and stabilisation is required to ensure patient safety
on EDs can be relieved when NPs manage lower priority during transport, including assessment of ABCs and suit-
cases. Waiting times and overall length of ED stay are able IV access. 48
significantly reduced when NPs manage triage category
3–5 presentations such as sprains and superficial If potential airway compromise is suspected, careful con-
wounds. 37 sideration should be given to an elective intubation rather
than an emergency airway intervention in a moving
vehicle or a radiology department. A laryngeal mask
RETRIEVALS AND TRANSPORT OF airway is not an acceptable method of airway manage-
CRITICALLY ILL PATIENTS ment for critically ill patients undergoing transport,
48
because of the associated problems of movement. A
The care of an acutely ill patient often includes transport, nasogastric or orogastric tube is inserted in all patients
either within a hospital to undergo tests and procedures requiring mechanical ventilation.
or between hospitals to receive a higher level of care or Fluid resuscitation and inotropic support are initiated
to access a hospital bed. The movement of critically prior to transporting the patient. Planning for the trip
ill patients places the patient at a higher risk of complica- needs to include adequate reserves of blood or other
tions during the transport period, 50-53 because of condi- IV fluid for use during transport. If the patient is com-
tion changes, inadequate available equipment to or bative or uncooperative, the use of sedative and/or
support from other clinicians, or the physical environ- neuromuscular blocking agents and analgesia may be
ment in the transport vehicle. For this reason the standard indicated. 51-53 A syringe pump with battery power is the
of care during any transport must be equivalent to, or most appropriate method for delivering medications for
better than that at the referring clinical area. 43,44 Safe sedation and pain relief. A Foley catheter is inserted for
transport of patients therefore requires adequate plan- transports of extended duration and all unconscious
ning and stabilisation from a team of staff with appropri- patients. 52-54
ate skills and experience. This section focuses on the
movement of critically ill patients by nurses, doctors and/ The patient’s medical records and relevant information
or paramedics between hospitals. 45,46 such as laboratory and radiology findings are copied for

588 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

the receiving facility, and other documentation includes method of managing large numbers of battlefield casual-
initial medical evaluation, and medical officer to medical ties. Today it is applicable for treating multiple victims of
officer communication, with the names of the accepting illness or injury outside and within the hospital setting.
doctors and the receiving hospital. 44,47 Variations exist between states and countries regarding
disaster victim triage classifications. It is therefore impor-
11,12
PATIENT MONITORING DURING TRANSPORT tant to be familiar with local plans and policy.
Critically ill patients undergoing transport receive the Triage of mass victims may be necessary in common situ-
same level of monitoring during transport as they would ations, like vehicle collisions with multiple occupants, as
have in a critical care unit. Equipment essential for trans- well as large-scale disasters, such as earthquakes, floods,
port includes: public transport incidents or explosions. The principles
of triage vary little, though the methods used to com-
l equipment for airway management, sized appropri- municate triage information and to match victims with
ately transported with each patient (check for opera- available resources may differ. Triage at the scene of a
tion before transport) major incident or disaster is commenced by the first
l portable oxygen source of adequate volume to provide qualified person to arrive (i.e. the one with the most
for the projected timeframe, with a 30-minute reserve medical training). This person is initially responsible
l a self-inflating bag and mask of appropriate size for performing immediate primary surveys on all victims
l handheld spirometer for tidal volume measurement and to determine and communicate the numbers and
l available high-pressure suction types of resources needed to provide initial care and
l basic resuscitation drugs, and supplemental medica- transport. 8
tions, such as sedatives and narcotic analgesics (con-
sidered in each specific case) In Australia and New Zealand, disaster systems have up
l a transport monitor, displaying ECG and heart rate, to five triage categories (depending on jurisdictional and
oxygen saturation, end-tidal CO 2 , and as many inva- local protocols). To provide the best level of care and
sive channels as required for pressure measurements. ensure the highest number of survivors, those who are
The monitor should have a capacity for storing and mortally injured but alive may be given a low treatment
reproducing patient bedside data and printouts during priority, though this will almost certainly ensure their
transport. 48 death. These decisions are therefore best made by an
experienced doctor. In a situation with a large number of
Monitoring equipment should be selected for its reliable casualties, one or more doctors should be present at the
operation under transport conditions, as monitoring can site to lead the triage effort. Further, it is not within the
be difficult during transport; the effects of motion, noise scope of practice of non-physician emergency personnel
and vibration can make even simple clinical observations to pronounce a patient dead, but properly trained ambu-
(e.g. chest auscultation or palpation) difficult, if not lance or rescue personnel can recognise the signs of death
49
impossible. As transport of mechanically-ventilated for the purposes of triage until doctors can formally
patients is associated with risk, 29,56,58,59 consistent ventila- declare death. 50,51
tion and oxygenation should be a goal; transport ventila-
tors provide more constant ventilation than manual
ventilation. An appropriate transport ventilator provides EMERGENCY DEPARTMENT RESPONSE TO AN
full ventilatory support, monitors airway pressure with a EXTERNAL DISASTER: RECEIVING PATIENTS
disconnect alarm, and should have adequate battery and Disasters may produce mass victims on a scale that means
gas supply for the duration of transport. 47 routine processes and practices in the ED and hospital
Adverse events during transport of critically ill patients will be overwhelmed. The ED response to an external
fall into two categories: 46,48 (1) equipment dysfunction, disaster forms part of the overall hospital response, out-
such as ECG lead disconnection, loss of battery power, lined in a hospital disaster plan. These plans are reviewed
loss of IV access, accidental extubation, occlusion of the regularly for currency, and practised for preparedness.
endotracheal tube, or exhaustion of oxygen supply (at The following aspects form part of the ED’s planning
least one team member should be proficient in operating and response to receiving patients from an external
51,52
and troubleshooting all equipment); and (2) physiologi- disaster.
cal deteriorations related to the critical illness.
Department Preparation
MULTIPLE PATIENT TRIAGE/DISASTER If the disaster site is close to the hospital, a significant
number of disaster victims will self-evacuate from the
Disaster triage is a process designed to provide the great- site and arrive at the hospital without any prehospital
est benefit to multiple patients when treatment resources triage, treatment or decontamination before any formal
and facilities are limited. Disaster triage systems differ notification has been received. In this instance the ED
from the routine triage system used within the ED (e.g. will need to declare the incident and commence the
48
the ATS); system care is focused on those victims who notification process required. The ED may be quickly
may survive with proper therapy, rather than on those overwhelmed with arriving patients; the closest local
who have no chance of survival, or who will live without medical facility may receive up to 50–80% of the
52
treatment. The system was first devised during war as a disaster victims within 90 minutes of the incident. On

Emergency Presentations 589

notification of a disaster response a number of key posi- Treatment
tions should be allocated (medical coordinator, nursing Treatment provided during a disaster will not reflect
coordinator, triage nurse, medical triage officer). These routine practices; priorities focus on resuscitation, iden-
personnel are senior staff with specific disaster training tification of serious injuries, identification of patients
and knowledge of the hospital’s disaster plan. 48,51 Nursing requiring urgent surgery and stabilisation of patients for
and medical coordinators are responsible for allocating transfer out of the ED. The best overall outcome during
staff to specific duties; all designated roles are outlined a disaster are achieved when the routine principles of
on action cards available for staff to read prior to com- resuscitation and management are adapted to reflect the
mencing their roles. 52 51,52
resources available.
The capacity of the ED to accommodate a large influx of
patients needs to be maximised. Patients currently in the
department are reviewed for a decision to admit. Patients Transfer from the ED
requiring admission are transferred out of the Depart- Patients are triaged, stabilised and transferred out to the
ment to a suitable location in the hospital. Patients suit- operating theatre or other clinical areas as soon as pos-
able for discharge or referral to their local medical officer, sible using designated transfer staff and a coordinated
including patients with minor complaints currently process outlined in the hospital plan. This will maintain
waiting, should be discharged or referred to community the effectiveness and efficiency of the department as
resources. A small number of patients may need to remain victims continue to arrive.
in the ED, and their care will need to be prioritised in
conjunction with arriving disaster victims. 50-52
Areas of the department are designated to accommodate RESPIRATORY PRESENTATIONS
the expected severity of the victims (e.g. resuscitation Patients with respiratory dysfunctions are a common
room for priority 1 patients, observation areas for priority presentation to the ED and are seen across all age
2). Walking wounded casualties with relatively minor groups. Respiratory symptoms can be associated with
injuries and who are unlikely to require admission to a broad range of underlying pathologies. This section
hospital are best accommodated in a treatment area will discuss the initial assessment and treatment of
outside the ED, as this cuts congestion and increases several common respiratory diseases seen in the ED.
the capacity for more significantly-injured victims to be Chapter 14 provides more detailed information regard-
managed. 51 ing respiratory diseases.
Additional staff members are notified from the current
staff lists to participate in the disaster management. Staff
members are allocated to teams to manage designated PRESENTING SYMPTOMS AND INCIDENCE
bed spaces within designated treatment areas. Additional Patients presenting with respiratory complaints can
staff from outside the ED may be deployed to assist; these display a range of symptoms (see Box 22.1), and these
staff should be teamed with routine ED staff, because of may vary based on the patient’s age, the underlying cause
the latter’s familiarity with the layout and location of of the symptoms and severity.
equipment and other resources. It is important to recog- Shortness of breath (SOB) or dyspnoea is a frequent
nise the need to replace staff to avoid fatigue, especially complaint for patients presenting to the ED. Respira-
in incidents of a protracted nature. Therefore, not all staff tory presentations are not isolated to any one specific
should be called in initially. Where possible, staff that
work together on a daily basis should work in teams
during the disaster period. 51,52
Triage and Reception BOX 22.1 Signs and symptoms commonly
Routine, day-to-day triage and reception processes will be associated with respiratory presentations
ineffective when receiving large numbers of disaster
victims. A registration process for disaster victims gener- l Shortness of breath
ally involves collecting minimal personal information l Dyspnoea (painful or difficulty breathing)
from the patients, where possible, and the allocation of l Decreased SaO 2
a prepared disaster hospital number used for identifica- l Cyanosis
8
tion and ordering investigations. Triage assessments will l Alteration in respiratory rate: tachypnoea/bradypnoea
often be undertaken by both a medical officer and a l Alterations in respiratory depth or pattern
nurse, and the process will be brief and focused. Most l Use of accessory muscles
victims will have been allocated a triage tag in the field, l Intercostal and/or subcostal recession
but are reevaluated for any changes, as their condition l Inability to speak in full sentences
may have deteriorated. Triage assessment is based on l Wheeze
observations of the nature and extent of the victims’ inju- l Stridor (upper airway respiratory disorders)
ries. Patients present in the ED prior to disaster notifica- l Alterations in level of consciousness
tion are considered part of the disaster event and triaged l Anxiety / feeling of impending doom
in the same manner. 4,7,8,52

590 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

patient population or age group and are encountered oxygen. Any potential detrimental effects are uncommon,
in patients across the lifespan. While dyspnoea is and concentration and time dependent with a slow onset;
commonly associated with respiratory conditions such this allows for monitoring (pulse oximetry, ABG analysis)
as asthma, pneumonia, chronic obstructive pulmonary and clinical review. 55,57
disease (COPD) and cardiac conditions, it has multiple
aetiologies and related to disease in almost any organ
system. A complaint of SOB is a significant symptom CANDIDATE DIAGNOSES AND MANAGEMENT
and is commonly associated with the need for hospital The common diagnoses related to patients who present
admission. 53-55 to ED with shortness of breath are asthma, respiratory
failure and pneumonia.
ASSESSMENT, MONITORING
AND DIAGNOSTICS Asthma
On arrival, patients with respiratory complaints are Asthma is a very common patient presentation to Austral-
assessed quickly using the ABC approach to determine asian EDs. Over 2.2 million Australians have asthma,
any potential life-threatening disturbance that requires with 16% of children and 12% of adults affected by the
immediate medical assessment and/or resuscitative inter- condition. 58-61 Asthma is a chronic inflammatory disease
vention. Initial assessment includes a thorough history of the airways with many cells and cellular elements
focused on the presenting complaints. A detailed history playing a role (mast cells, eosinophils, T lymphocytes,
often identifies the underlying process; however a high macrophages, neutrophils and epithelial cells). Inflam-
index of suspicion should be maintained for other poten- matory changes cause recurrent episodes of wheezing,
tial causes during initial assessment. 53,54 History focuses breathlessness, chest tightness and coughing associated
on the nature of symptoms, the timing of onset of symp- with widespread reversible airflow obstruction of the
toms, associated features, the possibility of trauma or airways. This airflow obstruction or excessive narrowing
aspiration and past medical history (particularly the pres- results from smooth muscle contraction and swelling of
ence of chronic respiratory conditions). During physical the airway wall due to smooth muscle hypertrophy,
examination, the patient assumes a position of comfort inflammatory changes, oedema, goblet cell and mucous
while inspection of the chest is undertaken, followed by gland hyperplasia and mucus hypersecretion. 61
auscultation, palpation and percussion (see Chapter 13 Normally, airways widen during inspiration and narrow
for more detail).
in expiration. In asthma, the above responses combine to
Patients with significant respiratory symptoms are best severely narrow or close the lumen of the bronchial pas-
managed in an acute monitored bed or resuscitation sages during expiration, with altered ventilation and air
area of the department. An initial set of observations trapping. 58-60 The causes of asthma are related to many
58
including heart rate, respiratory rate, blood pressure, factors, including allergy, infection (increased reaction
temperature and oxygen saturation is supported by con- to bronchoconstrictors such as histamine), 58,59 irritants
tinuous monitoring heart rate and oxygen saturation. (e.g. noxious gases, fumes, dusts, dust mites, powders),
Pulse oximetry plays an important role in the monitor- or heredity (although the exact role or importance of any
ing of the patient with a respiratory complaint, as rec- hereditary tendency is difficult to assess). 59
ognition of hypoxaemia is significantly improved when A patient usually has a history of previous asthma
it is used. 56
attacks. Often, an acute episode follows a period of
IV access enables collection of venous blood samples for exercise or exposure to a noxious substance, or a known
full blood count (FBC) and urea, electrolytes, creatinine allergen. 58,60 The onset of the asthma may be charac-
(UEC) where clinically indicated. A chest X-ray (CXR) is terised by vague sensations in the neck or pharynx,
ordered in most instances, and interpreted in relation to tightness in the chest with breathlessness, loose but
55
the clinical history and other examination findings. Spi- non-productive cough with difficulty in raising sputum,
rometry or peak flow measurements enable assessment difficulty breathing, particularly on expiration, with
of peak expiratory flow rate (PEFR), forced vital capacity increasing severity as the episode continues; apprehen-
(FVC) and forced expiratory volume in 1 second (FEV 1 ), sion and tachypnoea may follow as the patient becomes
to determine the nature and severity of the underlying hypoxic, with audible wheezing. 58,60 The characteristics
respiratory condition. These tests are however effort- and and initial assessment of acute mild, moderate and
technique-dependent and may not be able to be per- severe/life threatening asthma in adults and associated
55
formed by a patient who is acutely SOB. An arterial clinical management guidelines are outlined in
blood gas (ABG) is often indicated in patients with a Table 22.5. 61,62
significant respiratory presentation, and provides infor- Be alert to the high-risk patient whose ability to ventilate
mation on oxygenation, ventilation and acid–base is impaired: this is a life-threatening condition. These
status. 55
patients will exhibit an inability to talk, central cyanosis,
Oxygen therapy is commenced early for a patient present- tachycardia, use of respiratory accessory muscles, a silent
ing with signs of acute respiratory compromise, including chest on auscultation, and a history of previous intuba-
those with chronic obstructive pulmonary disease tion for asthma. 55,57-59 See Chapters 14 and 15 for ongoing
(COPD); importantly, patients with acute hypoxia require management.

Emergency Presentations 591



TABLE 22.5 Initial assessment and characteristics of acute asthma 61,62

Severity of attack
Symptoms Mild Moderate Severe or life-threatening
Able to talk in Sentences Phrases Words
Physical exhaustion No No Yes, may have paradoxical chest wall movement
Pulse oximetry (room air) >94% 90–94% <90%; cyanosis may be present
Pulse rate <100/min 100–120/min >120/min; below 60/min
Level of consciousness Normal May be agitated Confused, drowsy or agitated
Wheeze intensity Variable Moderate–loud Often quiet
Central cyanosis Absent May be present Likely to be present
Peak expiratory flow (% predicted) >75% 50–75% <50% or an inability to perform the test
Arterial blood gases Test not necessary If initial response is poor Yes




Acute Respiratory Failure (with or without chills), and mucoid, purulent or bloody
64
Acute respiratory failure occurs when the lungs provide sputum, with an abrupt or gradual onset. Physical
insufficient gas exchange to meet the body’s need for O 2 examination demonstrates tachypnoea, fever, tachycar-
consumption, CO 2 elimination, or both. Acute respira- dia, possible cyanosis, diminished respiratory excursion
63
tory failure results from a number of causes (see Chapter due to pleuritic pain, end-respiratory crackles or rales on
14). When alveolar ventilation decreases, arterial O 2 auscultation with bronchial breathing over areas of con-
64,66
tension falls and CO 2 rises. This rise in arterial CO 2 pro- solidation (see Chapter 13).
duces increased serum carbonic acid and pH falls, result- A CXR may reveal varying infiltrates: interstitial, segmen-
ing in respiratory acidosis. If uncorrected, low arterial tal or lobar; or may initially be clear until later in the
63
O 2 combines with low cardiac output to produce dimin- illness and following adequate rehydration. Venous
55
ished tissue perfusion and tissue hypoxia. Anaerobic blood samples will identify a raised white cell count and/
metabolism results, increasing lactic acid and worsening or leucocytosis. Blood cultures and sputum cultures assist
the acidosis caused by CO 2 retention. Other symptoms in identifying the causative organism. ABGs usually iden-
develop involving the central nervous and cardiovascular tify the degree of impaired gas exchange; hypoxaemia
57
systems. 59,60,63 ABGs confirm the diagnosis, with hyper- and hypocarbia may be present. 66
carbia (PaCO 2 >45 mmHg and hypoxaemia (PaO 2
<80 mmHg), and a low pH evident. A CXR identifies the Initial treatment involves administration of oxygen
specific lung disease. 63 therapy via face-mask, evaluated frequently in response
57
to ABG results and pulse oximetry. Treatment will also
Clinical management focuses on correction of hypercap- require IV fluid therapy to ensure adequate hydration,
nia, treatment of hypoxaemia, correction of acidosis, and and administration of antibiotics orally or parentally in
63
identification and correction of the specific cause (see accordance with antibiotic guidelines. Ventilatory support
Chapter 14). For a spontaneously breathing patient, may be required in some cases; in spontaneously breath-
administer oxygen by ventilation mask (24%) or nasal ing patients non invasive ventilation (NIV) via a face
cannula. Adjust oxygen therapy according to ABG find- mask should be used before invasive ventilation. Mechan-
ings at 15–20-minute intervals to achieve a PaO 2 of 85– ical ventilation is not normally required unless there is
90 mmHg. For a patient with inadequate respiratory underlying cardiopulmonary disease. 57,64,66
effort, non-invasive ventilation may be instituted. In an
apnoeic situation, initiate ventilatory assistance with
bag–mask ventilation prior to endotracheal intubation, CHEST PAIN PRESENTATIONS
then commence mechanical ventilation (see Chapter 15). Chest discomfort or pain is a common presenting com-
plaint to the ED and can be associated with a number of
Pneumonia different clinical conditions, several of which are associ-
Pneumonia is an acute inflammation of lung tissue ated with life-threatening pathology. Identification of
caused by a variety of viral and bacterial organisms, fungi cardiac-related chest pain is therefore important during
and parasites. 64-66 Pneumonia can occur in previously initial assessment, examining pain characteristics such as
healthy patients, but more often it is associated with intensity, location, radiation and other associated symp-
conditions that impair the body’s defence mecha- toms. Consider any presentation in which chest pain is a
nisms. 64,66 Predominant symptoms are a combination of feature as cardiac in origin until this has been ruled out
cough, chest pain (usually pleuritic), dyspnoea, fever or another cause confirmed.

592 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

DESCRIPTION OF PRESENTING SYMPTOMS Acute Coronary Syndrome
AND INCIDENCE Chest pain of cardiac origin results from reduced or
The incidents of acute chest pain presentations appear to obstructed coronary blood flow, commonly by athero-
be increasing as patients are more aware of the impor- sclerosis, but also coronary artery spasm or an
tance of early treatment for myocardial infarction due to embolism. 73-75 Acute coronary syndrome (ACS) collec-
67
public awareness campaigns. Up to 7% of all ED pre- tively describes unstable angina and acute myocardial
68
sentations are for complaints of chest pain. The pain or infarction (AMI). Angina (stable or unstable) is pain but
discomfort is often described in variety of ways; as pres- no damage to myocardial cells. A time-critical obstruction
sure, a weight on the chest, tightness, constriction about results in death or necrosis of a segment of myocardial
the throat, or an aching feeling. The pain may also be cell resulting in an acute myocardial infarction (AMI).
described in less typical terms such as epigastric pain, Coronary heart disease is the largest single cause of death
indigestion, stabbing pain, pleuritic or sharp. 69,70 Onset is and the most common cause of sudden death in Australia
usually gradual, reaching a peak over 2–3 minutes and and New Zealand. It is the leading cause of premature
76
last for several minutes or longer. 68,69 Pain may be mild death and disability in both countries, although death
to severe, and can be associated with physical exertion or rates have fallen since the 1960s. Over half of all coronary
emotional stress and may subside with rest, or be unpro- heart disease deaths were from AMI. ACS is the most
76
voked and may wake the patient from sleeping. Pain may common life-threatening condition seen in the ED
also radiate to an arm, to both arms, to the neck, jaw or and therefore represents an important area of clinical
back. 67,69,70 A patient may have a number of associated practice. 58,73,77 Chapters 9 and 10 provide additional
symptoms including: shortness of breath, nausea, vomit- information about presentations of cardiac dysfunction,
ing, weakness, dizziness, anxiety, feeling of impending including the pathophysiology, clinical manifestations
doom, palpitations and diaphoresis. 69,71 Up to 9% of and treatment.
patients diagnosed with an acute coronary syndrome
(ACS) may present with a number of these associated Initial management focuses on rapid identification of
symptoms but without chest pain; these patients tend to patients with AMI and their suitability for reperfusion
be elderly, female or diabetic. 69,70,72 therapy. Reperfusion therapy involves either thrombolysis
or percutaneous coronary intervention (PCI) (angio-
plasty ± stent). PCI is usually only available to patients
ASSESSMENT, MONITORING in larger centres with cardiac catheter facilities. Manage-
AND DIAGNOSTICS ment in the ED includes oxygen therapy, administration
Any patient presenting with a complaint of chest pain of aspirin 300 mg (if not already administered by prehos-
requires urgent assessment (within 10 minutes of arrival pital personnel) and pain relief (commonly IV morphine
to the ED). A patient with evidence of a disturbance in small incremental doses, and nitrates initially sublin-
to airway, breathing or circulation requires close moni- gual route). If pain persists despite IV morphine, IV
73
toring, immediate medical assessment and resuscitative nitrates may be indicated. Patient and family reassur-
interventions. Initial assessment includes a 12-lead ECG ance, information and emotional support is required to
and evaluation of the pain using the PQRST mnemonic allay anxiety and further stress.
shown in Table 22.3. The ECG should be rapidly evalu- Patients without initial evidence of AMI are stratified into
ated for presence of ST segment elevation or a new high-, intermediate- and low-risk groups based on the
left bundle branch block (LBBB) suggestive of an acute significance and duration of pain, ECG findings, past
myocardial infarction (AMI), as treatment for AMI is history, cardiovascular disease risk factors and cardiac
time critical. If the initial ECG is nondiagnostic and enzyme results. Specific treatment is guided by the associ-
symptoms persist, continue repeat ECGs at 15 minute ated risk pathway (see Chapter 10).
78
intervals. 68
Thoracic Aortic Dissection
Continuous cardiac monitoring is commenced to iden-
tify any life-threatening arrhythmias, along with supple- A tear in the intimal layer of the aortic wall results in
mental oxygen to improve PaO 2 and increase oxygen a thoracic aortic dissection (TAD): blood passes through
availability especially in the presence of myocardial isch- the tear; separates the intima from the vessel media or
aemia. An IV cannula is inserted and routine venous adventitia resulting in a false channel; and shear forces
blood samples are collected for cardiac enzymes: tropo- lead to dissection as blood flows through the false
69
nin T or troponin I. A physical examination may identify channel. Identification of this life threatening condi-
non-cardiac causes of the pain or complications associ- tion is important as patients often require immediate
ated with cardiac related conditions; 69,73 a number of sig- surgery; TAD is most common in men aged 50–70 years
nificant abdominal complaints may present with chest with a history of hypertension, while other risk factors
pain as a feature. 68,73 A CXR may also identify any poten- include Marfan’s disease, other connective tissue disor-
tial causes for the patient’s pain. ders, cocaine or ecstasy use, pregnancy and aortic valve
replacement. 69,72 TAD presents with acute and sudden
onset of severe pain (often described as sharp, tearing
CANDIDATE DIAGNOSES AND MANAGEMENT or ripping in nature) 69,72 which is maximal at symptom
Common cardiovascular diagnoses presenting to the ED onset. Pain is usually located in the midline, may be
include ACS and thoracic aneurysm. present in the back but rarely radiates. Pulse deficits or

Emergency Presentations 593

blood pressure differences (>20 mmHg) between the Administration of a narcotic analgesia in acute abdomi-
arms may be evident. CXR will be abnormal in 80–90% nal pain does not hinder assessment or obscure abdomi-
of cases; a widened mediastinum is present in 50% of nal findings, nor cause increased morbidity or mortality,
87
cases. 69,79 Diagnosis is confirmed by contrast CT. Man- and may allow for a better abdominal examination.
agement is aimed at aggressive control of blood pressure Incremental doses of a narcotic minimise pain but not
and pulse with sodium nitroprusside and beta blockers, palpation tenderness. Analgesics enable relaxation of the
relief of pain with narcotic analgesia and referral and/ patient’s abdominal muscles and decrease anxiety, poten-
or transport to cardiothoracic services for definitive sur- tially improving information obtained from the physical
gical intervention. 79 examination. 87
Venous blood samples are collected for full blood count
ABDOMINAL SYMPTOM (FBC), urea, electrolytes, creatinine (UEC), and amylase
85
PRESENTATIONS and lipase. A dipstick urinalysis can suggest specific
disease (e.g. leucocytes and/or blood with urinary tract
Acute abdominal pain is a common complaint, account- infection; haematuria with renal colic), within the context
85
ing for 5–8% of all presentations to the ED. 80,81 A specific of other clinical findings and formal microscopy.
cause for the presenting abdominal pain will not be Women of child-bearing age with abdominal pain provide
80
found in 30–40% of patients of all ages; for children a the challenge of a broader range of potential causative
diagnosis of non-specific abdominal pain accounts for up pathologies, although history and physical examination
82
to 60% of cases. About 20% of adult patients presenting are unreliable in determining pregnancy. If pregnancy
85
will require surgical intervention and/or hospital or a pregnancy-related disorder is possible, a urine
admission. 82,83 beta-human chorionic gonadotrophin (hCG) test is
performed. Test sensitivity is extremely high; a positive
Common causes in the elderly include biliary tract disease finding occurs within a few days of conception, and
(25%), diverticular disease (10%), bowel obstruction accuracy is com parable to blood sampling. An ectopic
84
(10%) or malignancy (13%). Elderly patients are more pregnancy may be missed if pregnancy is not considered;
likely to have catastrophic illnesses rarely seen in younger an ectopic pregnancy is extremely unlikely if the hCG
patients, including mesenteric ischaemia, leaking or rup- result is negative. 85
tured abdominal aortic aneurysm and myocardial infarc-
82
tion. 80,81,83 Up to a third require surgical intervention,
while 15% will not have a cause for their abdominal pain CANDIDATE DIAGNOSES AND MANAGEMENT
84
found. Presentations by elderly patients are often com- Common abdominal diagnoses for acute abdominal
plicated by a delay in seeking medical attention, atypical pain are abdominal aortic aneurysm, appendicitis and
presentations, associated medical conditions, medica- bowel obstruction.
tions and cognitive function.
Abdominal Aortic Aneurysm
ASSESSMENT, MONITORING Abdominal aortic aneurysm (AAA) is a common cause of
AND DIAGNOSTICS death in all patients over the age of 65 years and is

Patients presenting with abdominal pain are assessed responsible for 0.8% of all deaths. 82,88,89 The traditional
quickly for any disturbance to airway, breathing or circu- presentation is acute pain in the back, flank, or abdomen,
lation requiring close monitoring, immediate medical with hypotension and a palpable abdominal mass in the
88
assessment and/or resuscitative interventions. Abnormal older patient. Missed diagnoses primarily occur because
88
vital signs are suggestive of clinically significant abdomi- physical examination is frequently unreliable. Many
83
nal pain. A thorough history includes location and patients with dissecting AAA are misdiagnosed with renal
timing of onset, quantity, quality and radiation of pain, colic, because of haematuria present, no palpable pulsa-
88,89
associated symptoms, previous history and general state tile mass and flank pain. Other common misdiag-
of health. A complaint-specific history and physical noses include diverticulitis, gastrointestinal haemorrhage,
examination is performed for a differential diagno- acute myocardial infarction and musculoskeletal back
88
sis. 80,81,83 Physical assessment includes visual inspection pain. Abdominal aortic aneurysms are surgically
of the abdomen with the patient in a supine position, repaired more than any other type of aneurysm. A rup-
followed by auscultation, then gentle palpation and per- tured AAA is fatal unless a patient receives immediate
88,89
cussion of all four quadrants of the abdomen, working resuscitation and surgical intervention.
85
towards the area of reported pain (see Chapter 19 for
more details). While location of the pain is important, it Appendicitis
can be misleading, as various pathological processes can Appendicitis is the most common acute abdominal pain
localise to different areas of the abdomen (see Figure presentation that requires a surgical intervention. Diag-
86
22.1). An ECG is considered to rule out myocardial nosis is based on clinical assessment as there is no specific
ischaemia or infarction, as some cardiac patients may test available to confirm diagnosis. Appendicitis can
90
present with upper abdominal pain as the predominant mimic almost all acute abdominal pain presentations,
symptom (see previous section). Myocardial ischaemia and is frequently misdiagnosed as gastroenteritis during
may also be caused by the physiological stress of the the initial ED visit, or pelvic inflammatory disease or
intra-abdominal pathology. 80 urinary tract infection. Whilst a well-studied disease,
85

594 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E


Adult presentations with acute
abdominal pain


• Take a detailed history
• Perform a rapid physical assessment
• Obtain urine β-HCG from any woman of child-bearing age


Practice Tip
Always “suspect the worst”
and perform serial
evaluations when needed


Suspect ruptured
Suspect acute abdominal aortic Suspect ectopic
appendicitis 90 79,88,89 pregnancy 92
aneurysm

• Right lower quadrant pain • A clinical triad of: • In any woman of child bearing-age who
• A clinical triad of: - Abdominal pain. complains of abdominal pain.
- RLQ pain. - Pulsatile mass. • In the presence of abdominal pain,
- Abdominal rigidity. - Hypotension. amenorrhoea, and irregular vaginal
- Migration of the pain from the • In the presence of the following risk bleeding.
periumbilical area. factors: • When the pain is sharp, low
• History of: - Age > 50. and laterol.
- Nausea and vomiting appeared after - Smoking history. • In the presence of the
the pain has started. - History of hypertension. following risk factors:
- Psoas sign. - History of atherosclerosis. - Smoking.
- Rebound tenderness. - A positive family history of AAA. - Infectious disease.
• Symptoms are less than 2 days. - Maternal exposure to diethylstilboestrol.
• The condition should be suspected in - Tubal pathology, surgery or sterilisation.
pregnant women who exhibit new - A previous ectopic pregnancy.
abdominal pain. - More than one sexual partner.
- Infertility.
- Previous abdominal or pelvic surgery.



Practice Tip
• Be extremely cautious when assessing female and elderly patients because of high risk of misdiagnosis.
• The elderly are at particular risk of critical and severe conditions.
• Any patient with acute abdominal pain and abnormal vital signs should be triaged to be seen within 30 minutes or less.

86
FIGURE 22.1 An algorithm for triaging commonly missed causes of acute abdominal pain.

appendicitis continues to be a difficult ED diagnosis Ectopic Pregnancy
because of varied presentations. Women of childbearing
age with appendicitis are commonly misdiagnosed due An ectopic pregnancy is implantation outside the uterus;
to anatomical changes due to their pregnancy. Treatment most commonly in the fallopian tubes. Ectopic preg-
includes management of pain related symptoms and pro- nancies occur at a rate of about 11 : 1000 diagnosed
92
90
vision of intravenous hydration. Definitive treatment is pregnancies. Management is guided by the patient’s
surgical removal of the appendix. 90 haemodynamic state: stable patients with no tubular
ectopic may be managed with observation and drugs such
Bowel Obstruction as methotrexate; haemodynamically-unstable patients
will require resuscitation and surgical intervention.
92
A bowel obstruction commonly results from impaired
peristaltic movement, hernias, adhesions and neo-
91
plasms. Presentation includes poorly-localised colicky ACUTE STROKE
pain that increases in intensity and location, with subse-
91
quent abdominal swelling and vomiting of faecal fluid. Cerebrovascular disease is very prevalent in developed
93
Management includes both conservative options (man- countries; the third-largest cause of death in Australia
agement of symptoms, placement of a naso-gastric tube accounting for about 40,000 strokes (acute cerebrovascu-
and replacement of intravenous fluids) and surgical lar accident [CVA]), with 73% of these initial strokes. The
therapy for neoplasms or hernias. 91 two general stroke classifications are:

Emergency Presentations 595

99
l Ischaemic: are precipitated by disrupted blood flow to stroke presentation. IV access is obtained to administer
an area of the brain as a result of arterial occlusion. medications, and collect blood for electrolytes, haemato-
Acute ischaemic stroke presentations are now referred logy and coagulation studies. A blood sugar level test
to as a ‘brain attack’, to promote early presentation for will rule out hypoglycaemia or hyperglycaemia as a cause
access to time-critical treatments, 94,95 and because the of the presenting symptoms. Abnormal glucose levels
pathophysiology and current treatment of acute (isch- adversely affect cerebral metabolism. 99,94 After obvious
aemic) stroke mimics that of acute myocardial infarc- alternative diagnoses are excluded, a brain CT scan deter-
tion (‘heart attack’). From an ED perspective, serious mines whether a stroke is haemorrhagic or ischaemic in
long-term disability can be minimised if ischaemic origin. While a new-onset ischaemic stroke may not be
stroke is recognised and treated promptly; that is, evident for up to 24 hours, blood in the cranial cavity
within 3 hours of symptom onset. 96,97 will be apparent immediately. Patients with any sign of
l Haemorrhagic strokes are caused by rupture of a blood haemorrhage are excluded for fibrinolytic therapy. 95
vessel, which produces bleeding into the brain paren-
chyma. (Chapter 17 details the pathophysiological MANAGEMENT
processes). Acute ischaemic stroke (‘brain attack’) management
For patients diagnosed with a stroke, 30% will die in the includes timely administration of a fibrinolytic agent in
first year after their stroke, most (15–20%) within the first appropriately selected patients (see Box 22.2), which
30 days. Of the 70% who survive, 35% will remain per- facilitates reperfusion, minimises tissue damage and
manently disabled 1 year after a stroke, 10% of whom reduces long-term stroke sequelae. Longer times between
require care in a nursing home or other long-term symptom onset and fibrinolytic infusion are associated
facility. 98,99 with higher rates of morbidity and mortality. 94,98,99,102
Early presentation is therefore essential for appropriate
ASSESSMENT, MONITORING assessments and investigations (including CT scanning)
AND DIAGNOSTICS and thrombolytic administration to fall within the narrow
Symptoms of stroke are a common patient presentation treatment window. This has seen the emergence of acute
stroke units, with specialised teams dedicated to the rapid
to the ED; presenting signs vary from profound altera-
tions in level of consciousness and limb hemiplegia to
mild symptoms affecting speech, cognition or coordina-
tion. Symptoms may include confusion, dizziness, ataxia,
visual disturbances, dysphasia or receptive and expressive
aphasia, dysphagia, weakness, numbness or tingling of BOX 22.2 Criteria for administering
the face, arm or leg (usually unilateral). 97,98,100 As many fibrinolytic therapy in ischaemic stroke 101
disorders resemble a stroke presentation, emergency cli- Inclusion criteria (all must be positive):
nicians must quickly determine if another condition is l Age ≥18 years
responsible for the patient’s neurological deficits (e.g. l Clinical diagnosis of ischaemic stroke with measurable neu-
post-ictal phase following seizures, migraine with rological deficit
neurological deficits, hypoglycaemia or hyperglycaemia, l Time of symptom onset <180 min and well established
systemic infections, brain tumours, hyponatraemia,
hepatic encephalopathy). 93,97 Exclusion criteria (all must be negative):
l Evidence of intracranial haemorrhage on non-contrast
The focus of initial assessment is A, B, C, D (see Chapter head CT
24). Of note, for airway assessment, stroke symptoms l Only minor or rapidly improving stroke symptoms
include altered muscle function, affecting swallowing and l High suspicion of subarachnoid haemorrhage, even with
speech functions. A patient with a GCS score of 9 or normal CT
less may require intubation to protect and secure the l Active internal bleeding
airway. 99,101 The patient’s breathing pattern should be l Known bleeding condition, including but not limited to
assessed and continually monitored. Hypertension is platelets <100,000/mm 3
common, with the increase improving any cerebral isch- l Patient received heparin within 48 hr and had an elevated
aemia so this should not be lowered unless dangerously aPTT
94
high or contraindicated. Hypotension or dehydration l Current use of oral anticoagulants (e.g. warfarin)
decreases cerebral blood flow and perfusion and should l Recent use of anticoagulant and elevated PT (>15 sec) or
be corrected, although fluid replacement is instituted INR
100
with caution. Vital signs are documented every 15 l Intracranial surgery or serious head trauma, or previous
minutes during drug therapy to identify changes sugges- stroke within 3 months
tive of internal bleeding. Maintaining blood pressure l Major surgery or serious trauma within 14 days
less than 185/110 mmHg during fibrinolytic infusion l History of intracranial haemorrhage, arteriovenous malfor-
decreases the risk of intracerebral haemorrhage. 95
mation, or aneurysm
A thorough assessment of neurological disability should l Witnessed seizure at stroke onset
be undertaken, including a GCS (see Chapter 16). An l Recent acute myocardial infarction
ECG is recorded to detect any abnormal rhythm such as l SBP >185 mmHg or DBP >110 mmHg at time of treatment
atrial fibrillation (AF), which may be associated with

596 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

assessment and management of presentations (see
Chapter 17). TABLE 22.6 Acronyms outlining potential causes of
altered level of consciousness
OVERDOSE AND POISONING Acronym Cause Acronym Cause

Poisoning is a common clinical presentation in Australia T Trauma A Alcohol and
and New Zealand, accounting for 1–5% of admissions to other toxins
public hospitals. 103-105 Up to 25% of successful suicides I Infection E Endocrine
105
are due to poisoning. Current clinical management Encephalopathy
with supportive and/or symptomatic control has resulted P Psychogenic Electrolyte
in death rates as low as 0.5% for overdose admissions to Porphyria abnormality
105
hospitals. New Zealand has a similar poisoning pattern S Seizure I Insulin/diabetes
to Australia but much higher rates of admission and a Syncope
106
lower mortality rate than many countries. Common Space-occupying O Oxygen: hypoxia
of any cause
self-poisoning ED presentations include prescribed drugs, lesion Opiates
illicit drugs and ingestion of common dangerous sub-
stances (e.g. detergents, cleansers, psychotropic agents, U Uraemia
analgesics, insecticides, paracetamol, aspirin). 107
A range of artificial and naturally-occurring substances
can produce acute poisonings. The toxicity of a substance
depends on numerous factors, such as dose, route resuscitation may require removal of the toxin, counterac-
of exposure, and the victim’s preexisting conditions. tion of the poisoning by an antidote if available, and the
108-110
Poisoning, whether intentional or unintentional, can treatment or support of symptoms.
occur at any time, and may involve single or multiple Note that many drugs such as paracetamol may have
substances. 107-109 limited initial effects but serious, potentially fatal conse-
The vast amount of knowledge required on all poisons quences if not treated in a timely manner. 104,109,110 Once
prompted the development of poison control informa- ascertained that a patient does not have an immediate,
tion centres to provide specific information and guidance life-endangering problem, attention is directed towards a
for healthcare providers and the general public, on the more thorough assessment and identification of the toxin
management of a poisoned patient; to collect statistics on involved. Accurate history is often the most significant aid
toxic substances; and to educate the public on the preven- in directing care. If a history is unobtainable or uncertain,
108
tion or recognition of toxic exposures. Other initiatives there are several general guidelines available for dealing
to limit the incidence and severity of acute poisoning with a patient who has an altered mental state or con-
107,108,110
include the control of drugs, specific information on sciousness level (see Table 22.6).
labels, the introduction of blister packs and enforced Poisoning should always be considered for a patient
safety standards such as childproof caps. 108-110 with a sudden-onset, acute illness. If there is a strong
suspicion of poisoning, attempt to compare the patient’s
presentation with the suspected toxin and the likelihood
of exposure. Age and gender influence the types of pre-
sentation. Accidental poisonings are the most common
Practice Tip cause of medical emergencies in the paediatric patient
population. Childhood ingestions tend to be accidental
Australian Poisons Information: 131126
and to involve a single substance. Boys are more likely
Poisons Information New Zealand: 0800 POISON (0800 764766) to be the victims of poisoning than girls. Adult inten-
tional poisonings occur more often with adults, and
are more likely to involve multiple substances. 105-107
Women attempt suicide with poisons more often than
men, but men have a higher mortality rate. 105-107 Poison-
ASSESSMENT, MONITORING ings in the aged population are often complicated by
AND DIAGNOSTICS co-existing medical conditions, which may exaggerate
A poisoned patient may present with a wide range of the effects or impair the excretion of the substances
clinical features – from no symptoms through to a life- involved.
threatening condition or the potential to deteriorate
rapidly; patients should therefore always be assessed Previous History
immediately. Triage decisions are based on the potential Patients with existing medical conditions often have mul-
for rapid deterioration and the need for urgent interven- tiple medications that could be either intentionally or
tion. Resuscitation may be necessary before any further unintentionally ingested. Use of multiple drugs may
definitive care can be commenced. 107,109,110 Priorities cause untoward reactions. A patient with a history of
include assessment and maintenance of an airway, depression may attempt suicide with psychotropic
104
adequate ventilation and circulation. Successful drugs. 105-107 A quick onset and acute illness or condition

Emergency Presentations 597

raises the level of suspicion of a poisoning, especially if MANAGEMENT: PREVENTING
there is no history of previous signs or symptoms that TOXIN ABSORPTION
suggest another cause. If a patient presents with a history Initial and ongoing care of a victim follows three
of poisoning, the benefits and risks of treatment should principles: 104
be considered and therapy given if there is any doubt. 105,107
1. preventing further absorption of the toxin
Suspected Toxin 2. enhancing elimination of absorbed toxin from the
body
Rescue personnel, family or friends should bring any con-
tainer, plant product or suspected toxin with the patient 3. preventing complications by providing symptom-
to the hospital, as long as the substance presents no risk atic or specific treatments, including psychiatric
of contamination to the person retrieving it. If multiple management.
plants are growing together, a sample of each should be Ingested poisons are best removed while still in the upper
included. A child’s play area should be inspected for pos- gastrointestinal tract when possible. Emesis and gastric
sible sources of toxins. 107,108 lavage were utilised in the past to empty the stomach,
although a significant body of evidence now suggests that
Time of Poisoning these approaches are relatively ineffective and effective-
ness decreases rapidly after 1 hour. 107,108,110 Both the
History includes time of exposure, onset of symptoms
and time since treatment began. If the toxin was ingested, patient and substance should be evaluated for appropri-
108
determine the time since the last meal or alcohol con- ateness of gastric emptying. The patient’s consciousness
sumption. Alcohol is the most common drug taken with level, gag reflex and ability to vomit while protecting the
other intentional self-poisonings, can potentiate a range airway from aspiration is considered. Any central nervous
of medication effects and increase the incidence of vomit- system depressants are capable of obtunding the protec-
ing and potential aspiration. 108,110,112 Poisonings in chil- tive gag or cough reflex. If the ingested substance has a
dren tend to occur most often just prior to mealtimes, rapid onset of action (e.g. benzodiazepines), it is safer to
when they are hungry. Adults may take substances late in avoid emetics because of the risk of a sudden fall in the
the evening, fall asleep and be found several hours later. 104 level of consciousness.

Physical Assessment Ingested Poisons
Evaluate the substance ingested to determine whether
A thorough assessment may provide clues with an uncon-
scious, uncooperative or suspicious presentation. Assess gastric emptying is appropriate. Physical properties of a
for respiratory effort, skin colour, pupil size and reactivity, drug may make it more responsive to a particular type of
reflexes and general status. Auscultation of the lung fields, gastric emptying. For example, tricyclic antidepressants
the apical pulse and bowel sounds provide a baseline for tend to reenter the stomach acid after absorption into the
113
further assessment and clues to current problems. Check serum. Also consider the effects of substances on tissue.
the blood pressure as often as necessary to determine Corrosives, such as acids, alkalis and iron supplements,
cardiovascular stability. Percuss the thorax and abdomen produce irritation and tissue breakdown when in contact
to detect accumulations of fluid or air. 108,111 Needle marks, with the skin or mucous membranes. Recognition is
pill fragments, uneaten leaves or berries, or drug para- important, as therapy may cause further injury. Emesis
phernalia assist in a diagnosis. 108,111 The presence of pres- could be contraindicated, and a lavage tube may trauma-
sure areas on the skin may indicate how long the patient tise injured tissue. Waiting for emesis also causes further
has been unresponsive. Any odours are important to delay in definitive treatment. Other substances have
note; an oily-garlicky smell may be due to pesticides; natural emetic qualities if taken in sufficient doses (e.g.
108
other odours may indicate chronic medical disorders (e.g. hand soaps and liquid soap detergents).
fruity odour with diabetic ketoacidosis) or neglect of per- Evaluate other substances on an individual basis. Most
sonal hygiene. 112 petroleum distillates (e.g. furniture polish, cleaning
fluids) present a greater hazard for chemical pneumonitis
Diagnostics than a systemic intoxication. Even very small amounts
114
Toxicology screens include analysis of serum and urine can quickly disperse over the lung surface if accidentally
to determine the presence and amount of a substance. introduced into the trachea. Avoid emesis or lavage when
114
Laboratory levels are helpful but are considered in rela- the chance of aspiration is high. There are situations,
tion to the nature of the substance and its rate of metabo- however, when the amount, character or additional
lism. Certain substances are sequestered in fatty tissues chemicals present make it necessary to remove the
or bound to serum proteins, and may be present with ingested substance from the stomach.
104
a misleadingly low serum level. Serum electrolytes, Therapy can be based on the reported amount taken or
non-electrolytes, osmolality, arterial blood gases and time since ingestion. Time since ingestion is important to
urine electrolytes are used to determine a patient’s overall rule out the benefit of therapy, as the stomach tends to
status or response to therapy. Continuous cardiac moni- empty its contents after 1 hour unless the ingested sub-
toring supplemented with a 12-lead ECG or invasive stance slows gastric motility (e.g. narcotics slow peristalsis
monitoring devices may be required to guide symptom- and may be found in the stomach several hours after
atic care. 107,108,110 ingestion). A patient may also under-report the dosage
104

598 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

to avoid an obviously unpleasant experience. Although Contaminated linen and clothes should be sealed in a
conservative management with observation is appropri- bag and destroyed. 108,111
ate in certain situations, the risk of not treating might be
104
greater in others. If a large number of tablets or pills MANAGEMENT: ENHANCING TOXIN
are consumed at one time, they may clump together in ELIMINATION FROM THE BLOOD
the stomach and form a mass that is too large to pass out
of the pylorus (e.g. aspirin). 115 After a substance has entered the bloodstream, it is nor-
mally excreted from the body either in an unchanged
Once a substance enters the lower gastrointestinal tract, form or after liver metabolism and detoxification. Various
it can be absorbed into the mesenteric circulation. As metabolic byproducts are eliminated in the bile and
absorption can vary according to substance, slow-release faeces or urine. Urinary excretion of substances can be
characteristics, rate of peristalsis and the presence of other enhanced by increasing the filtration process (i.e. forced
substances, it is possible for a poison to be present in the diuresis: large volumes of IV solutions and/or diuretics),
bowel for an extended period of time. If intestinal motil- by inhibiting absorption in the renal tubules, or by stimu-
ity can be stimulated or the toxin permanently bound lating the secretion of substances into the urine. 108-110
until excretion, then further absorption is reduced. 108
Alkalinisation of Urine
Activated charcoal is a refined product with an enor-
mous surface area that binds to a large range of sub- Manipulation of the absorption or secretion process of a
stances to enhance elimination, and is the most effective drug can be assisted by chemically altering the structure
decontaminating agent currently available, when given of some substances. All substances break down into ions
early after ingestion. 107,108,110 A solution of either water at a specific pH for that substance. Altering the pH of
or sorbitol is mixed with 15–30 g of activated charcoal urine with acidifying or alkalising drugs allows the poison
to form a thick, liquid slurry which is given to a com- to be forced into an ion state and then excreted in the
pliant patient orally or through a nasogastric tube. It urine. This ‘ion trapping’ process is effective only for sub-
may be mixed with a cathartic, which reduces the time stances that are primarily eliminated by the kidneys 108-110
the substance or the charcoal is in contact with the (e.g. salicylates, tricyclic antidepressants have increased
bowel wall, although there is no evidence that this excretion due to urinary alkalisation). 104
116
improves clinical outcome. Effectiveness can be
improved through repeated administration of activated Haemodialysis or Haemoperfusion
charcoal, ensuring that the entire drug is absorbed, and If a dangerous amount of a poison is present or if renal
interrupting the drug reabsorption in the enterohepatic failure is evident, then haemodialysis or haemoperfusion
104
circulation. Cathartic agents such as sorbitol and poly- may be used to promote excretion. Dialysis is effective
ethylene glycol reduce gastric transit time; in theory in removing only substances that are reversibly bound
this limits absorption, although this has not significantly to serum proteins, or not stored in body fat. This is a
improved outcomes. 103,104 Unfortunately, not all poisons highly invasive approach and is normally reserved for
that are ingested can be bound by charcoal (e.g. alcohol, life-threatening cases (see Chapter 18 for further
heavy metals). 107,108,110 discussion). 107,108,110

Inhaled Poisons MANAGEMENT: PREVENTING
A patient poisoned by inhalation of toxic gases or powders COMPLICATIONS AND SPECIFIC
should be removed from the source as soon as it is safe SYMPTOMATIC CARE
to do so. Attempts to remove the substance, which is Supportive care is the key element in managing an acutely
usually a vapour, gas or fine particulate matter, from the poisoned patient. Once a patient has either ingested or
104
lungs are not normally useful. Staff involved in direct been exposed to many poisons, there are limited options
patient care should use contact precautions to reduce other than to treat the symptoms as they present or
their own contamination risks with unknown substances. become clinically significant (see Table 22.7).
Clothing for many inhaled poisons may contain signifi-
cant amounts of the poison and serve as a continuous Antidotes act to antagonise, compete with or override the
source of the toxin. Contaminated linen and clothes effects of the poison, although few specific antidotes exist
should be removed carefully, sealed in a bag and for toxins (see Table 22.8). In some cases, an absorbed
destroyed. 108,111 toxin can be rendered benign by the use of an antidote
(e.g. the interaction between naloxone and opiates).
104
Contact Poisons For chelating agents (desferrioxamine for iron poison-
Contact poisons are dangerous because of their ability to ing), a non-toxic compound is formed and safely elimi-
The effect of an antidote may
nated from the body.
107,108,110
enter the body via the skin or mucous membranes. All be only temporary if it has a shorter half-life than the
clothing and all of the toxic substance should be carefully poison. Most antidotes are given either in a specific dose
removed, preferably with an irrigating and neutralising or as a response to dose rate. 104
solution. Contact precautions to avoid direct skin contact
and reduce the risk of self-contamination are used. Cloth- For many poisonings, symptomatic care involves support
ing may contain significant residual amounts of the and protection of vital organ systems; frequent physical
poison and serve as a continuous source of the toxin. assessment of respiratory, cardiovascular and renal

Emergency Presentations 599



TABLE 22.7 Summary of the management of poisoning victims

Aim Action
Prevent absorption of toxin l Ingested toxins: activated charcoal is the most effective method of reducing adsorption.
l Inhaled toxins: remove victim from source of contamination and administer oxygen or provide fresh air.
l Contact toxins: remove any substances from the body surface, preferably with copious amounts of
irrigating fluid. Remove clothing and place in a sealed bag to reduce vapour hazards. Use special
caution with corrosive materials and pesticides.
Enhance elimination of the toxin Ingested or injected toxins: administer an antidote or antagonist if available (e.g. naloxone for opiates;
from the blood flumazenil for benzodiazepines 2–4). Employ forced diuresis, for acidification or alkalinisation of the
urine; and haemodialysis.
Prevent complications by providing Carefully monitor all vital systems. Continually reassess patient for changes or response to therapy.
symptomatic or specific Administer antidotes as prescribed. Provide symptomatic care as needed for: cardiac arrhythmias, CNS
treatment depression or stimulation, fluid and electrolyte imbalances, acid–base disturbances, renal function,
effects of immobility.




CENTRAL NERVOUS SYSTEM DEPRESSANTS
TABLE 22.8 Common emergency antidotes A large number of common medications are capable of
depressing levels of consciousness, thought processes, or
Poison Antidote important regulatory centres in the central nervous
Benzodiazepines Flumazenil system (CNS). Clinical findings can vary from class to
class or within the same drug family, as physical effects
Carbon monoxide Oxygen
are dependent on the chemical structure of the drug,
Insulin Dextrose dose, route of exposure and rate of metabolism. The
Opioids Naloxone chemical structure and/or purity of illicit drugs may also
be affected by variations or deliberate aberrations in the
Paracetamol N-Acetylcysteine 112,117-119
manufacturing process. Drugs in this section
Organophosphates Atropine and pralidoxime include sedatives, hypnotics, tranquillisers and narcotics
Tricyclic antidepressants Sodium bicarbonate (see Table 22.9).
Assessment
The predominant observed effect is an altered level of
function enables identification of any deterioration. Elec- CNS function. 112,118,119 A spectrum of physical findings is
trolyte and acid–base balance are monitored closely if possible with the selective action of the specific drug on
large volumes of fluids or drugs that alter serum pH are inhibitory or excitatory centres of the brain; effects can
administered. vary from mild euphoria to convulsions, or mild sedation
to coma, dependence, addiction and tolerance. Narcotics
A poisoning may be the physical manifestation of an
emergency or crisis that requires emotional support. An produce miosis (constriction of the pupil), and some
underlying emotional conflict or mental health problem patients experience nausea and vomiting due to
may exist, regardless of whether the poisoning was inten- stimulation of the chemoreceptor trigger zone in the
112,118,119
tional or accidental. Psychological care is therefore an medulla.
important component for all patients presenting with A narcotic overdose is distinctive: a decreased respiratory
poisoning. 107,108,110 Many facilities offer the services of a rate and tidal volume, miosis, hypotension, and an
mental health worker while the patient is still in the ED. altered level of consciousness. 112,118,119 However, other
If the patient’s condition is stable and the poisoning has factors may affect these findings:
not altered their mental state, early psychological inter-
vention is appropriate. l a decreased respiratory effort may produce hyper-
carbia, causing pupil dilation
For adult patients, the desire for treatment is not as l chronic narcotic users tend to have multiple problems
important as the manner in which treatment is received. associated with their drug use or lifestyle, which may
Even though patients may initially refuse care, if modify findings
approached in a non-threatening way and provided some l a sufficiently high quantity of CNS depressant will
form of control they will usually comply. If threatened depress vital regulatory centres in the brain
with force or restraints, they are placed in a difficult posi- l altered respirations cause hypoventilation, stasis of
tion of either submitting to coercion or resisting therapy secretions, and atelectasis; resultant hypoxia aggra-
for self-protection. A paediatric patient may be too young vates the sensorium and cerebral functioning 119
either to fully understand or to effectively cooperate (see l narcotics may produce idiopathic pulmonary
Chapter 26). oedema 112,118,119

600 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



TABLE 22.9 Assessment and management of specific drug overdoses

Type of poisoning General management Antidote Clinical considerations
CNS depressants Supportive care of airway, Naloxone hydrochloride Action of naloxone may be much shorter than the
(morphine, heroin, breathing, circulation (Narcan); specific reversal effect of the drug; the patient may need to be
methadone, oxycodone) agent observed for return of unconsciousness.
CNS stimulants Supportive care of airway, Benzodiazepines may be Reduce stimulation in the surrounding
breathing, circulation used to reduce symptoms environment; monitor CVS and temperature.
Salicylate Observe for hyperventilation Nil; charcoal may be used Monitor electrolyte changes and increases in fever.
and acid–base disturbances
Paracetamol Careful history required to N-Acetylcysteine Antidote must be given within the specified time
determine time and range; consider the effects of other drugs (e.g.
amount taken; initially paracetamol and codeine combinations);
vague symptoms monitor for signs of hepatotoxicity.
Carbon monoxide Supportive care of airway, High concentrations of Hyperbaric oxygen may be required; monitor
breathing, circulation oxygen therapy carboxyhaemoglobin; oxygen saturation
monitors will give erroneously high readings.
Organophosphates Decontamination; supportive Pralidoxime chloride; Maintain careful decontamination and personal
care of airway, breathing, benzodiazepines safety considerations.
circulation



l CNS depressants may cause peripheral vasodilation, exposure and a depressed immune response also predis-
with a resultant hypotension and tachycardia pose a patient to severe infections (e.g. hepatitis, osteo-
l arrhythmias may occur because of cardiac conduction myelitis, infective bacterial endocarditis, encephalitis/
effects or tissue hypoxia. 112,118,119 meningitis). 112,118,119



Practice tip
Practice tip
Comprehensive assessment of CNS function includes ob serving
for adequate respiratory function and levels of consciousness. Many patients with an overdose will not appreciate that their
narcotics have been reversed, and may awaken suddenly in a
frightened or agitated mood. Reassure them that they are safe
Patients with an altered level of consciousness are at risk and their privacy will be protected.
of injury from decreased sensory ability or prolonged
immobilisation. Reddened areas over bony prominences
or pressure points appear within a short time. Skin blis-
ters indicate altered blood flow, usually due to excessive Management
pressure. Actual skin breakdown can occur within 3 General principles apply for the management of a patient
hours. 112,118,119 If external pressure or altered circulation to with ingestion of a toxic substance with a reduced level
an extremity continues for over 4 hours, compartment of consciousness. Prevent continued absorption by
syndrome may develop. 112,118,119
administering activated charcoal for oral ingestions, and
provide symptomatic care 112,118,119 (see Table 22.9).
Effects of Multiple Drug Use
A patient who ingests a combination of drugs may CENTRAL NERVOUS SYSTEM STIMULANTS
experience toxicity because of additive or synergistic CNS stimulants increase the activity of the reticular acti-
effects. 112,118,119 Illicitly-produced drugs often have sub- vating system, promoting alertness and affecting the med-
stances added (e.g. glucose powders, icing sugar, talcum ullary control centres for respiratory and cardiovascular
powder) to dilute or ‘cut’ them, to increase the quantity function. Individuals using a CNS stimulant have an
of supply and profit for the supplier. 117,118 Users may also increased ability to perform muscular activity and a
intentionally inject other drugs (e.g. antihistamines, general sense of wellbeing. Many illegal stimulants
amphetamines, benzodiazepines) to modify or potenti- are poorly manufactured, with no guarantee of purity
ate the effects of narcotics. 112,118,119
or consistency in dosage. The possibility of overdose
is therefore always present, producing profound CNS
Potential for Acute or Active Infections excitation. 117,120,121 Commonly used stimulants include
The use of non-sterile solutions and equipment and the amphetamines, dextroamphetamine, methyphenidate,
sharing of injection equipment significantly increases the lysergic acid diethyamide (LSD), phencyclidine (PCP),
risk of acute or active infections. 112,118,119 Frequent caffeine, cocaine and methamphetamines. 112,118,119,125

Emergency Presentations 601

Assessment consciousness, seizure activity, or a loss of protective gag,
Both psychological and physical symptoms are produced. corneal and swallow reflexes. Nystagmus is a classic sign,
A patient may demonstrate repetitive, non-purposeful along with hypertension and an elevated body tempera-
movements, grind their teeth and appear suspicious ture. A significant rise in arterial pressure presents a risk
or paranoid of others. Physiological stimulation causes for intracerebral haemorrhage. One of the distinguishing
an increase in metabolism, with flushing, diaphoresis, features of amphetamines is their ability to produce coma
112,119
hyperpyrexia, mydriasis (excessive pupillary dilation) and without affecting respirations. The patient may be at
vomiting evident. Dizziness, loss of coordination, chest risk of dehydration and renal failure if muscle breakdown
pain, palpitations or abdominal cramps may also be has occurred. A high urine output should be maintained
present. During the acute phase of poisoning, severe and serum urea and creatinine levels monitored to detect
112,118,119
intoxication and loss of rational mental functioning may a decrease in renal function.
lead individuals to behave irrationally and even attempt Lower-dose intoxications do not produce unconscious-
suicide. Anxiousness and a general state of tension may ness but typically cause behavioural patterns that reflect
also lead the affected person to attempt to harm depersonalisation and distorted perceptions of events or
others. 112,118,119 Death is possible from cardiovascular col- other people. The patient’s physical and mental responses
lapse or as a sequela to convulsions and acute drug may be dulled and slow, or their behaviour abusive and
toxicity. 112,118,119 delusional. Intoxication is marked by paranoid thoughts,
with the patient responding to therapeutic or friendly
Management gestures with behaviours ranging from apprehension to
If a patient has ingested the drug, emesis or lavage is of aggressive hostility. To avoid stimulating the patient and
little value, and an individual risk–benefit assessment is intensifying their behaviour, use a quiet environment for
required. Gastric emptying may precipitate more severe initial assessment and treatment, although this is often
agitation with a concomitant rise in blood pressure, pulse difficult in the ED. 112,118,119
rate and metabolism. 112,118,119 Activated charcoal and
cathartics may be administered to promote elimination. Management
Note that there are no specific antidotes for CNS stimu- Gastric emptying is normally ineffective due to delays in
lants. Ongoing emergency management includes:
seeking treatment. If a patient presents early, activated
l support of vital functions 112,118,119 charcoal and cathartics are useful in preventing further
l reduction of external stimulation by locating the absorption. Noises, sights and sounds provoke paranoid
patient in a quiet, non-threatening environment ideation and may present a risk to staff and other
where a supportive person can attempt to calm and patients. ‘Talking down’ is usually not successful and
‘talk the person down’ while observing for untoward probably only serves to exacerbate the situation. If the
reactions patient is demonstrating hostile or self-abusive behav-
l sedation when necessary, although it is not desirable iour, restraints may be needed to protect him/her and
to give more medications in a precarious situation; any others present. The use of physical restraints is not
sedation may control seizures or keep the patient from without danger, and they should never be used as a sub-
self-harm. 112,118,119 stitute for a more desirable environment. If the threat of
danger or psychosis is significant, sedatives (diazepam,
AMPHETAMINES AND DESIGNER DRUGS haloperidol) may be necessary to control the patient’s
behaviour. Intravenous diazepam also controls frequent
Amphetamines and designer drugs have been drugs of 112,118,119
abuse for a number of years. Originally, many were seizure activity.
designed and introduced as anaesthetic agents, deconges-
tants or for other legitimate purposes. Amphetamines are SALICYLATE POISONING
chemically related to the anaesthetic ketamine, with a Aspirin is the most common form of salicylate in the
similar CNS response. 112,118,119 Most drugs in this group home and is found in many over-the-counter medica-
were discontinued or controlled because of the delirium tions, such as combination analgesics 122 and topical
and agitation experienced by patients who received them; ointments. Aspirin may be ingested orally, absorbed
paradoxically, these effects led to their popularity as through the rectal mucosa, or applied to the skin in
recreational drugs. 112,118,119 Amphetamines are synthetic topical preparations. Under normal circumstances, the
sympathomimetic drugs, available in oral, intranasal or kidneys serve as the principal organ of excretion. Aspirin
intravenous forms; crystalline rock forms such as ‘ice’ are was previously the most common poisoning in chil-
smoked. Death may occur from overdose, self-mutilation dren, 106,109,122 so legislation was implemented to limit
or dangerous activities such as diving into shallow waters the number of tablets per pack and to introduce packag-
or walking on traffic-laden roads. ing with childproof caps. In Australia, salicylate poison-
ing is now uncommon, accounting for only 0.3% of
Assessment calls to poison information centres. 106,122 The three
Depending on the dose, route and time since exposure, common types of aspirin overdose are: accidental inges-
a person exhibits characteristic behavioural and tion (more common in young children); intentional
physical changes. With high-dose intoxication, the patient ingestion (more common in adults); and chronic toxicity
has pronounced CNS involvement: altered levels of (occurs in any age group). 115,122

602 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Assessment, Monitoring and Diagnostics antipyretic agent. 109,124 The drug is absorbed in the
Intentional or accidental ingestion is straightforward, stomach and small bowel, with 98% metabolised by
with a clear history of poisoning. Chronic toxicity is the liver using one of two mechanisms: most by a
however often unrecognised. Individuals may not be pathway with breakdown into nontoxic byproducts;
aware of correct dosages, combine multiple drugs that the second hepatic pathway usually metabolises about
contain aspirin, or may have impaired excretion due to 4% of the drug, but the process has a toxic byproduct.
dehydration. The symptoms of chronic aspirin overdose The liver detoxifies this toxic byproduct by combining
(i.e. dehydration, lethargy, fever) resemble the original it with glutathione, a naturally-occurring substance. In
problem being treated, and some people will continue an overdose or when the minor pathway has already
treating themselves with aspirin for these symptoms. been stimulated (e.g. concomitant barbiturate use), more
Chronic toxicity has a higher mortality than acute paracetamol is metabolised by the secondary pathway
ingestion. 115,122,123 and the toxic byproduct accumulates, quickly consuming
the available glutathione, resulting in liver tissue
Aspirin is problematic if ingested in amounts greater than destruction. 109,124,126
150 mg/kg; toxicity presents with tachypnoea, fever, tin-
nitus, disorientation, coma and convulsions due to sys- Assessment, Monitoring and Diagnostics
temic effects of aspirin. 115,122,123 Acid–base disturbances
arise from direct stimulation on the respiratory centre in The amount of paracetamol ingested is best determined
the CNS; an increased rate and depth of respirations from patient history, as serum levels (although helpful)
cause hypocarbia and respiratory alkalosis, with renal can be easily distorted. A nomogram to plot measured
compensation by bicarbonate elimination. Salicylates, levels against time postingestion is a relative indicator
however, also alter metabolic processes, resulting in a of toxicity. A relatively small dose of 200 mg/kg
metabolic acidosis. Blood gases can therefore reflect aci- paracetamol is considered toxic, although hepatotoxicity
dosis, alkalosis or a combination. Tinnitus (ringing in the occurs after ingestion of 140 mg/kg or 10 g in a single
ears) is a symptom of the effect on the 8th cranial (acous- dose. 109,124,126
tic) nerve. 115,122,123 Liver function (liver enzymes, serum bilirubin, protein)
Aspirin also interferes with cellular glucose uptake, and coagulation tests (prothrombin time, partial throm-
causing initial hyperglycaemia. As cellular levels become boplastin time, platelets) identify the development of
depleted the patient demonstrates hypoglycaemic effects. hepatic dysfunction or damage. 109,124 The pattern of toxic
Later, serum levels may be either normal or hypoglycae- damage occurs over a characteristic three-phase course:
mic. 115,122,123 Patients may be nauseated and vomit after 1. First 24 hours: vague symptoms of nausea, vomit-
ingestion, causing fluid and electrolyte imbalance. 115,122,123 ing, and malaise.
Aspirin use is also associated with local tissue irritation, 2. 24–48 hours: above symptoms subside with onset
gastrointestinal bleeding, and platelet dysfunction, of right upper quadrant pain due to hepatic injury;
increasing risk of bleeding. Concomitant use of anti- urine output may decrease as paracetamol potenti-
coagulants therefore increases this risk. 115,122,123 ates the effect of antidiuretic hormone; liver
enzymes, bilirubin, proteins and clotting studies
Management may be abnormal.
Absorption can be reduced with activated charcoal, using 3. 60–72 hours: liver impairment becomes more
repeat doses for patients with signs of ongoing absorp- obvious, with jaundice, coagulation defects, hypo-
tion. 115,122,123 Urine alkalisation and forced diuresis can glycaemia and hepatic encephalopathy; renal
significantly increase elimination, as salicylates are weak failure or cardiomyopathy may also occur; death
acids excreted by the kidneys. 115,122,123 Haemodialysis from hepatic failure occurs in approximately 10%
is reserved for extreme cases with profound acidosis, of severe overdoses. 109,124-126
high blood levels, persistent CNS symptoms or renal
failure. 115,122,123 Management
As salicylates have no known specific antidote, 115,122,123 Absorption can be reduced with activated charcoal when
supportive therapy includes prevention of dehydration the patient presents to hospital early, however following
with careful monitoring of fluid output and adequate periods of 2 hours postingestion activated charcoal is
fluid replacement, monitoring serum electrolytes for unlikely to be effective. Haemodialysis with a charcoal
imbalance and replacement as needed. Evaluate ABGs to dialysate has been used to remove unchanged paracetamol
determine whether the patient continues to have meta- from the liver, but this does not remove the toxic
bolic effects from aspirin toxicity or is not responding to byproduct. Forced diuresis is also not effective, as
therapy. Control temperature elevations with external minimal paracetamol (about 2%) is removed by the
cooling methods if fever develops. kidneys. 126-128

Specific therapy is the use of an antidote, N-acetylcysteine,
PARACETAMOL POISONING which is structurally similar to glutathione and binds to
The incidence of paracetamol toxicity is associated with the toxic byproduct. When given within 24 hours of acute
approximately half of all Australasian toxic ingestions, ingestion, N-acetylcysteine is effective in preventing
due in part to its common availability as an analgesic/ hepatic damage. 126-128

Emergency Presentations 603

CARBON MONOXIDE POISONING
Carbon monoxide (CO) is a gaseous byproduct of incom- TABLE 22.10 Summary of assessment and
plete fuel combustion, and is present where there is a management of acid and alkali exposure
flame in a confined space with improper ventilation or
air exchange. Levels of CO can accumulate rapidly, and Nursing step Corrosive acids or corrosive alkalis
the gas is dangerous as it is colourless, odourless, tasteless Assessment l Burns to skin, mouth, pharynx or oesophagus
and non-irritating. 129-131 Common sources of CO are l Gastric irritation with nausea and vomiting
faulty radiant heaters, kerosene lamps, cooking stoves,
engine exhausts and fireplaces. Acute CO poisoning is the Management l Airway
most common form of successful poisoning in the USA, l Breathing
UK and Australia. 129-131 l Circulation
l Decontamination
Assessment, Monitoring and Diagnostics Prevent l Do not induce vomiting.
Haemoglobin has a 210–240 times greater affinity for CO absorption l Remove contaminated clothing.
than for oxygen, and shifts the oxygen–haemoglobin l Flush the skin with copious amounts of
water.
curve to the left (see Chapter 13). As CO displaces oxygen
from red blood cells, the patient experiences hypoxaemia Enhance l Administer chelating agents if they exist,
and hypoxia. 132-134 Headache, nausea and vague pains are elimination such as calcium gluconate for hydrofluoric
acid.
often experienced at onset of poisoning, with increasing
tiredness and sleepiness, difficulty concentrating, and Symptomatic l Protect burnt skin with sterile dressings.
failure to recognise the onset of poisoning. With higher management l Monitor respiratory status.
levels of inhalation, the patient may be tachypnoeic,
tachycardiac and experience loss of consciousness. A
characteristic red colour presents in the lips with skin
flushing. 132-134 The most important factors in determining oesophageal mucosa, presenting a risk for haemorrhage
CO poisoning are a history of exposure with an elevated and mediastinitis, and cardiac arrest as a result. 135-137 The
blood carboxyhaemoglobin level. 132-134 late sequelae of swallowing a corrosive substance involves
mucosal scarring with constriction and mechanical
Management obstruction of the oesophagus.
As CO is an inhaled toxin, the patient should be removed
from the contaminated environment to prevent further Assessment
absorption and allowed to breathe fresh air until 100% Physical findings are site-specific and relate to the type of
oxygen can be administered. Although this may be inef- exposure – ingestion, inhalation or contact (see Table
fective because of the bond between CO and haemoglo- 22.10). Ingested acids present as burns to the mouth and
bin, high-flow high-concentration oxygen administration pharynx. Patients who are able to vocalise complain of
134
will reduce the half-life of CO. Hyperbaric oxygenation pain, gastric irritation with vomiting and haematemesis.
is used to treat severe cases of CO poisoning, as pres- Fumes from an ingested substance may cause pneumoni-
surised oxygen reduces the half-life of the carboxyhaemo- tis. Contact with skin or the eyes is similar to other types
globin molecule and shortens the duration of effects. As of burns, with a sharply-defined blister or wound, inflam-
hyperbaric resources are not available at every facility, mation, pain and ulceration. Hypotension and cardiovas-
treatment depends on carboxyhaemoglobin serum levels, cular collapse are also possible when damage occurs to
time since exposure, transport time to the hyperbaric underlying vital structures. 135-137
chamber and the clinical symptoms of the patient. 132-134 Inhalation irritates respiratory tissues, producing direct
Patients should be monitored for adverse effects of damage, oedema and alterations in ventilation. Patients
hypoxia, as they may have convulsions, cardiac arrhyth- may initially experience coughing, choking, gasping for
mias and acid–base disturbances.
air and increased secretions. Evaluate for obvious tissue
CORROSIVE ACIDS injury, impaired respiratory function, and subsequent
effects of hypoxia and pulmonary oedema, which may
A range of substances have a similar ability to cause local occur up to 6–8 hours later. 135,137 Arterial blood gases,
tissue injury. Common acids involved in toxic emergen- ventilation studies, serial chest X-rays and frequent physi-
cies include acetic acid (vinegar); carbolic acid (phenol cal assessments are used to monitor for changes.
disinfectants); chlorine (swimming pools, sanitising
agents); hydrochloric acid (pools, cleaning agents); Management
hydrofluoric oxalic (laundry agents); sodium bisulphate
(toilet cleaning agents; converts to an acid when added Contaminated clothing should be removed to prevent
to water) and sulfuric acid (car battery acid). recontamination. Patients with external contamination
should be washed thoroughly to remove any remaining
Ingested corrosives produce immediate or late life- surface material that may come into contact with treating
threatening complications. In general, acids dissolve staff. For acid contact with skin or eyes, begin immediate
tissue and destroy haemoglobin. 135 Swallowing a strong flushing with a non-reactive liquid and continue to do so
acid can produce ulceration and perforation of oral and for at least 15 minutes to guarantee complete removal. In

604 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

most cases water will be the safest and best available gluconate may be required. Continue to monitor for sys-
liquid. Provide skin or eye protection with a sterile temic effects of perforation or tissue injury. 135
dressing. 135
PETROLEUM DISTILLATES
For ingested acids, emesis or lavage should not be
attempted, as the substance will cause additional damage Petroleum distillates are common substances, and
114
when ejected from the stomach. A gastric tube may also account for 7% of all poisonings. Typical petroleum
cause structural damage by penetrating or irritating friable products are benzene, fuel oils, petrol, kerosene, lacquer
tissues. 135-137 Do not attempt to neutralise the acid, as this diluents, lubricating oil, mineral oil, naphthalene, paint
may result in a chemical reaction and generate heat thinners and petroleum spirits. Toxicity depends on:
as a byproduct, with potential further burning and route of exposure (ingestion or aspiration); volatility
damage. 135-137 Suctioning of oral secretions should be (ease with which the substance evaporates); viscosity
done carefully and with as much visualisation of tissues (density or thickness); amount ingested; and presence of
as possible. A patient may be given water or milk to irri- other toxins. 114
gate the upper gastrointestinal tract, although extreme Products with a low viscosity are more likely to be aspi-
care is required to ensure that the airway is adequately rated and can quickly spread over the lung surface. Sub-
protected because of risk of aspiration. 135 stances with low viscosity and high volatility (e.g. benzene,
kerosene, turpentine) are toxic in doses as low as 1 mL/
CORROSIVE ALKALIS kg, with death from doses of 10–250 mL. Mortality is

Alkalis produce tissue destruction on contact by interact- increased if an additional toxic substance is present, or if
ing with fats and proteins and producing necrotic tissue. accidental aspiration occurs. 114
Alkalis involved in toxic emergencies include many
substances found around the house, such as ammonia Assessment
(detergents, cleaning agents); cement and builder’s Aspiration causes a pneumonitis with low-grade fever,
lime; low-phosphate detergents; sodium carbonate tachypnoea, coughing, choking, gagging and pulmonary
(dishwasher detergent); and sodium hypochlorite oedema as a late effect. 114,136 Immediately assess the
(laundry bleaches). 137 patient’s respiratory tract for possible aspiration; cough-
Skin contact and ingestion are the most common types ing, cyanosis or hypoxia may indicate aspiration or
137
of injury from an alkali; ingestion is most immediately chemical pneumonitis. As petroleum distillates are fat
life-threatening. Erosion of the oesophagus and stomach solvents and rapidly cross the lipid cell membrane, nerve
occurs if ingested orally, and peritonitis or mediastinitis tissue is especially sensitive to injury. A patient may
may develop as sequelae. Late effects are similar to those exhibit local effects, such as depressed nerve conduction;
produced by acids. Oesophageal strictures due to scarring or varied central effects, such as feelings of wellbeing,
are common post-ingestion. About 25% of patients who headache, tinnitus, dizziness, visual disturbances, through
137
ingest a strong alkali will die from the initial insult, to respiratory depression, altered levels of consciousness,
136
while 98% will develop strictures. 135-137 convulsions and coma.
Assessment Management
In the awake and alert patient, the decision to treat is
The immediate response to ingestion is increased secre-
tions, pain, vomiting or haemoptysis. Signs of perforation based on the physical properties of the substance, the
include fever, respiratory difficulty or peritonitis. Alkalis likelihood of aspiration or other complications, and the
136,137
and skin contact produce a soap-like substance because amount consumed. When preventing absorption,
of the interaction with tissue fats, giving a slimy, soapy carefully consider gastric emptying, as neither induced
feeling. 135,137 vomiting nor gastric lavage are recommended. If the
patient is lethargic or unconscious, an endotracheal tube
Management is placed for adequate airway protection, 114,135-137 although
this heightens the risk of aspiration as hydrocarbons
Induced vomiting or gastric lavage should not be adhere to the tube and increase the risk of chemical
attempted, as the alkalis will be neutralised by stomach pneumonitis. 114,135-137
acid, and lavage tubes may cause further tissue
damage. 135,137 External contact with alkalis requires ORGANOPHOSPHATES
copious irrigation at the point of contact; continue irriga- Organophosphates are a large and diverse group of chem-
tion for at least 15 minutes; for the eye, irrigation can be icals used in domestic, industrial and agricultural settings
for up to 30 minutes. Cover all wounds after irrigation (e.g. insecticides, herbicides). 103,104,138 Organophosphates
with sterile dressings to reduce the risk of infection.
are absorbed through the skin, ingested or inhaled.
A patient is deemed ‘nil by mouth’ until inspection of the Although most patients become symptomatic soon after
mouth and throat to determine the amount and extent ingestional exposure, the onset and duration of action
of burns. 135 An oesophagoscopy identifies the degree of depends on the nature and type of compound, the degree
injury and enables direct irrigation of any affected areas and route of exposure, the mode of action of the com-
of mucosa. 135 Alkalis that contain phosphates may pound, lipid solubility, and rate of metabolic degrada-
produce a systemic hypocalcaemia, and IV calcium tion. 103,139,140 The primary effect of organophosphates is

Emergency Presentations 605

binding and inactivation of acetylcholinesterase (AChE), enzyme activity). Levels do not, however, always correlate
a neurotransmitter that metabolises acetylcholine with clinical illness. 139
(ACh). 103,139,140
Mortality rates range from 3% to 25%, and are the most Management
common mode of suicide in some developing countries Initial priorities are ABC, in concert with D (danger), as
(e.g. Sri Lanka and Fiji). In one Australian study, 36% of organophosphates also present considerable risk to staff
patients had suicidal intentions, compared with 65–75% caring for the patient, especially during the initial phases
in developing countries. Men aged 30–50 years were of management. All patients’ clothing should be removed
141
more likely to attempt suicide with organophosphates. and considered hazardous waste. Patient decontamina-
Common complications include respiratory distress, sei- tion with soap and water is a priority, as soap with a high
zures and aspiration pneumonia, with respiratory failure pH breaks down organophosphates. 140,142 Staff should
the most common cause of death. 140 use personal protective equipment (PPE), such as neo-
prene or nitrile gloves, and gowns, when decontaminat-
ing patients. Charcoal cartridge masks for respiratory
Assessment, Monitoring and Diagnostics protection are used, although recent evidence suggests
Clinical findings of organophosphates are divided into that the nosocomial risk may not be as significant as once
142
three broad categories: thought.
1. Muscarinic effects; common manifestations are Intubation is commonly required after significant expo-
summarised by the mnemonic SLUDGE: Saliva- sure due to respiratory distress from laryngospasm, bron-
tion, Lacrimation, Urination, Defecation, GI upset, chospasm or severe bronchorrhoea. Continuous cardiac
pulmonary oEdema. 103,104,138,142 Other symptoms monitoring and an ECG are used to identify bradycardias.
include bradycardia, hypotension, bronchospasm, Activated charcoal is used for gastric decontamination for
cough, abdominal pain, blurred vision, miosis and patients who ingested organophosphate. The mainstay of
sweating. treatment is atropine and pralidoxime, with a benzodi-
138,139,142
2. Nicotinic effects: include muscle fasciculations, azepine used for seizure control. Atropine blocks
cramping, weakness and diaphragmatic failure. acetylcholine receptors and halts cholinergic stimulation.
Autonomic effects include hypertension, tachycar- Large doses of atropine are usually required (1–2 g IV),
dia, pupillary dilation and pallor. and repeated if muscle weakness is not relieved or the
3. CNS effects: include anxiety, restlessness, confu- signs of poisoning recur. Clearing of bronchial secretions
sion, ataxia, seizures, insomnia, dysarthria, tremors, is the endpoint of atropine administration, not pupil size
138,139,142
coma and paralysis; three types of paralysis may or absolute dose. Pralidoxime hydrochloride reac-
present: 103,104,138 tivates acetylcholinesterase and is effective in restoring
l type I: acute paralysis secondary to persistent skeletal muscle function, but is less effective at reversing
depolarisation at the neuromuscular junction; muscarinic signs. Over time, the bond between organo-
occurs shortly after exposure phosphate and cholinesterase becomes permanent and
142
l type II (intermediate syndrome): develops the effectiveness of pralidoxime diminishes. The
24–96 hours after resolution of acute choliner- current recommendation is for administration within 48
142
gic poisoning, and presents commonly as para- hours of poisoning. Benzodiazepines are clinically
lysis and respiratory distress. Proximal muscle indicated as the drug binds to specific receptor sites,
groups are involved, with relative sparing of potentiating the effects of gamma-aminobutyrate (GABA)
distal muscle groups; this may persist for up to and facilitating inhibitory transmitters for management
138,139,142
3 weeks of seizures.
l type III: organophosphate-induced delayed
polyneuropathy (OPIDP) occurs 2–3 weeks CHEMICAL, BIOLOGICAL AND RADIOLOGICAL
after exposure to large doses of certain organo- (CBR) EVENTS
phosphates. Distal muscle weakness with rela- Terrorist incidents and hoaxes involving toxic or infec-
tive sparing of the neck muscles, cranial nerves tious agents are frequent events, and there is now increased
and proximal muscle groups is characteristic. international attention paid to the potential risk of CBR
Recovery can take up to 12 months.
attacks. 143 While a nuclear weapon may be difficult for a
Laboratory diagnosis is based on measurement of cholin- terrorist group to obtain, there is evidence that groups
esterase activity using either erythrocyte or plasma levels; have attempted to acquire nuclear materials. 144,145 In addi-
erythrocyte cholinesterase is more accurate, but plasma tion, non-nuclear radioactive material may be easier to
cholinesterase is easier to test and is more widely avail- obtain and used in an explosive device (referred to as
able. Erythrocyte AChE is found in CNS grey matter, red ‘dirty bombs’). 144,145 Chemical agents or biological agents
blood cells, peripheral nerve and muscle. Plasma cholin- are also relatively easy to obtain, and pose a greater
esterase circulates in plasma and is found in CNS white threat. 143 The availability and the impact of chemical and
matter, pancreas and heart. 139-140 Levels of poisoning are biological threat materials are both relatively high, with
categorized as mild (cholinesterase activity is reduced to potentially devastating impacts. 143,146-149 As biological and
20–50% of normal; moderate (activity is 10–20% of chemical agents are dissimilar, each category is discussed
normal); or severe (less than 10% of cholinesterase separately, although there are common characteristics.

606 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Chemical Agents ENVENOMATION
Chemical agents are super-toxic chemicals used to poison Venomous animals can be land-based or marine-based,
mass victims. The chemicals are similar to hazardous and their distribution ranges from broad to very specific
industrial chemicals, but hundreds of times more toxic. locations. Exposure of humans to venom produces a large
For example, while the Sarin attack on the Tokyo subway and varied range of symptomatology, which often results
in 1995 killed 12 people, there were also 1039 injuries, in an emergency presentation. It is therefore important
and at least 4000 people with psychogenic symptoms. 147 for critical care nurses to be familiar with the types of
Sarin is approximately 60 times more toxic than methyl- potentially venomous animals inhabiting the catchment
isocyanate. To demonstrate this perspective: a leak of area of their health setting. Be familiar with the presenta-
methylisocyanate from a factory in Bhopal, India in 1984 tion and management of specific envenomations, includ-
caused 200,000 people to be affected, 10,000 severely ing antivenom availability. Contact the local poison
affected and 3300 deaths. Relatively small quantities of a information centre for advice from expert toxicologists
military grade chemical agent could therefore have the (see Online resources). Common envenomations across
same capability to produce large numbers of casualties Australia and New Zealand are described below.
(symptomatic and psychological). 147,148
Redback/Katipo Spider Bite
Biological Agents Description and incidence

Biological agents are living organisms or toxins with the
capacity to cause disease in people, animals or crops. The redback spider (Latrodectus hasseltii) is found through-
The toxins generally behave like chemical agents and out Australia but more commonly in temperate regions.
serve the same function: to poison people. 147,148 Biologi- Tasmania has the lowest incidence, while areas around
151
cal agents are relatively inexpensive to produce and have Alice Springs, Perth and Brisbane are especially infested.
the potential to be devastating in their effects. Organisms The redback spider is easily identifiable by the presence
such as anthrax, plague and smallpox have been the of a red, orange or brownish stripe on its characteristic
agents of greatest concern from terrorists’ potential use. 146 black, globular abdomen. The female is much larger than
Biological agents have the longest history of use, having the male; generally only the female is considered danger-
been available for centuries. 148 ous. Juveniles are smaller, more variably coloured, and
may lack any spots or stripes. Bites from both male and
juvenile spiders may result in symptoms, although these
Radiological Materials tend to be less significant than bites from a female. 152
Radiological materials pose both acute and long-term The redback spider has also become established outside
hazards to humans. Action is similar to some chemical Australia, including in New Zealand and Japan. 152,153
agents: cellular damage. A major difference is that the Although bites are rare, small populations of redback
radiological agents do not have to be inhaled or in skin spiders have been reported in Central Otago (South
contact to exert damage. 145 Deployment of a nuclear Island) and New Plymouth (North Island) since the early
weapon would be catastrophic; note evidence of events 1980s. 153 The only other venomous spider in New Zealand
like Hiroshima and Chernobyl. While very different, both is the Katipo (Latrodectus katipo) from the same genus as
events produced immediate injury and the long-term the redback. The katipo has a black, rounded body,
effects of ionising radiation on large populations. 146 Any slender legs and a red stripe on the abdomen. Adult males
radiological effects on human health from the 2011 and juveniles are black and white but are smaller than
tsunami in Japan and the subsequent damage to the females. The black katipo is a shy and non-aggressive
Fukushima nuclear reactors remains unclear at the time spider, found in coastal areas of New Zealand. They are
of writing. The event of most risk is likely to be a ‘dirty found in much of the North Island and on the South
bomb’ that combines conventional explosives with any Island as far south as Greymouth on the west coast and
available radioactive source. 146 Dunedin on the east coast. 154 Their habitat is generally
warm, sandy beaches and dunes, although environmen-
A CBR terrorism incident may or may not result in mass tal changes have resulted in increasingly scarce sightings
casualties and fatalities as intended. However, large and bites are rare. Symptoms of katipo spider bite are
numbers of psychological casualties are very likely and similar to those of the redback spider and where indi-
therefore, regardless of the effectiveness of the attack, and cated, redback antivenom is available to treat bites from
the number of people actually exposed to the agent, there both spiders in New Zealand.
will most likely be a mass casualty situation. 146 The psy-
chological implications of chemical and biological A redback spider bite is a frequent cause for ED presenta-
weapons may be worse than the physical ones. Chemical tions and the most clinically significant spider bite in
and biological weapons are weapons of terror; part of Australia. 152,155 Most bites are minor, with either minimal
their purpose is to wreak destruction via psychological or no symptoms and requiring no antivenom. In approxi-
means by inducing fear, confusion, and uncertainty in mately 20% of cases, significant envenomation occurs
150
everyday life. The long term social and psychological and antivenom administration is generally indicated,
effects of an episode of chemical or biological attack, real although death is extremely unlikely in untreated cases. 156
or suspected, would therefore be as damaging as the acute Redback antivenom is the most commonly administered
effects, if not more so. antivenom in Australia. 152

Emergency Presentations 607

Clinical manifestations anaphylactic reaction, although this is rare. An IV cannula
Envenomation by a redback spider is known as latrodec- is inserted and adrenaline 1 : 1000 is prepared for the
tism, as the venom contains excitatory neurotoxins that possiblity of anaphylaxis.
stimulate release of catecholamines from sympathetic The initial dose of Red Back Spider Antivenom is two
nerves and acetylcholine from motor nerve endings. 152,156 ampoules administered IM (500 units; approx 1.5 mL
Signs and symptoms associated with a significant enven- each ampoule), and symptoms should subside over the
omation are distinctive, and diagnosis is by clinical find- next 30–60 minutes. Complete resolution of symptoms
ings; initially a minor sting at the bite site, where the requires no specific further treatment. If there has not
spider may or may not have been seen. Over the first hour been complete resolution of symptoms after 2 hours a
the bite becomes progressively painful to severe, spread- further 2 doses of antinvenom are given. If after a further
ing proximally with and involving swollen and tender 2 hours there is incomplete resolution of symptoms or
local lymph nodes. Localised sweating at the bite site or no discernable response after 4 ampoules of antivenom,
limb or generalised sweating may appear, associated with expert advice should be sought via the local poison infor-
hypertension and malaise. Pain eventually becomes gen- mation centre. Patients who are symptom-free after 6
eralised and may be expressed as chest, abdominal, head hours of observation or the administration of antivenom
or neck pain suggestive of other acute conditions such as can be discharged home with instructions to represent
myocardial infarction. 155 should any symptoms return. Antivenom may be effective
Progression of symptoms generally occurs in less than 6 days after the bite (and possibly longer) however a larger
152,156
hours but may take up to 24 hours, while people with amount of antivenom is usually required.
minor untreated bites may experience symptoms for IV administration has been advocated in severe cases or
several weeks. 152,156 Other less common signs and symp- where there is poor response to IM administration. 152,156
toms include local piloerection, nausea, vomiting, head- The manufacturer recommends that for life-threatening
ache, fever, restlessness/insomnia, tachycardia, and envenomation the IV route may be used after first dilut-
neurological symptoms such as muscle weakness or ing the antivenom to 1 : 10 with Hartmann’s solution and
twitching. 152,157 administered over 20 minutes. 156,159 IV administration is
160
safe with reactions uncommon (less than 5%). No
Assessment significant benefit of IV administration over IM adminis-
Patients presenting with pain from a bite who have the tration was demonstrated in a randomised controlled
offending spider with them are straightforward in terms trial, so there is little evidence to justify one route of
of initial assessment. Identification of the spider is con- administration over another. 160 Redback spider antive-
firmed and a history of the event obtained, including the nom administration in various stages of pregnancy has
time of the bite and any first aid initiated. A brief assess- not been associated with direct or indirect harmful effects
ment of the bite site and the involved limb is undertaken, to the fetus. 152
including the extent of pain, presence of sweating and
painful tender lymph nodes, and a baseline set of vital
signs. Patients are then placed in a suitable area for Practice tip
medical assessment and ongoing observation. 157
Observations for the development or progression of symptoms
Adult patients presenting with vague limb pain, or pre- for a redback envenomation focuses on development of
verbal children who are ‘distressed’ and ‘cannot be local pain that spreads proximally and increases in intensity,
settled’, may be unaware that they have been bitten by a development of sweating either local or generalised and
redback. The pain may not have been felt at the time and hypertension.
no spider may have been seen. Thorough history-taking,
physical assessment and knowledge of latrodectism’s
effects enable detection of a suspected spider bite. 157 Funnel-web Spider Bite
Management Description and incidence
There is no recommended definitive first aid for a redback Funnel-web spiders are the most venomous spiders to
157,159,161
spider bite. Application of cold packs to the bite site and humans worldwide, and Australian funnel-web
administration of simple analgesia (e.g. paracetamol) spiders (Atrax or Hadronyche genera) are found primarily
may assist with local pain relief. The use of a pressure along the east coast. The Sydney funnel-web spider (Atrax
immobilisation bandage is not necessary, as symptom robustus) is found mainly within a 160 km radius of
progression is slow and not life-threatening, 152,156-158 and Sydney, while other species are found in eastern New
will cause further pain only in the affected limb. Remove South Wales and central and southern Queensland. The
any pressure bandage that was applied during first aid spider is large, black or dark brown, and approximately
after identification of the spider is confirmed. 152 3 cm long in the body. The cephalothorax is oval, smooth
and shiny, and the eyes are closely grouped. The abdomen
Presence of the above symptoms indicates systemic is similar in size to the thorax and is dull and hairy with
envenomation, requiring administration of redback spinnerets, that project noticeably behind the body. The
spider antivenom. 152,156 Prior to administration, the legs are moderately long and are black or dark plum in
patient should be placed in a clinical area with colour. Male spiders have longer legs, smaller abdomens
readily available resuscitation equipment to treat any and are significantly more toxic than females. 161

608 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Clinical manifestations antivenom may be required until all major symptoms
Funnel-web spider bites are potentially rapidly lethal; have resolved (severe bites often require eight
156,161,162
however, only 10–20% of bites result in systemic enven- ampoules). The antivenom dose for children is
156,161,162
omation, with the majority being minor and not requir- the same as the adult dose. First aid measures
ing antivenom. The bite is extremely painful, and fang such as a pressure immobilisation bandage can be
marks may be seen. Signs and symptoms of systemic removed after antivenom administration and the symp-
156
envenomation may appear within 10 minutes, and toms have stabilised; this may take several hours.
include perioral tingling and tongue fasciculation; Snake Bites
increased salivation, lacrimation, piloerection, sweating;
nausea, vomiting, headache; hypertension, tachycardia; Description and incidence
dyspnoea, pulmonary oedema; and irritability, decreased The Australian continent is inhabited by a large number
consciousness and coma. 156,162 Regardless of the presence of snakes (over 140 recognised snakes from 30 different
of symptoms, all possible funnel-web spider bites are species; 25% of all known venomous snakes, and 40% of
managed as a medical emergency. 156 all dangerous front-fanged snakes). 151,163 New Zealand
151
Assessment has no known venomous terrestrial snakes. Australian
Patients with suspected funnel-web spider bites are venomous snakes are found in both rural areas and resi-
dential and metropolitan areas, especially when in close
rapidly assessed for presence of any signs and symptoms proximity to bushland and in periods of drought. Distri-
of envenomation and allocated an ATS triage category of bution is within known geographical areas, and nurses
1–3, based on presenting symptoms. A pressure immo- require familiarity with the venomous snakes that inhabit
bilisation bandage is applied if this was not used during their locality of practice. The incidence of snakebite is
first aid. Patients with signs of envenomation are moved estimated at 500–3000 each year, with approximately
to a resuscitation area for immediate treatment, including 200–500 cases requiring treatment with antivenom. 164
urgent antivenom administration and management of There are on average 1–3 deaths per year, although this
the clinical effects of envenomation. Monitoring and may be higher due to unrecognised snake bites. 164
assessment for potentially serious manifestations focus
on ABC: Clinical manifestations
l airway compromise due to decreased level of con- The majority of snake bites do not result in significant
sciousness requiring airway protection with an airway envenomation. 165 Bites are generally recognised by the
adjunct or endotracheal intubation patient at the time because of associated pain, although
l breathing for respiratory compromise due to pulmo- some bites are unrecognised. The bite site may show
nary oedema, requiring CPAP or intubation/ventilation minimal to obvious signs of punctures or scratches, with
with PEEP (see Chapter 13) accompanying swelling and bruising. Multiple bites are
l circulatory compromise due to profound hypotension possible and are generally associated with major enven-
(although this is a late sign and hypertension is more omation. 156,165 Australian snake venoms contain a number
commonly seen), requiring IV access and volume of various toxins that are responsible for the systemic
replacement. Circulatory compromise/failure may effects 156,165,166 (see Table 22.11). Renal damage may occur
lead to cardiac arrest requiring cardiopulmonary as a consequence of myoglobinuria from severe rhabdo-
resuscitation (see Chapter 24). myolysis or haemoglobinuria associated with coagulopa-
thies, 165 leading to acute renal failure (see Chapter 18). 164
All patients require full monitoring with constant nursing
observation. A patient with no signs of envenomation on Assessment
arrival has a detailed history taken regarding the circum-
stances of the bite, the time, description of spider and any Patients presenting with snake bite(s) are allocated a high
first aid undertaken. The patient is then regularly assessed priority for assessment and treatment even if they appear
for any symptoms suggesting systemic envenomation. well on arrival. Patients who present without effective
After thorough medical assessment, if there are no signs first aid measures (the application of a pressure immo-
of systemic envenomation, any first aid such as a pressure bilisation bandage and splint) have these applied imme-
immobilisation bandage is removed and the patient diately. 165 The pressure immobilisation bandage is applied
observed for 6 hours. 156 With no diagnostic test for with a broad (15 cm) crepe bandage, commencing over
funnel-web spider envenomation and no venom detec- the bite site with the same pressure that would be used
tion procedure available, 156 clinical diagnosis is based on for a sprained ankle. The bandage is then extended to
the history and symptoms. cover the whole limb, including fingers/toes, and the
167
Management limb is splinted and immobilised. Correct application
of the pressure bandage is important, as any benefit is
For signs of systemic envenomation, two ampoules of lost with bandages that are too loose, not applied to the
167
funnel-web spider antivenom is administered slowly IV whole limb, or with no splinting or immobilistaion.
over 15–20 minutes; 161,162 premedication is not required, 156 Elasticised bandages are superior to crepe bandages in
although the patient is observed closely for anaphylaxis. obtaining and maintaining adequate pressure. 168 Do not
In severe envenomation associated with dyspnoea, pul- wash the wound prior to applying the pressure immobili-
monary oedema or decreased LOC, the initial antivenom sation bandage, as swabbing of the bite site is used when
dose should be doubled to four ampoules. 161,162 More performing venom detection. The patient should not

Emergency Presentations 609



TABLE 22.11 Characteristics and clinical manifestations of snake venom 156,165,166

Toxin Effects Signs and symptoms
Neurotoxin Blocks transmission at the neuromuscular junctions, causing l Ptosis (drooping of upper eyelids)
skeletal and respiratory muscle flaccid paralysis, either l Diplopia (double vision)
presynaptic and/or postsynaptic. l Ophthalmoplegia (partial or complete paralysis of
eye movements)
l Fixed, dilated pupils
l Muscle weakness
l Respiratory weakness, paralysis
Haemotoxin Causes coagulopathies, resulting in either: l Bleeding from bite wounds
l defibrination with low-fibrinogen, unclottable blood, but usually l Bleeding at venipuncture sites
with a normal platelet count; or l Haematura
l direct anticoagulation with normal fibrinogen and platelet count.
Both cause an elevated prothrombin ratio (INR).
Myotoxin Causes myolysis, resulting in generalised destruction of skeletal l Muscle weakness
muscles with high serum creatine kinase and leading to l Muscle pain on movement
myoglobinuria and occasionally severe hyperkalaemia. l Red or brown urine, which tests positively to blood





mobilise, to minimise distribution of any injected venom. To identify the likely snake involved and the correct anti-
Once applied the pressure immobilisation bandage is not venom required, a bedside snake venom detection kit
removed until the patient is in a hospital that is stocked (SVDK) is used at the bite site or with urine. A swab of
with antivenom. 164 the washings from the bite is collected by leaving the
pressure immobilisation bandage on and creating a
A brief and focused history explores the time and circum- window over the bite site to expose the area. Testing takes
stances of the bite, a description of the snake (colour, about 25 minutes. If there are signs of systemic envenom-
length), geographical location and the application of any ation, urine can be used to perform the test; blood should
first aid. The patient is assessed for general symptoms be avoided, as it is unreliable. A positive result indicates
including headache, nausea, vomiting, abdominal pain, that venom from a particular snake is present, but does
collapse, convulsions and anxiety (these alone do not not mean that systemic envenomation has occurred,
indicate envenomation), 164,165 as well as blurred or double while a negative result does not exclude systematic
vision, slurred speech, muscle weakness, respiratory dis- envenomation. 163,165
tress, bleeding from the bite site or elsewhere, and pain
and swelling at the bite site and associated lymph nodes.
Patients with suspected snake bite are located in an acute Practice tip
area with full monitoring available, with symptomatic
patients placed in a resuscitation area. The patient requires Whole blood clotting time is performed by drawing 10 mL
IV access and collection of blood for pathology tests venous blood and placing in a glass test tube. If the blood has
including FBC, UEC, CK and full coagulation studies. not clotted within 10 minutes, a coagulopathy is likely to exist,
Unnecessary venipunctures should be avoided, including suggesting envenomation. 166
sites where it may be difficult to control bleeding should
it occur. Healthcare settings with no ready access to
pathology services may need to perform whole blood In patients with known snake bite and systemic enven-
clotting time testing at the bedside to assess for any omation, antivenom administration is required if there is
coagulopathy. any degree of paralysis, significant coagulopathy, any
myolysis (myoglobinuria or CK >500), or unconscious-
All probable snake bites require observation for at least ness or convulsions. In an asymptomatic patient with
12 hours, as some serious symptoms may be delayed. 164,165 normal pathology and a negative or positive SVDK, it is
Assess for tachycardia, hypotension or hypertension, and likely that envenomation has not occurred. In this case,
a falling oxygen saturation, respiratory rate, forced vital the pressure immobilisation bandage is removed under
capacity (FVC) or peak expiratory flow rate (PEFR), indi- close observation in a resuscitation area. The patient is
cating respiratory muscle paralysis. 165 Frequent neuro- fully reevaluated including repeat blood test, assessing
logical observations focus on identification of muscle coagulation parameters, within 1–2 hours after removal
weakness and paralysis; note any ptosis, diplopia, of the pressure bandage. If the patient’s condition remains
dysphagia, slurred speech, limb weakness or an altered unchanged, further observation and repeat blood
level of consciousness. Insert an indwelling catheter for tests at 6 and 12 hours are required. Patients with no
close monitoring of urine output and presence of evidence of envenomation after 12 hours may be
any myoglobin. discharged. 163,167

610 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

Management Description and incidence
A patient with evidence of systemic envenomation Most stings occur during the summer months (Decem-
requires antivenom administration; monovalent antive- ber, January) in the tropical waters of northern Australia,
nom is used in preference to polyvalent antivenom when from Gladstone in Queensland around to Broome in
identity of the snake is known. Polyvalent antivenom is Western Australia, on hot, calm and overcast days when
a mixture of all monovalent antivenoms, and is therefore the jellyfish moves from the open sea to chase prey in
used for severe envenomation where the identity of the shallow water. 151,170,171 The exact incidence of stings is dif-
snake is unknown and the patient’s condition does not ficult to determine, but they are common in children.
allow time for a SVDK result, or where there is insufficient One ED reported 23 confirmed C. fleckeri stings in a
monovalent antivenom available. 163,165 Expert advice 12-month period. 172 There have been at least 63 con-
from a poison information centre may assist in identify- firmed deaths from envenomation by Chironex fleckeri in
ing the snake, based on known habitats and distribution the Indo-Pacific region.
as well as presenting symptoms.
Antivenom is always administered intravenously in a Clinical manifestations
diluted strength of 1 : 10 (or less if volume is a concern) Most stings are minor, with clinically significant stings
via an infusion. Administration is commenced slowly occurring from larger jellyfish. Stings generally occur on
while observing for signs of any adverse reaction. The the lower half of the body, and are characterised by
infusion rate can be increased if no reaction occurs, with immediate and severe pain. Pain increases in severity and
the whole initial dose administered over 15–20 minutes. may cause victims, especially children, to become inco-
The dose will vary depending on the type of antivenom, herent. While mechanisms of toxicity remain poorly
type of snake and number of bites; the use of 4–6 understood, death is thought to occur from central respi-
ampoules is not uncommon in severe envenomation. 156,165 ratory failure, or cardiotoxicity leading to A–V conduc-
Use of premedication before antivenom administration tion disturbances or paralysis of cardiac muscle. Victims
is controversial; at present the antivenom manufacturer may become unconscious before they can leave the water
does not recommend any premedication to reduce the following envenomation, and death can occur within
chance of anaphylaxis. Regardless of whether a premedi- 5 minutes. 170,171
cation is used, prepare to treat anaphylaxis. 165,169
The area of tentacle contact is seen as multiple linear
When the patient’s condition has stabilised after the lesions, purple or brown in colour. A pattern of transverse
initial dose of antivenom, the pressure immobilisation bars is usually seen along the lesions, along with an
bandage is removed, with continuous close observation intense acute inflammatory response, initially as a prompt
for any clinical deterioration caused by the release of and massive appearance of wheals followed by oedema,
venom contained by the pressure bandage. If deteriora- erythema and vesicle formation, which can lead to partial-
tion is evident, further antivenom and reapplication of or full-thickness skin death. 151,173
the pressure immobilisation bandage may be required. 163
Patients without signs of deterioration still require
ongoing observation in an HDU/ICU and repeat Assessment
pathology (coagulation studies) at 3 and 6 hours Patients presenting to ED after potential box jellyfish
post-antivenom administration. Ongoing observation sting are easily diagnosed based on the history, the pres-
and pathology studies will occur for at least 24 hours. 165 ence of pain and their skin lesions as outlined above.
Generally some form of prehospital management or
In children, management for snake bite is similar, with first aid will have been instituted. On arrival, patients
antivenom dosages the same as for an adult. Dilution with signs of clinically significant stings, alteration in
volume can be reduced (from 1 : 10 to 1 : 5) for consciousness, cardiovascular or respiratory function, or
children. 163 those with severe pain are seen immediately.
Box Jellyfish Envenomation
Chironex fleckeri (box jellyfish) is one of the world’s most Management
151
dangerous venomous animals. The jellyfish is a cubic Treatment focuses on appropriate first aid, administra-
(box-shaped) bell measuring 20–30 cm across and weigh- tion of adequate pain relief, symptomatic management
ing up to 6 kg. Four groups of tentacles, with up to 15 of cardiovascular and respiratory effects, and the admin-
tentacles in each group, can stretch up to 2 m and total istration of box jellyfish antivenom when indicated. First
length can exceed 60 m. Importantly, the animal is trans- aid measures include liberal application of vinegar to the
parent in water and is therefore difficult to identify. 170,171 sting area for 30–60 seconds. Vinegar inactivates the
The tentacles are covered with millions of stinging nema- undischarged nematocysts, so removal of any remaining
tocysts, each a spring-loaded capsule that contains a pen- tentacles should occur simultaneously to prevent further
etrating thread which discharges venom. Threads are envenomation. 151,173 Mild stings respond to the applica-
1 mm in length and capable of penetrating the dermis of tion of ice packs and simple oral analgesia, after the
adult skin. The tentacles also produce a sticky substance application of vinegar. 151,172 Patients with moderate to
that promotes adherence to a victim’s skin, causing some severe pain require IV narcotic analgesia. For patients
tentacles to be torn off and remain attached to the person, with continuing severe pain, antivenom is administered
where the nematocysts remain active. 151 along with continued parenteral analgesia. 171

Emergency Presentations 611

Patients are observed for the development of cardiorespi- Management
ratory symptoms, including arrhythmias. Management The mainstays of patient management are pain control
focuses on specific clinical effects, ranging from oxygen and symptom management. Application of vinegar as
administration and IV fluid resuscitation through to part of first aid is important, but due to delay in the pre-
intubation/mechanical ventilation or CPR. 151,173 Antive- sentation of symptoms following a sting this may be of
nom is indicated in patients with cardiorespiratory insta- limited value. 178 Pain is severe, and opioid analgesia may
bility, cardiac arrest or severe pain unrelieved by narcotic be required; if requirements for opioids are very high,
171
analgesia. Antivenom is carried by prehospital person- fentanyl is considered. 177 There is anecdotal evidence that
nel, and administration may occur prior to ED presenta- magnesium sulfate may have a role in the management
tion. A 20,000 unit ampoule of box jellyfish antivenom of Irukandji syndrome not responsive to the above treat-
is diluted in 10 mL isotonic saline and administered IV ments, but this remains unproven. 178
over 5–10 minutes. 172 The number of ampoules used
varies with clinical status: at least one for cardiorespira- Ciguatera
tory instability; up to three for life-threatening situations
with an inadequate response; and at least six for a cardiac Ciguatera is a type of seafood poisoning caused by the
arrest. 151,173 consumption of fish, especially certain tropical reef fish,
that contain one or more naturally-occurring neurotoxins
While the application of a pressure immobilisation from the family of ciguatoxins. Ciguatera is reported as
bandage to affected limbs after vinegar application was the most common form of seafood poisoning in the
previously recommended as a first aid intervention, there world, 180 and is considered a mild non-fatal disease, with
is little current evidence supporting this in box jellyfish a world wide mortality rate ranging from 0.1–20%.
181
stings, and its application may promote additional venom Ciguatera as a tropical disease confined to latitudes
release and therefore be potentially dangerous. 171,174 Some 35°N–35°S is no longer tenable, as tropical fish are now
animal research has suggested a role for magnesium marketed throughout the world and some species, like
sulfate in management for patients not responding to tuna, mackerel and dolphin fish, also migrate consider-
antivenom. 175 able distances. In Australia, there have been numerous
outbreaks of ciguatera poisoning in Sydney and as far
south as Melbourne. 181,182
Ciguatera toxins (ciguatoxins) are among the deadliest
Practice tip poisons known, reportedly 1000 times more potent than
arsenic. 183 These heat-stable toxins originate from a
The Australian Resuscitation Council currently recommends microorganism that attaches to certain species of algae in
that a pressure immobilisation bandage is not used in the man- tropical areas around the world; these toxins become
agement of jellyfish stings. 173,176 altered after ingestion by progressively larger fish up the
food chain. 174,181

Clinical manifestations and diagnosis
Irukandji Envenomation Ciguatera poisoning typically presents as an acute gastro-

The Irukandji is a small marine jellyfish, with stinging intestinal illness, followed by a neurological illness with
tentacles capable of causing intense pain and catechol- classical symptoms of heat and cold reversal of sensation
amine release. 177 that may last for a few days after consumption of con-
taminated fish 174 (see Table 22.12).

Description and incidence A patient may become sensitive to repeated exposure to
174,181
ciguatoxins;
additional exposure to poisoning from
Irukandji syndrome is a poorly-understood marine ciguatera may be more severe than the first episode.
envenomation encountered in far northern and north- Importantly, patients exposed to ciguatera suffer recur-
western areas of Australia. 178 Death is uncommon (two rences following the consumption of seemingly innocu-
recorded deaths in Australia), attributed to cerebral ous foods (e.g. nuts, nut oils, caffeine, alcohol, or animal
haemorrhage and is associated with other comorbid protein foods), 147,181,183 with relapses months or years
conditions. 179 after the initial poisoning. 183
Diagnosis is made on a patient’s history and clinical fea-
Assessment tures: consumption of fish followed by an acute gastroin-

People stung by an Irukandji may have no symptoms testinal and neurological illness. There is no conclusive
174,181
initially, but may develop symptoms up to one hour after diagnostic test for the presence of ciguatoxins.
being stung. Irukandji syndrome produces clinical fea-
tures of severe lower back pain, muscle cramps, raised Management
blood pressure, pulse and respiratory compromise, vom- Treatment of ciguatera poisoning is supportive care and
iting and anxiety. 177 A patient with suspected Irukandji symptom management. Mannitol has been recom-
envenomation is placed in an acute area with full moni- mended, although this is only effective if used in the first
toring available. 48–72 hours of the illness. 181,184

612 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



TABLE 22.12 Symptoms of Ciguatera 174

Gastrointestinal Neurological Cardiovascular Other symptoms
Abdominal pain Paraesthesias in extremities and around Bradycardia Dermatitis, rash, arthralgia and myalgia,
Nausea the mouth, tingling, burning, and pain Tachycardia general weakness, salivation, dyspnoea,
Vomiting Painful extremities Hypotension neck stiffness, headache, ataxia,
Diarrhoea Paradoxical temperature reversal where Hypertension sweating, metallic taste in the mouth
hot feels cold and cold feels hot Arrhythmia
Temperature sensitivity
Vertigo
Dental pain where teeth feel loose
Blurred vision
Tremor



NEAR-DROWNING medical conditions predispose a person to drowning and
DESCRIPTION AND INCIDENCE should be considered during management, including sei-
zures, arrhythmia (especially torsades de pointes associ-
Submersion incidents are frequent preventable events ated with long Q–T interval), coronary artery disease,
associated with significant mortality and morbidity, often depression, cardiomyopathy (dilated or hypertrophic
necessitating an ED presentation and subsequent hospi- obstructive), hypoglycaemia, hypothermia, intoxication
tal admission. In Australia, drowning is a relatively or trauma. 190
uncommon death (<1% of all reported deaths), but this Pulmonary manifestations after aspiration of fresh or salt
is significantly higher for children under 5 years (4.6 per water differ, as fresh water is hypotonic and when aspi-
100,000 population); 22% of all drowning deaths (over rated moves quickly into the microcirculation across
three times the adult rate). A higher incidence is seen in the alveolar–capillary membrane. With fresh water
males compared to females and a bimodal distribution aspiration, surfactant is destroyed, producing alveolar
of deaths is seen, with a peak in the toddler age group instability, atelectasis and decreased lung compliance
(0–4 years) and a second peak in young adolescent males and resulting in marked V/Q mismatching 185,186,190 (see
(15–19 years). 185-189 Chapter 13). In contrast, salt water has 3–4 times the
When near-drowning rates are added to drowning deaths, osmolality of blood, and when aspirated draws damaging
190
the incidence climbs to 24.5 per 100,000 population. protein-rich fluid from the plasma into the alveoli, result-
It is estimated that for every drowning death there are ing in both interstitial and alveoli oedema, with associ-
4–5 near-drowning hospital admissions and 14 ED ated bronchospasm and subsequent shunting and V/Q
presentations. 185-187 Near-drowning is also associated with mismatch. 185,186,190
high-impact injuries, especially boating or personal Despite these different physiological effects from aspi-
watercraft incidents and shallow-diving-related injuries. rated fresh and salt water, the resulting clinical manifesta-
Associated cervical spine injury is seen in 0.5% of near- tion is the same: profound hypoxaemia secondary to V/Q
drowning cases. 185 mismatch with intrapulmonary shunting (see Figure
CLINICAL MANIFESTATIONS 22.2). 185,186,190 Patients with evidence of fluid aspiration
The sequence of events in drowning has been identified often progress to develop severe ARDS within a very short
185
primarily by animal studies, highlighting an initial phase time. No significant effects on electrolytes are noted in
of panic struggling, some swimming movements and humans, as rarely more than 10 mL/kg and commonly
sometimes a surprise inhalation. There may be aspiration no more than 4 mL/kg of water is aspirated, while clini-
of small amounts of water at this time that produces cally significant electrolyte disturbances occur when over
185,186,190
laryngospasm for a short period. Apnoea and breath- 22 mL/kg has been aspirated.
holding occur during submersion and are often followed Cardiovascular effects are influenced by the extent and
by swallowing large amounts of water with subsequent duration of hypoxia, derangement of acid–base status,
vomiting, gasping and fluid aspiration. This leads to the magnitude of the stress response and hypothermia. 185
severe hypoxia, loss of consciousness and disappearance Ventricular arrhythmias and asystole may result from
of airway reflexes, resulting in further water moving into hypoxaemia and metabolic acidosis. Acute hypoxia results
the lungs prior to death. 185,186,190 in release of pulmonary inflammatory mediators, which
increase right ventricular afterload and decrease contrac-
Approximately 80–90% of submersion victims suffer ‘wet tility. 185,186,190 Hypotension is commonly seen due to
drowning’ as described above, with aspiration of water volume depletion secondary to pulmonary oedema,
into the lungs resulting from loss of airway reflexes and intracompartmental fluid shifts and myocardial
laryngospasm. Approximately 10–15% of victims have dysfunction. 185
sustained laryngospasm, and no detectable amount of
water will be aspirated (known as ‘dry drowning’), with Severe hypoxic and ischaemic injury is the most impor-
the resulting injury secondary to anoxia. 185,186 Preexisting tant factor related to outcome and subsequent quality of

Emergency Presentations 613


Aspiration may cause a rise in intracranial pressure (ICP). A 12-lead
Fresh water Salt water ECG identifies any arrhythmias (resulting from acidosis
and hypoxia rather than electrolyte abnormalities) and
the patient is managed conventionally (see Chapter
Bronchospasm Alveolar 11). 187 All patients require serial chest X-rays, as lung
Surfactant
Acute emphysema oedema fields often worsen in the first few hours. In clinically
significant submersions, the chest X-ray will typically
show bilateral infiltrates undifferentiated from other
V/Q-mismatch causes of pulmonary oedema.
Atelectasis
Compliance WOB MANAGEMENT

The condition of the patient, the environment and the
skill of the attending rescue personnel will influence pre-
hospital management of the postsubmersion patient, and
Hypoxia the adequacy of initial basic life support at the scene is
Acidosis the most important determinant of outcome. 188 The
Heimlich manoeuvre should not be performed in an
V/Q-mismatch, ventilation/perfusion mismatch; WOB, work of breathing.
attempt to remove aspirated water, as it is ineffective
FIGURE 22.2 Pathophysiology of respiratory failure due to fluid and likely to promote aspiration of gastric contents.
185
aspiration. Supplemental oxygen 100% is administered as soon
as possible. 188,189
For patients presenting to the ED in cardiac arrest, active
life. Other factors influencing the extent of injury include resuscitation measures continue (see Chapter 24),
water temperature and submersion time, stress during although the need for continued CPR is generally associ-
submersion, and coexisting cardiovascular and neuro- ated with a poor neurological outcome (submersions in
logical disease. 185,186,190 Prediction of death or persistent very cold water may have a better outcome). 188 The focus
vegetative state in the immediate period after near- of management for patients with spontaneous circulation
drowning is difficult. Patients awake or with only blunted includes respiratory support and the correction of
consciousness on presentation usually survive without hypoxia, neurological assessment and maintenance of
neurological sequelae. A third of patients admitted in optimal cerebral perfusion, cardiovascular support and
coma or after cardiopulmonary resuscitation will survive maintenance of haemodynamic stability, correction of
neurologically intact or with only minor deficits, while hypothermia and management of other associated
the remaining two-thirds of patients will either die or injuries.
remain in a vegetative state. 185
All patients require 100% supplemental oxygen via a
Hypothermia is a well-documented feature in submer- non-rebreathing mask initially. Patients without any
sion victims 185-189 (specific effects and management of respiratory symptoms should be observed for 6–12 hours,
hypothermia are covered later in this chapter). Incidents until there is a GCS >13, normal chest X-ray, no signs of
of submersion times of greater than 15 minutes where respiratory distress and a normal oxygen saturation on
victims recovered with a good neurological outcome all room air. 185-187 Alert patients unable to maintain adequate
occurred in very cold water (<10°C). While the exact oxygenation should be considered for CPAP or BiPAP
mechanisms in these outcomes is unclear, acute cold sub- prior to intubation (see Chapter 15).
mersion hypothermia may be protective against cerebral
insult by: very rapid cooling in victims with low levels of While cerebral oedema and intracranial hypertension is
subcutaneous fat who have aspirated a large amount of often seen in hypoxic neuronal injury, only general sup-
very cold water; induced muscle paralysis leading to portive measures are recommended as there is insuffi-
minimal struggling and very little oxygen depletion; and cient evidence to indicate that invasive ICP monitoring
the heart gradually slowing to asystole in the presence of and related management improve outcomes. 185-189 Any
profound hypothermia. 185-188 In these cases prolonged seizures should be promptly treated with appropriate
resuscitative efforts may be warranted, including active measures (see Chapter 17). Normocapnia is recom-
and aggressive re-warming interventions, that should not mended, although this needs to be balanced against any
be abandoned until the patient has been re-warmed to at permissive hypercapnia (cerebral vasodilation and
least 30°C. 187 increased ICP) for the management of any concomitant
ADS. Barbiturate-induced coma or corticosteroids are
190
ASSESSMENT not recommended as there is no evidence of improve-
189,190
Continuously monitor heart rate, BP and SaO 2 , and assess ment in outcome.
neurological status, including any seizure activity. Dete- Cardiovascular support may require a multifaceted
rioration is evident with a falling level of consciousness approach, initially by improving hypoxia and correcting
(LOC), a high alveolar–arterial (A–a) gradient, respira- circulating volume. Hypotensive patients require rapid
tory failure (PaCO 2 >45 mmHg) or worsening ABG volume expansion (crystalloid or colloid) and an indwell-
results. 187 Caution should be taken to avoid activities that ing catheter for hourly urine measurement. Patients with

614 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



TABLE 22.13 Physiological effects of hypothermia 191-197

Degree of hypothermia Mild (32–35°C) Moderate (28–32°C) Severe (<28°C)
General metabolic Shivering Raised oxygen consumption Normal metabolic functions fail
Raised oxygen consumption Acidosis
Hyperkalaemia
Cardiac Vasoconstriction Atrial arrhythmias Ventricular arrhythmias
Tachycardia Bradycardia Decreased cardiac output
Increased cardiac output
Respiratory Tachypnoea Decreased respiratory drive Apnoea
Bronchospasm
Neurological Confusion Lowered level of consciousness Coma
Hyperreflexia Hyporeflexia Absent reflexes
Coagulation Platelet dysfunction Increased haematocrit Lower bleeding times due to
Impaired clotting enzyme function failure of clotting systems
Increased blood viscosity




persistent cardiovascular compromise may require ino- Ambient temperatures need not be particularly low, as
tropic support in conjunction with invasive haemody- other contributing factors such as wind may be signifi-
namic monitoring. 185-189 cant. A patient with a decreased LOC may present with
191
hypothermia after lying on a cool surface. As a person’s
Patients presenting with associated high-impact or
shallow-diving mechanisms should have cervical spine core temperature drops, progressive cardiac abnormali-
immobilisation instituted with the application of a rigid ties occur; normal sinus rhythm may progress to sinus
cervical collar, especially for complaints of neck pain or bradycardia, T wave inversion, prolonged P–R and Q–T
191
an altered level of consciousness (see Chapter 17). The intervals, atrial fibrillation and ventricular fibrillation.
management of hypothermia and re-warming methods A QRS abnormality, the Osborn wave (positive deflection
outlined below are appropriate for the management of at the junction of the QRS and ST segment), is frequently
194
near-drowning. described as being characteristic of cold injury.
Metabolic acidosis and blood-clotting abnormalities are
HYPOTHERMIA common, and hypoglycaemia (depletion of glycogen
stores caused by excessive shivering) or hyperglycaemia
DESCRIPTION AND INCIDENCE (inhibition of insulin action due to the lowered tempera-
Cold injury is a common problem in Australia and New ture) may occur. 191-197 The physiological alterations that
Zealand, despite the relatively warm weather zones in the accompany lowering of core temperature to below 30°C
former. The very young and very old are most susceptible are summarised in Table 22.13.
191
to injury. A normal core temperature of 37°C has a MANAGEMENT
variation of 1–2°C. Temperature maintenance is essential
for normal homeostatic functioning, and normal adap- A patient with severe hypothermia may appear dead:
tive mechanisms can respond to reductions in ambient cold, pale, stiff, with no response to external stimulation.
temperature. Hypothermia is a body temperature below Successful resuscitation of patients has occurred at tem-
35°C (measured centrally by oesophageal or rectal peratures as low as 17°C, due to the low body tempera-
probe), and occurs with exposure to low ambient tem- ture protecting vital organs from hypoxic injury. 192-196 This
peratures that are influenced by low environmental tem- is reflected in the anecdotal phrase, ‘patients are not dead
peratures, humidity, wind velocity, extended exposure until they are warm and dead’. 193 In most cases, therefore,
time or cold water immersion. 191-193 resuscitation should continue until the patient’s core
temperature reaches 30°C. 192-196
CLINICAL MANIFESTATIONS If a patient’s core temperature is below 32°C, ‘core
When skin temperature is reduced after exposure to the rewarming’ is indicated. This approach is favoured, as
cold, sympathetic stimulation occurs causing peripheral experimental evidence indicates that return to normal
vasoconstriction, decreased skin circulation and shunting cardiovascular function is more rapid with temperature
of blood centrally to vital organs. Blood pressure, heart rises of up to 7.5°C per hour. 191,192 A number of invasive
rate and respiratory rate rise, and shivering (involuntary internal warming options are available, including perito-
clonic movements of skeletal muscle) stimulates meta- neal dialysis and haemodialysis, although the most effec-
bolic activity to produce heat and blood flow to striated tive of all internal methods is cardiopulmonary bypass,
muscles 191,192 to maintain a normal core temperature. If as it transfers heat at a rate several times faster than
continued exposure to cold occurs these compensatory any other methods available (approximately 7.5°C per
functions fail, and hypothermia results. 191-193 hour). 195 While the technique is efficient, it is obviously

Emergency Presentations 615

more invasive and carries associated risks, and so is impaired neurological function. 198 Heat stroke is a pro-
reserved for profoundly hypothermic patients. 191 found disturbance of the body’s heat-regulating ability,
and is often referred to as ‘sunstroke’, although it relates
External warming is indicated only if the core tempera-
ture is above 32°C, as this may cause vasodilation and to the body’s inability to dissipate heat, loss of sweat
hypovolaemic shock. Shunting of cold peripheral blood function and severe dehydration, rather than actual sun
198,199
to the core may also lead to further chilling of the exposure.
myocardium and ventricular fibrillation. 191,192 External
warming using warm blankets, forced warm air blankets, Management
and heat packs in contact with the patient’s body should Initial management of the hyperthermic patient focuses
raise body temperature by approximately 2.5°C per on airway, breathing and circulation, 198,199 with correction
hour. 191,192 Inhalation rewarming with oxygen warmed to of urgent physiological states such as hypoxia, severe
42–46°C is also effective, as around 10% of metabolic potassium imbalances and acidosis. A heat-stressed
heat is lost through the respiratory tract. 195 patient can have large fluid losses and require prompt
fluid resuscitation, preferably isotonic sodium chloride
HYPERTHERMIA AND HEAT ILLNESS solution. 198,199 Total water deficit should be corrected

DESCRIPTION AND INCIDENCE slowly; half of the deficit is administered in the first 3–6
199
hours, with the remainder over the next 6–9 hours.
Heat-related illness is common in Australia, although
there are only limited deaths. 198,199 Alterations in thermo- Rapid cooling is the second priority: lowering core tem-
regulatory function cause varying degrees of heat illness, perature to <38.9°C within 30 minutes improves survival
198
categorised as three types: heat cramps, heat exhaustion and minimises end-organ damage. The ideal goal is
199
and heat stroke. 198,199 Excess exposure to heat substan- to reduce the core temperature by 0.2°C/min. Non-
tially increases fluid and electrolyte losses from the invasive external methods of cooling include removal of
body. 198,199 The loss of both fluids and electrolytes in clothing and covering the patient with a wet, tepid sheet.
addition to impaired organ function lead to the compli- Ice packs can be placed next to the patient’s axillae, neck
cations of heat illnesses. Factors contributing to heat and groin. Invasive cooling measures such as iced gastric
illness include elevated ambient temperature, increased lavage, iced peritoneal lavage and cardiopulmonary
heat production due to exercise, infection, and drugs such bypass are reserved for the patient who fails to respond
199
as amphetamines, phenothiazines or other stimulants. 198 to conventional cooling methods. Core body tempera-
Impaired heat dissipation is caused by exposure to ture should be monitored using a continuous rectal or
high ambient temperatures with high humidity, a failure tympanic probe. No randomised clinical trials have com-
199
of acclimatisation, excessively heavy clothing, inade- pared the effectiveness of different cooling methods.
quate fluid intake leading to dehydration and sweat
dysfunction. 198 SUMMARY
CLINICAL MANIFESTATIONS This chapter has provided an overview of important ED
systems and processes, outlining the practice of initial
Environmental heat illness is more likely to develop assessment and prioritisation of patients presenting to
when the ambient temperature exceeds 32–35°C and the the ED through the unique nursing process of triage. The
humidity is greater than 70%. 198,199 Assessment of the role of the emergency nurse, including aspects of extended
patient’s physical state and vital signs including GCS practice and the role of the emergency nurse practitioner,
score provides evidence of hypovolaemia and shock.
were described. The initial ED management of common
Heat exhaustion is a more severe form of heat illness and emergency presentations were outlined reflecting current
is associated with severe water or salt depletion due to practice and based on the latest available evidence.
excessive sweating and a temperature below 40°C. Com-
bined water and salt loss causes muscle cramps, nausea The emergency environment is dynamic, and it was
and vomiting, headache, dizziness, weakness, fainting, beyond the scope of this chapter to describe the full
thirst, tachycardia, hypotension, profuse sweating, but extent of emergency nursing practice and the clinical
with normal neurological function. Haemoconcentration entities that they manage. It is therefore important for
is noted if body water has been sufficiently depleted, a critical care nurse to be familiar with the content pro-
while serum sodium can be either high or low depending vided in the other chapters in this text, as well as other
on the relative amounts of salt and water lost. 198 resources. As noted at the beginning of this chapter,
other common presentations to the ED, such as trauma
Heat stroke is the most severe and serious form of and cardiorespiratory arrest, are described in Chapters
heat-related illness, with temperatures above 41°C and 23 and 24.

616 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



Case study
0750h 0815h
Maria Baxter, a 42-year-old woman, presented to the ambulance The Poisons Information Hotline was contacted for advice, with the
bay of the ED with her family in a private car for evaluation after a following information provided:
suspected overdose of insecticide. Maria’s partner and sister l symptoms may have a delayed onset
approached the triage area stating that the patient had taken l the solution contains active metabolites
‘another overdose and was vomiting’. At this stage they gave no l a serum cholinesterase level should be collected
warning to the emergency staff of the type of ingestion. The initial l an oral dose of activated charcoal should be administered
history was difficult due to the dysfunctional communication by l a dose of atropine may be given as a heart rate response test
the family members present. Questioning of Maria’s sister by the l administration of pralidoxime was suggested if there was no
triage nurse revealed that the patient had deliberately drunk response to atropine or an exacerbation of symptoms was
approximately one cup of ‘insect killer’. seen.
The triage nurse protected herself (minimally) with a pair of gloves 0825h
and a patient gown, then went to assess Maria, who was sitting in Maria’s pulse rate was noted to be 110 beats/min. A dose of atro-
the backseat of the car. On initial triage assessment, the patient pine 0.5 mg IVI was administered and her pulse rate rose to 125. A
was alert and able to talk, stating that she ‘felt unwell’ and relaying chest X-ray was also ordered.
what had happened. The triage nurse noted that the patient had
vomited recently and that there was a strong smell of a garlicky 0830h
oil-type substance coming from the car. The triage nurse immedi- Maria developed mild sweating of the face and forehead. There
ately removed herself from the area and contacted the shift coor- was no increase in salivation but a large amount of clear saliva was
dinator of the ED to inform her of the incident, the need for noted on the tongue. No muscle fasciculations were evident, and
assistance and that staff should adopt a standard approach to a Maria’s pupils fluctuated from 4 mm to 1 mm in size. On ausculta-
chemically contaminated patient. tion her chest was clear, and good power was evident in all limbs.
Maria remained in the car while staff prepared a treatment area At this time, staff discussed Maria’s progress with her concerned
that was isolated from the department (a single room with family, including the potentially serious nature of the ingestion,
negative-pressure air flow and high-volume air extraction). Staff and offered emotional support.
also applied personal protective equipment (PPE) to guard them 0845h
selves from contamination with the substance. Three suitably-
clothed nursing staff helped Maria from the car. After minimal Maria developed widespread muscle tremors but retained good
assessment, she was taken to an external shower, where she had muscle strength, including the ability to cough and maintain ade-
her clothing removed and placed in a sealed contaminated-waste quate respiratory function. Her pulse rate rose to 144 beats/min
bag. The patient was then given a shower using warm, soapy water. with a blood pressure of 140/90 mmHg. A pralidoxime loading
It was noted at this point that an oily substance on and around her dose was ordered (1 g in 100 mL isotonic saline) and commenced
mouth and hands turned white when water was applied. This was over 30 minutes, followed by a pralidoxime infusion (at 400 mg/h).
thoroughly removed and Ms Baxter was placed in the isolation 0850h
room of the ED.
An ICU review was requested and Maria was seen by the intensive
0803h care consultant. The consultant agreed with the current manage-
Maria was formally triaged with an ATS of 2, based on her exposure ment plan and accepted Maria as a suitable admission to the ICU.
to the chemical and the level of response required. Her initial At that time a bed was available and ready. The earlier chest X-ray
observations were: alert with pink, warm and dry skin; pulse 72 was reviewed and noted to be clear. The ICU consultant also noted
beats/min; blood pressure 117/71 mmHg; oxygen saturation that the ECG showed a sinus tachycardia with no rhythm distur-
100%. Cardiac monitoring and supplemental oxygen therapy (6 L/ bances. At this time, emergency staff caring for Maria began com-
min via Hudson mask) were commenced. An IV cannula was plaining of nausea and headaches. A rotation of the staff caring for
inserted by an ED nurse and venous blood samples were collected Maria was commenced.
for haematology and biochemistry.
0900h
0810h Maria had an increase in sweating, further diarrhoea, had devel-
Initial medical assessment noted the following additional history: oped a cough, and increased salivation which required suctioning.
l Maria vomited twice, once in the car and once in the ED; this But Maria was still able to talk, and her GCS remained at 15. Other
was followed by an episode of diarrhoea. observations were: heart rate 130, respiratory rate 24, blood pres-
l Maria had taken an intentional ingestion of chlorpyrofos, esti- sure 140/95, and oxygen saturation 99%.
mated to be approximately half a cup at 0630–0645h. Maria
stated that she wanted to kill herself. 0910h
l The family appeared asymptomatic. With an ICU bed available, a transfer to the ICU was undertaken.
l On the container supplied by the family, the information label Maria was transferred with full monitoring and resuscitation equip-
read ‘Super Buffalo Fly Insecticide, 20% chlorpyrofos, 65% ment and with the ICU consultant, emergency physician and an
liquid hydrocarbon’. emergency nurse escort.

Emergency Presentations 617



Case study, Continued
0915h extubation, Maria complained of a headache and generalised
Maria’s condition suddenly deteriorated during transport to the weakness, but was able to eat, drink and mobilise. She spent a total
ICU. Her level of consciousness decreased, along with her respira- of 5 days in the ICU before being discharged to the mental health
tory effort. She was noted to be profoundly weak, with widespread service.
piloerection and muscle tremors. Assisted ventilation with bag– Mental health admission summary
valve–mask resuscitator commenced. Maria was diagnosed as having a maladaptive situational response
0920h and moderate depression with ongoing suicidal thoughts. She
On arrival in the ICU Maria was unable to protect her airway due stated to staff that she would not use insect killer again and had
to profound weakness and a reduced GCS. She was intubated with no other formal plan of how she might harm herself. The mental
midazolam 3 mg and vecuronium 10 mg given for induction. health admission was for a total of 5 days. At hospital discharge
Maria had no suicidal ideation. A community mental health team
Summary of ICU admission follow-up was arranged.
Maria required 3 days of ventilation. A pralidoxime infusion was
required for 2 days due to depleted cholinesterase levels. On





Research vignette

Fry MM, Rogers T. The transitional emergency nurse practitioner framework. The advanced role had made a significant contribution
role: implementation study and preliminary evaluation. Austral- towards meeting local service needs.
asian Emergency Nursing Journal 2009; 12(2): 32–7.
Critique
Abstract This paper described the implementation and evaluation of an
Background extended practice emergency nursing role, a transitional emer-
An implementation study was undertaken to develop and gency nurse practitioner (TENP). The role of the emergency nurse
employ Transitional Emergency Nurse Practitioners (TENPs) to practitioner and other extended practice roles have been described
address increased service demands. The TENP role was to be a in this chapter. This specific role was created due to the lack of
new advanced practice role, which was based on a Nurse Prac- available authorised emergency nurse practitioners, state health
titioner (NP) framework. The implementation study provided a funding and a need to meet an increase in service demand. This
roadmap for the introduction of the new nursing role. The imple- paper explored a number of features associated with this single
mentation study aimed to i) develop an integrated and supported site implementation.
Transitional Emergency Nurse Practitioner Role; ii) provide a
framework for practice and knowledge development; and iii) An initial six-month implementation plan was described, including
undertake a six month preliminary evaluation of the TENP work a communication strategy; a consultative process to define the
performance. TENP role and scope of practice; education; ongoing support struc-
tures; and assessment and feedback mechanisms. A framework for
Methods the role of the TENP was presented which focused on three main
The study describes the communication strategy, the consultative patient groups:
process for role definition, education, ongoing support structures 1. a ‘see and treat’ group consisting of minor illness and traumatic
and assessment and feedback mechanisms embedded in the conditions and where minimal medical supervision would be
implementation process. In addition, a six month mixed method required
preliminary evaluation was undertaken as a part of the implemen- 2. a ‘collaborative’ group of more complex patients where signifi-
tation plan. The preliminary evaluation included review of TENP cant collaboration with senior medical staff would be required
managed patient groups; peer audit of TENP documentation; a 3. a ‘consultative’ patient group where the TENPs would supervise
senior emergency physician survey of TENP work performance; or assist junior medical and nursing staff in various clinical
and review of TENP investigations and referrals. procedures.
Results The scope of practice for these patient groups was depicted in a
TENPs managed the care of, or were involved with 2730 patients role model. This framework and scope of practice provide clear
(10%) of which 68% (n = 1987) were in the ‘See and Treat’ group information and assistance for other sites considering implementa-
and 32% (n = 721) were the ‘Collaborative’ (742) and ‘Consultative’ tion of a similar role. The framework and scope of practice is an area
(22) groups. TENPs managed an average of 20 patients per 15 hour for further study and evaluation.
work day. Work performance evaluation identified the role was safe
and efficient and the staff supported the new role. A subsequent six-month postimplementation evaluation of the
role explored the total numbers of patients seen by the TENP, as
Conclusions noted in the Abstract. Of interest only a very small number of
The implementation study provided an effective framework for patients were seen in the consultative group (n = 22). There was no
the introduction of a transitional nursing role based on a NP discussion regarding the possible reasons for the small patient

618 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E



Research vignette, Continued
number in this group or whether consideration should be given to of supervision, diagnostic accuracy, quality of documentation,
refining the role model and scope of practice. The role was also appropriateness of investigations, medications required and an
evaluated using a peer audit process of TENP documentation for area for comments. The TENPs were rated 6–9 for supervision
appropriateness and adherence to policy and guidelines. The requirements and 7–9 for diagnostic accuracy, documentation
audits examined components of history, examination, investiga- quality, medications required and investigations and pathology
tion, diagnostic interpretation, management plans, patient dis- ordered. Once again the exact number of surveys conducted was
position and patient referral. Audit scores ranged from 22–25 not reported and validation of the survey tool was not described.
(maximum possible audit score was 25). The number of documen- Unfortunately, patient satisfaction of the role, and representation
tation audits conducted was not stated, and an in-depth descrip- rates of patients treated by the TENPs, were not studied.
tion or validity testing of the audit tool were not discussed. The Overall, this paper detailed a framework and scope of practice for
latter is another topic of potential research.
the successful implementation of a TENP role. Other emergency
Evaluation also included a survey of the TENP work performance departments wishing to implement extended nursing practice
by 5 senior emergency physicians, using a 10-point scale (10 = roles could consider the implementation described here. The
minimal supervision required and/or patient management perfor- paper also supports the benefits, safety and success of the
mance by the TENP was appropriate). The survey examined levels extended nursing practice roles.




Learning activities

1. Review your department’s plan for the management of a 7. Are there specific antidotes for organophosphate poisoning?
potentially chemical-contaminated patient. Explain your answer.
2. Outline what PPE your department has available for staff use. 8. Outline the effects of atropine administration in the context of
3. Describe the routes by which organophosphates can be this poisoning. What are the endpoints for atropine therapy?
absorbed. 9. How does pralidoxime work?
4. In the case study, why did Maria have her clothing removed 10. Outline the preparation for the safe transport of critically
and then washed with soapy water before entering the ED? unwell patients. Consider in your response the patient’s condi-
5. Given the symptoms described for Maria, outline the musca- tion, the personnel required and the equipment.
rinic and nicotinic effects displayed with the poisoning in this 11. Maria’s family members requested to visit her during the initial
case study. management in the ED. How would you handle this request?
6. List the common acronyms outlining the muscarinic and nico-
tinic effects displayed with organophosphate poisoning.


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Trauma Management 23





Louise Niggemeyer
Paul Thurman




The injury epidemiology for trauma differs with severity.
Learning objectives The majority of trauma patients requiring admission to
an ICU are those with more serious injuries that are asso-
After reading this chapter, you should be able to: ciated with motor vehicles, motorbikes and pedestrian
l identify the benefits and limitations of an organised trauma collisions. Falls, collisions and assaults are less common,
system but still frequent, causes of trauma requiring critical care
l describe the rationale for a systematic approach to the admission. A significant proportion of injured patients
patient who has sustained injuries admitted to critical care have experienced neurotrauma,
l discuss the benefits of appropriate nursing care of the while other common injuries include multiple fractures
patient with serious injury and/or multitrauma and injury to internal organs in the thorax and abdomen.
l describe the acute nursing management of the patient The systematic organisation of trauma systems and
with multiple serious fractures improved delivery of prehospital care has resulted in
l describe the acute nursing management of patients with improved survival of trauma patients in recent years.
burn injuries, abdominal injuries and chest trauma Consequently, a greater number of patients with severe
l describe the nurse’s role in managing the trauma patient multiple injuries are now admitted to critical care units.
undergoing interim damage-control surgery. These patients generally require complex nursing care,
often for lengthy periods, both within the critical care
unit and beyond. This chapter reviews the common trau-
matic injuries that result in admission to critical care and
outlines the principles of management.
Key words
TRAUMA SYSTEMS AND PROCESSES
trauma
multitrauma A trauma system can be defined as:
transport an assembly of health care processes intended to improve sur-
fractures vival among injured patients by reducing the time interval
spinal injuries between injury and definitive treatment, and by assuring that
burns appropriate resources and personnel are immediately available
damage-control surgery when a patient presents to a hospital’.
8, p. 643
Without trauma systems in place, a range of organisa-
tional and clinical errors in the management of trauma
INTRODUCTION patients have been identified. These errors occur at all
stages of care, including prehospital, emergency, operat-
Trauma refers to physical injury that is caused by mechan- ing theatre, intensive care unit, wards, and during trans-
ical injury, also known as kinetic injury. Injury remains fers between hospitals. The majority of errors identified
9
the leading cause of death in adults under 45 years of age, were errors in management of patients, although approxi-
and is a leading cause of preventable mortality and mor- mately 20% of errors occurred as a result of system inad-
bidity in Australia and New Zealand, as well as the rest equacies. A smaller number of technique or diagnostic
1-4
of the world. Furthermore, injury represents a major errors occurred.
cost to injured individuals, the healthcare system and
5,6
society. More than 5.2 million people throughout the Over the past 20 years there has been increasing emphasis
world die due to injury, with 90% occurring in low- to on the development of trauma systems that cover geo-
middle-income countries. According to the World Health graphical areas, such as a nominated state or region. The
Organization, injury accounts for 16% of the world’s introduction of trauma systems has resulted in a 15–30%
disease burden. 7 reduction in the risk of death, primarily in the area of 623

624 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

10
preventable deaths. Although this reduction appears healthcare facilities may occur for clinical reasons, such
11
widespread, it has not been replicated in remote areas, as specialist or higher levels of care being required, or for
and is limited by the lack of examination of deaths that non-clinical reasons, such as bed availability. It is prefer-
occur before a patient reaches hospital or after discharge. able for patient transfer to be for clinical reasons only;
Additionally, the lack of examination of functional out- however non-clinical transfer is sometimes unavoidable.
comes limits interpretation of the trauma system, as it is Secondary transport of critically injured patients may
not clear whether the patients who survive have altered occur via either ground or air (by fixed-wing or helicop-
functional capacity. Despite these limitations, there is ter). The decision as to what form of transport to use will
widespread agreement on the benefits of trauma system depend on:
implementation, although the contribution of nursing
care in such trauma systems is rarely considered or mea- l the condition of the patient
sured. Furthermore, the precise components of a trauma l the potential impact of the transport medium on the
system that prove beneficial have not been identified. 12 patient
l the distance to be covered
PREHOSPITAL CARE l the urgency of the transport
The debate regarding the relative benefits of stabilising a l the environmental conditions
patient at the scene versus proceeding to the hospital as l the resources available
13
quickly as possible, is not new. Benefits are somewhat l the expertise of the respective transport teams.
dependent on the proximity of effective trauma facilities, Amenities such as landing sites, particularly for helicop-
the level of knowledge and skills of the prehospital per- ters, being in close proximity to healthcare facilities must
sonnel available and the specific injuries and condition also be considered. Different jurisdictions activate air
of the patient. The principle of the ‘golden hour’ remains retrieval using helicopters when the distance for the trans-
in place today and suggests that, in order to improve port is beyond a certain point, with the minimum dis-
outcomes, definitive care should be provided to patients tance ranging from 16–80 km. 14,15,19,20
as soon as possible, and preferably within 1 hour of the
injury being sustained. 13,14 In countries with large dis- It is essential that the standard of care is not compro-
tances and sparse populations this aim presents particular mised during transport of critically injured patients.
challenges and cannot be met in many regions. Despite Minimum standards exist that outline the requirements
these distances and transport challenges, recognition of for transport of critically injured patients, and these
life-threatening conditions, application of appropriate should be referred to for full details. 13,18,19 The following
emergency interventions and prompt transport to the principles apply during such phases of care:
nearest appropriate hospital remain the principles of pre- l There must be adequate preparation of the patient and
hospital care. 13-15 equipment.
In a number of regions, processes are in place to facilitate l Transport must occur by personnel with appropriate
prehospital admission: personnel can notify the receiving levels of expertise.
hospital in advance, for those patients who meet pre- l Necessary equipment, including batteries and pumps,
defined criteria. Identified patients generally have severe should be secured.
physiological compromise, or injuries from high-velocity l Patients should be stabilised prior to transport (whilst
causes that result in significant injury and associated poor balancing the need for timely transport).
outcomes. Early notification allows the assembly of a l Monitoring of relevant aspects of the patient’s care is
multidisciplinary group of health professionals who can essential.
provide immediate, expert assessment, resuscitation and l Adequate vascular access and airway control must be
treatment of critically injured patients. 16,17 Such trauma secured prior to commencing transport.
teams have been shown to provide benefit in the early l Effective communication is mandatory between refer-
management of multiply-injured trauma patients, and ring, transporting and receiving personnel.
are reviewed later in this chapter. 10,16 l Documentation, including X-rays and scans, should
accompany the patient and should cover the patient’s
TRANSPORT OF THE CRITICALLY status, assessment and treatment before, during, and
ILL TRAUMA PATIENT on completion of, the transport.
Transport of critically injured patients occurs at two stages l Relatives should be informed of the transfer, includ-
in the patient’s care. Primary transport occurs from the ing destination, and provided with assistance for
18
place of injury to the first healthcare facility to provide their own travel arrangements. Checklists itemising
care to the patient; this is sometimes referred to as pre- many of these principles, sometimes attached to an
hospital transport. Secondary transport occurs between envelope containing all transfer documentation, are
healthcare facilities; this is sometimes referred to as inter- often used to ensure that all necessary actions are
20
hospital transport. This chapter concentrates on second- undertaken.
ary transport, although many of the principles are similar
for both stages of transport. Intrahospital transport prin- TRAUMA RECEPTION
ciples are also relevant for critically injured patients being Reception of the trauma patient at the emergency depart-
transferred within departments in a healthcare facility ment of the hospital is generally performed by the triage
(see Chapter 6). Transport of a patient between nurse, although in the severely injured patient it is usual

Trauma Management 625

for a multidisciplinary team to receive the patient and Radiological and Other Investigations
commence assessment and treatment concurrently. In the Initial radiological investigations will usually be per-
setting of a mass-casualty incident, triage may be per- formed in the emergency department using portable
formed in the field.
equipment. A radiographer is often a member of the
The formal process of triage provides a means of cate- trauma team that is activated on notification of the immi-
gorising patients based on threat to life. Although there nent arrival of a severely-injured trauma case. Radiologi-
are many different triage systems in use, within Australia cal investigation will be dependent on the type of injury
and New Zealand, the five-level triage categorisation of sustained, but will generally consist of a portable X-ray
23
the Australasian Triage Scale (ATS) is widely used. See of the injured area/s if these include the chest, cervical
Chapter 22 for further description of the ATS. spine or pelvis. Other X-rays at this stage are rarely benefi-
cial, or rarely change the course of treatment.
Primary Survey If the patient is sufficiently stable after the secondary
Priorities of care are similar to those in all health settings, survey, more extensive investigation in the radiology
with airway, breathing and circulation taking precedence, department should be undertaken. This will include CT
and disability and exposure/environment being part of scans. It is essential that clinicians consider investigations
the primary survey (see Chapter 22). These components carefully, to ensure that all necessary imaging is under-
of care will often occur simultaneously rather than taken; for example, where a CT scan of the brain is
sequentially. Compromise to airway and breathing may required it is often prudent to also undertake a CT scan
result from direct injury, for example to the trachea, or of the cervical spine. However care should be taken to
indirectly through decreased level of consciousness. avoid investigations that will not change the planned
Compromise to circulation is usually as a result of sig- treatment but may delay urgent interventions such as
nificant blood loss, although it may occur as a result of surgery. Current controversies in radiation exposure and
injuries, such as cardiac contusions in chest trauma, or lifetime-associated cancer risks need to be considered.
21
the patient’s preexisting disease. The priorities of care Furthermore, the implications of moving the patient on
during this time reflect the principles of care in any and off imaging tables for repeated imaging is problem-
setting, and include: atic. The patient should be accompanied and monitored
l maintaining life, with priority given to airway, breath- by an appropriately competent nurse during all transfers
ing and circulation for investigation. Where the patient is requiring ongoing
l treating immediate problems such as bleeding advanced life support such as fluid resuscitation or airway
l preventing complications or further compromise. monitoring, it may also be appropriate for a medical
officer to accompany the patient.
Secondary Survey Further radiological investigation may be required as
Following stabilisation of the life-threatening problems part of the tertiary survey. This will depend on the radio-
identified during the primary survey, patients should logical examinations that have been undertaken as part
undergo a secondary survey (see Chapter 22). This is a of the secondary survey, the treatment that has already
systematic examination of the body regions to identify been administered and the current condition of the
injuries that have not yet been recognised. It is essential patient.
that both the front and the back of the patient, as well as
areas covered by clothing, are examined during this Focused assessment with sonography for trauma
process.
Where abdominal trauma is suspected, a focused assess-
Tertiary Survey ment with sonography for trauma (FAST) examina-
A tertiary survey should be conducted on, or soon after, tion 22,23 is likely to be used as part of the secondary survey
the arrival of trauma patients in the ICU. The purpose to determine whether free fluid is present in the abdomi-
of this third survey is to identify injuries that have not nal cavity. The abdomen is scanned in four zones – peri-
yet been detected, assess initial response to treatment cardial, Morison’s pouch (right upper quandrant),
and plan assessment and management strategies for splenorenal (left upper quadrant), and pelvis (Douglas’
future care. pouch). This generally takes 1–2 minutes when per-
formed by an experienced, credentialled clinician. Find-
The tertiary survey consists of another head-to-toe physi- ings are regarded as positive (fluid [blood] observed),
cal examination, assessment of the patient’s condition in negative or equivocal. Technical difficulties can be expe-
the context of his/her earlier condition and the treatment rienced with obese patients. While a positive FAST is
that has been administered, a full review of all diagnostic useful in identifying if a patient should receive urgent
information gained so far, and acquisition of the patient’s surgical intervention, a negative FAST does not rule out
past health history if family members or friends are avail- significant abdominal trauma, and the low sensitivity of
22
able. A systematic approach will minimise the number of FAST remains a concern for trauma clinicians. Where a
injuries that are not identified during the first 24 hours patient is undergoing a prolonged trauma resuscitation
of care. It is also important to repeat the tertiary survey phase, there may be an indication to repeat the FAST after
after the patient regains consciousness and begins to 20 minutes. The use of FAST examination outside the
mobilise. Joint injuries may only become apparent during trauma resuscitation and reception phase is occurring
weight-bearing movements. more often and can be undertaken in any clinician setting

626 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

of other injuries, for example neurological trauma or
TABLE 23.1 Criteria for activation of trauma teams 26,27 skeletal trauma, will vary for each individual patient and
will be dependent on the physiological impact of the
Physiological criteria Injury criteria injuries. Neurological and spinal cord injury are reviewed
in Chapter 17.
Heart rate <50 or >120 Penetrating injury to head, neck
beats/min or torso
Respiratory rate <10 or >29 Burn to ≥20% body surface area MECHANISM OF INJURY
breaths/min Fall ≥5 metres The most common causes of traumatic injury include
Systolic blood pressure Multiple trauma
<90 mmHg Crush or degloving injury to road traffic crashes, falls and collisions. While falls
Glasgow Coma Scale Score <10 extremity account for the greatest number of injuries requiring hos-
28
Skin pale, cool or moist Amputation proximal to the wrist pitalisation, injuries sustained in road traffic crashes
Paralysis or ankle tend to be more severe given the high velocity of the
Trauma arrest Motor vehicle crash with ejection trauma, and account for the greatest number of major
injuries, including those injuries requiring a critical care
admission. 28-30
The mechanism of injury is recognised as affecting both
where there is a suspicion of internal haemorrhage or survival and requirement for admission to the intensive
pneumothorax. 24
care unit. Patients who are injured in a road traffic crash
TRAUMA TEAMS experience a similar mortality to those injured through
falls (approx 3% in all patients and 10–17% in major
There are a number of different ways to organise the early injury patients), with both groups having a higher mor-
care of trauma patients. The most common method used tality than patients injured in assaults and collisions with
is through the establishment of multidisciplinary trauma objects (<1% in all patients and 12% in major injury
teams that can provide immediate, expert assessment, patients). 28,29 The older age group, with associated comor-
resuscitation and treatment of traumatised patients, espe- bidities, is likely to account for many of the deaths in the
cially those with multiple injuries. Many hospitals that group injured through falls. In addition, patients injured
receive trauma cases operate trauma teams that are either in road traffic crashes tend to spend longer in the inten-
activated or placed on standby, via pagers or telephone, sive care unit than patients injured through falls or
based on communications from paramedic personnel in assaults and collisions, and experience a greater number
25
the prehospital setting. This activation is based on a of injuries. 28
combination of physiological and injury criteria (see
Table 23.1). Age is sometimes added to the patient crite- GENERIC NURSING PRACTICE
ria, with those under 5 years or over 65 years receiving Nursing care of trauma patients is characterised by the
particular attention. A number of hospitals have two need to integrate practices directed towards limiting the
levels of trauma team activation, with more severe impact of the injury and healing injuries to multiple
injuries activating the full trauma team and less severe body areas in a complex process. The delivery of critical
activating a partial team. The use of two-tiered trauma care services must be systematic and must cross depart-
team activation has not been shown to affect patient mental and team barriers to achieve a coordinated
outcomes. 17 approach. This section outlines the principles of care
relevant to all trauma patients, including positioning,
COMMON CLINICAL PRESENTATIONS mobilisation, and prevention or minimisation of the

Trauma generally occurs to a specific area of the body trauma triad components of hypothermia, acidosis and
(e.g. the chest or the head) or consists of an injury caused coagulopathy.
by a specific external cause (e.g. burns). This section has
been arranged according to these specific types of injury, Positioning and Mobilisation of
including skeletal, chest, abdominal and from burns. the Trauma Patient
Specific considerations relating to penetrating injuries Appropriate positioning and mobilisation provides a sig-
have been covered separately, although the majority of nificant challenge for nurses involved in the acute care of
care for patients with penetrating injuries will follow the the trauma patient. Positioning refers to the alignment
principles of the area for injury. For example, a patient and distribution of the patient in the bed, for example
with a penetrating injury of the abdomen will generally supine, Fowler, semirecumbent or prone. In addition to
be cared for in the same way as all patients with abdomi- these fundamental nursing postures, there is positioning
nal trauma. of the limbs (i.e. elevated arms and legs). Mobilisation
refers to the movement of joints by the patient, to shift
Patients with multitrauma will also be cared for accord- from one place to another. This movement may be
ing to the principles of care for each specific injury, restricted to rolling within the bed, or moving out of
although consideration of priorities is essential. Care the bed.
should follow the common principles of airway, breath-
ing and circulation, therefore concentrating on respira- The principles of positioning and mobilisation are gener-
tory and circulatory compromise first, before moving on ally not different from those in other critically ill patients,
to the treatment of other injuries. The relative importance and should incorporate the need to:

Trauma Management 627


Cervical Spine Immobilisation Procedure
Cervical spine immobilisation should be performed as a team. Generally, four people should work together.
1. Leader is positioned at the head of the patient and positions his or her hands on each side of the patient’s head, with thumbs along
the mandible and fingers behind the head on the occipital ridge. Maintain gentle but firm stabilization of the patient’s neck
throughout the entire procedure.
2. Assess the patient’s motor and sensory level by asking the patient to wiggle his or her toes and fingers. Touch the patient’s arms
and legs to determine sensory response.
3. Apply and secure appropriate fitting cervical collar. Follow the directions for sizing that comes with each collar. An ill-fitting collar
can cause pain, occlude the patient’s airway, or fail to give appropriate immobilisation.
4. Straighten the patient’s arms and legs and position team members so that the patient may be rolled on the backboard as a unit.
5. The patient’s head should be immobilised until the straps are correctly placed. The straps should be placed so that the patient is secured
to the backboard at the shoulders, hips, and proximal to the knees.
6. The patient’s head should be further immobilised with head blocks or towel rolls. Tape or straps should not be placed across the chin.
7. The patient’s head should be manually immobilised until the head and neck are immobilised.
8. The patient’s motor and sensory function should be reassessed after the patient is immobilised.
9. Some patients such as those with a compromised airway or neck deformities may not be able to tolerate laying flat.
10. Massive neck swelling that may result from a penetrating injury may prohibit the use of a cervical collar. Towel rolls and tape may
be safer method of securing the patient to the board and allow for evaluation of the patient’s injury.
Modified from Emergency Nurses Association: Trauma nursing core course provider manual, ed 5, Des Plaines, III, 2000, The Association.
78
FIGURE 23.1 Spine Movement Precautions.


l promote the patient’s comfort The two methods available for moving the trauma patient
l maintain the patient’s and staff members’ safety are staff manual handling and lifting hoists. Generally,
l prevent complications trauma patients can be log-rolled (see Figure 23.1 for
l facilitate delivery of care. initial care and p. 635 for later care) as frequently as
required for nursing care. Any restrictions to patient posi-
Difficulty in positioning and mobilisation is often expe- tioning and weight bearing due to injuries or physiologi-
rienced when there is concern for the stability of the cal status must be considered through this process; it is
patient’s cervical spine, particularly in unconscious essential that care be taken to prevent any worsening of
patients. Specific protocols for confirming the absence of injuries due to handling of the patient. Knowledge of the
injury to the cervical spine in unconscious patients, or position restrictions for each limb, including all weight-
those complaining of cervical soreness or abnormal neu- bearing joints and the vertebrae, is imperative to avoid
rology, vary between institutions and regions, but gener- secondary iatrogenic injury. Certain injuries will impose
ally incorporate the following principles: 31
position and mobility restrictions (see Table 23.2).
l Obtain a detailed history of the injury wherever pos-
sible, including specific investigation of mechanisms
of injury that might exert force on the cervical spine. Practice tip
A high index of suspicion should remain, particularly
in the setting of injuries often associated with cervical When planning positioning and mobilisation of the trauma
spine injury, including craniofacial trauma rib frac- patient, ascertain the weight-bearing status of each injured
tures, pneumothoraces and damage to the great vessels limb, then determine positions or methods of mobilisation that
and/or trachea. are appropriate.
l Undertake plain X-rays of the full length of the spine,
interpreted by a radiologist.
l Where any abnormality exists in clinical or radiologi-
cal assessment, or the patient remains unconscious, a Practice tip
CT or MRI may be undertaken, and this must be
reported on by a radiologist. The NEXUS low-risk criteria have been widely accepted as iden-
l A correctly fitted hard collar should remain in place tifying patients in whom further examination is unnecessary
only until the patient is appropriately reviewed and and cervical spine injury can be excluded on the basis of clinical
the chance of a cervical spine injury is eliminated. If examination. These criteria include absence of midline cervi-
82
a collar is required for more than 4 hours, a long-term cal spine tenderness, no focal neurological deficit, no intoxica-
collar (e.g. Philadelphia, Aspen or Miami J) should tion, no painful distracting injury and normal alertness.
be used.
l Maintain appropriate pressure area care to areas under
the hard collar as well as usual pressure points until The ‘Trauma Triad’
cervical clearance is gained. 32
The critically injured patient can experience the ‘trauma
The practice of maintaining a patient in a hard collar for triad’ of hypothermia, acidosis and coagulopathy. While
days without active attempts to gain cervical clearance it is possible to experience these pathophysiological con-
should be avoided at all costs. ditions individually, they often occur simultaneously.