History of Triage

Triage was first described in 1797 during the Napoleonic wars by Surgeon Marshall Larrey, Napoleon’s chief medical officer,⁷ who introduced a system of sorting casualties that presented to the field dressing stations. His aims were military rather than medical, however, so the highest priority were given to soldiers who had minor wounds and could be returned quickly to the battle lines with minimal treatment.^1,8

The documented use of triage was limited until World War I, when the term was used to describe a physical area where sorting of casualties was conducted, rather than a description of the sorting or triage process itself.⁸ Triage continued to develop into a formalised assessment process, with subsequent adoption for initial categorising of patient urgency and acuity within most civilian EDs.^1,7,8

Development of Triage Processes in Australia and New Zealand

Australia is a world leader in the development of emergency triage and patient classification systems. In the late 1960s patients presenting to ‘casualty’ departments in Australia were not always triaged,^1,2,4,5 with many EDs using random models of care; ambulance presentations were given priority and the ‘walking wounded’ seen in order of arrival. In the mid-1970s, staff at Box Hill Hospital in Melbourne developed a five-tiered system that included a time-based scale and different colours on the medical record to indicate priority.^1,7,8 Subsequent modification and refinement led to the Ipswich Scale in the 1970s–80s.^1,2,4,5,7 These early triage systems reinforced the concepts developed by Larrey, and established a process for patients’ presentations to be seen in order of clinical priority rather than time of attendance. In the 1990s the impact of community expectations and national health policy led to further enhancements of triage systems in Australia, and the Ipswich triage scale was adapted into the national triage scale (NTS). The NTS was subsequently tested and demonstrated to have the essential characteristics of utility, reliability and validity.^{1,2,4,5,7,9–11} In 1993, the NTS was adopted by the Australasian College for Emergency Medicine (ACEM) in its triage policy,⁷ and subsequently renamed the Australasian triage scale (ATS) as it was implemented in most EDs in Australia and New Zealand (see Table 22.1).⁴

TABLE 22.1 Australasian triage code

The ATS is now a world-leading, reliable and valid triage classification system for emergency patients, with demonstrated predictive properties for severity of illness, mortality and the need for admission.^5,7,9–11 When properly applied, presenting patients should receive the same triage score no matter which ED they present to.^5,9,11

The Process of Triage

All patients presenting to an ED are triaged on arrival by a suitably experienced and trained registered nurse.^2,10 This assessment represents the first clinical contact and the commencement of care in the department. The ideal features of a triage area are: a well-signposted location close to the patient entrance; ability to conduct examination and primary treatment of patients in privacy; a close physical relationship with acute treatment and resuscitation areas; and appropriate resources including an examination table, thermometer, a sphygmomanometer, stethoscope, glucometer and pulse oximetry.^2,4,10

As the first clinician in the ED to interview the patient, the triage nurse gathers and documents information from the patient, family and friends, or prehospital emergency personnel. Professional maturity is required to manage the stress inherent in dealing with an acutely ill patient and family members (under significant stress themselves), while rapidly making informed judgement on priorities of care for a wide range of clinical problems.¹⁰

The triage nurse receives and records information about the patient’s reason for presentation to the ED, beginning with a clear statement of the complaint in the patient’s own words, followed by historical information and related relevant details, such as time of onset, duration of symptom/s, and what aggravates or relieves the symptom/s. A brief, focused physical assessment including vital signs may be undertaken to identify the urgency and severity of the condition, and may be collected as part of the triage process to inform decision making.^5,10,11 Triage assessment generally should be no longer than 2–5 minutes, balancing between speed and thoroughness.¹¹ From the information collected, the triage nurse determines the need for immediate or delayed care,^1–3 and assigns the patient a 1–5 ATS category in response to the statement: This patient should wait for medical assessment and treatment no longer than ….¹¹

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 possible to categorise the patient correctly in all instances, but it is better to allocate priority on a conservative basis and err on the side of a potentially more serious problem.^3,8,10,11 Importantly, a triage allocation is dynamic and can be altered at any time.^5–8 If a patient’s condition changes while waiting medical assessment/treatment, or if additional relevant information becomes available that impacts on the patient’s urgency the patient should be re-triaged to a category that reflects the determined urgency.^11,12 Frequent, ongoing observation and assessment of patients is therefore routine practice following the initial triage assessment.

The premise for a triage decision is that utilisation of valuable healthcare resources provide the greatest benefit for the neediest, and that persons in need of urgent attention always receive that care.^{1,2,4,5,11,12} Triage encompasses the entire body of emergency nursing practice, and nurses complete a comprehensive triage education program prior to commencing this role. A formal national triage training resource has been developed that provides the essential education components to promote consistency in application of the ATS.^11,12

Triage Categories

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 assessment of airway, breathing, circulation and disability remains the cornerstone of patient assessment in any clinical context, including triage.

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

Patient History/interview

The triage interview provides the basis for data gathering and clinical decision making regarding patient acuity. After an introduction, the triage nurse asks person-specific open-ended questions. Use of close-ended questions or summative statements enables clarification and confirmation of information received, and to check understanding by the patient.¹² Privacy is important to ensure that the patient is comfortable in answering questions of a personal nature. Most EDs need to balance providing an area that is private and accessible, yet safe for staff to work in relative isolation.

A large component of the triage assessment may be based on subjective data, which are then compared and combined with the objective data obtained through the senses of smell, sight, hearing and touch to determine a triage category: pulse, blood pressure, respiratory rate and characteristics, oxygen saturation, capillary return, temperature, blood glucose level. One aspect of the history that is difficult to quantify is intuition. This is that ‘sixth sense, or gut feeling’ that tells us that something not yet detectable 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 feel right’.^6,11,12

Primary Survey

While taking a patient history, the triage nurse also simultaneously conducts a primary survey. As noted earlier, airway, breathing, circulation and neurological function (deficit) is observed. If any major problem is observed, the interview is ceased and the patient is transferred immediately to the acute treatment or resuscitation area.⁸

Secondary Survey and Physical Examination

A secondary survey, involving a concise, systematic physical examination, is conducted after the patient history and primary survey have been completed. The equipment used includes a thermometer, stethoscope, oxygen saturation monitor and sphygmomanometer, in combination with clinical skills. This examination is not comprehensive but focuses on the presenting complaint while avoiding tunnel vision and wrong conclusions.^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 should reflect a system of rapid assessment that is reproducible and adaptable to a variety of presentations.

Approaches to Triage Assessment

A range of approaches to nursing assessment is applicable to triage assessments (see Table 22.3).⁸ Body systems approach enables systematic examination of each body system to discover abnormalities (i.e. central nervous system, cardiovascular system, respiratory system, gastrointestinal system, etc.).^6,11,12 See also the relevant ‘system-based’ chapters.

TABLE 22.3 Aids to triage assessment

Mental Health Presentations

Patients with psychiatric problems presenting to an ED should be triaged, assessed and treated as for other presenting patients, with particular attention to appropriate initial medical assessment and management.^6,11,12 Resources outlining specific mental health triage category descriptors are readily available, and relate specific aspects of mental health presentation with clinical urgency and triage categories (see Table 22.4), including an outline of suggested responses, such as patient placement requirements based on the level of risk and urgency.^6,11–14

TABLE 22.4 Examples of a mental health triage tool¹³

Nurse-Initiated X-Rays

Nurse-initiated radiology ordering enables investigations of extremities, joints such as hips and shoulders, the chest and abdomen according to clinical protocols that list inclusion and exclusion criteria¹⁹ based on findings from the ACN’s history-taking and clinical examination. The inclusion criteria reflect well-established clinical indicators. While nurse-initiated radiology ordering is often undertaken as an extended triage nurse function, it can be performed by any accredited nurse. The use of nurse-initiated radiology, especially in association with extremity injuries, is safe and accurate, reducing both waiting time and department transit time and improving both patient and staff satisfaction.^17,19–21

Nurse-Initiated Analgesia

Although pain is a common complaint in the majority of patients presenting to the ED,^22,23 management has previously been insufficient, especially in relation to the timeliness, adequacy and appropriateness of analgesia administered,^22,23 and resulting in poor patient satisfaction.²² To address these findings, many EDs developed nurse-initiated analgesia protocols, standing orders or pathways. Nurse-initiated analgesia protocols enable designated emergency nurses to implement analgesia regimens prior to assessment by a medical officer. These protocols are locally derived and note patient inclusion and exclusion criteria for managing mild, moderate or severe pain in both adult and paediatric patients, and often include administration of an antiemetic.^22,23 A numerical pain rating scale or a visual analogue scale is used to direct the type and route of analgesia administration. Severe pain protocols outline incremental intravenous narcotic administration, including incremental and total maximum administration dosages. After administration of the initial dose, the administering nurse gives subsequent incremental doses in response to a reevaluation of the patient’s pain score and vital signs (pulse, blood pressure and respiratory rate). Protocols directed towards moderate and minor pain may include either single or incremental IV analgesia or oral analgesia. Nurse-initiated analgesia protocols have also been found to be safe and effective and to shorten the time ED patients wait for analgesia,^23,24 which should assist in improving patient outcomes and satisfaction.

Clinical Initiative Nurse

The clinical initiative nurse (CIN) is a specific advanced practice role introduced to primarily provide care for waiting-room patients awaiting medical officer assessment. The role was initially introduced into levels 5 and 6 metropolitan and several large rural EDs in New South Wales, to manage and reduce ED waiting times and associated patient distress, improve ‘time seen’ rates, patient service satisfaction and patient outcomes (key performance indicators). These and similar roles are now being implemented nationally.²⁵ The role includes initiation of treatment for lower-acuity waiting-room patients, following advanced practice protocols. The treatment provided by the CIN includes ordering of radiology and/or pathology investigations, administration of oral analgesia, review and reassessment of waiting patients (particularly those who have waited longer than their triage benchmark time), and providing information and education to waiting patients and carers regarding waiting times, ED processes and patient education. The role acts as an adjunct to the triage role, and maintains a close working relationship with the triage nurse.^25–27 The CIN role has contributed to timely access to interventions, investigations and care for waiting patients, increases autonomous practice, independent decision making and enhances patient advocacy. The role also provides opportunity for the clinical and professional development of emergency nurses.²⁶

Nurse Practitioner

The nurse practitioner (NP) level of health care is one of the most important developments in contemporary nursing and marks the opportunity for significant reform in Australian health care. Nurse practitioners, while well established in North America, the UK and parts of Europe, are a relatively recent development in Australia. Introduction of the NP level of service has been a function of individual states rather than a national government process, and consequently implementation throughout Australia has been gradual, with title protection and practice privileges now legislated in five states over a 15-year period.

Introduction of the NP has been complicated by existing nomenclature relating to advanced practice roles in nursing, with titles such as advanced specialist, clinical nurse consultant, clinical nurse specialist and advanced practice nurse used interchangeably and at times problematically in the literature,^28,29 including internationally.³⁰ Consensus is gradually emerging that the NP role is evolving and developing globally as the most significant of the advanced practice roles in modern health care.²⁹

The NP scope of practice is determined by the clinical setting of the authority to practise. There are three points in this central to the nature of the role:

National and international experience has demonstrated a specific service that is highly regarded^32–35 and in demand.^36,37 The NP service provides care to many underserviced groups such as the homeless,³⁸ women and children, the elderly,³⁹ rural and remote communities^36,40 and specialist services in acute care areas.⁴¹ Nurse practitioners are effective in managing common acute illnesses and injuries and stable chronic conditions,³⁹ and provide an emphasis on health promotion and assessment and disease prevention.⁴²

The Australian experience has demonstrated that pressure on EDs can be relieved when NPs manage lower priority cases. Waiting times and overall length of ED stay are significantly reduced when NPs manage triage category 3–5 presentations such as sprains and superficial wounds.³⁷

Retrievals

Australasia has a variety of retrieval or transport models, although most retrieval teams comprise doctors, nurses and paramedics with specialised training in critical care. The skills of the escort personnel need to match the acuity of the patient, so that they can respond to most clinical problems.^47,48 Retrieval team staff therefore need to deliver high-level critical care equal to the standard of the receiving centre, but need to be familiar with the challenges associated with working outside the hospital environment. Standards for the transport of critically ill patients have been established by the College of Critical Care Medicine (CICM) and the Australian College of Emergency Medicine (ACEM).⁴⁸

When transporting an unstable patient it is essential that a minimum of two people focusing solely on the clinical care aspects of the patient are present, in addition to other staff transporting the patient and equipment. The transport team leader is usually a medical officer with advanced training in critical care medicine, or for the transport of critical but stable patients, a registered nurse with critical care experience. The skillset includes advanced cardiac life support, arrhythmia interpretation and treatment and emergency airway management.⁴⁸

Preparing a Patient for Interhospital Transport

Adequate and considered preparation of the transport of a critically ill patient from one hospital area to another should be appropriately planned and not compromised by undue haste. While strong evidence to support a ‘scoop and run’ approach to patients in the field exists, this principle does not apply to interhospital or intrahospital transport of a critically ill patient. Appropriate evaluation and stabilisation is required to ensure patient safety during transport, including assessment of ABCs and suitable IV access.⁴⁸

If potential airway compromise is suspected, careful consideration should be given to an elective intubation rather than an emergency airway intervention in a moving vehicle or a radiology department. A laryngeal mask airway is not an acceptable method of airway management for critically ill patients undergoing transport, because of the associated problems of movement.⁴⁸ A nasogastric or orogastric tube is inserted in all patients requiring mechanical ventilation.

Fluid resuscitation and inotropic support are initiated prior to transporting the patient. Planning for the trip needs to include adequate reserves of blood or other IV fluid for use during transport. If the patient is combative or uncooperative, the use of sedative and/or neuromuscular blocking agents and analgesia may be indicated.^51–53 A syringe pump with battery power is the most appropriate method for delivering medications for sedation and pain relief. A Foley catheter is inserted for transports of extended duration and all unconscious patients.^52–54

The patient’s medical records and relevant information such as laboratory and radiology findings are copied for the receiving facility, and other documentation includes initial medical evaluation, and medical officer to medical officer communication, with the names of the accepting doctors and the receiving hospital.^44,47

Patient Monitoring During Transport

Critically ill patients undergoing transport receive the same level of monitoring during transport as they would have in a critical care unit. Equipment essential for transport includes:

Monitoring equipment should be selected for its reliable operation under transport conditions, as monitoring can be difficult during transport; the effects of motion, noise and vibration can make even simple clinical observations (e.g. chest auscultation or palpation) difficult, if not impossible.⁴⁹ As transport of mechanically-ventilated patients is associated with risk,^29,56,58,59 consistent ventilation and oxygenation should be a goal; transport ventilators provide more constant ventilation than manual ventilation. An appropriate transport ventilator provides full ventilatory support, monitors airway pressure with a disconnect alarm, and should have adequate battery and gas supply for the duration of transport.⁴⁷

Adverse events during transport of critically ill patients fall into two categories:^46,48 (1) equipment dysfunction, such as ECG lead disconnection, loss of battery power, loss of IV access, accidental extubation, occlusion of the endotracheal tube, or exhaustion of oxygen supply (at least one team member should be proficient in operating and troubleshooting all equipment); and (2) physiological deteriorations related to the critical illness.

Emergency Department Response to an External Disaster: Receiving Patients

Disasters may produce mass victims on a scale that means routine processes and practices in the ED and hospital will be overwhelmed. The ED response to an external disaster forms part of the overall hospital response, outlined in a hospital disaster plan. These plans are reviewed regularly for currency, and practised for preparedness. The following aspects form part of the ED’s planning and response to receiving patients from an external disaster.^51,52

Presenting Symptoms and Incidence

Patients presenting with respiratory complaints can display a range of symptoms (see Box 22.1), and these may vary based on the patient’s age, the underlying cause of the symptoms and severity.

Shortness of breath (SOB) or dyspnoea is a frequent complaint for patients presenting to the ED. Respiratory presentations are not isolated to any one specific patient population or age group and are encountered in patients across the lifespan. While dyspnoea is commonly associated with respiratory conditions such as asthma, pneumonia, chronic obstructive pulmonary 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 and is commonly associated with the need for hospital admission.^53–55

Assessment, Monitoring and Diagnostics

On arrival, patients with respiratory complaints are assessed quickly using the ABC approach to determine any potential life-threatening disturbance that requires immediate medical assessment and/or resuscitative intervention. Initial assessment includes a thorough history focused on the presenting complaints. A detailed history often identifies the underlying process; however a high index of suspicion should be maintained for other potential causes during initial assessment.^53,54 History focuses on the nature of symptoms, the timing of onset of symptoms, associated features, the possibility of trauma or aspiration and past medical history (particularly the presence of chronic respiratory conditions). During physical examination, the patient assumes a position of comfort while inspection of the chest is undertaken, followed by auscultation, palpation and percussion (see Chapter 13 for more detail).

Patients with significant respiratory symptoms are best managed in an acute monitored bed or resuscitation area of the department. An initial set of observations including heart rate, respiratory rate, blood pressure, temperature and oxygen saturation is supported by continuous monitoring heart rate and oxygen saturation. Pulse oximetry plays an important role in the monitoring of the patient with a respiratory complaint, as recognition of hypoxaemia is significantly improved when it is used.⁵⁶

IV access enables collection of venous blood samples for full blood count (FBC) and urea, electrolytes, creatinine (UEC) where clinically indicated. A chest X-ray (CXR) is ordered in most instances, and interpreted in relation to the clinical history and other examination findings.⁵⁵ Spirometry or peak flow measurements enable assessment of peak expiratory flow rate (PEFR), forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV₁), to determine the nature and severity of the underlying respiratory condition. These tests are however effort- and technique-dependent and may not be able to be performed by a patient who is acutely SOB.⁵⁵ An arterial blood gas (ABG) is often indicated in patients with a significant respiratory presentation, and provides information on oxygenation, ventilation and acid–base status.⁵⁵

Oxygen therapy is commenced early for a patient presenting with signs of acute respiratory compromise, including those with chronic obstructive pulmonary disease (COPD); importantly, patients with acute hypoxia require oxygen. Any potential detrimental effects are uncommon, and concentration and time dependent with a slow onset; this allows for monitoring (pulse oximetry, ABG analysis) and clinical review.^55,57

Candidate Diagnoses and Management

The common diagnoses related to patients who present to ED with shortness of breath are asthma, respiratory failure and pneumonia.

Description of Presenting Symptoms and Incidence

The incidents of acute chest pain presentations appear to be increasing as patients are more aware of the importance of early treatment for myocardial infarction due to public awareness campaigns.⁶⁷ Up to 7% of all ED presentations are for complaints of chest pain.⁶⁸ The pain or discomfort is often described in variety of ways; as pressure, a weight on the chest, tightness, constriction about the throat, or an aching feeling. The pain may also be described in less typical terms such as epigastric pain, indigestion, stabbing pain, pleuritic or sharp.^69,70 Onset is usually gradual, reaching a peak over 2–3 minutes and last for several minutes or longer.^68,69 Pain may be mild to severe, and can be associated with physical exertion or emotional stress and may subside with rest, or be unprovoked and may wake the patient from sleeping. Pain may also radiate to an arm, to both arms, to the neck, jaw or back.^67,69,70 A patient may have a number of associated symptoms including: shortness of breath, nausea, vomiting, weakness, dizziness, anxiety, feeling of impending doom, palpitations and diaphoresis.^69,71 Up to 9% of patients diagnosed with an acute coronary syndrome (ACS) may present with a number of these associated symptoms but without chest pain; these patients tend to be elderly, female or diabetic.^69,70,72

Assessment, Monitoring and Diagnostics

Any patient presenting with a complaint of chest pain requires urgent assessment (within 10 minutes of arrival to the ED). A patient with evidence of a disturbance to airway, breathing or circulation requires close monitoring, immediate medical assessment and resuscitative interventions. Initial assessment includes a 12-lead ECG and evaluation of the pain using the PQRST mnemonic shown in Table 22.3. The ECG should be rapidly evaluated for presence of ST segment elevation or a new left bundle branch block (LBBB) suggestive of an acute myocardial infarction (AMI), as treatment for AMI is time critical. If the initial ECG is nondiagnostic and symptoms persist, continue repeat ECGs at 15 minute intervals.⁶⁸

Continuous cardiac monitoring is commenced to identify any life-threatening arrhythmias, along with supplemental oxygen to improve PaO₂ and increase oxygen availability especially in the presence of myocardial ischaemia. An IV cannula is inserted and routine venous blood samples are collected for cardiac enzymes: troponin T or troponin I. A physical examination may identify non-cardiac causes of the pain or complications associated with cardiac related conditions;^69,73 a number of significant abdominal complaints may present with chest pain as a feature.^68,73 A CXR may also identify any potential causes for the patient’s pain.

Candidate Diagnoses and Management

Common cardiovascular diagnoses presenting to the ED include ACS and thoracic aneurysm.

Assessment, Monitoring and Diagnostics

Patients presenting with abdominal pain are assessed quickly for any disturbance to airway, breathing or circulation requiring close monitoring, immediate medical assessment and/or resuscitative interventions. Abnormal vital signs are suggestive of clinically significant abdominal pain.⁸³ A thorough history includes location and timing of onset, quantity, quality and radiation of pain, associated symptoms, previous history and general state of health. A complaint-specific history and physical examination is performed for a differential diagnosis.^80,81,83 Physical assessment includes visual inspection of the abdomen with the patient in a supine position, followed by auscultation, then gentle palpation and percussion of all four quadrants of the abdomen, working towards the area of reported pain⁸⁵ (see Chapter 19 for more details). While location of the pain is important, it can be misleading, as various pathological processes can localise to different areas of the abdomen (see Figure 22.1).⁸⁶ An ECG is considered to rule out myocardial ischaemia or infarction, as some cardiac patients may present with upper abdominal pain as the predominant symptom (see previous section). Myocardial ischaemia may also be caused by the physiological stress of the intra-abdominal pathology.⁸⁰

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

Administration of a narcotic analgesia in acute abdominal pain does not hinder assessment or obscure abdominal findings, nor cause increased morbidity or mortality, and may allow for a better abdominal examination.⁸⁷ Incremental doses of a narcotic minimise pain but not palpation tenderness. Analgesics enable relaxation of the patient’s abdominal muscles and decrease anxiety, potentially improving information obtained from the physical examination.⁸⁷

Venous blood samples are collected for full blood count (FBC), urea, electrolytes, creatinine (UEC), and amylase and lipase.⁸⁵A dipstick urinalysis can suggest specific disease (e.g. leucocytes and/or blood with urinary tract infection; haematuria with renal colic), within the context of other clinical findings and formal microscopy.⁸⁵ Women of child-bearing age with abdominal pain provide the challenge of a broader range of potential causative pathologies, although history and physical examination are unreliable in determining pregnancy.⁸⁵ If pregnancy or a pregnancy-related disorder is possible, a urine beta-human chorionic gonadotrophin (hCG) test is performed. Test sensitivity is extremely high; a positive finding occurs within a few days of conception, and accuracy is comparable to blood sampling. An ectopic pregnancy may be missed if pregnancy is not considered; an ectopic pregnancy is extremely unlikely if the hCG result is negative.⁸⁵

Candidate Diagnoses and Management

Common abdominal diagnoses for acute abdominal pain are abdominal aortic aneurysm, appendicitis and bowel obstruction.

Assessment, Monitoring and Diagnostics

Symptoms of stroke are a common patient presentation to the ED; presenting signs vary from profound alterations in level of consciousness and limb hemiplegia to mild symptoms affecting speech, cognition or coordination. Symptoms may include confusion, dizziness, ataxia, visual disturbances, dysphasia or receptive and expressive aphasia, dysphagia, weakness, numbness or tingling of the face, arm or leg (usually unilateral).^97,98,100 As many disorders resemble a stroke presentation, emergency clinicians must quickly determine if another condition is responsible for the patient’s neurological deficits (e.g. post-ictal phase following seizures, migraine with neurological deficits, hypoglycaemia or hyperglycaemia, systemic infections, brain tumours, hyponatraemia, hepatic encephalopathy).^93,97

The focus of initial assessment is A, B, C, D (see Chapter 24). Of note, for airway assessment, stroke symptoms include altered muscle function, affecting swallowing and speech functions. A patient with a GCS score of 9 or less may require intubation to protect and secure the airway.^99,101 The patient’s breathing pattern should be assessed and continually monitored. Hypertension is common, with the increase improving any cerebral ischaemia so this should not be lowered unless dangerously high or contraindicated.⁹⁴ Hypotension or dehydration decreases cerebral blood flow and perfusion and should be corrected, although fluid replacement is instituted with caution.¹⁰⁰ Vital signs are documented every 15 minutes during drug therapy to identify changes suggestive of internal bleeding. Maintaining blood pressure less than 185/110 mmHg during fibrinolytic infusion decreases the risk of intracerebral haemorrhage.⁹⁵

A thorough assessment of neurological disability should be undertaken, including a GCS (see Chapter 16). An ECG is recorded to detect any abnormal rhythm such as atrial fibrillation (AF), which may be associated with stroke presentation.⁹⁹ IV access is obtained to administer medications, and collect blood for electrolytes, haematology and coagulation studies. A blood sugar level test will rule out hypoglycaemia or hyperglycaemia as a cause of the presenting symptoms. Abnormal glucose levels adversely affect cerebral metabolism.^99,94 After obvious alternative diagnoses are excluded, a brain CT scan determines whether a stroke is haemorrhagic or ischaemic in origin. While a new-onset ischaemic stroke may not be evident for up to 24 hours, blood in the cranial cavity will be apparent immediately. Patients with any sign of haemorrhage are excluded for fibrinolytic therapy.⁹⁵

Management

Acute ischaemic stroke (‘brain attack’) management includes timely administration of a fibrinolytic agent in appropriately selected patients (see Box 22.2), which facilitates reperfusion, minimises tissue damage and reduces long-term stroke sequelae. Longer times between symptom onset and fibrinolytic infusion are associated with higher rates of morbidity and mortality.^94,98,99,102 Early presentation is therefore essential for appropriate assessments and investigations (including CT scanning) and thrombolytic administration to fall within the narrow treatment window. This has seen the emergence of acute stroke units, with specialised teams dedicated to the rapid assessment and management of presentations (see Chapter 17).

Assessment, Monitoring and Diagnostics

A poisoned patient may present with a wide range of clinical features – from no symptoms through to a life-threatening condition or the potential to deteriorate rapidly; patients should therefore always be assessed immediately. Triage decisions are based on the potential for rapid deterioration and the need for urgent intervention. Resuscitation may be necessary before any further definitive care can be commenced.^107,109,110 Priorities include assessment and maintenance of an airway, adequate ventilation and circulation.¹⁰⁴ Successful resuscitation may require removal of the toxin, counteraction of the poisoning by an antidote if available, and the treatment or support of symptoms.^108–110

Note that many drugs such as paracetamol may have limited initial effects but serious, potentially fatal consequences if not treated in a timely manner.^104,109,110 Once ascertained that a patient does not have an immediate, life-endangering problem, attention is directed towards a more thorough assessment and identification of the toxin involved. Accurate history is often the most significant aid in directing care. If a history is unobtainable or uncertain, there are several general guidelines available for dealing with a patient who has an altered mental state or consciousness level^107,108,110 (see Table 22.6).

Poisoning should always be considered for a patient 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 presentation. Accidental poisonings are the most common cause of medical emergencies in the paediatric patient population. Childhood ingestions tend to be accidental and to involve a single substance. Boys are more likely to be the victims of poisoning than girls. Adult intentional 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 Poisonings in the aged population are often complicated by co-existing medical conditions, which may exaggerate the effects or impair the excretion of the substances involved.

Management: Preventing Toxin Absorption

Initial and ongoing care of a victim follows three principles:¹⁰⁴

Ingested poisons are best removed while still in the upper gastrointestinal tract when possible. Emesis and gastric lavage were utilised in the past to empty the stomach, although a significant body of evidence now suggests that these approaches are relatively ineffective and effectiveness decreases rapidly after 1 hour.^107,108,110 Both the patient and substance should be evaluated for appropriateness of gastric emptying.¹⁰⁸ The patient’s consciousness level, gag reflex and ability to vomit while protecting the airway from aspiration is considered. Any central nervous system depressants are capable of obtunding the protective gag or cough reflex. If the ingested substance has a rapid onset of action (e.g. benzodiazepines), it is safer to avoid emetics because of the risk of a sudden fall in the level of consciousness.

Management: Enhancing Toxin Elimination from the Blood

After a substance has entered the bloodstream, it is normally excreted from the body either in an unchanged form or after liver metabolism and detoxification. Various metabolic byproducts are eliminated in the bile and faeces or urine. Urinary excretion of substances can be enhanced by increasing the filtration process (i.e. forced diuresis: large volumes of IV solutions and/or diuretics), by inhibiting absorption in the renal tubules, or by stimulating the secretion of substances into the urine.^108–110

Management: Preventing Complications and Specific Symptomatic Care

Supportive care is the key element in managing an acutely poisoned patient. Once a patient has either ingested or been exposed to many poisons, there are limited options other than to treat the symptoms as they present or become clinically significant (see Table 22.7).

TABLE 22.7 Summary of the management of poisoning victims

Antidotes act to antagonise, compete with or override the effects of the poison, although few specific antidotes exist for toxins (see Table 22.8). In some cases, an absorbed toxin can be rendered benign by the use of an antidote (e.g. the interaction between naloxone and opiates).¹⁰⁴ For chelating agents (desferrioxamine for iron poisoning), a non-toxic compound is formed and safely eliminated from the body.^107,108,110 The effect of an antidote may be only temporary if it has a shorter half-life than the poison. Most antidotes are given either in a specific dose or as a response to dose rate.¹⁰⁴

TABLE 22.8 Common emergency antidotes

For many poisonings, symptomatic care involves support and protection of vital organ systems; frequent physical assessment of respiratory, cardiovascular and renal function enables identification of any deterioration. Electrolyte and acid–base balance are monitored closely if large volumes of fluids or drugs that alter serum pH are administered.

A poisoning may be the physical manifestation of an emergency or crisis that requires emotional support. An underlying emotional conflict or mental health problem may exist, regardless of whether the poisoning was intentional or accidental. Psychological care is therefore an important component for all patients presenting with poisoning.^107,108,110 Many facilities offer the services of a mental health worker while the patient is still in the ED. If the patient’s condition is stable and the poisoning has not altered their mental state, early psychological intervention is appropriate.

For adult patients, the desire for treatment is not as important as the manner in which treatment is received. Even though patients may initially refuse care, if approached in a non-threatening way and provided some form of control they will usually comply. If threatened with force or restraints, they are placed in a difficult position of either submitting to coercion or resisting therapy for self-protection. A paediatric patient may be too young either to fully understand or to effectively cooperate (see Chapter 26).

Central Nervous System Depressants

A large number of common medications are capable of depressing levels of consciousness, thought processes, or important regulatory centres in the central nervous system (CNS). Clinical findings can vary from class to class or within the same drug family, as physical effects are dependent on the chemical structure of the drug, dose, route of exposure and rate of metabolism. The chemical structure and/or purity of illicit drugs may also be affected by variations or deliberate aberrations in the manufacturing process.^{112,117–119} Drugs in this section include sedatives, hypnotics, tranquillisers and narcotics (see Table 22.9).

Central Nervous System Stimulants

CNS stimulants increase the activity of the reticular activating system, promoting alertness and affecting the medullary control centres for respiratory and cardiovascular function. Individuals using a CNS stimulant have an increased ability to perform muscular activity and a general sense of wellbeing. Many illegal stimulants are poorly manufactured, with no guarantee of purity or consistency in dosage. The possibility of overdose is therefore always present, producing profound CNS excitation.^117,120,121 Commonly used stimulants include amphetamines, dextroamphetamine, methyphenidate, lysergic acid diethyamide (LSD), phencyclidine (PCP), caffeine, cocaine and methamphetamines.^{112,118,119,125}

Amphetamines and Designer Drugs

Amphetamines and designer drugs have been drugs of abuse for a number of years. Originally, many were designed and introduced as anaesthetic agents, decongestants or for other legitimate purposes. Amphetamines are chemically related to the anaesthetic ketamine, with a similar CNS response.^112,118,119 Most drugs in this group were discontinued or controlled because of the delirium and agitation experienced by patients who received them; paradoxically, these effects led to their popularity as recreational drugs.^112,118,119 Amphetamines are synthetic sympathomimetic drugs, available in oral, intranasal or intravenous forms; crystalline rock forms such as ‘ice’ are smoked. Death may occur from overdose, self-mutilation or dangerous activities such as diving into shallow waters or walking on traffic-laden roads.

Salicylate Poisoning

Aspirin is the most common form of salicylate in the home and is found in many over-the-counter medications, such as combination analgesics¹²² and topical ointments. Aspirin may be ingested orally, absorbed through the rectal mucosa, or applied to the skin in topical preparations. Under normal circumstances, the kidneys serve as the principal organ of excretion. Aspirin was previously the most common poisoning in children,^106,109,122 so legislation was implemented to limit the number of tablets per pack and to introduce packaging with childproof caps. In Australia, salicylate poisoning is now uncommon, accounting for only 0.3% of calls to poison information centres.^106,122 The three common types of aspirin overdose are: accidental ingestion (more common in young children); intentional ingestion (more common in adults); and chronic toxicity (occurs in any age group).^115,122

Paracetamol Poisoning

The incidence of paracetamol toxicity is associated with approximately half of all Australasian toxic ingestions, due in part to its common availability as an analgesic/antipyretic agent.^109,124 The drug is absorbed in the stomach and small bowel, with 98% metabolised by the liver using one of two mechanisms: most by a pathway with breakdown into nontoxic byproducts; the second hepatic pathway usually metabolises about 4% of the drug, but the process has a toxic byproduct. The liver detoxifies this toxic byproduct by combining it with glutathione, a naturally-occurring substance. In an overdose or when the minor pathway has already been stimulated (e.g. concomitant barbiturate use), more paracetamol is metabolised by the secondary pathway and the toxic byproduct accumulates, quickly consuming the available glutathione, resulting in liver tissue destruction.^109,124,126

Carbon Monoxide Poisoning

Carbon monoxide (CO) is a gaseous byproduct of incomplete fuel combustion, and is present where there is a flame in a confined space with improper ventilation or air exchange. Levels of CO can accumulate rapidly, and the gas is dangerous as it is colourless, odourless, tasteless and non-irritating.^129–131 Common sources of CO are faulty radiant heaters, kerosene lamps, cooking stoves, engine exhausts and fireplaces. Acute CO poisoning is the most common form of successful poisoning in the USA, UK and Australia.^129–131

Corrosive Acids

A range of substances have a similar ability to cause local tissue injury. Common acids involved in toxic emergencies include acetic acid (vinegar); carbolic acid (phenol disinfectants); chlorine (swimming pools, sanitising agents); hydrochloric acid (pools, cleaning agents); hydrofluoric oxalic (laundry agents); sodium bisulphate (toilet cleaning agents; converts to an acid when added to water) and sulfuric acid (car battery acid).

Ingested corrosives produce immediate or late life-threatening complications. In general, acids dissolve tissue and destroy haemoglobin.¹³⁵ Swallowing a strong acid can produce ulceration and perforation of oral and oesophageal mucosa, presenting a risk for haemorrhage and mediastinitis, and cardiac arrest as a result.^135–137 The late sequelae of swallowing a corrosive substance involves mucosal scarring with constriction and mechanical obstruction of the oesophagus.

Assessment

The immediate response to ingestion is increased secretions, pain, vomiting or haemoptysis. Signs of perforation include fever, respiratory difficulty or peritonitis. Alkalis and skin contact produce a soap-like substance because of the interaction with tissue fats, giving a slimy, soapy feeling.^135,137

Management

Induced vomiting or gastric lavage should not be attempted, as the alkalis will be neutralised by stomach acid, and lavage tubes may cause further tissue damage.^135,137 External contact with alkalis requires copious irrigation at the point of contact; continue irrigation for at least 15 minutes; for the eye, irrigation can be for up to 30 minutes. Cover all wounds after irrigation with sterile dressings to reduce the risk of infection.

A patient is deemed ‘nil by mouth’ until inspection of the mouth and throat to determine the amount and extent of burns.¹³⁵ An oesophagoscopy identifies the degree of injury and enables direct irrigation of any affected areas of mucosa.¹³⁵ Alkalis that contain phosphates may produce a systemic hypocalcaemia, and IV calcium gluconate may be required. Continue to monitor for systemic effects of perforation or tissue injury.¹³⁵

Assessment

Aspiration causes a pneumonitis with low-grade fever, tachypnoea, coughing, choking, gagging and pulmonary oedema as a late effect.^114,136 Immediately assess the patient’s respiratory tract for possible aspiration; coughing, cyanosis or hypoxia may indicate aspiration or chemical pneumonitis.¹³⁷ As petroleum distillates are fat solvents and rapidly cross the lipid cell membrane, nerve tissue is especially sensitive to injury. A patient may exhibit local effects, such as depressed nerve conduction; or varied central effects, such as feelings of wellbeing, headache, tinnitus, dizziness, visual disturbances, through to respiratory depression, altered levels of consciousness, convulsions and coma.¹³⁶

Management

In the awake and alert patient, the decision to treat is based on the physical properties of the substance, the likelihood of aspiration or other complications, and the amount consumed.^136,137 When preventing absorption, carefully consider gastric emptying, as neither induced vomiting nor gastric lavage are recommended. If the patient is lethargic or unconscious, an endotracheal tube is placed for adequate airway protection,^{114,135–137} although this heightens the risk of aspiration as hydrocarbons adhere to the tube and increase the risk of chemical pneumonitis.^{114,135–137}

Assessment, Monitoring and Diagnostics

Clinical findings of organophosphates are divided into three broad categories:

Laboratory diagnosis is based on measurement of cholinesterase activity using either erythrocyte or plasma levels; erythrocyte cholinesterase is more accurate, but plasma cholinesterase is easier to test and is more widely available. Erythrocyte AChE is found in CNS grey matter, red blood cells, peripheral nerve and muscle. Plasma cholinesterase circulates in plasma and is found in CNS white matter, pancreas and heart.^139–140 Levels of poisoning are categorized as mild (cholinesterase activity is reduced to 20–50% of normal; moderate (activity is 10–20% of normal); or severe (less than 10% of cholinesterase enzyme activity). Levels do not, however, always correlate with clinical illness.¹³⁹

Management

Initial priorities are ABC, in concert with D (danger), as organophosphates also present considerable risk to staff caring for the patient, especially during the initial phases of management. All patients’ clothing should be removed and considered hazardous waste. Patient decontamination with soap and water is a priority, as soap with a high pH breaks down organophosphates.^140,142 Staff should use personal protective equipment (PPE), such as neoprene or nitrile gloves, and gowns, when decontaminating patients. Charcoal cartridge masks for respiratory protection are used, although recent evidence suggests that the nosocomial risk may not be as significant as once thought.¹⁴²

Intubation is commonly required after significant exposure due to respiratory distress from laryngospasm, bronchospasm or severe bronchorrhoea. Continuous cardiac monitoring and an ECG are used to identify bradycardias. Activated charcoal is used for gastric decontamination for patients who ingested organophosphate. The mainstay of treatment is atropine and pralidoxime, with a benzodiazepine used for seizure control.^138,139,142Atropine blocks acetylcholine receptors and halts cholinergic stimulation. Large doses of atropine are usually required (1–2 g IV), and repeated if muscle weakness is not relieved or the signs of poisoning recur. Clearing of bronchial secretions is the endpoint of atropine administration, not pupil size or absolute dose.^138,139,142 Pralidoxime hydrochloride reactivates acetylcholinesterase and is effective in restoring skeletal muscle function, but is less effective at reversing muscarinic signs. Over time, the bond between organophosphate and cholinesterase becomes permanent and the effectiveness of pralidoxime diminishes.¹⁴² The current recommendation is for administration within 48 hours of poisoning.¹⁴² Benzodiazepines are clinically indicated as the drug binds to specific receptor sites, potentiating the effects of gamma-aminobutyrate (GABA) and facilitating inhibitory transmitters for management of seizures.^138,139,142

Chemical Agents

Chemical agents are super-toxic chemicals used to poison mass victims. The chemicals are similar to hazardous industrial chemicals, but hundreds of times more toxic. For example, while the Sarin attack on the Tokyo subway in 1995 killed 12 people, there were also 1039 injuries, and at least 4000 people with psychogenic symptoms.¹⁴⁷ Sarin is approximately 60 times more toxic than methylisocyanate. To demonstrate this perspective: a leak of methylisocyanate from a factory in Bhopal, India in 1984 caused 200,000 people to be affected, 10,000 severely affected and 3300 deaths. Relatively small quantities of a military grade chemical agent could therefore have the same capability to produce large numbers of casualties (symptomatic and psychological).^147,148

Biological Agents

Biological agents are living organisms or toxins with the capacity to cause disease in people, animals or crops. The toxins generally behave like chemical agents and serve the same function: to poison people.^147,148 Biological agents are relatively inexpensive to produce and have the potential to be devastating in their effects. Organisms such as anthrax, plague and smallpox have been the agents of greatest concern from terrorists’ potential use.¹⁴⁶ Biological agents have the longest history of use, having been available for centuries.¹⁴⁸

Radiological Materials

Radiological materials pose both acute and long-term hazards to humans. Action is similar to some chemical agents: cellular damage. A major difference is that the radiological agents do not have to be inhaled or in skin contact to exert damage.¹⁴⁵ Deployment of a nuclear weapon would be catastrophic; note evidence of events like Hiroshima and Chernobyl. While very different, both events produced immediate injury and the long-term effects of ionising radiation on large populations.¹⁴⁶ Any radiological effects on human health from the 2011 tsunami in Japan and the subsequent damage to the Fukushima nuclear reactors remains unclear at the time of writing. The event of most risk is likely to be a ‘dirty bomb’ that combines conventional explosives with any available radioactive source.¹⁴⁶

A CBR terrorism incident may or may not result in mass casualties and fatalities as intended. However, large numbers of psychological casualties are very likely and therefore, regardless of the effectiveness of the attack, and the number of people actually exposed to the agent, there will most likely be a mass casualty situation.¹⁴⁶ The psychological implications of chemical and biological weapons may be worse than the physical ones. Chemical and biological weapons are weapons of terror; part of their purpose is to wreak destruction via psychological means by inducing fear, confusion, and uncertainty in everyday life.¹⁵⁰ The long term social and psychological effects of an episode of chemical or biological attack, real or suspected, would therefore be as damaging as the acute effects, if not more so.

Redback/Katipo Spider Bite

Funnel-web Spider Bite

Snake Bites

Description and incidence

Most stings occur during the summer months (December, January) in the tropical waters of northern Australia, from Gladstone in Queensland around to Broome in Western Australia, on hot, calm and overcast days when the jellyfish moves from the open sea to chase prey in shallow water.^151,170,171 The exact incidence of stings is difficult to determine, but they are common in children. One ED reported 23 confirmed C. fleckeri stings in a 12-month period.¹⁷² There have been at least 63 confirmed deaths from envenomation by Chironex fleckeri in the Indo-Pacific region.

Clinical manifestations

Most stings are minor, with clinically significant stings occurring from larger jellyfish. Stings generally occur on the lower half of the body, and are characterised by immediate and severe pain. Pain increases in severity and may cause victims, especially children, to become incoherent. While mechanisms of toxicity remain poorly understood, death is thought to occur from central respiratory failure, or cardiotoxicity leading to A–V conduction disturbances or paralysis of cardiac muscle. Victims may become unconscious before they can leave the water following envenomation, and death can occur within 5 minutes.^170,171

The area of tentacle contact is seen as multiple linear lesions, purple or brown in colour. A pattern of transverse bars is usually seen along the lesions, along with an intense acute inflammatory response, initially as a prompt and massive appearance of wheals followed by oedema, erythema and vesicle formation, which can lead to partial- or full-thickness skin death.^151,173

Assessment

Patients presenting to ED after potential box jellyfish sting are easily diagnosed based on the history, the presence of pain and their skin lesions as outlined above. Generally some form of prehospital management or first aid will have been instituted. On arrival, patients with signs of clinically significant stings, alteration in consciousness, cardiovascular or respiratory function, or those with severe pain are seen immediately.

Management

Treatment focuses on appropriate first aid, administration of adequate pain relief, symptomatic management of cardiovascular and respiratory effects, and the administration of box jellyfish antivenom when indicated. First aid measures include liberal application of vinegar to the sting area for 30–60 seconds. Vinegar inactivates the undischarged nematocysts, so removal of any remaining tentacles should occur simultaneously to prevent further envenomation.^151,173 Mild stings respond to the application of ice packs and simple oral analgesia, after the application of vinegar.^151,172 Patients with moderate to severe pain require IV narcotic analgesia. For patients with continuing severe pain, antivenom is administered along with continued parenteral analgesia.¹⁷¹

Patients are observed for the development of cardiorespiratory symptoms, including arrhythmias. Management focuses on specific clinical effects, ranging from oxygen administration and IV fluid resuscitation through to intubation/mechanical ventilation or CPR.^151,173 Antivenom is indicated in patients with cardiorespiratory instability, cardiac arrest or severe pain unrelieved by narcotic analgesia.¹⁷¹ Antivenom is carried by prehospital personnel, and administration may occur prior to ED presentation. A 20,000 unit ampoule of box jellyfish antivenom is diluted in 10 mL isotonic saline and administered IV over 5–10 minutes.¹⁷² The number of ampoules used varies with clinical status: at least one for cardiorespiratory instability; up to three for life-threatening situations with an inadequate response; and at least six for a cardiac arrest.^151,173

While the application of a pressure immobilisation bandage to affected limbs after vinegar application was previously recommended as a first aid intervention, there is little current evidence supporting this in box jellyfish stings, and its application may promote additional venom release and therefore be potentially dangerous.^171,174 Some animal research has suggested a role for magnesium sulfate in management for patients not responding to antivenom.¹⁷⁵

Description and incidence

Irukandji syndrome is a poorly-understood marine envenomation encountered in far northern and northwestern areas of Australia.¹⁷⁸ Death is uncommon (two recorded deaths in Australia), attributed to cerebral haemorrhage and is associated with other comorbid conditions.¹⁷⁹

Assessment

People stung by an Irukandji may have no symptoms initially, but may develop symptoms up to one hour after being stung. Irukandji syndrome produces clinical features of severe lower back pain, muscle cramps, raised blood pressure, pulse and respiratory compromise, vomiting and anxiety.¹⁷⁷ A patient with suspected Irukandji envenomation is placed in an acute area with full monitoring available.

Management

The mainstays of patient management are pain control and symptom management. Application of vinegar as part of first aid is important, but due to delay in the presentation of symptoms following a sting this may be of limited value.¹⁷⁸ Pain is severe, and opioid analgesia may be required; if requirements for opioids are very high, fentanyl is considered.¹⁷⁷ There is anecdotal evidence that magnesium sulfate may have a role in the management of Irukandji syndrome not responsive to the above treatments, but this remains unproven.¹⁷⁸

Clinical manifestations and diagnosis

Ciguatera poisoning typically presents as an acute gastrointestinal illness, followed by a neurological illness with classical symptoms of heat and cold reversal of sensation that may last for a few days after consumption of contaminated fish¹⁷⁴ (see Table 22.12).

A patient may become sensitive to repeated exposure to ciguatoxins;^174,181 additional exposure to poisoning from ciguatera may be more severe than the first episode. Importantly, patients exposed to ciguatera suffer recurrences following the consumption of seemingly innocuous foods (e.g. nuts, nut oils, caffeine, alcohol, or animal protein foods),^147,181,183 with relapses months or years after the initial poisoning.¹⁸³

Diagnosis is made on a patient’s history and clinical features: consumption of fish followed by an acute gastrointestinal and neurological illness. There is no conclusive diagnostic test for the presence of ciguatoxins.^174,181

Management

Treatment of ciguatera poisoning is supportive care and symptom management. Mannitol has been recommended, although this is only effective if used in the first 48–72 hours of the illness.^181,184