more_vertThe findings of the study by Sarah McNab and colleagues (March 28, p 1190)1 showed a substantial effect of isotonic fluid maintenance in children admitted to hospital. In the study, the number of patients who received emergency surgery between the two study groups, isotonic hydration with 140 mmol/L of sodium and hypotonic hydration with 77 mm/L of sodium, was significantly different (67 [20%] of 338 patients in the isotonic group vs 92 [27%] of 338 patients in the hypotonic group, p=0·02). I believe that this difference might have caused the difference in the number of patients with hyponatraemia because of the following reasons: the release of antidiuretic hormone is stimulated by surgical stress (eg, pain, narcotic use, and blood loss), which is experienced by many children undergoing surgery;2 previous studies3,4 suggest that the presence of hypotonic intravenous fluid during the perioperative period is associated with an increased risk of hyponatraemia; and the results of McNab’s study suggest that the risk of hyponatraemia might be greatest in the first 6 h of the study period in both treatment groups.
Preference: Emergency Medicine
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[World Report] Tackling the UK’s alcohol problems
A new UK unit, which takes alcohol-dependent patients straight out of the emergency setting to a specialist detox centre, is a promising approach, say experts. Nayanah Siva reports.
Penetrating neck injury in an isolated medical setting
Clinical record
A 34-year-old man presented to a small rural emergency department at 21:45, arriving by private car from a bush campsite some 45 minutes’ drive away. An empty “stubbie” beer bottle had been recapped and thrown on the fire. It subsequently exploded, showering glass fragments onto surrounding people, one of whom sustained a small penetrating neck injury (PNI) with a piece of glass lodging in his anterior neck.
On arrival at the hospital, the patient had removed the glass and was clutching his neck with paper towels, describing a feeling of blood in the back of his throat, with associated haemoptysis.
He had a Glasgow Coma Scale score of 15, with normal vital signs, and was found to have a 1 cm wound just above his cricoid cartilage slightly to the right of midline. There was minimal active bleeding externally, but air occasionally bubbled from the wound and surgical emphysema was palpable on the right side of his neck. He was most comfortable slightly head down on his right side, and was maintaining O2 saturation of 99% in room air, with no clinical evidence of pneumothorax.
In consultation with Adult Retrieval Victoria, the attending anaesthetic-trained rural general practitioner decided to proceed to rapid sequence intubation (RSI) with an oral endotracheal tube (ETT) before evacuation to a tertiary centre.
With assistance from the nursing staff and a second anaesthetic-trained rural GP, the patient was pre-oxygenated with deep spontaneous breaths and a successful RSI under direct laryngoscopy was performed. For easier insertion, a size 7.5 cuffed ETT was placed. Blood was present on the vocal cords, but the oropharynx was clear.
Mechanical ventilation was carried out initially with a portable unit (Weinmann Medumat Standard-a), on minute volume cycle with a minimum available pressure of 20 cm H2O. Subsequent chest x-ray showed extensive surgical emphysema (Figure) and air mediastinum, at which point he was moved to the operating theatre to allow lower pressure ventilation using an anaesthetic ventilator. The ETT was shifted further down the trachea to tamponade the site of traumatic injury, and reduce bleeding and tissue emphysema.
Assisted ventilation at the hospital continued until 01:38, when the retrieval team arrived by road ambulance some 4 hours later.
He was transferred by road ambulance to the tertiary hospital, arriving at 04:22, where investigation with computed tomography (CT) angiography excluded any vascular injury. A surgical tracheostomy and tracheal repair was undertaken at 12:40 later that day. He spent over 24 hours in the intensive care unit on mechanical ventilation before making a full recovery.
Penetrating neck injury is commonly related to violence in countries such as the United States and South Africa,1 but it is rarer in Australia. This case report highlights the challenges and importance of initial management of a PNI in an isolated medical service, and the importance of health education around campfire safety.
The initial management of a PNI in a patient with a patent airway and who is haemodynamically stable with no signs of vascular injury is generally now considered to involve CT vascular imaging and selective surgical management.2,3 In an isolated medical facility without access to these services, management options are more limited. Initial treatment involves management of actual and potential airway complications together with stabilisation of vascular injury and resultant haemorrhage, with a plan for early evacuation to an appropriate tertiary facility for definitive care.
Our patient was haemodynamically stable and clinically had no obvious evidence of a significant vascular injury. The penetrating glass fragment was described as small, although not seen by the medical staff as the patient had removed it before arrival. The ongoing haemoptysis and palpable surgical emphysema suggested airway injury, and potential risks associated with haematoma formation and airway obstruction during transport led to the decision to perform rapid sequence endotracheal intubation. This is thought to be the safest initial airway management when anatomical structures are preserved,2,4 although definitive surgical airway management would be required at the tertiary centre.
Incorrect ETT placement, inadequate seal, or excessive ventilator pressure, may lead to acute deterioration where tracheal injury exists. This is particularly important in a remote medical setting, where considerable delay can occur before transport to an appropriate tertiary care facility, which could have become a critical issue in our case had the patient not been haemodynamically stable.
Despite standard transport immobilisation protocols, the literature recommends that cervical spine immobilisation is not required unless focal neurological deficits are present.2 Penetrating neck injuries (particularly stabbing) rarely cause spinal cord injury,5 and cervical collars can impede airway visualisation or evidence of other injuries. Our patient had no clinical evidence of spinal cord injury and no mechanism of injury to suggest one, so a cervical collar was not applied, making it easier to intubate as well as to monitor and assess the injury site.
Many outdoor recreation activities involving campfires occur in isolated environments, with limited access to medical and emergency services. In such situations, burns are an increasing concern,6 either from falls or exploding containers.7 This case demonstrates the additional risk of projectiles from exploding containers irresponsibly placed into fires. Although common sense dictates that it is risky to throw sealed containers into open fires, anecdotally it is often done when alcohol consumption is combined with open fires in a relaxed bush environment.
This case suggests that appropriate initial management of PNIs in an isolated rural setting can include careful endotracheal intubation until later surgical management with a definitive surgical airway. In addition, it reinforces the public health message that responsible behaviour reduces risk — particularly when setting an example and providing health education messages to the next generation. This case was unusual, but the clinical and public health lessons it provides are perhaps generalisable.
Lessons from practice
- Management of penetrating neck injury in an isolated setting involves stabilisation and endotracheal intubation.
- Cervical spine immobilisation is not required with penetrating neck injury unless focal neurological deficits are present.
- Rapid sequence intubation is a useful skill for general practitioners to have when working in a rural setting.
Alcohol-based hand sanitiser: a potentially fatal toy
We present a case of acute ethanol toxicity in a preschool child who developed depressed mental status and hypotension and required inotrope support as a result of ingesting an alcohol-based hand sanitiser
Clinical record
In September 2014, a 3-year-old girl was brought by her parents to the emergency department (ED) with an acutely altered level of consciousness. The history from the parents stated that the young girl had been playing with an alcohol-based hand sanitiser (ABHS; 70% ethanol, 375 mL [Figure]) with her 1-year-old sibling while the parent was in the room. Ingestion of the ABHS had not been witnessed.
On assessment she had a patent airway, a respiratory rate of 18 breaths/min, an oxygen saturation level of 96% on room air, heart rate of 97 beats per minute, blood pressure of 95/54 mmHg and a temperature of 35.5°C. Her Glasgow coma scale (GCS) score was 10/15 (motor response, 5; verbal response, 3; eye response, 2). Her eyes showed alternating disconjugate gaze, with pupils equally constricted at 2 mm. Her pupils dilated in response to noxious stimuli (eg, trapezius squeeze test). The patient’s medical history included normal development, no infectious contacts, and she was fully vaccinated and had no surgical history. No odour of ethanol was appreciated on her breath or her clothing. Her 1-year-old sibling was behaving normally.
A blood glucose test at the bedside gave a concentration of 4.6 mmol/L (reference interval [RI], 4.4–6.1 mmol/L), and a venous gas analysis showed a pH of 7.34 (RI, 7.33–7.44), a normal Pco2 of 44 mmHg, a bicarbonate level of 23 mmol/L (RI, 24–28 mmol/L)and a base deficit of − 3 mmol/L (RI, − 2 to 2) with an increased anion gap of 17 mEq/L (RI, 4–12 mEq/L).
Her measured serum osmolality was abnormal at 357 mmol/L (RI, 265–295 mmol/L). She had a normal haemoglobin concentration, platelet count and white cell count with no evidence of left shift. Results of an electrolyte assay included an abnormal serum sodium concentration of 151 mmol/L (RI, 135–145 mmol/L) and a chloride concentration of 111 mmol/L (RI, 98–106 mmol/L), with normal concentrations of potassium, urea, creatinine and C-reactive peptide (7 mg/L; RI, < 8 mg/L). Liver enzymes were not analysed. An electrocardiogram was normal. A computed tomography scan of her brain without contrast showed no acute intracranial injury. Within an hour of ED admission, the patient developed hypotension (70/22 mmHg) which was treated with two fluid boluses of normal saline (20 mL/kg each) and peripheral adrenaline infusion (0.05 µg/kg/h).
Treating physicians deemed that she was not clinically septic, dehydrated or severely injured based on her history and serial examinations paired with investigations. However, they had a high suspicion of intoxication. Subsequently, her serum ethanol concentration just before adrenaline administration was reported as 260 mg/dL (legal blood ethanol level for drivers in the state of Victoria, < 50mg/dL).
She was admitted to the paediatric intensive care unit (PICU) without intubation. No additional blood ethanol concentration tests were performed. A peripheral blood culture was negative, and serial blood gas measurements showed a normal venous lactate level and gradual normalisation of pH and sodium and chloride concentrations over the following 15 hours. The patient’s condition improved (at 5 hours after her PICU admission, her GCS score was 15/15, she was normotensive without inotrope support and was mobilising) and she was discharged within 24 hours.
Hand hygiene with alcohol-based hand sanitiser (ABHS) is encouraged in health, education and day-care facilities, workplaces and the home.1,2 The active ingredient of ABHS is ethanol or isopropanol at a concentration of 60% to 95%. The increasing intentional ingestion of these products by teenagers, and consequences, have been well reported.3 The Victorian Poisons Information Centre received a total of 15 729 calls in 2013 relating to children aged under 5 years, and reported that topical antiseptics/hand sanitisers was the fifth most frequent source of poison to which this age group was exposed.4
Our unique case shows the toxic effects of ABHS. The patient had altered Glasgow coma scale scores, associated hypotension, hypernatraemia, hyperchloraemia and one of the highest serum ethanol concentrations yet reported in this age group. A surprising feature was the ingestion of an ABHS that comprised 70% ethanol despite parental supervision of play. The hyperchloraemia and hypernatraemia might be explained by the suppression of antidiuretic hormone by ethanol, resulting in water diuresis, with loss of more water than sodium or chloride and the lack of further fluid intake.5 Strict fluid output was not recorded to confirm this.
A published review of Ovid MEDLINE, EMBASE and CINAHL databases shows that ingestion of household products containing ethanol by children is an increasingly common occurrence, and that there is a paucity of studies from outside North America.6 This review includes two retrospective studies from North American poison centres that report a lack of significant effects from unintended paediatric ingestion of ABHS.6 A previously published case reports mild hypothermia, hypokalaemia and the necessity for mechanical ventilation for airway protection during transport to another facility after ABHS ingestion.7
We used a modified Widmark formula to estimate the minimum weight of ethanol needed to be ingested as follows:
Weight of alcohol ingested in grams = (blood ethanol concentration in mg/dL × total body water in litres)/the percentage of water in blood (which is 80.65%).
The patient’s height was 95 cm (50th centile) and her weight was 16 kg, giving an estimated total body water volume of 9.4 L. To achieve a blood ethanol concentration of 260 mg/dL, she would have needed to ingest 30.3 g of ethanol ([260 mg/dL × 9.4 L]/80.65 = 30.3 g).8,9 This equates to a consumption of a minimum 55 mL of an ABHS comprising 70% alcohol (55.3 g ethanol per 100 mL).8
Currently, the only highlighted label on the ABHS indicates that the liquid is flammable (Figure). This may be insufficient to convey the toxic potential of ABHSs to parents, carers and children.
Lessons from practice
- Contrary to perceptions, preschool children are able to ingest enough alcohol-based hand sanitiser to develop severe ethanol toxicity.
- There should be an increased awareness of the hazards associated with alcohol sanitiser ingestion.
Non-admitted patient care 2013–14: Australian hospital statistics
In 2013–14, about 46 million occasions of service were provided for non-admitted patients by 558 public hospitals, including:-6 million occasions of service for emergency care -18 million for outpatient care -22 million for other non-admitted patient care. For the first time, information is also included about the patient’s age and sex, their Indigenous status, how the service was delivered and how it was funded.
Australia’s hospitals 2013–14: at a glance
Australia’s hospitals 2013–14 at a glance provides information on Australia’s public and private hospitals. In 2013–14, there were 9.7 million hospitalisations, including 2.5 million involving surgery. Public hospitals provided care for 7.2 presentations to emergency departments, with 74% of patients seen within recommended times for their triage category and about 73% were completed within 4 hours. This publication is a companion to the 2013–14 Australian hospital statistics suite of publications.
[Case Report] Eosinophilic myocarditis: a paraneoplastic event
In September, 2014, a 55-year-old woman presented to our emergency department with a 2 month history of worsening dyspnoea. She was a smoker with a 19 pack-year history but no other risk factors for pulmonary or cardiovascular disease. On examination her blood pressure was 90/60 mm Hg, heart rate 130 beats per min, and oxygen saturation 92% on room air. She had jugular venous distension and reduced breath sounds bilaterally but no pitting oedema of the legs. Laboratory tests showed an increased leucocyte count (18·9 × 109/L) with neutrophilia (79%) and normal eosinophils, raised C-reactive protein (36 mg/L), and raised troponin T (354 ng/L).
MERS: worst may be past
The World Health Organisation has indicated that the Middle East Respiratory Syndrome (MERS) outbreak that has so far claimed 24 lives in South Korea may have passed its peak.
While warning that it was critical health authorities closely monitor the situation, the WHO’s Emergency Committee has nonetheless declared that South Korean efforts to track and quarantine infected people had “coincided with a decline in the incidence of cases”.
Since the first case was reported in South Korea last month, 166 people in the North Asian country are confirmed to have been infected with MERS, including 30 currently receiving treatment, while a further 5930 are in quarantine at home or in medical facilities.
Fears that the disease might spread further in the region were fuelled earlier this week when Thai officials reported a visiting businessman from Oman had fallen ill with the disease, and 59 people who had been in contact with have been placed in quarantine.
But the WHO praised South Korean health authorities for rapidly alerting their Chinese counterparts about an infected traveller, who was quickly located and isolated.
The World Health Organisation’s Emergency Committee, which met earlier this week to discuss the outbreak, said it was not yet serious enough to warrant the declaration of a public health emergency, and advised that travel restrictions and airport screening were not necessary.
Nonetheless, the Committee warned the outbreak was “a wake-up call” for governments about the speed with which serious infectious diseases could spread “in a highly mobile world”.
“All countries should always be prepared for the unanticipated possibility of outbreaks of this and other serious infectious diseases,” it said. “The situation highlights the need to strengthen collaboration between health and other key sectors, such as aviation, and to enhance communication processes.”
No cases have been reported in Australia, and a Federal Health Department spokeswoman said the risk of MERS arriving in Australia was considered to be low, at least for the time being.
But health and border protection authorities are on alert for the disease, and the Federal Government is planning to warn Australians travelling overseas, particularly to the Middle East as part of the Hajj pilgrimage, about MERS and what precautions they need to take to minimise the chances of infection.
Though Korean authorities have been praised for the strength of recent actions to control the spread of MERS, serious shortcomings in their initial response have been blamed for helping the outbreak gain momentum.
The WHO Emergency Committee detailed a number of factors that helped the disease spread, including ignorance of MERS among health workers and the broader public; “suboptimal” infection prevention and control measures in hospitals; keeping patients infected with MERS in crowded emergency departments and wards for extended periods; the behaviour of patients in going to several different doctors and hospitals for treatment; and the custom of family and friends staying with their infected loved ones in hospital.
“There are still many gaps in knowledge regarding the transmission of this virus between people, including the potential role of environmental contamination, poor ventilation and other factors,” the Committee said, though adding that there was no evidence of sustained transmission in the community.
Adrian Rollins
Consensus guidelines for the investigation and management of encephalitis
A summary of a position paper for Australian and New Zealand practitioners
Encephalitis is caused by inflammation of the brain and is a challenging condition for clinicians to identify and manage. It manifests as a complex neurological syndrome with protean clinical manifestations that may be caused by a large number of aetiologies, many without effective treatments. It can be fatal and survivors often experience significant neurological morbidity. Studies have shown variable quality in case management in multiple settings,1–3 emphasising the need for consensus guidelines.
The need for guidelines is also important because encephalitis is a marker of emerging and re-emerging infectious diseases, and is therefore a syndrome of public health importance. There are unique infectious aetiologies in Australia — including Hendra virus, Australian bat lyssavirus, Murray Valley encephalitis virus and West Nile virus (Kunjin virus) infections — that require early identification, reporting and specialist clinical and public health responses. Regionally, causes of encephalitis with potential for introduction into and epidemic activity in Australia include Japanese encephalitis virus, enterovirus 71, dengue virus and Nipah virus. There is also a rapidly growing list of immune-mediated encephalitides that are important because of their potential response to immunomodulatory treatments and their association with underlying tumours.
“encephalitis is a marker of emerging
and re-emerging infectious diseases”
Although comprehensive guidelines have been published elsewhere, including recent international consensus guidelines,4 these are detailed and lack a specific geographic focus. As a result, we have developed a concise guideline for clinicians in Australia and New Zealand5 (doi: 10.1111/imj.12749) that provides a substantial update to previous guidance published in the Journal.6
The guideline was developed by the Australasian Society for Infectious Diseases Clinical Research Network (ASID CRN) Encephalitis Special Interest Group with subsequent, multiple rounds of consultation involving the ASID Guidelines Committee, the Public Health Association of Australia, the Australian and New Zealand Association of Neurologists and the Australasian College for Emergency Medicine.
Main recommendations
The guideline principally consists of two algorithms. The first algorithm addresses the patient with possible meningoencephalitis — a scenario that is frequently encountered in emergency departments. This algorithm is designed to assist clinicians to: consider encephalitis within a wide differential diagnosis, perform appropriate specimen sampling and investigations, and initiate antimicrobial therapy promptly (including acyclovir for possible herpes simplex virus [HSV] encephalitis). In most patients with possible meningoencephalitis, an alternative diagnosis will be made. The algorithm aims to discriminate between patients in whom encephalitis can be excluded and those who require a more detailed assessment. The second algorithm addresses the patient in whom encephalitis is considered likely. This algorithm provides a robust clinical case definition of encephalitis, identifies key first-line (universal) diagnostic tests (Box), outlines a process of excluding HSV disease, and formulates an approach of directed (second- and third-line) diagnostic testing based on risk factors, clinical features and radiological features.
In addressing these scenarios, the guideline answers the following questions:
- What features are important to consider during history-taking and examination?
- In which patients should magnetic resonance imaging be performed?
- What are the common abnormalities evident in cerebrospinal fluid?
Furthermore, it provides advice on the tests that should be done to diagnose the most common causes of encephalitis and defines specific patient subpopulations to highlight differences in aetiology (to help prioritise testing). These subpopulations include: children and neonates, immunocompromised patients, overseas travellers and immigrants, and patients residing in tropical Australia.
The guideline considers the particularly vexing question of the contemporary role of brain biopsy by presenting evidence of its yield in cohorts of patients who have encephalitis. It also introduces the various immune-mediated encephalitides, describes their clinical features and, in doing so, assists the clinician in deciding when to perform specific antibody studies. From a treatment perspective, the guideline defines optimal therapy for HSV encephalitis and outlines possible treatment strategies for other infectious and immune-mediated causes based on lower-quality evidence. In particular, it suggests when to consider empiric antimicrobial therapy and immunomodulatory therapies.
Encephalitis presents a complex challenge to clinicians. Its possibility must be suspected in a variety of presentations, and it requires the performance of a detailed clinical assessment, consultation, and judicious investigation. Unnecessary delays must be avoided, and it is essential to institute empiric therapies appropriately and provide high-quality supportive management. Optimal application of current knowledge is likely to improve diagnosis; however, even with an extensive diagnostic work-up, definitive aetiology may not be identified for 30%–40% of patients with encephalitis.7 Novel agents and a changing geographical distribution of known diseases are likely to be identified with improved surveillance; these possibilities should be considered where unexplained encephalitis clusters occur.
Box anchor (office use only)
Recommended first-line investigation of encephalitis in Australia and New Zealand*5
* Table reproduced with permission from: Britton PN, Eastwood K, Paterson B, et al; Australasian Society of Infectious Diseases; Australasian College of Emergency Medicine; Australian and New Zealand Association of Neurologists; Public Health Association of Australia. Consensus guidelines for the investigation and management of encephalitis in adults and children in Australia and New Zealand (Internal Medicine Journal, Wiley Publishing Asia Pty Ltd, © Royal Australasian College of Physicians 2015).
[Correspondence] Training children in cardiopulmonary resuscitation worldwide
In Europe and the USA, 700 000 people die after out-of-hospital cardiac arrest and unsuccessful cardiopulmonary resuscitation (CPR) every year,1 about 2000 deaths per day. These estimates apply to many other parts of the world. This cause of death is probably the third most common cause of death in developed countries, after all cancers combined and other cardiovascular causes.1 When professional emergency medical services arrive after cardiac arrest—which can be after 8–12 min or more—the brain has already started to die.