Guidelines and statements

Paediatric empyema thoracis occurs in 0.7% of pneumonias in Australia and general paediatricians may only see a few cases in their career. A recent survey demonstrated a lack of consensus in management across Australia, highlighting the need for a local guideline. Empyema is an accumulation of infected fluid in the pleural space caused by a disruption in the equilibrium of pleural fluid secretion and absorption by the pleural lymphatic drainage system. Children with empyema typically present with symptoms and signs of pneumonia. A persistent fever despite 48 hours of appropriate antibiotic treatment may indicate development of empyema. Children with empyema should be managed in a hospital with paediatric expertise — preferably by or in consultation with respiratory paediatricians, and in conjunction with paediatric surgeons (recommendation [R], strong; evidence [E], low quality). If feasible, children should be transferred to a tertiary paediatric centre; treatment of paediatric empyema is very different to that of adult disease. A chest x-ray should be carried out for children in whom empyema is suspected (R, strong; E, high quality); a routine lateral film is not needed. A lateral decubitus or erect film may be used to differentiate a simple parapneumonic effusion from an empyema if ultrasound is not available (R, strong; E, none). Daily x-rays are not necessary to monitor progress as changes on chest x-ray lag behind clinical status (R, strong; E, none). Ultrasound is the central investigation in the management of paediatric empyema; it should be used for all children with empyema as it is the best technique for differentiating pleural fluid and consolidation, estimating effusion size and grading complexity, demonstrating the presence of fibrinous septations and guiding chest drain placement (R, strong; E, high quality). A preoperative chest computed tomography (CT) scan should not be routinely performed (R, strong; E, moderate quality) but should be reserved for complicated cases in which the condition has not responded to treatment or there is concern that another pathological condition, such as a tumour, is involved. Blood tests such as blood culture (R, strong; E, high quality), full blood count and measurement of C-reactive protein level (R, strong; E, none) may help in supporting the diagnosis and monitoring the progress of the disease, but there is no role for routine blood tests. Children with empyema should receive high-dose, intravenous antibiotic therapy to ensure pleural penetration (R, strong; E, high quality). The majority of causative organisms in Australia are Streptococcus pneumoniae (in particular, serotypes 1, 3 and 19A), Streptococcus pyogenes, methicillin-sensitive Staphylococcus aureus and methicillin-resistant S. aureus (MRSA). In the absence of a positive culture result, the initial choice depends on the local hospital infection control policy for managing community-acquired pneumonia. Appropriate antibiotics should cover at least S. pneumoniae and S. aureus (R, strong; E, high quality). Consideration should be given to coverage of MRSA for children from communities with a high prevalence of MRSA (R, strong; E, high quality). Anaerobic infection should be considered in children who are at risk of aspiration. Macrolides should be used when Mycoplasma pneumoniae is thought to be the causative organism but should not be used routinely (R, weak; E, moderate quality). Moderate to large effusions require drainage. There is no role for diagnostic thoracocentesis. If there is a need to access the pleural cavity, the placement of a drain should be considered, thus ensuring that the child undergoes only one invasive intervention (R, strong; E, high quality). Pleural fluid should be sent for cytological testing, microscopic examination and culture, including culture for Mycobacterium tuberculosis (R, strong; E, high quality). Ideally, pleural fluid should be tested using enhanced molecular techniques such as polymerase chain reaction (R, strong; E, high quality). There is currently no role for pleural biochemical markers to guide therapy in children (R, weak; E, low quality). Chest drainage with a large bore drain alone is not recommended (R, strong; E, moderate quality). Instead, percutaneous small bore drainage with a fibrinolytic agent (preferably urokinase) or video-assisted thoracoscopic surgery (VATS) is recommended (R, strong; E, moderate quality). Open thoracotomy is not recommended as it has largely been superseded by the use of VATS. Children with an oxygen saturation level below 93% on room air should be given supplemental oxygen (R, strong; E, high quality). Other standard therapy includes fluid replacement (R, strong; E, none), use of antipyretic agents (R, strong; E, none specific to empyema) and analgesia (R, strong; E, none). There is no role for chest physiotherapy — apart from early mobilisation and encouragement of deep breathing and coughing, particularly after surgical intervention or tube drainage (R, strong; E, low quality) — and no indication for routine bronchoscopy in children with empyema (R, strong; E, weak). If a child has been afebrile for 24 hours, a change from intravenous to oral antibiotic therapy can be considered (R, weak; E, none). The choice of oral antibiotic depends on the organism identified (if any) or the class of antibiotic that was successfully used by intravenous therapy. There is no consensus on duration of oral antibiotic therapy, which varies from 1 week to 6 weeks (R, weak; E, none). A follow-up chest x-ray should be carried out 4–6 weeks after discharge from hospital to confirm that changes are resolving (R, weak; E, none). Further imaging is not required unless there are persistent clinical symptoms or complications (R, weak; E, none). There is no need for routine investigations to identify a possible underlying cause in previously healthy children without a history of recurrent infections (R, weak; E, very low quality). The full position statement is available at http://www.thoracic.org.au/ professional-information/position-papers-guidelines.

on behalf of the Australian Research Network in Empyema (ARNiE)

Haemoglobin A1c (HbA1c — a term that is sometimes used interchangeably with “glycated haemoglobin”) measurements are an indicator of time-averaged blood glucose levels (previous 2–3 months), and are used as the best marker of long-term diabetes control. A recent consensus statement on the worldwide standardisation of HbA1c measurement1 has updated previous international recommendations on the standardisation of HbA1c measurement and reporting.2 Here, we provide the rationale and guidance for implementation of HbA1c reporting in the new Système International (SI) units in Australia. This article represents the views of the Australasian Association of Clinical Biochemists, the Australian Diabetes Educators Association, the Australian Diabetes Society and the Royal College of Pathologists of Australasia, and was prepared by a working party of representatives of these organisations. The International HbA1c Consensus Committee recommends that all HbA1c levels be reported in SI units (mmol/mol, no decimal places) — with results directly traceable to the International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) reference method — and in the currently used, National Glycohemoglobin Standardization Program (NGSP) units (percentage, one decimal place). We recommend that dual reporting in Australia begins in July 2011, and that reporting of percentages ceases 2 years later. In New Zealand, dual reporting commenced in August 2009. The key reasons for implementing this recommendation in Australia are that: the SI units relate to a scientifically valid measure of HbA1c; the SI units remove potential confusion between HbA1c values as a percentage and blood glucose values in mmol/L; the change is in keeping with the international consensus statement;1 and the change has already been initiated in New Zealand and a number of countries in the European Union. Until now, all HbA1c measurements performed in Australia have been reported as percentages (HbA1c as a percentage of total haemoglobin) that are aligned with those produced in the Diabetes Control and Complications Trial.3 These units and this standardisation have been promoted by the NGSP in the United States, and the activities of this organisation have produced marked improvement in the accuracy of HbA1c results worldwide. More recently, the IFCC has developed a reference method that is more specific for HbA1c and more analytically robust.4 The IFCC method is now used as the reference system by the NGSP and for all routine methods for measurement of HbA1c, although a numerical conversion is required during the calibration process. The changes recommended here will provide results that are directly aligned with the IFCC method. As the IFCC method is more specific for HbA1c, not measuring several other haemoglobin–sugar complexes, the results are 10% to 40% lower than those from the NGSP system, depending on HbA1c concentration. Because reporting these results as percentages may lead to confusion (eg, producing a result of 5.3% rather than 7.0%), the units are changed to mmol/mol (millimoles HbA1c per mole of total haemoglobin [53 mmol/mol in the previous example]), which is consistent with the SI units recommended for use in Australia. There is a linear relationship between results from the two methods, and the “master equation” is used to convert results between the two methods: HbA1c SI unit (mmol/mol) = 10.93 × HbA1c NGSP unit (%) − 23.50.5 To make the conversion easier for clinicians, it is important to translate current treatment advice to the new units. A general conversion table for clinical use is provided in Box 1. The general HbA1c target of ≤ 7.0% for patients with type 1 and type 2 diabetes mellitus equates to ≤ 53 mmol/mol, although these values need to be individualised for patients. The recently updated diabetes treatment guidelines are shown with SI units in Box 2 and Box 3,6 and recommendations for reporting HbA1c levels in Australia are summarised in Box 4. In addition, supporting material for doctors and patients will be presented in SI units in the future. The routine reporting of an estimated average glucose (eAG) value may be useful for consultations with individual patients. However, the working party strongly agrees with the revised consensus statement that routine reporting of eAG with all requests for HbA1c analysis is not appropriate.1 The reasons for this include variability in the methods used to measure eAG, the risk of confusing a measure of long-term glycaemia (eAG) with a measure of short-term blood glucose control (actual blood glucose level), and its lack of applicability in the majority of patients with type 2 diabetes (in whom blood glucose levels are not measured at frequent intervals).7 Nonetheless, eAG values will be used as an educational tool at the discretion of individual clinicians, who can assist patients to understand the significance and limitations of the result. 1 Conversion table for haemoglobin A1c (HbA1c) values HbA1c as percentage (old units) HbA1c in mmol/mol (new units) 5.0 31 6.0 42 6.5 48 7.0 53 8.0 64 9.0 75 10.0 86 11.0 97 12.0 108 2 Recommended haemoglobin A1c (HbA1c) target ranges for patients with type 1 diabetes6 HbA1c target General target ≤ 53 mmol/mol, ≤ 7.0%* Specific clinical situations Pregnancy or planning pregnancy ≤ 53 mmol/mol, ≤ 7.0%*† Children and adolescents ≤ 58 mmol/mol, ≤ 7.5%* Recurrent severe hypoglycaemia or hypoglycaemia unawareness ≤ 64 mmol/mol, ≤ 8.0% Patients with major comorbidities likely to limit life expectancy Symptomatic therapy of hyperglycaemia‡ and avoidance of ketosis * Achievement of HbA1c targets must be balanced against risk of severe hypoglycaemia. † An HbA1c level of ≤ 42 mmol/mol (≤ 6.0%) is desirable if it can be achieved safely. ‡ Where practical, suggest blood glucose target level < 15 mmol/L to help minimise risk of infection. 3 Recommended haemoglobin A1c (HbA1c) target ranges for patients with type 2 diabetes6 HbA1c target General target ≤ 53 mmol/mol, ≤ 7.0%* Specific clinical situations Diabetes of short duration† and no clinical cardiovascular disease Requiring lifestyle modification ± metformin ≤ 42 mmol/mol, ≤ 6.0%* Requiring any antidiabetic agents other than metformin or insulin ≤ 48 mmol/mol, ≤ 6.5%* Requiring insulin ≤ 53 mmol/mol, ≤ 7.0%* Pregnancy or planning pregnancy ≤ 42 mmol/mol, ≤ 6.0%* Children and adolescents ≤ 53 mmol/mol, ≤ 7.0%* Diabetes of longer duration† or clinical cardiovascular disease (any therapy) ≤ 53 mmol/mol, ≤ 7.0%* Recurrent severe hypoglycaemia or hypoglycaemia unawareness (any therapy) ≤ 64 mmol/mol, ≤ 8.0% Patients with major comorbidities likely to limit life expectancy‡ (any therapy) Symptomatic therapy of hyperglycaemia§ * Achievement of HbA1c targets must be balanced against risk of severe hypoglycaemia, especially among older people. † In an older adult, long duration might be considered to be > 10–20 years, but for a person who develops type 2 diabetes at a young age, it might be considerably longer. ‡ Examples of major comorbidities include chronic medical conditions, such as chronic kidney disease stages 4 or 5; heart failure stages III or IV (New York Heart Association grading); incurable malignancy; and moderate to severe dementia. § Where practical, suggest blood glucose target level < 15 mmol/L to help minimise risk of infection. 4 Recommendations for reporting haemoglobin A1c (HbA1c) levels in Australia From July 2011, HbA1c levels should be reported in both National Glycohemoglobin Standardization Program units (percentage) and the Système International (SI) units (mmol/mol) by all pathology laboratories and, where possible, from point-of-care devices. The period of dual reporting will be 2 years, after which only the SI units will be used. These recommendations are consistent with international recommendations and are already in place in New Zealand.

Graham R D Jones MB BS, DPhil, FRCPA, Chemical Pathologist · George Barker BHSc, CDE-RN, NP · Ian Goodall BSc, FAACB, FFRCPA · Hans-Gerhard Schneider MD, FRACP, FRCPA · Mark D S Shephard MAACB, FFRCPA, PhD · Stephen M Twigg MB BS, PhD, FRACP