SAJCC Vol 33, No 1 (2017) by HMPG

SAJCC SOUTHERN AFRICAN JOURNAL OF CRITICAL CARE

JULY 2017 Vol. 33 No. 1 • Glucose control • Arterial line damping • Abdominal hypertension • Obstetrics in the ICU • Nursing DNR patients • Contaminated nebulisers

THE OFFICIAL JOURNAL OF THE CRITICAL CARE SOCIETY OF SOUTHERN AFRICA

SAJCC SOUTHERN AFRICAN JOURNAL OF CRITICAL CARE

The Official Journal of the Critical Care Society of Southern Africa July 2017 Vol. 33 No. 1

CONTENTS 2

EDITORIAL

Sugar, Pressure and Pregnancy W L Michell

ARTICLES

4 Glycaemic control in a cardiothoracic surgical population: Exploring the protocol-practice gap D Maharaj, H Perrie, J Scribante, F Paruk

8 Analysis of damping characteristics of arterial catheter blood pressure monitoring W H Rook, J D Turner, T H Clutton-Brock 12 Obstetric patients admitted to the intensive care unit of Dr George Mukhari

Academic Hospital, Ga-Rankuwa, South Africa

M Motiang 15 C orrelation between different methods of intra-abdominal pressure

monitoring in varying intra-abdominal hypertension models

D Wise, R N Rodseth, L Correa-Martin, F M Sanchez Margallo, P Becker, G Castellanos, R M L N Malbrain 19 Lived experiences of Rwandan ICU nurses caring for patients with a do-not-

resuscitate order E Nankundwa, P Brysiewicz

23 C ontamination of nebulisers and surrounding air at the bedside of

mechanically ventilated patients L van Heerden, H van Aswegen, S van Vuuren, R Roos, A Duse

CASE REPORT

28 The treatment of autonomic dysfunction in tetanus L Maryke Spruyt, T van den Heever G

LETTER TO THE EDITOR

32 The need for setting standards in critical care transfers Venter, D Stanton, N Conradie, L Jordaan, C Venter, M Venter, W Stassen M Photo credit: Intensivecarehotline.com Articles listed in: EXCERPTA MEDICA (EM BASE), BIOLOGICAL ABSTRACTS (BIOSIS), SCIENCE CITATION INDEX (SCISEARCH), CURRENT CONTENTS/CLINICAL MEDICINE, SCIENTIFIC ELECTRONIC LIBRARY ONLINE (SCIELO) Published by the Health and Medical Publishing Group Pty Ltd, Co registration 2004/022032/07, a subsidiary of the South African Medical Association, Suite 11, Lonsdale Building, Gardener Way, Pinelands, 7405. All letters and articles for publication must be submitted online at www.sajcc.org.za. Tel: 072 635 9825. E-mail: publishing@hmpg.co.za

EDITOR W L Michell FFA (Crit Care) University of Cape Town

DEPUTY EDITOR B Morrow BSc (Physio), PhD University of Cape Town

NURSING SCIENCE EDITOR P Brysiewicz RN, PhD University of KwaZulu-Natal

ASSOCIATE EDITORS A Argent FCPaeds (Cert Crit Care), MD University of Cape Town

P D Gopalan FCA (Crit Care) University of KwaZulu-Natal

L Hill RD, PhD CriticalPoint Critical Care Nutrition Consultancy

I A Joubert FCA (Crit Care) University of Cape Town

R Mathiva FCPaeds (Crit Care) University of the Witwatersrand

M Mer FCP (Pulm) (Cert Crit Care) University of the Witwatersrand

S Mokgokong MMed (Neurosurg), DSc University of Pretoria

F Paruk FCOG (SA) (Cert Crit Care), PhD University of Pretoria

H Perrie RN, MSc University of the Witwatersrand

G Richards FCP(SA), PhD University of the Witwatersrand

J Scribante RN, MSc University of the Witwatersrand

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EDITORIAL

Sugar, Pressure and Pregnancy Controlling blood glucose is one of the banes in the life of the intensive care unit (ICU) nurse. The story of tight glucose control started in 2001, when Van den Berghe et al.[1] published the startling finding that maintaining tight glucose control in the range of 4.5 - 6.0 mmol/L in a surgical ICU dramatically decreased mortality. ICUs across the world began implementing tight glucose control strategies accordingly, but the expected improved outcome was not realised. This observation was confirmed by the multi-centered NICE-SUGAR trial,[2] which showed that the intervention actually increased mortality and the increased deaths were linked to an unacceptably high incidence of hypoglycaemic events. In this issue of SAJCC, we publish a study by Maharaj et al.,[3] showing that protocol violations in blood glucose control in a cardiothoracic ICU are very common and results in wide swings in glucose levels. It appears that unless there is a high ratio of expert nurses available, the tight protocol does more harm than good. ICUs that are still trying to follow the tight range should adjust their targets immediately. The current Surviving Sepsis guidelines recommend that blood glucose be controlled using a protocolised approach: a target of <10.0 mmol/L should be maintained and that arterial blood should be used for the measurement if an arterial catheter is in place.[4] This is more easily achievable than tight glucose control and allows nurses more time to perform other, important procedures. Once technology allows us to close the loop between continuous glucose monitoring and insulin pump control, we should consider revisiting tight control. Arterial catheters are widely used in ICUs for monitoring blood pressure and for arterial blood sampling. The problem of under- and overdamping of the intra-arterial blood pressure monitoring system was first comprehensively studied in 1981, and intensivists and anaesthesiologists were well aware of the problem.[5] Because this phenomenon leads to inaccurate systolic and diastolic readings, while minimally affecting mean blood pressures, we have more recently tended to ignore damping issues and to use mean pressures as the main therapeutic target in managing the critically ill patient. However, the increasing use of the invasive arterial pressure trace for monitoring stroke volume and intravascular volume responsiveness means that we must, once again, pay attention to this issue, as these techniques rely on accurate systolic and diastolic readings, as well as a true depiction of the pressure curve. In this issue of SAJCC, we publish a survey of intra-arterial pressure monitoring systems in an ICU.[6] Only 19% of systems were appropriately damped, with the rest being over- or under-damped. Overdamping can be corrected by paying attention to details, such as under-pressurised flush bags, blood clots, bubbles, and malpositioned catheters. Underdamping is caused by resonance in the system, which can be controlled by a propriety device inserted between the arterial catheter and the transducer.[7] One solution may be for monitor manufacturers to develop software that could detect the presence of an over- or underdamped system and possibly even correct for this error. Obstetric patients form a greater proportion of the ICU population in developing countries when compared with developed countries. In this issue, we publish a study by Motiang[8] of 210 obstetric patients admitted to a tertiary-level ICU over a 4-year period. The patients were young, with an average admission time of 24 hours and a mortality

rate of only 9%. The most common reason for ICU admission was pre-existing cardiac disease and the second most frequent reason was preeclampsia, which was probably the reason for the main cause of death – intracerebral haemorrhage. This study suggests that obstetric patients are worthwhile occupiers of ICU beds and systems should be in place for them to have rapid access to critical care when it is required. The problem of abdominal hypertension and the development of abdominal compartment syndrome is now well recognised, but the accurate measurement of intra-abdominal pressure is crucial for the diagnosis. Bladder catheters are usually used, as direct measurement is too invasive. It is important to strictly follow international guidelines to ensure reliable readings.[9] For a variety of reasons, where the transvesical route cannot be used, the transgastric route is recommended. The animal model published in this issue is reassuring, as it confirms that there are no significant differences between the three methods of intra-abdominal pressure measurement in two different abdominal hypertension models.[10] Finally, I recommend reading Nankundwa’s[11] qualitative study on the emotional response of nurses caring for patients with do-not-resuscitate orders. Poor communication between the medical and nursing staff was reported to be the main source of emotional distress. As one subject stated, ‘Usually the decision is made by doctors and nurses are the ones to implement it’. This highlights the importance of honest, open communication and respect among healthcare professionals, including doctors and nurses, working in critical care – for the benefit of both patients and staff.

W Lance Michell Editor lance.michell@uct.ac.za S Afr J Crit Care 2017;33(1):2. DOI:10.7196/SAJCC.2017.v33i1.337

1. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med 2001;345(19):1359-1367. https://doi.org/10.1056/nejmoa011300 2. The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009;360(13):1283-1297. https://doi.org/10.1056/nejmoa0810625 3. Maharaj D, Perrie H, Scribante J, Paruk F. Glycaemic control in a cardiothoracic surgical population: Exploring the protocol-practice gap. S Afr J Crit Care 2017;33(1):4-7. https://doi. org/10.7196/SAJCC.2017.v33i1.280 4. Rhodes A, Evan LE, Alhazzani W, et al. Surviving Sepsis Campaign: International guidelines for management of sepsis and septic shock: 2016. Intensive Care Med 2017;43(3):304-377. https://doi. org/10.1007/s00134-017-4683-6 5. Gardner RM. Direct blood pressure measurement – dynamic response requirements. Anesthesiol 1981;54(3):227-236. https://doi.org/10.1097/00000542-198103000-00010 6. Rooke WH, Turner JD, Clutton-Brock TH. Analysis of damping characteristics of arterial catheter blood pressure monitoring in a large intensive care unit. S Afr J Crit Care 2017;33(1):8-10. https:// doi.org/10.7196/SAJCC.2017.v33i1.300 7. Todorovic M, Jensen EW, Thøgersen C. Evaluation of dynamic performance in liquid-filled catheter systems for measuring invasive blood pressure. Int J Clin Monit Comput 1996;13(3):173178. https://doi.org/10.1023/a:1016903508976 8. Motiang M. Obstetric patients admitted to intensive care unit of Dr George Mukhari Academic Hospital, Ga-Rankuwa, South Africa. S Afr J Crit Care 2017;33(1):12-14. https://doi.org/10.7196/ SAJCC.2017.v33i1.281 9. Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: Updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013,39(7):11901206. https://doi.org/10.1007/s00134-013-2906-z 10. Wise RD, Rodseth RN, Correa-Martin L, et al. Correlation between different methods of intraabdominal pressure monitoring in varying intra-abdominal hypertension models. S Afr J Crit Care 2017;33(1):15-18. https://doi.org/10.7196/SAJCC.2017.v33i1.327 11. Nankundwa E, Brysiewicz P. Lived experiences of Rwandan ICU nurses caring for patients with a do-not-resuscitate order. S Afr J Crit Care 2017;33(1):19-22. https://doi.org/10.7196/SAJCC.2017. v33i1.281

SAJCC July 2017, Vol. 33, No. 1

Marketing Code Authority Member

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

ARTICLE

Glycaemic control in a cardiothoracic surgical population: Exploring the protocol-practice gap D Maharaj,1 MB BCh, DA, MMed (Anaesth), FCA; H Perrie,1 MSc; J Scribante,1 MCur; F Paruk,2 MB ChB, FCOG, Cert Crit Care, MD 1 2

Department of Anaesthesiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Department of Critical Care, Faculty of Health Sciences, University of Pretoria, South Africa

Corresponding author: D Maharaj (maharajdyuti@gmail.com)

Background. Glycaemic control constitutes an important component in the management of critically ill patients. As such, all healthcare workers involved in the management of critically ill patients need to ensure that it is achieved adequately. To avoid glucose variability and to maintain normoglycaemia, evidence-based protocols are implemented to guide clinical care. However, it has been suggested that with the use of protocoldirected therapy, protocol-practice gaps are common and therefore protocol adherence must be audited regularly. The aim of this study was to evaluate adherence to the glucose control protocol by nurses in the cardiothoracic intensive care unit (ICU) at a tertiary academic hospital. Methods. A retrospective study involving the review of ICU charts of all post-cardiac surgery patients ≥16 years admitted to the cardiothoracic ICU during March 2011. A convenience sampling method was used. Results. A total of 741 glucose readings for 22 patients were evaluated. The median (interquartile range) glucose reading was 7.8 mmol/L (6.7 9.3 mmol/L). Overall, 411 (55.5%) protocol violations were recorded and 629 (84.9%) of the total readings were abnormal. Protocol violations were similar between the day and night staff; 188 (54.7%) and 223 (58.5%) were recorded, respectively (p=0.256). Of the readings, 464 (62.6%) were conducted by ICU-trained nurses and 245 (33.2%) by non-ICU-trained nurses. There were fewer protocol violations recorded by the ICU-trained nurses compared with the non-ICU-trained nurses, i.e. 53.3% and 63.7%, respectively (p<0.05). Conclusion. Adherence to the glucose-control protocol was suboptimal. These results may suggest that the training and education of healthcare workers in implementing protocols is an ongoing and dynamic process, and that there is a need for the regular evaluation of protocol adherence in order to identify protocol-practice gaps. S Afr J Crit Care 2017;33(1):4-7. DOI:10.7196/SAJCC.2017.v33i1.280

Landmark studies conducted within the last two decades have been instrumental in informing the critical care discipline regarding the importance of glycaemic control.[1-4] While it is evident that optimal glucose targets remain undetermined, it is clear that specific patient populations do require meticulous glycaemic control. The cardiothoracic population is a classic example where perioperative hyperglycaemia has been clearly demonstrated to be associated with an increase in both morbidity and mortality.[5,6] As such, cardiothoracic units emphasise the importance of postoperative glycaemic control and, in particular, the avoidance of a glucose level >10 mmol/L. In the intensive care unit (ICU) setting, adherence to protocols is often suboptimal. This has been borne out in numerous studies assessing adherence to nutrition and sedation protocols.[7] The use of protocols simplifies processes, standardises care, facilitates patient safety, and reduces costs. The lack of adherence can hinder the success of any protocol.[8] In the resource-constrained South African context, adherence to protocols may also be influenced by the shortages of ICU-trained nurses, as well as the high workload burden. Taking these factors into account, and considering the importance of adherence to glucose control protocols – its impact on morbidity and mortality – as well as the recognised occurrence of protocol-practice gaps, we undertook a study to evaluate the adherence to the glucose control protocol in a cardiothoracic ICU setting.

Methods

A retrospective, contextual, single-centre, descriptive design was used in this study. The study was conducted in the cardiothoracic ICU of a quaternary, academic hospital. At the time of the study, an average of 21 cardiac operations were performed monthly (>16-year age group) and the nurse-to-patient ratio was 1:1 in the ICU. Nurses allocated to patient care were from all nursing categories, including agency nurses – enrolled, registered, and registered critical care nurses. A consecutive, convenience sampling method was used. The ICU charts of all postcardiac surgery patients who were ≥16 years old and who had been admitted to the ICU during March 2011, as well as the demographics of the nurses working in the ICU at the time, were analysed. At the time of the study, the glucose control protocol defined a target blood glucose range of 4.1 - 6 mmol/L (Table 1). The exclusion criteria were children <16 years old, and post-thoracic surgery patients. Therefore, 14 patients were excluded from the study: 12 paediatric cardiac, and 2 thoracic patients. Approval to conduct this study was obtained from the Human Research Ethics Committee (Medical) of the University of the Witwatersrand (ref. no. M120109) and other relevant authorities. The data collection procedure involved the utilisation of two data collection sheets; one for the collection of data from the ICU charts, and another to capture the demographics of the nurses assigned to patient care during the research period. Both the ICU charts and nurses received study numbers, and no identifiable information was recorded.

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Results

During the data collection period, 22 patients were admitted, of whom 13 (59.1%) were male and 9 (40.9%) were female. The mean age of patients was 48.5 years and the age range was 17 - 76 years. The median (interquartile range (IQR)) length of stay in ICU was 4 (3 - 5) days, with 2 patients staying in the ICU for >20 days. The surgical procedures performed included 17 (77.3%) valvular procedures, 3 (13.6%) coronary artery grafts, and 2 (9.1%) ‘other’ procedures. The median (IQR) blood glucose concentration was 7.8 (6.7 - 9.3) mmol/L (Fig. 1). The glucose

Table 1. Glucose control protocol in ICU Blood glucose (mmol/L) Rapidly acting insulin (U) <4 Nil. Treat as hypoglycaemia: 1. Call medical doctor 2. Administer 25 mL of DW50% 3. Recheck BG every 15 min until >5 mmol/L 4. Thereafter recheck BG hourly 4.1 - 6.0 0 6.1 - 8.0 1 8.1 - 10.0 2 10.1 - 12.0 4 12.1 - 14.0 6 14.1 - 16.0 8 16.1 - 18.0 10 18.1 - 20.0 12 >20 12 (Call medical doctor)

readings ranged from 3.1 to 17.8 mmol/L. Table 2 shows the number of glucose readings obtained within the different glucose ranges. According to the glucose control protocol in place at the time of the study, 629 (84.9%) of the readings were abnormal, i.e. outside the required glucose range. The target range of 4.1 – 6.0 mmol/L was only observed in 112 (15.1%) of the glucose readings. Hypoglycaemia, defined at the time of the study as a glucose value of <4.0 mmol/L, was observed in 7 (0.9%) readings. Interestingly, had the results been analysed using the currently employed glucose control protocol, 279 (37.7%) readings would have been within the target range, which is presently defined as 6.1 - 8.0 mmol/L. During the study period, a total of 741 glucose readings were recorded, of which 411 (55.5%) readings were in violation of the glucose control protocol. Eighteen (2.4%) readings were never recorded. Fig. 2, which does not include the unknown readings, shows the number of glucose readings obtained for each patient and the proportion of protocol violations per patient. Unknown values are not shown on this figure. Among the 411 protocol violations, the daytime nursing staff violated the protocol 188 (54.7%) times, and the night-time nursing staff violated the protocol 223 (58.8%) times (χ22(1)=1.29; p=0.26) (Table 3). There 20 16 (2.1%) unknown values for this variable. were The ICU-trained nursing staff recorded 464 (62.6%) readings, while the non-ICU-trained nursing staffed recorded 246 (33.2%) readings. 15 ICU-trained nursing staff violated the protocol 247 (53.4%) times and the non-ICU-trained staff violated the protocol for 156 (63.7%) glucose

Median blood glucose values (mmol/L)

The ICU unit manager allocated study numbers to the nurse and therefore the authors were blinded to the nurses’ identification. Only the authors had access to the raw data. Anonymity, confidentiality, and privacy of patients and nurses were therefore maintained. Data were manually entered into a Microsoft Excel 2010 spreadsheet, and subsequently analysed STATA 11 (STATA Corp., USA). The results of the study were analysed using descriptive and inferential statistics. Comparisons were made using the χ2 test and p-values <0.05 were considered statistically significant. Missing data were included in the analysis and were recorded as ‘unknown’.

Table 2. Glucose results by category (N=741) Glucose category Number of glucose (mmol/L) readings, n (%) 5 <4 7 (0.9) 4.1 - 6.0 112 (15.1) 6.1 279 (37.7) 0 - 8.0 8.1 - 12.0 1 2 3 4 5 6 300 7 8 (40.5) 9 10 11 12 13 14 12.1 - 14.0 26 (3.5)Patient number 14.1 - 16.0 6 (0.8) 16.1 - 18 11 (1.5) >18 0 (0)

Normal range No Yes Outliers No No 15 16 17 18 19 20 21 22 No No No No

ICU = intensive care unit; U = unit(s); DW50% = 50% dextrose water; BG = blood glucose. No protocol violation Protocol violation 160 140

15 Glucose readings, n

Median blood glucose values (mmol/L)

120 100 80 60 40

Outliers 0 1 2

4 5

6 7 8

9 10 11 12 13 14 15 16 17 18 19 20 21 22 Patient number

Fig. 1. Median (interquartile range) glucose value per patient.

0 1 2 3

4 5 6 7

8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Patient number

Fig. 2. Protocol violations with respect to number of glucose readings per patient.

No protocol violation

Protocol violation

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Table 3. Association between nurse shift and ICU training in protocol violations Variable Nurse shift Day Night ICU-trained Non-ICU-trained

Glucose readings, n (%)

No protocol violations, n (%)

Protocol violations, n (%)

345 (46.6) 380 (51.2) 464 (62.6) 245 (33.2)

156 (45.4) 156 (41.2) 216 (46.7) 89 (36.3)

188 (54.7) 223 (58.5) 247 (53.3) 156 (63.7)

readings (χ2(1)=6.97; p=0.008) (Table 3). There were 31 (4.2%) unknown values for this variable.

Discussion

In this study, there were 411 (55.5%) protocol violations. This value is higher than that reported by Taylor et al.[9] and Rood et al.,[10] who reported glucose protocol violations of 47% and 44%, respectively. A study by Oeyen et al.,[11] as well as the NICE-SUGAR trial[13] reported a much lower protocol violation rate of 29%. Possible reasons for the lower proportion of violations are that, compared with our setting, these were large-centre trials conducted in developed countries that had adequate resources. It has also been shown that patients enrolled in prospective research studies receive a higher standard of care, which may influence protocol adherence. Shift work, and in particular working night shifts, is recognised as a source of distress for nurses.[12] In a study of 23 Australian nurses, getting less sleep was significantly related to an increased likelihood of nursing error and a decreased likelihood of identifying colleagues’ errors.[13 ] However, in this study, there was no statistically significant difference between day and night staff violations (p=0.26). According to the South African National Audit of Critical Care Resources in 2007, there is a national shortage of critical care nurses.[14] As a result, there is a risk of increased workload and burnout.[15] Furthermore, with staff shortages and the implementation of many protocols in ICUs, critical care nurses are under constant pressure to deliver safe and effective care to critically ill patients, as well as to impart their skills and knowledge to non-ICU-trained nurses. It is important to note that, although there was a nurse patient ratio of 1:1 during the study period, these nurses were from all nursing categories, including agency staff - enrolled nurses, registered nurses, and registered critical care nurses are allocated to patients. In this study, we also compared protocol violations between ICU-trained and non-ICU-trained nurses and, after reviewing the literature, were not surprised to find that there were more protocol violations by the non-ICU-trained nurses (p=0.008) included in our study. For a protocol to be efficiently developed and implemented, its feasibility should be tailored according to resource availability within the specific setting. All healthcare workers involved in patient care need to work together in order to facilitate this process. Protocol violation may, or may not, compromise patient care. According to Wong et al.,[16] ‘one of the cardinal concepts (borrowed from industry), in patient safety, is systems analysis. This is the concept that system failure, not individual human failure, is to blame for many of the adverse events occurring in healthcare. The problem is not “bad people”; the problem is that the system needs to be made safer ... To err is human.’ Cabana et al.[17] assessed the knowledge, attitude, and behaviour of physicians, and identified barriers to adherence to practice guidelines. In their model, barriers to knowledge included lack of awareness and familiarity with guidelines. Barriers to attitude included lack

p-value 0.26 0.008

of agreement with guidelines, lack of self-efficacy, lack of outcome expectancy, lack of motivation, and resistance to changing previous practice. The behaviour attributes included external barriers with factors related to patients (e.g. patient expectation), the practice environment (e.g. lack of time and resources) and the guidelines themselves (e.g. conflicting recommendations). One of the most consistent findings in research on health services is the gap between evidence and practice.[17] Evidence-based protocols and guidelines are utilised to assist not only with patient clinical management and to reduce the guess-work from patient care, but also to reduce the workload on nursing staff as a short-term solution to skilled staff shortages.[17] The finding of a substantial proportion of protocol violations in the ICU highlights the necessity of further education and ongoing assessments of implemented protocols by all healthcare workers involved in patient care. Education of healthcare workers and followup questionnaires on the understanding and implementation of local protocols should also be considered. Evaluation and identification of the factors responsible for protocol violations, and the subsequent targeting of the identified factors, are imperative to improve adherence to any protocol. As proposed by Cabana et al.[17] the knowledge, attitudes and behaviour of healthcare workers should also be evaluated when implementing a protocol. Furthermore, a systems analysis approach should be considered for implementation of future protocols.[15] Despite emphasis on the need for protocol-driven ICUs to reduce the work burden, standardise care, and avoid delay in treatment to allow for better communication and improved outcomes, it remains unknown whether the protocols and protocol adherence translate into improved clinical outcomes. According to Kollef,[18] who conducted numerous studies on the potential of protocols to improve outcomes in ICUs, although the overall quality of evidence supporting the efficacy of protocols may be less than ideal, the reported success following their implementation supports the use of this tool in critically ill patients. Complex critical illnesses, such as sepsis, require multiple therapies and interventions to optimise clinical outcomes, and protocols appear to deliver recommended therapies and possibly improve patient outcomes. A large number of studies involving computerised and closed-loop protocol implementation showed improved adherence to the protocol. This should guide future research into protocol implementation.[9] The results of this study must be interpreted with caution. The study was conducted contextually – in an academic institute in a cardiothoracic ICU with the study population being cardiac patients – and our results may not be extrapolated to the general population. A retrospective research design, although it can offer valuable results, has limitations: the study design does not allow for the determination of causation, only association, and the quality of the data cannot be controlled by the researcher.

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Conclusion

This study explored the protocol-practice gap in a single ICU and found that, as has been observed elsewhere, adherence to protocols was poor. Further studies should be designed to explore the reasons for the gap in adherence and non-compliance. An understanding of the underlying reasons would allow for the implementation of strategies to reduce the gap in practice. The training and education of healthcare workers in implementing protocols is an ongoing and dynamic process, and regular evaluation is essential in identifying the protocol-practice gap. Acknowledgements. None. Author contributions. All authors contributed equally to the preparation of the manuscript. Funding. None. Conflicts of interest. None. 1. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy critically ill patients. N Engl J Medicine.2001;345(19):1359-1367. https://doi.org/10.1056/nejmoa011300 2. Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy in the medical ICU. N Engl J Med 2006;354(5):449-461. https://doi.org/10.1056/nejmoa052521 3. Brunkhorst FM, Engel C, Bloos F, et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. New Engl J Med 2008;358(2):125-139. https://doi.org/10.1056/nejmoa070716 4. Preisr JC, Devos P, Ruiz-Santana S, et al. Impact of tight glucose control by intensive insulin therapy on ICU mortality and the rate of hypoglycemia: Final results of the Glucontrol study. Intensive Care Med 2007;33(Suppl 2):S189.

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5. Lazar HL, Chipkin SR, Fitzgerald CA, et al. Tight glycemic control in diabetic coronary artery bypass graft patients improves perioperative outcomes and decreases recurrent ischemic events. Circulation 2004;109(12):1497-1502. https://doi.org/10.1161/01.cir.0000121747.71054.79 6. Ingels C, Debaveye Y, Milants I, et al. Strict blood glucose control with insulin during intensive care after cardiac surgery: Impact on 4-year survival, dependency on medical care, and quality-oflife. Eur Heart J 2006;27(22):2716-2724. https://doi.org/10.1093/eurheartj/ehi855 7. Compton F, Bojarski C, Siegmund B, Van der Giet M. Use of a nutrition support protocol to increase enteral nutrition delivery in critically ill patients. Am J Crit Care 2014;23(5):369403. https://doi.org/10.4037/ajcc2014140 8. Plost G, Nelson DP. Empowering critical care nurses to improve compliance with protocols in the intensive care unit. Am J Crit Care 2007;16(2):153-156. 9. Taylor BE, Schallom ME, Sona CS, et al. Efficacy and safety of an insulin infusion protocol in a surgical ICU. J Am Coll Surg 2006;202(1):1-9. https://doi.org/10.1016/j.jamcollsurg.2005.09.015 10. Rood E, Bosman RJ, van der Spoel JI, Taylor P, Zandstra DF. Use of a computerized guideline for glucose regulation in the intensive care unit improved both guideline adherence and glucose regulation. J Am Med Info Assoc 2005;12(2):172-180. https://doi.org/10.1197/jamia.m1598 11. Oeyen SG, Hoste EA, Roosens CD, Decruyenaere JM, Blot SI. Adherence to and efficacy and safety of an insulin protocol in the critically ill: A prospective observational study. Am J Crit Care 2007;16(6):599-608. 12. The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. New Engl J Med 2009;360(13):1283-1297. https://doi.org/10.1056/nejmoa0810625 13. McVicar A. Workplace stress in nursing: A literature review. J Adv Nurs 2003;44(6):633-642. https://doi.org/10.1046/j.0309-2402.2003.02853.x 14. Scribante J, Bhagwanjee S. National audit of critical care resources in South Africa: Nursing profile. S Afr Med J 2007;97(12):1315-1318. 15. Dorrian J, Lamond N, van den Heuvel C, Pincombe J, Rogers AE, Dawson D. A pilot study of the safety implications of Australian nurses' sleep and work hours. Chronobiol Int 2006;23(6):11491163. https://doi.org/10.1080/07420520601059615 16. Wong DA. It’s more than human error: A systems approach to patient safety. Spine Line 2002;20-21. 17. Cabana MD, Rand CS, Powe NR, et al. Why don't physicians follow clinical practice guidelines? A framework for improvement. JAMA 1999;282(15):1458-1465. https://doi.org/10.1001/ jama.282.15.1458 18. Kolleff MH. Clinical practice improvement initiatives: Don’t be satisfied with early results. Chest 2009;136(2):335-338. https://doi.org/10.1378/chest.09-0637

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This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

ARTICLE

Analysis of damping characteristics of arterial catheter blood pressure monitoring in a large intensive care unit W H Rook,1 BMedSc, MB ChB, PhD; J D Turner,2 BMedSc, BMBS; T H Clutton-Brock,3 MB ChB Department of Critical Care, University Hospitals Leicester, Leicester, UK Department of Anaesthesia. University Hospitals Nottingham, Nottingham, UK 3 Department of Critical Care, University Hospitals Birmingham, Birmingham, UK 1 2

Corresponding author: W H Rook (whrook@gmail.com)

Background. For many reasons, the invasive measurement of systolic and diastolic blood pressure should be accurate. Accuracy is determined, in part, by the damping characteristics of the arterial catheter blood pressure monitoring system. Objectives. To ascertain the damping characteristics of arterial catheter blood pressure monitoring in a large tertiary intensive care unit (ICU) and to elicit any causes of under- or over-damping of the measurement systems. Methods. A cross-sectional, observational study of arterial line measurements in a large general ICU. The coefficient of damping (CoD) was calculated from the waveform generated from a ‘fast flush’. Results. Thirty systems (19%) were adequately damped (CoD 0.4 - 0.8), 56 (37%) were overdamped, and 68 (44%) were underdamped. We did not find that poor damping characteristics were associated with the age of the arterial catheter or the type of catheter used. Conclusion. Most systems observed in this study were inappropriately damped, which would result in the inaccurate display of the waveform and systolic and diastolic pressures. S Afr J Crit Care 2017;33(1):8-10. DOI:10.7196/SAJCC.2017.v33i1.300

Haemodynamic instability is a feature of many admissions to the intensive care unit (ICU), and indeed theatres frequently require active management to ensure adequate and acceptable cardiac output and perfusion pressure, whilst preventing excessively high pressures. Thus, real-time, accurate measurement of arterial blood pressure (ABP) is vitally important for making clinical decisions. This becomes especially important where the clinical condition requires ABP to be tightly regulated around a target, such as in therapeutic hypotension in trauma,[1] or where decision-making is based on arterial waveform characteristics such as when using pulse-contour analysis.[2] Real-time monitoring of ABP is commonly carried out invasively in theatres and ICUs using an arterial catheter placed within a peripheral artery, most commonly the radial artery, connected via fluid-filled tubing to a pressure transducer. Unfortunately, the method for monitoring ABP invasively is subject to distortions that can reduce the accuracy of the measurement, i.e. damping and resonance.[3-5] In this setting, damping refers to anything which absorbs energy within the oscillating system, resulting in an artificial reduction in the measured amplitude of the oscillating arterial pressure waveform, i.e. the pulse pressure. Conversely, resonance refers to an artificial amplification of the oscillating arterial pressure waveform when this waveform occurs at a similar frequency to the natural frequency of the measurement system, resulting in an exaggeration of the amplitude of the arterial pressure waveform. The extent to which a system is damped is described by the coefficient of damping (CoD), while the frequency of oscillation that the system resonates at, is known as the natural frequency (ωn). Importantly, a certain amount of damping, where the CoD is ~0.7, is required for accurate blood pressure measurement; enough to damp artificial distortion inherent to the measurement system, but not so much that the true pressures and details of the arterial waveform are misrepresented.

In 1903, Frank[6] originally described the manner by which a system must respond to an oscillatory waveform to accurately measure ABP. This was later updated by Gardner, [4] who described the range of natural frequency and CoD that would give adequate response characteristics to accurately measure blood pressure; a ωn of >10Hz is almost always required. The range of CoD that would give accurate ABP readings increases as ωn increases, but 0.4 - 0.8 will give an accurate reading in the majority of cases.[4] A number of factors are thought to contribute to suboptimal damping; air bubbles within the tubing system dramatically increase the CoD, as do blood clots – both resulting in overdamping, while excessive lengths of tubing reduce the CoD, resulting in underdamping.[4,7] The aim of this prospective study was to carry out an evaluation of whether the arterial blood pressure monitoring systems used in a large tertiary hospital ICU had appropriate CoDs to accurately measure ABP and produce a reliable pulse contour. Secondary aims of the study were to examine the hypothesis that the time the arterial catheter had been in place, the site of the catheter, and the type of catheter used would affect the CoD.

Methods

Ethical approval was obtained from the University of Birmingham Research Ethics Committee to carry out this audit, with no requirement for individual patient consent. On randomly selected days, all patients in the Queen Elizabeth Hospital Birmingham Critical Care Unit, with an arterial line in situ were audited. Basic details were recorded: age, working diagnosis, site of arterial cannula, date and time of insertion, hours since insertion, type of cannula (manufacturer, gauge, length). The CoD was measured using the ‘fast flush’ method described by Jones and Pratt[8] and by McGhee and Bridges.[7] Briefly, the flush valve on the back of the BD DTX Plus Disposable Pressure Transducer (BD

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Biosciences, UK) was opened to allow a fast flush of normal saline (0.9% NaCl), and then closed, to create a decaying waveform before the system returned to the normal monitoring of ABP. The flush was performed thrice. The resulting waveforms were displayed on the patient monitor, were anonymously photographed, and the resulting images analysed using ImageJ software (v1.44, NIH, USA) to measure the amplitude of the two initial oscillations in pixels (A1 and A2, Fig. 1). The CoD was then calculated according the formula described by Gilbert, as follows:[9]

CoD = – In

(A2 / A1) π2+[In(A2 / A1) ]2

Where no oscillations occur, it is known that the CoD is ≥1, and in these instances the CoD was recorded as 1.0.[9] Statistical analysis was performed using Aabel version 3 statistical analysis software (Gigawiz Ltd., USA). Factorial ANOVA or linear regression analysis were used as appropriate and as detailed, with results considered statistically significant if p<0.05.

Results

A total of 154 patients with invasive blood pressure measurements were included in the study; 143 had BD Floswitch 20 g 4.5 cm arterial cannulae (BD Biosciences, UK), 10 had Vygon 20 g 8.0 cm arterial cannulae (Vygon UK Ltd., UK), and 1 had a 5Fr 20 cm femoral PiCCO line (Phillips Healthcare, UK). A total of 143 patients had catheters in the radial artery, 9 had brachial artery catheters, and 2 had femoral artery catheters. Fifty-six (37%) damping assessments had a CoD ≥1, i.e. no oscillations occurred on the fast flush test. It was not possible to quantify the CoD in these patients, but they were classified as overdamped. Of the remaining 98 patients, the mean (standard deviation, SD) CoD was 0.35 (0.20). Of these, 30 (19%) had a CoD in the recommended range of 0.40 - 0.80 and 68 (44%) were underdamped (CoD <0.4) (Fig. 1). There were no damping measurements in the 0.8 - 1.0 range. There was no statistically significant relationship observed between the duration an arterial catheter had been in situ and its CoD, and there were no statistically significant differences between the CoDs recorded in the different arterial lines.

Outside reference range for acceptable damping Within reference range for acceptable damping

Frequency

This study examined the CoD in a large sample of patients in the ICU setting (N=154). Importantly, we found that of the 154 damping measurements, only 30 (19%) had a CoD judged to be adequate for providing an accurate, reliable measure of ABP. This shows that a significant proportion of invasive blood pressure management does not conform to the standards required for accurate monitoring. This is significant for at least three reasons. Firstly, although overor underdamping affects mean arterial pressure (MAP) minimally, it leads to large inaccuracies in measurements of systolic and diastolic blood pressure,[7] both of which are key measured variables used to direct therapy, especially fluid resuscitation. Secondly, poor damping reduces the reliability of pulse pressure measurements, and thus removes another important clinical indicator. Finally, it makes the use of pulse contour analysis for the estimation of cardiac output impossible, as this relies on accurate, optimally-damped ABP measurements. A number of papers have previously called for routine monitoring of arterial line damping.[4,7,9] This is underlined by the findings of Romagnoli et al.,[10] who found that systolic pressure (mean (SD)) was overestimated by 28 (15) mmHg in patients with underdamped ABP waveforms when compared with those with appropriately damped systems. Routine monitoring would ensure that inappropriately damped lines are recognised and, at the very least, taken account of, if not corrected or replaced. Further, our study indicates the need for national standards and guidelines to direct clinically acceptable standards of invasive ABP monitoring, which are thus far unavailable. Importantly, our new evidence makes it clear that further studies are required to assess the impact of poor damping characteristics on clinical care and outcomes.

Study limitations

Firstly, owing to the limited resolution of the patient monitoring screens, it was sometimes impossible to measure A2 in cases where the oscillations were very small. These would typically have represented CoDs between 0.9 and 1.0 and would therefore have fallen outside the required range for accurate measurement. Secondly, blood pressure was not recorded in this study, which necessitates further investigations to examine the clinical implications of our findings. Currently, invasive ABP measurement is considered the ‘gold standard’.[11] It would be of interest to compare oscillometrically derived v. invasively derived ABP, and to examine over- or underdamped measurement systems lead to a disparity in the measured ABP Lastly, although the patients’ broad diagnosis was recorded, no attempt was made to record specific blood pressure targets. The authors were therefore unable to detail for how many patients accurate blood pressure measurement was of critical importance, and for how many it was less important. However, it is important to note that all patients were critically unwell, by virtue of the fact that they were treated in the ICU.

Conclusion

This study showed that the majority of arterial catheter blood pressure monitoring systems in our ICU were either over- or underdamped, resulting in inaccurate systolic and diastolic pressure readings.

0 0.0 - 0.1

0.1 - 0.2 0.2 - 0.3

0.3 - 0.4

0.4 - 0.5 0.5 - 0.6

0.6 - 0.7 0.7 - 0.8

0.8 - 0.9

0.9 - 0.1

Coefficient of damping

Fig. 1. Frequency histogram detailing CoD in the 98 patients in which it was possible to measure it.

Discussion

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Acknowledgements. The authors wish to thank all nursing staff who assisted with the collection of the data. Author contributions. THC-B & WHR: Design, data collection, analysis, manuscript preparation. JDT: Data collection and analysis.

ARTICLE Funding. None Conflict of interest. None. 1. Dutton RP. Resuscitative strategies to maintain homeostasis during damage control surgery. Br J Surg 2012;99(Suppl 1):21-28. https://doi.org/10.1002/bjs.7731 2. Alhashemi JA, Cecconi M, Hofer CK. Cardiac output monitoring: An integrative perspective. Crit Care 2011;15(2):214. https://doi.org/10.1186/cc9996 3. Kleinman B. Understanding natural frequency and damping and how they relate to the measurement of blood pressure. J Clin Monit 1989;5(2):137-147. https://doi.org/10.1007/bf01617889 4. Gardner RM. Direct blood pressure measurement â&#x20AC;&#x201C; dynamic response requirements. Anaesthesiol 1981;54(3):227-236. 5. Stoker MR. Principles of pressure transducers, resonance, damping and frequency response. Anaesth Intensive Care Med 2004;5(11):371-375. https://doi.org/10.1383/anes.5.11.371.53397

6. Frank O. Kritic der elastischen manometer. Zeitschrift FĂźr Biologie 1903;44:445-613. 7. McGhee BH, Bridges EJ. Monitoring arterial blood pressure: What you may not know. Crit Care Nurse 2002;22(2):60-79. 8. Jones A, Pratt O. Physical principles of intra-arterial blood pressure measurement. Anesthesia Tutorial of the Week, 2009: www.frca.co.uk/Documents/137%20Physical%20principles%20of%20 intra-arterial%20blood%20pressure%20measurement.pdf (accessed 21 April 2015). 9. Gilbert M. Principles of pressure transducers, resonance, damping and frequency response. Anaesth Intensive Care Med 2012;13(1):1-6. https://doi.org/10.1016/j.mpaic.2011.10.010 10. Romagnoli S, Ricci Z, Quattrone D, et al. Accuracy of invasive arterial pressure monitoring in cardiovascular patients: An observational study. Crit Care 2014;18(6):644. https://doi. org/10.1186/s13054-014-0644-4 11. Ward M, Langton JA. Blood pressure measurement. Cont Educ Anaesth Crit Care Pain 2007;7(4):122-126. https://doi.org/10.1093/bjaceaccp/mkm022

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This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

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Obstetric patients admitted to the intensive care unit of Dr George Mukhari Academic Hospital, Ga-Rankuwa, South Africa M Motiang, MB ChB, MMed (Anaesth) Department of Intensive Care, Sefako Makgatho Health Science University, Pretoria, South Africa Corresponding author: M Motiang (mammie@telkomsa.net)

Background. Pregnancy is a natural physiological process that normally ends uneventfully. However, there are instances where admission to an intensive care (ICU) is required. Objectives. To determine the spectrum of disease requiring ICU admission in obstetric patients, condition on discharge, maternal mortality, and the cause of maternal death. Methods. A retrospective study of all pregnant and postpartum patients admitted from January 2008 to December 2011 was conducted. Outcome measures were the spectrum of disease, ICU interventions, and maternal outcomes. Results. In total, 210 patients were reviewed. The mean age was 28.15 (standard deviation (SD) 6.97) years. Twelve (5.7%) patients were admitted at a mean (SD) gestational age of 25.33 (6.56) weeks, 94.2% (n=198) were postpartum, and 88.6% (n=186) were post-caesarean section. Pre-existing cardiac disease (44.3%, n=93), eclampsia and preeclampsia (20%, n=42), obstetric haemorrhage (16.2%, n=34), and pulmonary oedema (6.2%, n=13) were the most common causes of admission. Sixty-one percent (n=128) of patients received ventilatory support. The median length of ICU stay was 24 hours (range 1 - 17 days). Eighty-seven percent (n=183) of the patients were haemodynamically stable. Maternal mortality was 9% (n=19). Conclusion. Cardiac disease in pregnancy was the most common diagnosis in patients admitted to our ICU, followed by eclampsia and preeclampsia. Most of the patients (87.1%) were haemodynamically stable and needed minimal intervention, as confirmed by their short periods of stay in ICU. Although the mortality rate in our institution was higher than that observed in developed countries, it was lower than rates reported in other South African studies. This study has found that many of the patients were admitted to ICU for monitoring purposes only and did not require ICU level of care. S Afr J Crit Care 2017;33(1):12-14. DOI:10.7196/SAJCC.2017.v33i1.279

Pregnancy represents a unique alteration in physiology that usually proceeds to its completion without complication. However, there are instances where complications, sometimes life-threatening, can occur that require intensive care with invasive monitoring and mechanical ventilation.[1] Critically ill obstetric patients are significantly different from the average patient admitted to the intensive care unit (ICU). They present a challenge to the critical-care physician, owing to their unique physiology and the specific medical disorders that sometimes occur during pregnancy and the peripartum period.[2] The challenges faced in the treatment of these patients are even greater owing to the fact that two lives are simultaneously endangered. Pregnant patients account for a small number of ICU admissions in developed countries (â&#x2030;¤2%) but they can reach up to 10% or more in developing countries.[3] Studies conducted in South Africa (SA) indicate admission rates of 6.7 - 13.6%.[4,5] The most common causes of admission to ICU for obstetric patients are eclampsia, severe preeclampsia, haemorrhage, anaesthetic complications, congenital and valvular heart disease, cardiomyopathy, and puerperal infections.[4-8] The overall maternal mortality rate in ICU varies from 0 - 38%. Local studies have reported a mortality rate in the range of 21 - 38%.[4-6] In view of the aforementioned, a retrospective study was undertaken at Dr George Mukhari Academic Hospital (DGMAH), Ga-Rankuwa,

SA. DGMAH is a tertiary hospital that receives 32% of obstetric referrals from neighbouring provinces. The aim was to determine the spectrum of diseases requiring ICU admission in obstetric patients, condition on discharge, maternal mortality, and the cause of maternal death.

Methods

The study was conducted at DGMAH, a 22-bed multidisciplinary ICU academic centre in Ga-Rankuwa, SA. The hospital is affiliated to Sefako Makgatho Health Sciences University. The ICU beds at DGMAH serve all surgical disciplines, internal medicine, obstetrics and gynaecology, as well as the paediatrics wards. An average of 720 patients are admitted to this ICU per annum; obstetrics patients represent 11.6% of all ICU admissions, which accounts for 0.92% of all deliveries. Thirty-two percent of obstetrics patients are referrals from nearby provinces like North West, Limpopo and Mpumalanga. A retrospective study of all pregnant and postpartum patients admitted to this multidisciplinary ICU over a 4-year period, from 1 January 2008 to 31 December 2011, was conducted. The study was approved by the Medunsa Research and Ethics Committee (MREC) of the university (ref. no. MREC/ M/31/2013:IR). Data were collected from the acuity book, which is used to record all daily admissions to ICU. Further data were extracted from the standard ICU flow chart, TPH254 (81/524737), as well as from the medical records section of the hospital. The data included basic

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demographic data, obstetric and medical history (weeks of gestation, mode of delivery, pre-existing medical conditions), diagnosis, length of stay in the ICU, length of stay on mechanical ventilation, haemodynamic stability, ICU outcome, condition on discharge, and cause of death. The reasons for ICU admission were sorted in descending order according to the frequency of occurrence. For each reason, a 95% confidence interval (CI) was calculated for the percentage of occurrence. Data analysis was performed usig Statistical Analysis System release 9.2 (SAS Institute Inc., USA).

Table 3. Causes of maternal mortality (N=19) Cause Intracerebral bleed Cardiogenic shock DIC Hypovolaemic shock Respiratory failure Hepatorenal failure

n (%) 7(36.8) 5 (26.3) 3 (15.8) 2 (10.5) 1 (5.3) 1 (5.3)

*DIC = disseminated intravascular coagulation.

Results

A total of 248 obstetric patients were admitted during the study period, of whom 210 had complete medical records. Fifteen percent (n=38) of the patients were excluded from the study due to incomplete records. The demographic characteristics of the participants are shown in Table 1. The mean age was 28.15 (standard deviation (SD) 6.97) years. Twelve (5.7%) patients were admitted at a mean (SD) gestational age of 25.33 (6.56), 94.2% (n=198) were postpartum, and 88.6% (n=186) were postcaesarean section. Pre-existing cardiac disease 44.3% (n=93/210), eclampsiapreeclampsia 20% (n=42), obstetric haemorrhage 16.2% (n=34) and pulmonary oedema 6.2% (n=13) were the most common causes of admission. Of the 93 patients who had pre-existing cardiac disease, mixed mitral valve disease accounted for 52% (n=48). The remaining 13.3% (n=28) of patients were admitted because of extrauterine pregnancy, a ruptured uterus, puerperal sepsis, pulmonary disease, anaesthetic complications, and kyphoscoliosis (Table 2). Eighteen (8.6%) women had an associated medical illness, other than cardiac, prior to pregnancy, with HIV infection being the most common (7.1%; n=15), followed by epilepsy. Sixty-one percent (n=128) of patients received ventilatory support, for a median (range) period of 1 (1 - 13) day. The median length of ICU stay was 24 hours (range 1 - 17 days). Eighty-seven percent (n=183) of the patients were haemodynamically stable. Maternal mortality was 9% (n=19). The major cause of death was intracerebral haemorrhage (36.8%; n=7), followed by cardiogenic shock

Table 1. Patient characteristics (N=210) Age (years), mean (SD) Mode of delivery, n (%) Normal vaginal delivery Caesarean section Time of admission, n (%) Antepartum Postpartum

28.15 (6.97) 24 (11.4) 186 (88.6) 12 (5.7) 198 (94.2)

Table 2. Diagnosis on admission (N=210) Diagnosis Cardiac Eclampsia and pre-eclampsia Obstetric haemorrhage Pulmonary oedema Pulmonary disease Kyphoscoliosis Ruptured uterus Extrauterine pregnancy Anaesthetic complications Puerperal sepsis

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n (%) 93 (44.3) 42 (20.0) 34 (16.2) 13 (6.2) 9 (4.3) 6 (2.9) 5 (2.4) 4 (1.9) 3 (1.4) 1 (0.5)

Table 4. Discharge condition (N=191) Condition Normal Hypoxic ischaemic brain injury Left ventricular hypertrophy Pseudobulbar palsy Renal failure

n (%) 182 (95.3) 5 (2.7) 2 (1.0) 1 (0.5) 1 (0.5)

(26.3%; n=5) (Table 3). A total of 191 (90.6%) patients were discharged, of whom 182 (95.3%) were in a stable condition. Five patients suffered hypoxic ischaemic brain injury, two had left ventricular hypertrophy, one developed pseudobulbar palsy, and the other suffered renal failure. Hypoxia developed as a result of difficult intubation in the operating room (n=2) and convulsions in eclampsia (n=3). Hypoxic ischaemic brain injury had been confirmed by computed tomography scans. All five patients were discharged with a tracheostomy mask. The patient who developed renal failure had to be dialysed (Table 4).

Discussion

Cardiac disease in pregnancy was the most common reason for admission in our patients, with mixed mitral disease as the predominant lesion, followed by peripartum cardiomyopathy. This is in agreement with the findings of Trikha and Singh.[8] In a study conducted in Belgium, it was found that pre-existing and acquired cardiopathies are the main reason for admission to an ICU in a developed country, and have surpassed hypertensive disorders and haemorrhage.[9] The second most common reason for admission was eclampsia and preeclampsia (20.0%), followed by obstetric haemorrhage (16.2%). Afessa et al.[10] investigated the clinical course and outcome of critically ill obstetric patients treated in an ICU. They reported that obstetric patients with pre-existing medical problems were more likely to require intensive care support than those without pre-existing medical conditions. We had 48.6% patients with cardiac and pulmonary problems requiring ICU support. A study undertaken at Tygerberg Hospital, Cape Town, SA, demonstrated a significant reduction in maternal deaths when patients were managed in an obstetric critical care unit.[11] Tygerberg Hospital is one of only two hospitals in SA that have a dedicated obstetric ICU in the public health sector. The first unit was opened at Groote Schuur Hospital in Cape Town, SA, with reported benefits in terms of continuity of care provided before and after delivery, as well as intensive observation that allowed for prevention or early recognition and treatment of complications.[12] Our study had 198 (94.3%) patients admitted postpartum, 88.6% of them post caesarean section. In a 5-year review of obstetrics patients requiring critical care, 66% of the women admitted were postpartum. This is likely related to the significant haemodynamic

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changes which occur in the postpartum period, including 65% increase in cardiac output, acute blood loss at delivery and a decrease in plasma protein oncotic pressure, which may exacerbate symptoms in patients with underlying cardiovascular or pulmonary dysfunction.[13] One hundred and eighty-three (87.1%) of our patients were, however, haemodynamically stable. Most of the patients were referred to ICU owing to a high risk for cardiovascular compromise due to pre-existing cardiac lesions. Kilpatrick et al.[13] reported on a relatively small number of obstetric patients that required ICU admission. Pre-eclampsia was the single most common precipitating factor, accounting for 33% of obstetric diagnoses. They concluded that if expertise with insertion and monitoring of central venous and arterial lines were available in the labour and delivery units, relatively few women would require transfer to the ICU.[13] Preeclampsia and eclampsia accounted for 20% of admissions in our study. In a study by Karnad et al.,[14] obstetric disorders accounted for 80% of their ICU admissions. Pulmonary oedema owing to valvular heart disease was one of the most common medical disorders. In our study, 6.2% of the patients with pre-eclampsia also had pulmonary oedema. Karnad et al.[14] reported a mortality rate of 21.6%, attributed to inadequate utilisation of prenatal services as well as a delay of more than 24 hours between the onset of acute illness and ICU admission. In this study, 61% (n=128) of patients received ventilatory support for a maximum of 13 days and a median of 1 day. Other studies have reported ventilatory support of their patients in the range of 18.6% to 67%.[1,3,10,15-18] The median length of ICU stay in this study was 24 hours, up to a maximum of 17 days. The patient who was hospitalised for 17 days was eventually discharged with a tracheostomy mask. She had suffered hypoxic brain injury following an eclamptic convulsion. Between 2011 and 2013, the five most common causes of maternal deaths in SA were non-pregnancy-related infections (mainly HIV infection), obstetric haemorrhage, complications of hypertension in pregnancy, medical and surgical disorders, and pregnancy-related sepsis. There has been a 25% reduction in deaths due to HIV infections, most likely due to an efficient screening and treatment programme.[19] A study by Chweneyagae et al.[7] found HIV infection to be the most important condition contributing to maternal death in SA. Our maternal mortality was 9% over a period of 4 years. Seven (36.8%) patients died due to an intracerebral bleed in eclampsia. This may indicate failure to lower the blood pressure timeously and judiciously, as well as a lack of obstetric emergency training skills. Preeclampsia-eclampsia also accounted for the highest number of deaths in a study conducted in a tertiary hospital in the Limpopo Province, SA.[4] In order to reduce maternal mortality, Moran et al.[20] concluded that interventions to scale up emergency obstetrics skills training must happen alongside interventions to strengthen other components of the health system. This involves training healthcare workers in essential steps in the management of obstetric emergencies (ESMOE), team training using emergency obstetric simulation training (ESOT) and having appropriate policies and standard operating procedures in place. Ntuli et al.[4] reported a mortality rate of 34.8%, which was higher than the mortality rate observed in our study, and that reported at King Edward VIII Hospital in Durban, SA,[5] but similar to the findings at Johannesburg Hospital, SA.[6] They[4] attributed this to lack of proper antenatal care, limited specialist obstetric and critical care specialist support, and poor transport. Our mortality rate was low compared with other SA studies,[4-6] but relatively high when compared with developed countries. Australia reported a 0% mortality over a period of 8 years.[21]

Conclusion

Cardiac disease in pregnancy was the most common diagnosis in patients admitted to our ICU, followed by eclampsia and preeclampsia. Most of the patients (87.1%) were haemodynamically stable and needed minimal intervention, as confirmed by their short periods of stay in ICU. Even though the mortality rate in our institution was higher than that observed in developed countries, it was lower than rates reported in other SA studies. This study has found that many of the patients were admitted to ICU for monitoring purposes only and did not require ICU level of care, whereas other SA units admitted patients with higher acuity of illness. It is therefore recommended that proper screening of ICU referrals be conducted before admission, with a view to sparing ICU beds for the most deserving patients. Healthcare workers involved in obstetrics should also undergo training in ESMOE. Acknowledgements. The author would like to thank Prof. HS Schoeman for statistical analysis and Prof. CT Sehoole for review of different drafts of this article. Author contributions. MM conceptualised the study and wrote the manuscript. Funding. None. Conflict of interest. None. 1. Collop NA, Sahn SA. Critical illness in pregnancy. An analysis of 20 patients admitted to a medical intensive care unit. Chest 1993;103(5):1548-1552. https://doi.org/10.1378/chest.103.5.1548 2. Soubra SH, Guntupalli KK. Critical illness in pregnancy: An overview. Crit Care Med 2005;33(10):S248-S255. https://doi.org/10.1097/01.ccm.0000183159.31378.6a 3. Vasquez DN, Estenssoro E, Canales HS, et al. Clinical characteristics and outcomes of obstetric patients requiring ICU admission. Chest 2007;131:718-724. https://doi.org/10.1378/chest.06-2388 4. Ntuli TS, Ogunbanjo G, Nesengani S, Maboya E, Gibango M. Obstetric intensive care admissions at a tertiary hospital in Limpopo Province, South Africa. S Afr J Crit Care 2015;31(1):8-10. https:// doi.org/10.7196/SAJCC.164 5. Platteau P, Engelhardt T, Moodley J, Muckart JJ. Obstetric and gynaecological patients in an intensive care unit: A 1 year review. Trop Doctor 1997;27(4):202-206. https://doi. org/10.1177/004947559702700406 6. Taylor R, Richards GA. Critically ill obstetric and gynaecological patients in the intensive care unit. S Afr Med J 2000;90(11):1140-1144. 7. Chweneyagae D, Delis-Jarrosay N, Farina Z, et al. The impact of HIV infection on maternal deaths in South Africa. S Afr J Obstet Gynaecol 2012;18(3):70-76. https://doi.org/10.7196/sajog.581 8. Trikha A, Singh PM. The critically ill obstetric patient – recent concepts. Indian J Anaesth 201;54(5):421-427. https://doi.org/10.4103/0019-5049.71041 9. De Greve M, Van Mieghem T, Van Den Berghe G, Hanssens M. Obstetric admissions to the intensive care unit in a tertiary hospital. Gynecol Obstet Invest 2016;81(14):315-320. https://doi. org/10.1159/000431224 10. Afessa B, Green B, Delke I, Koch K. Systemic inflammatory response syndrome, organ failure, and outcome in critically ill obstetric patients treated in an ICU. Chest 2001;120(4):1271-1277. https:// doi.org/10.1378/chest.120.4.1271 11. Langenegger E. The impact of a new South African obstetric critical care unit at Tygerberg Hospital: A comparison of patient outcomes before and after. Int J Gynecol Obstet 2012;119(Suppl 3):S396-S397. https://doi.org/10.1016/s0020-7292(12)60814-5 12. Johanson R, Anthony J. Obstetric intensive care at Groote Schuur Hospital, Cape Town. J Obstet and Gynaecol 1995;15(3):174. https://doi.org/10.3109/01443619509015490 13. Kilpatrick SJ, Matthay MA. Obstetric patients requiring critical care; a five year review. Chest 1992;101(5):1407-1412. https://doi.org/10.1378/chest.101.5.1407 14. Karnad DP, Lapsia V, Krishnan A, Salvi VS. Prognostic factors in obstetric patients admitted to an Indian intensive care unit. Crit Care Med 2004;32(6):1294-1299. https://doi.org/10.1097/01. ccm.0000128549.72276.00 15. Zwart JJ, Dupuis JRO, Richters A, Ory F, van Roosmalen J. Obstetric intensive care unit admission: A 2-year nationwide population-based cohort study. Intensive Care Med 2001;36(2):256-263. https://doi.org/10.1007/s00134-009-1707-x 16. Leung NYW, Lau AC, Chan KK, Yan WW. Clinical characteristics and outcomes of obstetric patients admitted to intensive care unit: A 10-year retrospective review. Hong Kong Med J 2010;16(1):18-25. 17. Lataifeh I, Amarin Z, Zayed F, Al-Mehaisen L, Alchalab H, Khader Y. Indications and outcome for obstetric patients’ admission to intensive care unit: A 7-year review. J Obstet Gynaecol 2010;30(4):378-382. http://dx.doi.org/10.3109/01443611003646298 18. Gupta S, Naithani U, Doshi V, Bhargava V, Vijay BS. Obstetric critical care: A prospective analysis of clinical characteristics, predictability, and fetomaternal outcome in a new dedicated obstetric intensive care unit. Indian J Anaesth 2011;55(2):146-153. http://dx.doi.org/10.4103/00195049.79895 19. National Committee for Confidential Enquiry into Maternal Deaths. Saving Mothers 2011-2013: Sixth report on the confidential enquiries into maternal deaths in South Africa - short report. http://www.doh.gov.za (accessed 29 November 2016). 20. Moran NF, Naidoo M, Moodley J. Reducing maternal mortality on a countrywide scale: The role of emergency obstetric training. Best Pract Res Clin Obstet Gynaecol 2015;29(8):1102-1118. [https://dx.doi.org/10.1016/j.bpobgyn.2015.08.002] 21. Siram S, Robertson MS. Critically ill obstetric patients in Australia: A retrospective audit of 8 years’ experience in a tertiary intensive care unit. Crit Care Resusc 2008;10(2):120-124.

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Correlation between different methods of intraabdominal pressure monitoring in varying intraabdominal hypertension models R D Wise,1 MB ChB, FCA, Cert Crit Care, MMed, Dip Obst, Dip PEC; R N Rodseth,1 MB ChB, FCA, Cert Crit Care, MMed, MSc, PhD; L Correa-Martin,2 DVM, PhD; F M Sanchez Margallo,2 DVM, PhD; P Becker,3 PhD; G Castellanos,4 MD, PhD; M L N G Malbrain,5 MD, PhD 1

Pietermaritzburg Metropolitan Department of Anaesthetics, Critical Care and Pain Management, Pietermaritzburg, South Africa, and Discipline of Anaesthesiology and Critical Care, School of Clinical Medicine, University of KwaZulu-Natal, Durban, South Africa 2 Laparoscopy and Anaesthesiology Research Department, Jesús Usón Minimally Invasive Surgery Centre, Cacères, Spain 3 Department of Statistics, University of Pretoria, South Africa 4 Department of Surgery, Virgen de la Arrixaca University Hospital, Murcia, Spain 5 Medical and Surgical ICU and High Care Burn Unit, Ziekenhuis Netwerk Antwerpen, Antwerpen, Belgium Corresponding author: R D Wise (robertwise@webafrica.org.za)

Background. Advances in intra-abdominal pressure (IAP) measurement have enabled better monitoring and physiological manipulation of patients with intra-abdominal hypertension or abdominal compartment syndrome. This study aimed to determine the correlation between transvesical (TV), transgastric (TG) and direct transperitoneal (TP) IAP monitoring at different IAPs in porcine models. Objectives. To assess the statistical agreement between TV, TG and TP pressure monitoring in a pneumoperitoneum and an intestinal obstruction intra-abdominal hypertension model at different IAPs. Methods. Fifty-nine pigs were divided into six groups: a control group (Cr; n=5), three pneumoperitoneum groups at pressures of 20 mmHg, 30 mmHg, and 40 mmHg (Pn20, Pn30, Pn40; n=40), and two intestinal-occlusion groups at pressures of 20 mmHg and 30 mmHg (Oc20, Oc30; n=14). IAP was simultaneously measured in each pig using the three methods at different times. The control group did not have any intervention to increase the IAP. Intra-class correlation was used to assess agreement between the methods. Results. At pressures >20 mmHg, all three methods showed good correlation with each other (Pn20=0.87; Pn30=0.96; Pn40=0.88; Oc20=0.69; Oc30=0.86). Correlation between TP and TG (Cr=0.0; Pn20=0.85; Pn30=0.94; Pn40=0.90; Oc20=0.78; Oc30=0.78); TP and TV (Cr=0.0; Pn20=0.83; Pn30=0.95; Pn40=0.86; Oc20=0.59; Oc30=0.88); and importantly between TV and TG (Cr=0.0; Pn20=0.95; Pn30=0.98; Pn40=0.88; Oc20=0.69; Oc30=0.91) was good. Conclusion. All three measurement methods showed good correlation at pressures >20 mmHg and were unaffected by the type of IAP model. These results suggest that either transvesical or transgastric pressure measurements can be used for IAP measurement when TP pressures are >20 mmHg. S Afr J Crit Care 2017;33(1):15-18. DOI:10.7196/SAJCC.2017.v33i1.327

Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) have been highlighted as major causes of morbidity and mortality in intensive care unit (ICU) patients.[1,2] Awareness of this clinical problem has improved through the publication of consensus documents, guidelines and the work of the World Society of Abdominal Compartment Society (WSACS, www.wsacs.org).[2] Recently, the introduction of the polycompartment syndrome concept, where increased compartment pressures in one region impact negatively on other regions, has been highlighted.[3] Advances in IAP measurement have enabled better monitoring and physiological manipulation of patients with IAH or ACS. Accurately measured IAP (IAP) is central to the management of patients with IAH and ACS. IAP can be measured through direct intraperitoneal measurement, or indirect measures using a hollow viscus such as the bladder, stomach, rectum or uterus. Traditionally, the gold standard for measuring IAP has been via a Foley catheter in the bladder.[2] However, circumstances may arise where this method is not viable and alternative methods must be used.

This study aimed to compare the statistical agreement between transvesical (TV), transgastric (TG) and direct transperitoneal (TP) IAP monitoring. Measurements were taken in two different porcine IAH models (i.e. a pneumoperitoneum model and an intestinal obstruction mode) at different IAPs.

Methods

This study was carried out in strict accordance with the recommendations in the Royal Decree 1201/2005 of 10 October 2005 on the protection of animals used for experimentation and other scientific purposes. All experimental protocols were approved by the Committee on the Ethics of Animal Experiments of Minimally Invasive Surgery Centre Jesús Usón, and by the Council of Agriculture and Rural Development of the Regional Government of Extremadura (ref. no. ES100370001499). Fifty-nine white female pigs (24.1 kg; range 17.3 - 33 kg) were fasted for 24 hours before receiving premedication with intramuscular atropine (0.04 mg/kg), diazepam (0.4 mg/kg) and ketamine (10 mg/ kg). Induction and anaesthesia were the same as described previously

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1.2 1.0

Correlation

by Correa-Martin et al.[4] Briefly, the animals were pre-oxygenated with a factional inspired oxygen of 1.0 (fresh-gas flow of 3 - 5 L/min), before administration of propofol 1% (3 mg/kg), after which their tracheas were intubated and their lungs mechanically ventilated. Anaesthesia was maintained with isoflurane (minimum alveolar concentration of 1.25) and 0.9% sodium chloride intravenous fluids (2 mL/kg/h). Intraoperative analgesia was provided with an infusion of remifentanil (0.3 Îźg/kg/min). On completion of the study, the animals were euthanised following the guidelines of the American Veterinary Medical Association Panel on Euthanasia[5] using potassium chloride (KCl, 1 - 2 mmol/kg).[4]

Study design

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TP v. TV

0.4

TV v. TG

Fig. 1. Comparison of intra-class correlation between three modalities (transperitoneal, transgastric, transvesical) used for the measurement of IAP in two different porcine models. (IAP = intra-abdominal pressure; TP = transperitoneal; TG = transgastric; TV = transvesical; Pn20 = pneumoperitoneum model, pressure 20 mmHg; Pn30 = pneumoperitoneum model, pressure 30 mmHg; Pn40 = pneumoperitoneum model, pressure 40 mmHg; Oc20 = intestinal obstruction model, pressure 20 mmHg; Oc30 = intestinal obstruction model, pressure 30 mmHg.)

Oc30

Correlation

Oc20 Pn40

TP v. TV TP v. TG

Pn30

TP v. TG v. TV

Pn20 Control 0

Statistical analysis

Intra-class correlation was used to assess agreement between the three pressure measurement methods. This inferential method was selected because the quantitative measurements of IAP were made on grouped subjects. It was used to identify how closely the groups resembled each other. Correlation could therefore be investigated based on the varying pressure models. In addition, the subjects had a fixed degree of relatedness. As the test subjects were organised into related groups, we used intraclass correlation to assess the degree of agreement between the three pressure-measurement methods. This allowed the determination of the correlation between the three groups. TV and TG measurements were compared with the TP measurements that were considered the most accurate. Analysis was performed using STATA 13 (Stata Corp., USA).[7]

TP v. TG

0.2

Data collection

IAP was measured simultaneously at 30-minute intervals in each pig using the 3 methods (i.e. TP, TV and TG). The direct TP technique, a direct measure of IAP, was considered the gold standard. TP measurements were achieved using a Jackson-Pratt catheter inserted laparoscopically into the abdominal cavity and placed on the liver.[4] TV measurements were achieved using a manual manometer system with a Foley catheter in the bladder and urine drainage bag. TG measurements were made through a gastric balloon catheter (placed endoscopically) connected to an electronic pressure transducer (Spiegelberg Pharma, Germany).[6] The TG measurements were graphically recorded in real time.

TP v. TG v. TV

0.6

Co nt ro l Pn 20 Pn 30 Pn 40 Oc 20 Oc 30

The pigs were divided into six groups: a single control group (Cr; n=5), three pneumoperitoneum groups with IAP of 20 mmHg, 30 mmHg, and 40 mmHg (Pn20, Pn30, Pn40; n=40) and two mechanical intestinal-occlusion groups with IAP of 20 mmHg and 30 mmHg (Oc20, Oc30; n=14). Correa-Martin et al.[4] have previously described the pneumoperitoneum and mechanical obstruction models. The pneumoperitoneum model was achieved using an insufflation technique with laparoscopy, while the mechanical obstruction model was achieved by placing a laparoscopic suture at the ileocaecal valve, with 0.9% saline infused into the bowel. The subjects were then maintained at the required IAP for up to 5 hours. IAP was measured simultaneously using the three different methods under investigation. Multiple physiological parameters, together with blood samples, were measured every 30 minutes. Measurements were initiated (parameter T1) once IAP stabilised.[4] The control group received the same anaesthetic as the experimental groups, with the same 30-minute physiological measurements as the experimental groups. The control group did not have any intervention to increase the IAP.

0.8

0.5

1.0

1.5

Fig. 2. Comparison of intra-class correlation between the different IAP measurement techniques in the different models of ACS. (ACS = abdominal compartment syndrome; TP = transperitoneal; TG = transgastric; TV = transvesical; Pn20 = pneumoperitoneum model, pressure 20 mmHg; Pn30 = pneumoperitoneum model, pressure 30 mmHg Pn40 = pneumoperitoneum model, pressure 40 mmHg; Oc20 = intestinal obstruction model, pressure 20 mmHg; Oc30 = intestinal obstruction model, pressure 30mmHg.)

Results

In the first comparison among TP v. TG v. TV v. control, there were 2 087 observations. When comparing TP against TG, there were 1 392

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observations. Likewise, when comparing TV against TG there were 1 392 comparisons. The first comparison between all three methods of pressure measurement (TP v. TG v. TV) showed very poor correlation in the control group (variance fraction = 0.0). Therefore the relationship between the variables measured was weak, with variability in the changes in IAP between the groups. Comparison amongst the other groups showed good correlation (Pn20=0.87; Pn30=0.96; Pn40=0.88; Oc20=0.69; Oc30=0.86). A comparison between TP and TG had similar results with good correlation (Cr=0.0; Pn20=0.85; Pn30=0.94; Pn40=0.90; Oc20=0.78; Oc30=0.78). The analysis between TP and TV also showed good correlation (Cr=0.0; Pn20=0.83; Pn30=0.95; Pn40=0.86; Oc20=0.59; Oc30=0.88). Good correlation was shown between the TV and TG models (Cr=0.0; Pn20=0.95; Pn30=0.98; Pn40=0.88; Oc20=0.69; Oc30=0.91). All models correlated better at higher pressures.

Discussion

IAH and ACS negatively impact morbidity and mortality in ICU patients.[8-10] The 2013 updated WSACS guidelines recommend IAP monitoring when there is any known risk factor for the development of IAH/ACS in critically ill or injured patients.[2] The findings of Cheatham et al.[1] support the routine monitoring of IAP, as this allows the implementation of early management protocols, thereby improving patient survival. Finding a simple, reliable and reproducible measuring technique for the measurement of IAP is important, as it is well recognised that clinical examination is not reliable.[11,12] Repeated or continuous IAP pressure monitoring via the trans-bladder route is recommended by the WSACS, and is probably still the most commonly used technique.[13-15] This study found good correlation between TP, TG and TV methods at IAPs >20 mmHg. This supports the hypothesis that IAPs can be accurately measured for intermittent readings via any of these routes. TV pressure monitoring is ideal for most patients at risk of developing IAH/ACS because a urinary catheter is likely to have been placed. The bladderâ&#x20AC;&#x2122;s anatomical position, compliance and relatively low wall tension when drained or filled with a small volume (25 mL) of room or body temperature saline makes it suitable for indirect pressure measurements.[2,16,17] Like all available techniques, none are without limitations, and the stimulation of detrusor contraction should always be considered, with a 60-second pause after instillation of saline before reading the pressure. The results from the TV and TP comparisons confirm this route as reliable when compared with direct IAP measurements. However, it may not always be possible to use the TV route. Alternative techniques to TV pressure measurements should also be simple and cost-effective. These different methods are simply classified into direct and indirect techniques.[16] Alternative invasive and noninvasive techniques have been explored, with the TV route maintaining popularity.[18,19] Invasive (direct) measurement usually only occurs after placement of an intraperitoneal catheter, such as in continuous peritoneal dialysis, continuous paracentesis or experimentally in laboratory research.[16] Other routes that have been considered include both rectal and uterine, but these costly and often complicated methods have obvious practical limitations in critically ill patients. Inferior vena cava pressure is another direct technique, but introduces additional risks of bloodstream infections, bleeding and additional costs and risks of needlestick injuries.[15] Microchip transducer-tipped catheters, although able

to provide alternative solutions to continuous IAP monitoring, are expensive and are not frequently used.[15] The TG route for IAP monitoring has also been investigated. Its appeal is similar to that of the bladder â&#x20AC;&#x201C; most patients at risk will already have access to this hollow organ via a nasogastric tube, placement is easy, it is relatively inexpensive and there is no needle-stick risk. However, previous studies examining the TG route have been small, with limited numbers of paired readings being analysed.[6,20-22] Gastric tonometry balloons and regular nasogastric tubes have also been used. Disadvantages compared with the bladder include the need to remove air before instillation of fluid, contractility of the muscular stomach wall, an exit through the pylorus, a dependence on the patient achieving enteral tolerance, and difficulty with continuous monitoring. However, if this route correlates well with TV readings, it may provide a very useful method for intermittent IAP monitoring when bladder monitoring is not possible. Such a scenario may occur during surgical procedures. Predicting the likelihood of a polycompartment syndrome using IAPs provides useful additional information when deciding on abdominal closure. Correlation between TG and TV measurements was good at pressures >20 mmHg. This supports the hypothesis that IAP can be accurately measured for intermittent readings via the TG route. Clinically applicable routes (TV and TG) can therefore be used for intermittent intraabdominal measurements. Despite limitations, both techniques may be useful in different settings. Continuous IAP measurements are probably easiest using the TV technique, whereas intermittent measurements can be achieved using either TV or TG methods. In this study, the intra-abdominal hypertension model did not influence correlation. Future studies should investigate intraoperative IAP limits (measured via the nasogastric tube) when closing the abdomen following surgery to provide clinical guidance for surgeons and anaesthesiologists when faced with this clinical dilemma.

Limitations

Despite being a large-animal study, limitations include the small number of subjects studied and the limited duration of measurements: the design of the study was not tested beyond 5 hours of initiation of IAH. Furthermore, a gastric balloon tonometry device was used and not a standard nasogastric tube, but it seems unlikely that this would make a difference to pressure readings.

Conclusions

Correlation between all three methods of IAP measurement (TP, TG and TV) was good at pressures >20 mmHg. However, correlation was poor at low IAPs. These findings were independent of the IAP model used. TG and TV techniques both have utility in the clinical setting, with TG pressure monitoring offering an attractive alternative for intermittent pressure monitoring when the TV route is not possible. The TG route may be most useful in patients undergoing surgery where the TV route is not accessible. Acknowledgements. None. Conflict of interest. MLNG Malbrain is the founding president and member of the executive committee of the WSACS and current treasurer. He is a member of the medical advisory board of Pulsion Medical Systems (Maquet Getinge Group) and consults for ConvaTec, Acelity, Spiegelberg and Holtech Medical. He is a member of the executive committee of the International Fluid Academy (IFA). The IFA is integrated within the not-for-profit charitable organisation iMERiT (International Medical Education and Research Initiative) under Belgian Law. The IFA website (http://www.fluidacademy.

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org) is now an official SMACC (Social Media and Critical Care)-affiliated site and its content is based on the philosophy of FOAM (Free Open Access Medical Education – #FOAMed). All other authors declare that they have no financial or personal relationships that may have inappropriately influenced them in writing this paper. Author contributions. RW, RNR, GC, MLNGM contributed to analytical design and manuscript drafting and review. LC-M, FMSM, GC contributed to experimental design, data collection, and manuscript review. PB contributed to analytical design, statistical analysis and the manuscript. Funding. This work was supported by one grant from Extremadura Regional Government through the Plan Regional de Investigación de Extremadura (PRI09A161 to Minimally Invasive Surgery Center Jesús Usón). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 1. Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Crit Care Med 2010;38(7):402-407. http:// doi.org/10.1097/CCM.0b013e3181b9e9b1 2. Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: Updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013;39(7):11901206. http://doi.org/10.1007/s00134-013-2906-z 3. Malbrain ML, Roberts DJ, Sugrue M, et al. The polycompartment syndrome: A concise state-of-theart review. Anaesthesiol Intensive Ther 2014;46(5):433-450. http://doi.org/10.5603/AIT.2014.0064 4. Correa-Martin L, Parraga E, Sanchez-Margallo FM, et al. Mechanical intestinal obstruction in a porcine model: Effects of intra-abdominal hypertension. A preliminary study. PloS One 2016;11(7):e0148058. http://doi.org/10.1371/journal.pone.0148058 5. American Veterinary Medical Association: Guidelines for the Euthanasia of Animals. 2013 edition. Schaumburg, United States: American Veterinary Medical Association. 6. Correa-Martin L, Castellanos G, Garcia M, Sanchez-Margallo FM. Renal consequences of intraabdominal hypertension in a porcine model. Search for the choice indirect technique for intraabdominal pressure measurement. Actas Urol Esp 2013;37(5):273-279. http://doi.org/10.1016/j. acuro.2012.06.001

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7. StataCorp: Stata Statistical Software: Release 13. College Station, TX: StataCorp LP. 8. Malbrain ML, Chiumello D, Pelosi P, et al. Prevalence of intra-abdominal hypertension in critically ill patients: A multicentre epidemiological study. Intensive Care Med 2004;30(5):822829. http://doi.org/10.1007/s00134-004-2169-9 9. Zhang HY, Liu D, Tang H, Sun SJ, et al. Prevalence and diagnosis rate of intra-abdominal hypertension in critically ill adult patients: A single-center cross-sectional study. Chin J Traumatol 2015;18(6):352-356. https://doi.org/10.1016/j.cjtee.2015.11.015 10. Malbrain ML, Chiumello D, Pelosi P, et al. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: A multiple-center epidemiological study. Crit Care Med 2005;33(2):315-322. http://doi.org/10.1097/01.CCM.0000153408.09806.1B 11. Kirkpatrick AW, Brenneman FD, McLean RF, Rapanos T, Boulanger BR. Is clinical examination an accurate indicator of raised IAP in critically injured patients? Can J Surg 2000;43:207-211. 12. Castillo M, Lis RJ, Ulrich H, Rivera G, Hanf C, Kvetan V. Clinical estimate compared to intraabdominal pressure measurement. Crit Care Med 1998;26((Suppl 1)):78A. 13. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from the International Conference of Experts on intra-abdominal hypertension and abdominal compartment syndrome. II. Recommendations. Intensive Care Med 2007;33(6):951-962. http://doi.org/10.1007/s00134-007-0592-4 14. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International Conference of Experts on intra-abdominal hypertension and abdominal compartment syndrome. I. Definitions. Intensive Care Med 2006;32(11):1722-1732. http://doi.org/10.1007/s00134-006-0349-5 15. Malbrain ML. Different techniques to measure intra-abdominal pressure (IAP): Time for a critical re-appraisal. Intensive Care Med 2004;30(7):357-371. http://doi.org/10.1007/s00134-003-2107-2 16. De Keulenaer BL, Regli A, Malbrain ML. Intra-abdominal measurement technique: Is there anything new? Am Surg 2011;77(July Suppl):S17-S22. 17. De Waele JJ, De Laet I, Malbrain ML. Rational intra-abdominal pressure monitoring: How to do it? Acta Clin Belg 2007;62(Supp1:16-25). http://doi.org/10.1179/acb.2007.62.s1.004 18. Van Ramshorst GH, Salih M, Hop WC, et al. Noninvasive assessment of intra-abdominal pressure by measurement of abdominal wall tension. J Surg Res 2011;171(7):240-244. http://doi. org/10.1016/j.jss.2010.02.007 19. Kim KS, Seo JH, Kang JU, Song CG. Implementation of a multi-functional ambulatory urodynamics monitoring system based on newly devised abdominal pressure measurement. J Med Syst 2010;34(6):1011-1021. http://doi.org/10.1007/s10916-009-9318-1 20. Debaveye Y, Bertieaux S, Malbrain M. Simultaneous measurement of intra-abdominal pressure and regional CO2 via a gastric tonometer. Intensive Care Med 2000;26(Suppl3):S324. 21. Sugrue M, Buist MD, Lee A, Sanchez DJ, Hillman KM. Intra-abdominal pressure measurement using a modified nasogastric tube: Description and validation of a new technique. Intensive Care Med 1994;20:588-590. 22. Collee GG, Lomax DM, Ferguson C, Hanson GC. Bedside measurement of intra-abdominal pressure (IAP) via an indwelling naso-gastric tube: Clinical validation of the technique. Intensive Care Med 1993;19:478-480.

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Lived experiences of Rwandan ICU nurses caring for patients with a do-not-resuscitate order E Nankundwa,1 RN, M Critical Care & Trauma Nursing; P Brysiewicz,2 PhD 1 2

School of Nursing and Midwifery, School of Medicine and Health Sciences, University of Rwanda, Kigali, Rwanda School of Nursing and Public Health, University of KwaZulu-Natal, Durban, South Africa

Corresponding author: P Brysiewicz (brysiewiczp@ukzn.ac.za)

Background. Do not resuscitate (DNR) is the policy and practice of deliberately not attempting to resuscitate a person whose heart has stopped beating. Research on nursing care for patients designated with DNR orders has been conducted since the late 1980s; however, no study appears to have been carried out in the Rwandan setting. Purpose. The purpose of this study was to explore the lived experiences of nurses caring for a patient with a DNR order in an intensive care unit (ICU) in Kigali, Rwanda, in order to suggest nursing recommendations. Methods. Using a phenomenological approach, two semi-structured interviews were conducted with each participant to explore their lived experiences of caring for patients with DNR orders. The sample comprised six nurses from an ICU in a large tertiary-level hospital in Kigali, Rwanda. Results. The data were organised into categories based on a review of the data from the interviews of the six participants. The categories were: feeling emotional distress; barrier to optimal care; and not part of decision-making. Conclusion. DNR orders are a fairly new concept in Rwanda and the practice of DNR orders in ICU is very demanding for the staff, especially the ICU nurses. Additional education about DNR orders as well as policies to guide its implementation could assist ICU nurses in their difficult work. S Afr J Crit Care 2017;33(1):19-22. DOI:10.7196/SAJCC.2017.v33i1.281

Do not resuscitate (DNR) is the policy and practice of deliberately not attempting to revive a person whose heart has stopped beating, i.e. to withhold resuscitation.[1] The DNR decision does not signify abandonment of the patient, but is rather part of the actions that favour the patientâ&#x20AC;&#x2122;s wellbeing in order to make a peaceful death possible.[2] DNR can in fact play an active role in patient care although its interpretation can modify the therapeutic approaches to patient care. This may lead to inadequate treatment,[3] and may cause the healthcare team to do less than their best for the patient, which may lead to abandonment of the patient.[4] End-of-life decisions are complex for any healthcare worker, especially for the intensive care unit (ICU) nurse, as they have to shift the treatment from aggressive life-saving therapy to end-of-life care. [5] It has been shown that many doctors and nurses feel unprepared to facilitate end-of-life decision-making and are unclear regarding some of the legal aspects of the DNR order.[6] The decision to not resuscitate is difficult to reach, therefore a DNR order should be based on a proper agreement between all the members of the healthcare team, the patient, and their family, where possible. The procedure of this decision-making must be clear and well documented, although communication about DNR can be challenging and highly stressful. Many studies illustrate that nurses, patients and family involvement in this decision making process is low, with the doctor as the major decision-maker.[7,8] Nursesâ&#x20AC;&#x2122; voices are often absent in such end-of-life decision-making.[3,7] It is recommended that the DNR decision is made involving the whole team looking after the patient and it should then be written clearly in the patientsâ&#x20AC;&#x2122; notes, and regularly reviewed.[9] Rwanda is a small country located in East Africa. After the genocide in 1994, the country experienced many challenges involving access to

quality healthcare and lack of human resources. Intensive care medicine or critical care services are poorly developed, or at best still in their infancy. Special ICUs, such as neurological and neonatal ICUs, are still a novel concept and there is a severe lack of experienced and specially trained medical and nursing staff in the ICUs.[10] Research conducted regarding DNR policies has shown that in some low- and middleincome countries like Rwanda, guidelines to support the DNR decision and end-of-life care do not exist or their development is still in the early stages.[7,8,11] In Rwanda, people tend to deny death, believing that medical science can cure any patient. Death is often seen as a failure of the healthcare system, rather than a natural aspect of life. This belief affects all healthcare professionals, including nurses, because they consider that if a patient is in hospital the purpose is to restore life and not allow them to die.[12] Research on nursing care for patients designated with DNR orders has been conducted since the late 1980s; however, no study appears to have been carried out in the Rwandan healthcare setting, although DNR orders are commonly used in some of the hospitals. This study may provide more information about the practice of DNR orders from the perspective of the nurses working in the ICU and may add to a limited body of knowledge. The purpose of the study was to explore the lived experiences of nurses caring for a patient with a DNR order in an ICU in Kigali, Rwanda.

Methods

Using a phenomenological approach,[10] two in-depth individual interviews were conducted with each participant to explore their lived experiences of providing care to patients with a DNR order in the

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ICU. The use of this approach allowed the researchers to gain a deeper understanding of the participants’ experiences.

Research setting

The study was conducted with nurses working in the seven-bedded ICU of a 200-bed tertiary hospital in Kigali, Rwanda. The ICU at the hospital is a medical-surgical unit, receiving both adult and paediatric patients. The ICU receives patients with life-threatening conditions directly into the ICU or from other departments within the hospital. At the time of this research study, hospital records indicated that ~20 patients were admitted to the ICU monthly.

Study sample

Purposive sampling was used to include nurses working in the ICU in the research setting, who were registered with the Rwanda Nursing Council, had at least 6 months’ experience in the ICU, and expressed interest in participating in the study. The final decision about sample size was based on evidence of data saturation, which was said to have occurred when no new information of significance was obtained and the participants started to repeat facts which were already submitted by other participants during the interviews.[13] In the current study six participants were interviewed.

Data collection

Following ethical approval and permission from the university research committee and the hospital administration, the researcher facilitated access to the participants through their ICU unit manager. Interviews were held with the cooperation of the unit manager in a quiet, distraction-free venue close to the ICU, between August and September 2011. Two semi-structured individual interviews were conducted with each participant and lasted ~25 - 30 minutes. The interviews were conducted in either English or Kinyarwanda, depending on the preference of the participant, and the researcher was fluent in both languages. The interview started with the following question: ‘Please can you tell me about your most recent experience of nursing a patient with a DNR order in the ICU?’ Further questions were then asked as to whether the DNR order influenced the nursing care in any way, and if the participants had any nursing recommendations for the use of the DNR order in an ICU. All interviews were recorded with the permission of the participants. The second interviews were then used to verify the findings from the first interview. The researcher was known to the participants, as she had previously worked in the units. This was found to facilitate access to the participants, build rapport, and did not appear to negatively influence the data-collection process. However, it may have influenced the participants’ responses as they may have provided answers that they thought the researcher wanted to hear.

Data analysis

All interviews were transcribed into written English text by the researcher and a language expert from a local university checked the transcripts for accuracy. The data were then manually analysed using Giorgi’s phenomenological approach.[14] The researchers read and reread the interviews several times to get a sense of the whole. The text was divided into units and then transformed into meaning by selecting descriptive quotations from the text. The meanings were then grouped together and developed into categories to create a general description of the nurses’ experience.[14]

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Trustworthiness

Credibility was achieved through prolonged engagement as the researcher had previously developed a rapport with the participants while working with them as a student, after which she spent 2 months collecting the data. This helped to ensure that rich, useful data were collected. All the potential participants approached were given the opportunity to refuse participation in the study, so that those interviewed were willing and interested to participate. It was emphasised to the participants that they should be frank in telling their stories and that there was no correct answer. Frequent debriefing sessions were held between the researchers to discuss the developing ideas and interpretations, and to challenge assumptions. Feedback was provided to the participants regarding the categories emerging from the data in order to obtain their reactions and to explore whether the interpretations were a good representation of their reality.[15] In an attempt to ensure dependability, the researchers described the decision-making processes and the context of the research study in detail. Transferability was ensured by providing a sufficiently detailed description of the research process to aid the reader in deciding if the findings could be transferred to a similar context. Confirmability was ensured by undertaking an audit trail and providing information regarding the path that the researchers took and how they arrived at their interpretations.[15]

Ethical considerations

Permission to conduct the study was obtained from the ethics research committee at the University of Rwanda, as well as the hospital where data collection took place. Participation was voluntary and written informed consent was obtained from all participants, who were informed of their right to withdraw from the research at any time. Confidentiality was assured through use of pseudonyms so that data could not be traced back to individuals. The data were kept in a secure place, available only to the research team.

Results

The data were organised into categories based on a review of the data obtained from the interviews of the six participants (Table 1). Three categories emerged from the data: • feeling emotional distress • barrier to optimal care • not part of decision-making.

Feeling emotional distress

The participants referred to the emotional distress they experienced while providing care to a DNR patient. They viewed the DNR orders as permitting death to occur and giving permission to terminate a patient’s life. One of the participants said: ‘When the decision are made [it] is ... too hard and painful … eeeeh … I can’t believe it because it is like he said the death is coming up and we can’t do anything … to the patient.’ (Dan) Another said: ‘Watching their death is a very difficult experience ...eeeeeeh … and when you know that patient with cardiac arrest will not receive CPR.’ (Leon) Participants felt despair while caring for the DNR patients because there was no longer anything they could do for the patient: ‘When we consider that restore [restoring] to health is no longer possible for patient with DNR we feel desperation and disappointed.’ (Nana)

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‘ When a patient is designated with a DNR order, I feel not comfortable to discover that really there is no hope that the patient will recover … he is really departed.’ (Sifa) A participant also went further to explain feeling a moral conflict with the DNR decision, i.e. whether to act on the decision or not. He said: ‘As nurses, our moral[s] may be in conflict with the decision because we are left with the decision of whether to initiate the CPR or not, many times we attempt the CPR … and believe that those patients can recover.’ (Dan) ‘I'm worrying about them … because withdrawing … looks like killing [the] patient.’ (Leon)

Barrier to optimal care

The participants described how the presence of a DNR order became a barrier to providing optimal care for the patient. Participants felt that patients with a DNR order could receive less intensive care and some of the daily nursing activities would not be performed as well as usually done. A participant said: ‘Yeah … It can influence the nursing care for instance, vital sign monitoring are not well performed. You can’t do pressure area care to prevent bed sores. You can’t feed him via nasogastric tube. Sometimes we can’t concentrate on urine output, or fluid intake … Yeah … It continue[s] to affect some range of nursing care.’ (Dan) Participants mentioned that DNR orders resulted in the patient being abandoned by the staff: ‘Another factor influencing nurse’s care for DNR patients is that the decision make(s) the patient abandoned, so the effect is that (the) patient receive(s) less attention. (Jacques) ‘Yeah … there is a change … patients without a DNR will be treated differently.’ (Leon) Another participant mentioned: ‘ I think there is a general feeling that DNR have a negative impact on care. I personally was unable to care for the patient because I could not ignore the medical doctor for making this decision.’ (Jacques)

Not part of decision-making

Participants explained that the doctors were the ones who made the end-of-life DNR decisions and nurses were expected to adhere to these decisions, whether they agreed with them or not. Participants explained: ‘Usually the decision is made by doctors and nurses are the one[s] to implement it. (Nana)

Table 1. Profile of the participants Pseudonym Jacques Leon Kazi Nana Sifa Dan

Age 30s 30s 20s 20s 20s 30s

Gender Male Male Male Female Female Male

ICU = intensive care unit; RN = registered nurse.

Level of education RN RN RN RN RN RN

ICU Experience 4 years 3 years 5 years 6 years 2 years 4 years

This lack of involvement was mentioned by two other participants: ‘Most of the time we are not part of the discussion and the views of nurses are ignored. The doctors are the one who make this order.’ (Jacques) ‘Normally physician, anesthesiologist, and neurosurgeons, after patient assessment make the decision; nurses are not included in the discussion, it’s very painful.’ (Dan) The participants went further to explain that the DNR decisions were not always documented or were unclear in the patients’ files. This lack of documentation created problems at times: ‘Sometime we apply resuscitation measures wrongly because it is not written in the patient records.’ (Leon) A participant explained a possible reason for why the DNR order was not documented: ‘Listen … the doctors fear to write do not resuscitate … I think its Rwandan culture. We … I always feel God may be the one who can decide about life and dying … they are not sure about the decision and think: How can I make this decision? Perhaps he will survive.’ (Dan)

Discussion

In this study, participants described their emotional distress in response to DNR orders for patients in their care. Studies have shown that when the DNR decision is written it is followed by the real probability of death, and this makes nurses feel morally discouraged, with feelings of stress, frustration, anger, sadness, helplessness, and moral distress. Moral distress is associated with the powerlessness of the nurse to influence the end-of-life decisions, especially when they believe that the care provided to the patient is in conflict with patients’ families’ wishes, or that the nurse is powerless to carry out what they believe to be right.[16,17] To address this issue, ethical education in nursing practice is essential for nurses working in ICUs, where ethical decision-making is needed on a regular basis.[18] Some healthcare providers consider that DNR orders result in the patient being abandoned and some doctors perceive that patients with a DNR order receive less attention from the nurses. This was confirmed in a study describing the medical handover from the night staff team, where patients with DNR orders were not recorded, as the team had decided that these patients did not need to be assessed and treated like other patients.[19] Petriş et al.[1] agreed that the DNR order is akin to organising death. In contrast, a systematic review showed that DNR orders were found to be associated with lower quality of care, but an increased quality of life.[20] Following the clear decision of DNR, the care of the patient becomes calmer and the nurses then have more time to be with the patient and family, with more active communication, instead of focusing on technical medical tasks.[18,21] The nurses in the current study described how they were not part of the DNR decision-making process. This was in agreement with the findings of another study,[22] which highlighted the dissatisfaction of nurses during the DNR decision-making process due to inadequate collaboration, including failure to consider nurses' opinions. As a consequence, the nurse then feels uncomfortable and frustrated because they feel that the doctors do not listen to their concerns.[23] Miscommunication between nurses and doctors may affect the relationship with patients, particularly in instances where they have different opinions about the plan of care. Our results illustrate that discussion and decision-making regarding DNR orders were directed by the doctors; the nurses’ input was limited. Many researchers agree

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that DNR decisions are usually made by physicians alone.[24] Moreover, another study has shown that doctors avoid discussion and the involvement of nurses and patients’ families in this process for fear of destroying hope and the therapeutic relationship.[21] Nurses who deliver terminal care in an ICU must plan the key interventions to improve the quality of care. Nurses believe that they know the patient best, but are often not solicited by the doctors when making decisions regarding care.[25] Several studies agree that DNR orders are often not recorded and that doctors wait until the patient shows definite signs of deterioration, or until the patient is clearly dying, to do so. It may then be too late to complete the process of adequate collaborative discussion and documentation.[4,7,8] Pettersson et al.[21] state that the lack of a clear decision regarding a DNR order, or inadequate reporting and documentation of this order, creates obstacles to providing high-quality nursing care and could result in unintended CPR.

Study recommendations

Implementation of training related to DNR orders is needed for all health professionals working in ICU, specifically regarding how to collaborate as a team regarding these decisions. The rationale for DNR orders needs to be better articulated and understood by all healthcare professionals working in the ICU. Additional information on how to cope with such stressful situations also needs attention. In addition, nurses need training on how to communicate with the rest of the healthcare team and the patients’ families about DNR decisions. The nursing care of a patient with a DNR order at the end of life should be incorporated into the curriculum of nurses at all levels of nursing education. Policies to guide DNR orders in ICU should be developed and implemented to assist all healthcare professionals.

Study limitations

This research was conducted in the ICU of one tertiary hospital in Rwanda, and thus only reflects the experience of nurses working there. The presence of the researcher could have influenced the participants’ responses, in that the participants may have provided answers in accordance with what they thought the researcher wanted to hear.

Conclusion

DNR orders are a fairly new concept in Rwanda and the practice of DNR orders in ICU is very demanding for the staff, especially the ICU nurses. Additional education about DNR orders as well as policies to guide their implementation could assist the ICU nurses in their difficult work.

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Acknowledgements. None. Author contributions. Both EN and PB (research supervisor) contributed to all aspects of the study and writing of the manuscript. EN collected the data. Funding. None. Conflict of interest. None. 1. Petris A, Cimpoeşu D, Costache I, Rotariu I. Do not resuscitate decision: Ethical issues during cardiopulmonary resuscitation. Rev Rom Bioet 2011;9(2):99-108. 2. Rudnick A, Wada K. Introduction to bioethics in the 21st century. In: Rudnick A, ed. Bioethics in the 21st Century. InTech, 2011. http://dx.doi.org/10.5772/19392 3. Coffey A, McCarthy G, Weathers E, et al. Nurses' preferred end-of-life treatment choices in five countries. Int Nurs Rev 2013;60(3):313-319. https://dx.doi.org/10.1111/inr.12024 4. Bach V, Ploeg J, Black M. Nursing roles in end-of-life decision making in critical care settings. West J Nurs Res 2009;31(4):496-512. https://dx.doi.org/10.1177/0193945908331178 5. Sham CO, Cheng YW, et al. Do‐not‐resuscitate decision: The attitudes of medical and non‐ medical students. J Med Ethics 2007;33(5):261-265. https://doi.org/10.1136/jme.2005.014423 6. Shanawani H, Wenrich MD, Tonelli MR, Curtis R. Meeting physicians responsibilities in providing end-of-life care. Chest 2008;133(3):775-786. https://doi.org/10.1378/chest.07-2177 7. Miller S, Dorman S. Resuscitation decisions for patients dying in the community: a qualitative interview study of general practitioner perspectives. Palliat Med 2014;28(8):1053-1061. https:// dx.doi.org/10.1177/0269216314531521 8. Chen YY, Gordon NH, Connors AF, Garland A, Chang SC, Youngner SJ. Two distinct do-notresuscitate protocols leaving less to the imagination: An observational study using propensity score matching. BMC Med 2014;12:146. https://dx.doi.org/10.1186/s12916-014-0146-x 9. Cardozo M. What is a good death? Issues to examine in critical care. Br J Nurs 2005;14(20):10501060. https://doi.org/10.12968/bjon.2005.14.20.20046 10. Munyiginya P, Brysiewicz P, Mill J. Critical care nursing practice and education in Rwanda. S Afr J Crit Care 2016;32(2):55-57. https://dx.doi.org/10.7196/SAJCC.2016.v32i2.272 11. Cohn S, Fritz ZB, Frankau JM, Laroche CM, Fuld JP. Do Not Attempt Cardiopulmonary Resuscitation orders in acute medical settings: a qualitative study. QJM 2013;106(2):165-177. https://dx.doi.org/10.1093/qjmed/hcs222 165-177 12. Searight HR, Gafford J. Cultural diversity at the end of life: Issues and guidelines for family physicians. Am Fam Physician 2005;71(3):515-522. https://doi.org/10.4135/9781452204819.n6 13. Onwuegbuzie AL, Leech NL. Sampling designs in qualitative research: Making the sampling process more public. Qual Rep 2007;12(2):238-254. 14. Dowling M. From Husserl to van Manen. A review of different phenomenological approaches. Int J Nurs Stud 2007;44:131-142. https://dx.doi.org/10.1016/j.ijnurstu.2005.11.026 15. Shenton AK. Strategies for ensuring trustworthiness in qualitative research projects. Educ Inform 2004;22(2):63-75. https://doi.org/10.3233/efi-2004-22201 16. Shoorideh FA, Ashktorab T, Yaghmaei F, Alavi Majd H. Relationship between ICU nurses' moral distress with burnout and anticipated turnover. Nurs Ethics 2015;22(1):64-76. https://dx.doi. org/10.1177/0969733014534874 17. Browning AM.CNE article: Moral distress and psychological empowerment in critical care nurses caring for adults at end of life. Am J Crit Care 2013,22(2):143-151. https://dx.doi.org/10.4037/ ajcc2013437 18. Park YR, Kim JA, Kim K. Changes in how ICU nurses perceive the DNR decision and their nursing activity after implementing it. Nurs Ethics 2011;18(6):802-813. https://dx.doi. org/10.1177/0969733011410093 19. Fritz Z, Fuld J. Ethical issues surrounding do not attempt resuscitation orders: Decisions, discussions and deleterious effects. J Med Ethics 2010;36(10):593-597. https://dx.doi.org/10.1136/ jme.2010.035725 20. Brinkman-Stoppelenburg A, Rietjens JAC, van der Heide A. The effects of advance care planning on end-of-life care: A systematic review. J Palliat Med 2014;28(8):1000-1025. https://dx.doi. org/10.1177/0269216314526272 21. Pettersson M, Hedstrom M, Hoglund AT. Striving for good nursing care: Nurses' experiences of do not resuscitate orders within oncology and hematology care. Nurs Ethics 2014;21(8):902-915. https://dx.doi.org/10.1177/0969733014533238 22. Ferrand E, Lemaire F, Regnier B, et al. Discrepancies between perceptions by physicians and nursing staff of intensive care unit end-of-life decisions. Am J Respir Crit Care 2003;167(10):13101315. https://dx.doi.org/10.1164/rccm.200207-752OC 23. Martin B, Koesel N. Nurses’ role in clarifying goals in the intensive care unit. Crit Care Nurses 2010;30(3):63-72. https://dx.doi.org/10.4037/ccn2010511 24. Vermoch K, Anason B. Understanding global end-of-life care practices: IHF 2014 research project. World Hosp Health Serv 2015;51(4):4-10. 25. Espinosa L, Young A, Symes L, Haile B, Walsh T. ICU nurses’ experiences in providing terminal care. Crit Care Nurs Q 2010;33(3):273-281. https://dx.doi.org/10.1097/CNQ.0b013e3181d91424

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Contamination of nebulisers and surrounding air at the bedside of mechanically ventilated patients L van Heerden,1 MSc Physiotherapy; H van Aswegen,1 PhD; S van Vuuren,2 PhD, R Roos,1 PhD; A Duse,3 MSc Med FCPath (Microbiol)

Department of Physiotherapy, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Department of Pharmacy and Pharmacology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 3 Department of Clinical Microbiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 1 2

Corresponding author: H van Aswegen (Helena.vanaswegen@wits.ac.za)

Background. The delivery of aerosolised medication, as performed by nurses and physiotherapists in intensive care units (ICUs), forms an important component of patient care. Objectives. To determine the presence of contamination of nebulisers used within a ventilator circuit; to describe the protocol and clinical practice regarding decontamination and storage of these devices; and to identify micro-organisms colonising contaminated nebulisers and the surrounding air at patientsâ&#x20AC;&#x2122; bedsides. Methods. A cross-sectional multicentre observational study was conducted, including site and equipment sampling to determine contamination. ICU managers were interviewed to determine the decontamination and storage protocols used for nebulisers in their units. Swabs were taken from nebuliser chambers and streaked onto blood agar plates (BAPs). An air sampler was used to collect air samples from the surrounding bedside environment. The BAPs were incubated for bacterial and fungal contamination. Species of colonies observed in these samples were identified. Results. Sixty-one nebulisers from seven ICUs were sampled (Micro Mist n=37; Aeroneb n=24). Half of the nebulisers (Micro Mist (n=19, 51.4%)); Aeroneb (n=12, 50%)) and most air samples (n=60, 98%)) presented with contamination. All participating ICUs reported decontamination and storage protocols, but visual inspection of nebulisers suggested that the protocols were not observed. Nebulisers rinsed with alcohol and left open to the environment to dry had the lowest contamination rates. Coagulase-negative Staphylococcus species (spp.) were mostly found in the surrounding air and Aeroneb samples, and Enterococcus spp. were mostly found in the Micro Mist nebulisers. Conclusion. Although decontamination and storage protocols for nebulisers were in place, nebuliser and air contamination was high, possibly due to poor staff adherence. S Afr J Crit Care 2017;33(1):23-27. DOI:10.7196/SAJCC.2017.v33i1.295

Aerosol delivery of pharmacological agents is an important adjunctive therapy frequently used in patient care during mechanical ventilation (MV).[1] Information on the frequency of use of aerosol drug delivery for patients on MV in South African (SA) intensive care units (ICUs) is currently not available. Nebulisation is the process whereby liquid medications are aerosolised in order to enhance their penetration into the lower respiratory tract of patients with, for example, lower airway obstruction, pulmonary infection, or needing mucolysis of obstructive pulmonary secretions.[2] A range of aerosol devices is used for the administration of medication to patients during the period of MV. These devices include jet nebulisers (e.g. Micro Mist (Hudson RCI, USA)), vibrating-mesh nebulisers (e.g. Aeroneb (Aerogen, USA)), ultrasonic nebulisers and pressurised metered-dose inhalers used with a spacer.[1-3] Internationally the Micro Mist nebuliser is mostly used in ICU settings, followed by ultrasonic nebulisers and, more recently, vibrating-mesh nebulisers.[3-5] Ellis et al. [6] reported that Micro Mist and ultrasonic nebulisers were mostly used in participating private- and public-sector ICUs in Johannesburg during the time of their survey. Conventionally, physiotherapists and ICU nurses are responsible for the administration of nebulised drug therapy to patients on MV. The study by Ellis et al.[6] is one of the few identified that investigated the prevalence of nebuliser contamination and decontamination and storage protocols for nebulisers used within a ventilator circuit. In this study, nebulisation was mainly performed using Micro Mist

nebulisers, and more than half of these nebulisers (52%) presented with bacterial growth. Contaminated nebulisers stored in sterile drapes on top of the ventilator had higher bacterial concentrations than those that were contaminated but not stored under a drape. None of the public- or private-sector ICUs surveyed in this study had a nebuliser decontamination and/or storage protocol in place.[6] Contaminated nebulisers have been linked to the development of hospital-acquired and ventilator-associated pneumonia.[7,8] Ventilatorassociated pneumonia (VAP) is an infection that occurs more than 48 hours after intubation, and represents 86% of pneumonias acquired in the hospital.[7] Contaminated hospital air and water are also known as environmental reservoirs contributing to the development of nosocomial pneumonia.[8] The extent of microbial contamination of bedside surfaces and the surrounding air of patients in ICUs in Taiwan was studied. The authors noted that Pseudomonas aeruginosa was the most frequently detected and abundant bacterium in the samples collected.[9] There is currently no information available regarding the association between micro-organisms cultured from contaminated nebulisers used in MV circuits and air samples taken from around the ICU patientâ&#x20AC;&#x2122;s bedside. The research questions for this study were: 1. What is the presence of nebuliser contamination after use in a ventilator circuit? 2. Are nebuliser decontamination and storage protocols in place and implemented in clinical practice?

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3. Is there an association between decontamination practices and nebuliser contamination? 4. Which micro-organisms colonise contaminated nebulisers and the surrounding air at patients’ bedsides?

Methods

A cross-sectional multicentre observational study was done. Ethical clearance (ref. no. M120514) was obtained from the Human Research Ethics Committee at the University of the Witwatersrand (Wits). Permission to conduct the study at the respective hospitals was received from the hospital manager or chief executive officer and the specific ICU manager. All hospital managers and unit managers provided written informed consent before data collection commenced. Sixteen hospitals (private and public sector) in Pretoria, SA, were approached for participation in the study. Four private hospitals provided consent. The inclusion criteria for this study were having nebulisers in the ICU at the time of audit that had been used within a ventilator circuit attached to an endotracheal or a tracheostomy tube. Nebulisers of patients nursed in isolation cubicles were excluded from the study owing to known diagnosed infections. The unit audit tool used by Ellis et al.[6] was reviewed and adapted to meet the objectives of this study. The tool assessed information related to the ICU environment, number of staff on duty, presence of nebuliser decontamination and storage protocols and observations made regarding nebuliser storage. Using this tool, unit managers of participating ICUs were interviewed (once-off) to determine the existence of decontamination and storage protocols for nebulisers in their respective units. After the interview, the unit manager indicated which patients were receiving MV at the time, and identified the nebulisers stored at their bedsides. Visual inspection of each nebuliser was done to identify the presence of remaining liquid in the nebuliser reservoir, and to observe the storage procedure. Nebuliser swabs were collected first. The Micro Mist nebuliser was removed from the oxygen tubing and/or covering and placed on sterile gauze on a sterile workstation. The easy-seal threaded cap was removed and placed on the sterile gauze. The base plate was then removed without touching the sides of the chamber and also placed on the sterile gauze. A sterile swab was dipped into the residual solute within the reservoir of the nebuliser and immediately streaked across a sterile blood agar plate (BAP). This procedure was repeated twice in order to collect two sets of BAPs. If the reservoir was dry or there was less than 2 ml of liquid in the reservoir, 2 ml of 0.9% sodium chloride solution was added to the reservoir. Each nebuliser was reassembled and returned to the patient’s bedside in its original position and condition. The Aeroneb nebuliser is manufactured to stay attached within the ventilator circuit,[10] and only its plug was opened for swabbing. The Surface Air System (SAS) sampler (SAS International PBI, Italy) was used to collect air samples. The SAS sampler was programmed to sample a constant 200 L of air for each air sample taken.[11] The aspirating metal head and chamber of the SAS sampler were disinfected with 70% alcohol before each sampling procedure. After the device was air dried, a BAP was inserted. Two air samples were taken at each selected bedside, no more than 1 m away from the ventilator. The BAPs were put in individualised resealable plastic bags and stored upside down in a cooler box for safe transportation to the laboratory for incubation. One air BAP and one nebuliser BAP were incubated at 25°C for 7 days for possible fungal contamination, and the others incubated at 37°C for 24 hours for possible bacterial contamination. After incubation, the number of colony-forming units was counted on each BAP, and each colony was described according to elevation,

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colour, shape, size, surface, margins, density, pigments and the presence of haemolysis. The five most frequently observed colonies cultured from the air, as well as nebuliser, for each hospital were selected for identification. Bacterial isolates were identified using conventional, internationally accepted microbiological techniques, including Gram stain microscopy and biochemical reactions. All Gram-negative organisms were identified on the MicroScan Walkaway 96 (Dade-Behring, USA) using the Microscan Rapid Negative ID Type 3 (RNID3) (Dade-Behring, USA) and API (Biomerieux, France) systems. Gram-positive organisms were identified through various testing algorithms. Colonies were then identified with the API20C AUX system (Biomerieux, France). Gram-positive cocci were tested for catalase production with hydrogen peroxide (Diagnostic Media Products, SA). The Prolex latex agglutination test (Prolab-diagnostics, UK) was used to distinguish Staphylococcus aureus from coagulasenegative Staphylococci. Catalase-negative organisms were tested on both bile aesculin plates (Diagnostic Media Products, SA) and with the PYR 50 test (Remel, USA) to differentiate between Streptococci and Enterococci. Streptococci and Enterococci were not identified further, and thus reported as either Streptococcus or Enterococcus species (spp).

Statistical analysis

Data from the participating hospitals were pooled and analysed as such to maintain hospital anonymity. Descriptive statistics were used to analyse data, and these are presented as frequencies and percentages. The Fischer’s exact test was used to ascertain the association between the contamination of Micro Mist nebulisers and storage protocol, by using the following variables: stored wet, stored in a glove, stored under a sterile drape and stored open to the environment. Statistical significance was set at a p-value <0.05.

Results

Ninety-two patients across the participating seven ICUs received aerosol therapy. Sixty-one nebulisers (Micro Mist (n=37, 61%); Aeroneb (n=24, 39%)) were sampled. The types of ICUs included were cardiac, medical, surgical, trauma, neurology and two mixed units. Fig. 1 outlines the

Hospitals approached for participation Private hospitals (n=12) Public hospitals (n=4)

No feedback received • Private hospitals (n=8) • Public hospitals (n=4)

Hospitals that consented (n=4)

ICU beds screened (n=440)

Patients receiving MV (n=132)

Patients receiving aerosol therapy (n=92)

Hospital 1 Nebulisers sampled (n=12)

Hospital 2 Nebulisers sampled (n=12)

Hospital 3 Nebulisers sampled (n=32)

Nebulisers excluded (n=31)

Hospital 4 Nebulisers sampled (n=5)

Fig.1. Flow diagram summarising hospital recruitment procedure and nebulisers and air samples swabbed.

ARTICLE

process of hospital recruitment, the number of nebulisers and air samples included and swabbed and reasons for exclusion. Thirty-one (51%) of the nebulisers swabbed presented with contamination. Both types of nebulisers presented with contamination: Micro Mist (n=19, 51%) and Aeroneb (n=12, 50%). Contamination was found in the majority of air samples (n=60, 98%). Six decontamination and storage protocols for Micro Mist nebulisers were identified in the seven ICUs included, as in some hospitals, different ICUs used the same protocols. No decontamination and storage protocols were reported for the Aeroneb nebulisers by any of the unit managers. The respective decontamination and storage protocols are outlined in Table 1. Storage protocol 1 stipulated that Micro Mist nebulisers were to be left open to the environment. However, it was observed that Micro Mist nebulisers were not stored on a hook at the bedside, but left open in a petri dish. In protocol 2, used in two ICUs in the same hospital, the Micro Mist nebulisers were not dried before they were stored under a sterile cloth. According to the unit manager, these sterile cloths were replaced every week. In protocol 3, the Micro Mist nebulisers were to be stored inside an acceptor bag; however, no acceptor bag was observed during data collection in that specific ICU. Using the unit audit tool developed for this study, four types of storage methods (stored in a latex glove, under a sterile cloth, open to the environment or in a paper bag) were defined for visual inspection of each nebuliser in the unit on the day of audit. Although most of the protocols in the ICUs included drying of the Micro Mist nebulisers,

most of them, as well as the Aeroneb nebulisers, were found to be wet during visual inspection. Thirty-three (89%) of the 37 Micro Mist nebulisers, and 20 of the 24 (83%) Aeroneb nebulisers, had retained fluid in their chambers on visual inspection, before the nebulisers were swabbed. Most Micro Mist nebulisers were stored in a latex glove (n=20). More than a third of the Micro Mist nebulisers stored in a glove presented with bacterial growth (n=7, 35%), and almost half presented with fungal contamination (n=9, 47%). Nebulisers stored under a sterile cloth had the highest percentage of bacterial (n=4, 44%) as well as fungal contamination (n=6, 67%). Nebulisers stored open to the environment resulted in the least bacterial (n=2, 29%) and fungal contamination (n=2, 29%). One nebuliser was left in the ventilator circuit, and presented with fungal contamination. Five Micro Mist nebulisers were stored connected to the oxygen port of the ventilator. Only one of these presented with both bacterial and fungal contamination. There was no significant association between latex glove storage and bacterial growth (p=0.72), or between storage under a sterile cloth and bacterial growth (p=0.62). When nebulisers were stored open to the environment, no significant association was observed between the storage method and bacterial growth (p=0.59). For some Micro Mist nebulisers, both bacterial and fungal growth was observed on the same BAP (n=11, 58%). On separate BAPs, only fungal (n=6, 32%) or bacterial growth (n=2, 11%) was observed. For the Aeroneb nebuliser the following contamination was observed: bacterial and fungal growth (n=9, 75%), fungal growth only (n=1, 8%)

Table 1. Type of decontamination and storage protocols used as reported by the unit managers Hospital 1

Protocol 1

Nebulisers assessed, n 12

Rinsed Yes

Method of decontamination 70% alcohol

Dried nebuliser Yes

Drying method Paper towel

Yes

Provac water

None

Yes

Paper towel

Wash with Bioscrub once a day None

Yes

Paper towel

Yes

Saline or sterile water

None

Yes

Wash with Bioscrub after aerosolisation

Yes

Paper towel

Method of storage Connected to the oxygen output of the ventilator, stored on a hook at the bedside and open to the environment Connected to oxygen, taken apart and left to dry under a sterile cloth Stored in acceptor (sterile) bag Stored in a glove connected to the oxygen output Stored in a glove connected to the oxygen output Stored in a glove connected to the oxygen output

Table 2. Microorganisms identified in nebulisers and air samples Contamination area

Microorganism No growth Empedobacter brevis Stenotrophomonas spp. Staphylococcus aureus Coagulase-negative Staphylococcus Enterococcus spp. Neisseria spp. Pseudomonas stutzeri Brevundimonas vesicularis Bacillus spp. Micrococcus spp.

Micro Mist nebuliser (n=17), n (%) 7 (41) 2 (12) 1 (6) 0 0 2 (12) 1 (6) 0 0 0 0

Aeroneb (n=12) 3 (25) 0 0 1 (8) 4 (33) 2 (17) 0 0 0 0 0

Air surrounding bedside (n=50) 15 (30) 0 0 1 (2) 8 (16) 2 (4) 3 (6) 4 (8) 1 (2) 1 (2) 1 (2)

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ARTICLE

and bacterial growth only (n=2, 17%). When storage protocol 1 was followed, the least amount of contamination was found (n=3/12, 25%). Storage protocols 2 and 3 resulted in the most bacterial and/or fungal contamination: n=8/12 (67%) and n=4/5 (80%), respectively. Ten different micro-organisms were identified in the sampled nebulisers and surrounding air (Table 2). Coagulase-negative Staphylococcus (CoNS) was the most commonly identified in air samples (n=8, 16%), followed by Pseudomonas stutzeri (n=4, 8%) and Neisseria spp. (n=3, 6%). Coagulase-negative Staphylococcus was the most common organism identified in Aeroneb nebulisers (n=4, 33%), whereas Empedobacter brevis and Enterococcus spp. were the most frequently encountered bacterial contaminants in Micro Mist nebulisers (n=2, 12% each). In two instances the same micro-organism was identified in the chamber of a nebuliser and its surrounding air. Enterococcus spp. were identified in a Micro Mist nebuliser and its surrounding air, and CoNS was identified in an Aeroneb and its surrounding air.

Discussion

Contamination was found in half of the Micro Mist and Aeroneb nebulisers used within a ventilator circuit, and in most of the samples taken of the surrounding air at patients’ bedsides. Visual inspection of the nebulisers stored by patients’ bedsides showed that the nebuliser storage protocols of the ICUs were not being consistently observed, which could imply low levels of staff adherence to nebuliser decontamination and storage protocols. This would have to be investigated in more depth in future studies. This study is the first to report the presence of contamination of Aeroneb nebulisers used within a ventilator circuit. The presence of contamination found in Aeroneb nebulisers was similar to that found in Micro Mist nebulisers. This finding was noteworthy, as one would expect less contamination to occur, as the inner portion of the Aeroneb nebuliser does not make contact with the outside environment. This suggests that keeping Aeroneb nebulisers connected in the ventilator circuit does not reduce the risk of contamination. Peckham et al.[12] also expressed their surprise at finding similar rates of contamination between conventional and mesh technology nebulisers used at home by adults with cystic fibrosis. None of the three public-sector or six private-sector hospital ICUs assessed by Ellis et al.[6] had nebuliser decontamination and storage protocols in place. In contrast, all ICUs that participated in this study had decontamination and storage protocols for Micro Mist nebulisers in place. The decontamination and storage protocols for Micro Mist nebulisers differed between hospitals, and within ICUs in the same hospital. It should be noted that most nebulisers were stored wet, and therefore it seemed that protocols were not being adhered to. Three different rinsing solutions were noted in the protocols identified. Different cleaning practices of nebulisers used in ICUs and wards are reported in the literature. In a single-centre study performed in India, Jadhav et al.[13] found a reduction in bacterial (87% - 12%) and fungal (75% - 15%) colonisation rates of nebulisers used in ICUs and the wards when nebulisers were washed with soap and distilled water and then disinfected with 70% alcohol. These results were obtained when their staff were educated on performing effective and prompt hand hygiene with alcohol-based hand wash before and after handling the nebulisers.[13] Another protocol noted the following with regards to cleaning of reusable nebulisers in a hospital setting: clean, disinfect, rinse with sterile water after each use and air-dry.[14] If a mask or mouthpiece was used during aerosol therapy, these devices would be wiped down with

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70% alcohol after each use. The author encouraged good handwashing hygiene practices, and suggested that the inside of the nebuliser should not be touched when left out to dry or during reassembly.[14] The importance of good handwashing hygiene and the wearing of gloves when handling a nebuliser should not be ignored as a potential means to lessen nebuliser contamination. In this study, the lowest amount of nebuliser contamination occurred when nebulisers were left open to the environment to air dry, which is congruent with research evidence.[14] An explanation for this finding is that exposure to light contributes to the inhibition of bacterial growth.[15] Micro Mist nebulisers that were stored under a sterile cloth presented with a higher percentage of fungal and bacterial contamination, similar to Ellis et al.’s[6] findings. Drying is an important component of decontamination protocols, as devices left wet can result in increased contamination,[16] as confirmed by this study’s findings. Although identical micro-organisms were identified in both nebulisers and the surrounding air in two instances in the current study, it cannot be assumed that the surrounding air was the only contributor to nebuliser contamination, or vice versa, as results showed that different decontamination and storage methods play an important role in the presence of contamination. Of concern is the relatively high level of contamination found in the air surrounding the ICU beds, as this could potentially pose a number of health risks to ICU staff and to patients’ visitors as well. It is known that epidemic pneumonia outbreaks in ICUs occur as a result of contamination of respiratory-therapy equipment, medical aerosols, water and air.[8] Therefore, staff or visitors with lower immunity might be at greater risk of falling ill. Further research into this aspect of exposure and risk profiling is needed. Staphylococcus aureus and CoNS, Enterococcus, Stenotrophomonas and Neisseria spp. are known causes of VAP.[17] Enterococcus and CoNS were identified in nebulisers and air samples in this study. A limitation of this study is that no data were collected regarding the patients’ infection status at the time of the audit. It is therefore unclear whether the presence of these organisms was as a result of patients having VAP at the time of nebuliser and air assessment, or if the patients were still at risk of developing VAP due to the presence of these organisms. However, when organisms are found in nebulisers and the surrounding air, it can be assumed that the organism would most likely be a contaminant.[13] The frequency of CoNS cultured in air samples in this study is of concern. Qudiesat et al.[18] reported CoNS as one of the microorganisms most detected in air samples in government and private healthcare settings, which included ICUs, in Jordan.[18] In contrast, in Taiwan, Pseudomonas aeruginosa was reported as the most frequent and abundant micro-organism found in air samples in ICUs.[9]Another limitation of the current study is that the ICUs studied were all from the private healthcare setting. Therefore, results cannot be extrapolated to public-sector ICUs. Recommendations for clinical practice are that nebulisers used within a ventilator circuit should be wiped dry and stored open to the environment, to ensure that the lowest amount of contamination occurs. Unit managers should ensure that ICU nurses are educated on nebuliser decontamination, and that storage protocols are in place. Physiotherapists are responsible for staying abreast of protocols in the ICUs where they work. Furthermore, these protocols need to be implemented, and regular audits of adherence conducted in order to reduce the risk of infection to patients and staff. A longitudinal design to investigate staff adherence and the association between patient diagnosis and micro-organisms identified in nebulisers and the surrounding air at the bedside is recommended.

ARTICLE

Conclusion

Nebuliser decontamination and storage protocols were recorded in the participating ICUs, but the presence of air and nebuliser contamination was of concern. The micro-organisms identified in both nebulisers and air samples are associated with the development of VAP. The possible reason for increased contamination appeared to be poor staff adherence to recorded protocols. Acknowledgements. Unit managers and staff of the participating ICUs for their assistance. Author contributions. LVH collected data and assisted in statistical analysis and write-up of the manuscript; HvA and SVV conceptualised the research question, assisted with statistical analysis and write-up of manuscript; SVV and LVH were responsible for incubation and culturing of specimens; RR assisted with statistical analysis and write-up of manuscript; AD assisted with identification of bacterial colonies and write-up of manuscript. Funding. LVH received funding for this work from the Wits University Faculty of Health Sciences Medical Research Endowment Fund, and the Cardiopulmonary Physiotherapy Rehabilitation Group of the SA Society of Physiotherapy. SVV received funding for this work from the National Research Foundation. None of the funding sources had input in the content of this manuscript. Conflict of interest. None. 1. Ehrmann S, Roche-Campo F, Papa G, et al. Aerosol therapy during mechanical ventilation: an international survey. Intensive Care Med 2013;39(6):1048-1056. http://dx.doi.org/10.1007/ s00134-013-2872-5

2. Kallet R. Adjunct therapies during mechanical ventilation: airway clearance techniques, therapeutic aerosols, and gases. Respir Care 2013;58(6):1053-1071. http://dx.doi.org/10.4187/respcare.02217 3. Ari A, Areabi H, Fink B. Evaluation of aerosol generator devices at 3 locations in humidified and non-humidified circuits during adult mechanical ventilation. Respir Care 2010;55(7):837-844. 4. Dhand R. Aerosol delivery during mechanical ventilation: From basic techniques to new devices. J Aerosol Med Pulm Drug Deliv 2008;21(1):45-60. http://dx.doi.org/10.1089/jamp.2007.0663 5. Robinson B, Athota K, Branson R. Inhalational therapies for the ICU. Curr Opin Crit Care 2009;15(1):1-9. http://dx.doi.org/10.1097/MCC.0b013e3283220e34 6. Ellis A, Van Aswegen H, Roos R, et al. Contamination and current practice in decontamination of nebulisers in ventilated patients. S Afr J Physiother 2013;Wits Special Edition:10-14. 7. Rotstein C, Evans G, Born A, et al. Clinical practice guidelines for hospital-acquired pneumonia and ventilator-associated pneumonia in adults. Can J Infect Dis Med Microbiol 2008;19(1):19-53. 8. Safdar N, Crnich C, Maki D. The pathogenesis of ventilator-associated pneumonia: its relevance to developing effective strategies for prevention. Respir Care 2005;50(6):725-739. 9. Huang P, Shi Z, Chen C, et al. Airborne and surface-bound microbial contamination in two intensive care units of a medical centre in central Taiwan. Aerosol Air Qual Res 2013;13(3):10601069. http://dx.doi.org/10.4209/aaqr.2012.08.0217 10. Tatham A. Aerogen: Pioneering aerosol drug delivery. 2014. https://www.aerogen.com/aerogenpublications-area (accessed 5 August 2016). 11. Perdelli F, Dallera M, Luisa C, et al. A new microbiological problem in intensive care units: Environmental contamination by MRSA with reduced susceptibility to glycopeptides. Int J Hyg Environ Health 2008;211(1-2):213-218. https://doi.org/10.1016/j.ijheh.2007.04.002 12. Peckham D, Williams K, Wynne S, et al. Fungal contamination of nebuliser devices used by people with cystic fibrosis. J Cyst Fibros 2016;15:74-77. http://dx.doi.org/10.1016/j.jcf.2015.06.004 13. Jadhav S, Sahasrabudhe T, Kalley V, et al. The microbial colonization profile of respiratory devices and the significance of the role of disinfection: A blinded study. J Clin Diagn Res 2013;7(6):10211026. http://dx.doi.org/10.7860/JCDR/2013/5681.3086 14. Oâ&#x20AC;&#x2122;Malley CA. Device cleaning and infection control in aerosol therapy. Respir Care 2015;60(6):917930. http://dx.doi.org/10.4187/respcare.03513 15. Sagripanti JL, Vossa L, Marshall HJ, et al. Inactivation of vaccinia virus by natural sunlight and by artificial UVB radiation. Photochem Photobiol 2013;89(1):132-138. http://dx.doi.org/10.1111/ j.1751-1097.2012.01207.x 16. Oâ&#x20AC;&#x2122;Malley C. Infection control in cystic fibrosis: cohorting, cross-contamination, and the respiratory therapist. Respir Care 2009;54(5):641-655. http://dx.doi.org/10.4187/aarc0446 17. Joseph NM, Sistla S, Dutta TK, et al. Ventilator-associated pneumonia: A review. Eur J Intern Med 2010;21(5):360-368. http://dx.doi.org/10.1016/j.ejim.2010.07.006 18. Qudiesat K, Abu-Elteen K, Elkarmi A, Hamad M, Abussaud M. Assessment of airborne pathogens in healthcare settings. Afr J Microbiol 2009;3:66-67. http://www.academicjournals.org/journal/ AJMR/article-abstract/5BC5AEF12241 (accessed 5 August 2016).

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This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

CASE REPORT

The treatment of autonomic dysfunction in tetanus G L Maryke Spruyt, MB ChB, MMed (Surg); T van den Heever, MB ChB, MMedSc (Crit Care) Department of Critical Care, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa Corresponding author: T van den Heever (theavdheever@gmail.com)

We report a case of generalised tetanus in a 50-year-old female patient after sustaining a wound to her right lower leg. She developed autonomic dysfunction, which included labile hypertension alternating with hypotension and sweating. The autonomic dysfunction was treated successfully with a combination of morphine sulphate infusion, magnesium sulphate, and clonidine. She also received adrenaline and phenylephrine infusions as needed for hypotension. We then discuss the pathophysiology, clinical features and treatment options of autonomic dysfunction. S Afr J Crit Care 2017;33(1):28-31. DOI:10.7196/SAJCC.2017.v33i1.274

Despite extensive vaccination programmes worldwide that have resulted in a significant decline in the incidence of tetanus, this preventable disease remains a challenge, especially in developing regions of the world. In 2013, a total of 103 cases of tetanus were reported in Europe and 457 cases in the Americas, compared twith 4 153 cases in South-East Asia and 6 508 cases in Africa.[1] In South Africa (SA), the incidence of tetanus has decreased from a total of 356 cases in 1980 to 38 in 2002 and only 2 cases in 2014.[2] Although it could be regarded as a rare disease in SA, patients presenting with tetanus are still seen occasionally. Tetanus is a notifiable disease in SA. According to the National Health Act No. 61 of 2003, it has to be reported to appropriate local, provincial and national health authorities. However, notification from the public sector is often lacking due to uncertainty of the channels to be followed to report notifiable diseases,[3] probably more so in rural areas. It is therefore not an overstatement to suggest that tetanus may have a higher incidence in SA than reflected by official statistics.

Case description

A 50-year-old female presented to our intensive care unit (ICU) at the Universitas Academic Hospital Complex in Bloemfontein, South Africa (SA), with generalised tetanus after sustaining a wound to her right lower leg. On day 11 she developed autonomic dysfunction, which included labile hypertension alternating with hypotension and sweating. The autonomic dysfunction was treated successfully with a combination of morphine sulphate infusion (27 mg/day as constant infusion), magnesium sulphate (16.8 - 40.8 g/day as constant infusion titrated to maintain a level of 2 - 4 mmol/L) and oral clonidine (75 µg in three divided doses per day). She also received adrenaline and phenylephrine infusions as needed for hypotension. The tetanus was complicated by rhabdomyolysis, which responded to aggressive fluid management. The duration of autonomic instability was 18 days. On day 39 after admission she was discharged to the ward. Informed consent was obtained from the patient to use her information for a case study. Ethical approval (ref. no. ECUFS 226/2014) to report this case was obtained from the Ethics Committee of the Faculty of Health Sciences, University of the Free State in Bloemfontein, SA.

Discussion

Pathophysiology

The spores of Clostridium tetani are found in soil, faeces and street dust. Entry into the body is usually through lacerations, minor cuts

and wounds, or injections.[4,5] Cases have resulted from wounds that were considered too trivial to warrant medical attention.[6] Two toxins are produced by the tetanus bacillus, namely tetanospasmin and tetanolysin.[7] Tetanospasmin is extremely potent and as little as 240 g is sufficient to obliterate the entire world population.[4,5] For the purpose of this case study, we looked at the pathophysiology and treatment of autonomic dysfunction in tetanus.

Autonomic dysfunction

The pathogenesis of autonomic dysfunction in tetanus is unclear. Several theories have been proposed, including damage to brain stem and hypothalamic nuclei, and direct disturbances in autonomic nerves (by tetanospasmin).[8] Autonomic dysfunction is characterised by sympathetic overdrive as well as a parasympathetic component.[9,10] Tetanospasmin blocks the inhibitory transmitter release from the presynaptic terminal of inhibitory spinal interneurons, resulting in sympathetic overdrive.[4,9] There is selective inhibition of the inhibitory reflex in the central nervous system (CNS). The resulting motor neuron overactivity causes excessive secretion of acetylcholine.[11] This cholinergic effect causes parasympathetic overactivity. The development of sympathetic overdrive presents between 7 and 14 days after the onset of muscle spasms,[12,13] and is characterised by tachycardia and precipitous systolic arterial pressure changes from minute to minute.[9] During autonomic instability there is an increase in noradrenaline and adrenaline levels indicative of both adrenal medullary and neuronal involvement.[13] Urinary catecholamine excretion in tetanus has been found to exceed that in other critically ill patients.[14] The systemic vascular resistance (SVR) may initially be low, but rises as the disease progresses. This high SVR then becomes labile and can vary widely within minutes. As a result of this high and widely variable SVR, perfusion may become dependent on adequate myocardial contractility. The use of beta-adrenergic blockers in this situation, with the negative inotropic effect, may precipitate cardiovascular collapse by reducing cardiac output.[7,9]

Clinical features

Tetanus is characterised by rigidity, muscle spasms and increased urinary excretion of catecholamines. Tonic muscular spasms may

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CASE REPORT

be confused with tonic-clonic convulsions. These muscular spasms may either be spontaneous or triggered by touch, visual, auditory or emotional stimuli.[7] Autonomic dysfunction may occur, and does not necessarily correlate with the severity of tetanus. Wassay et al.[8] reported autonomic dysfunction in a third of tetanus cases. Autonomic dysfunction presents as labile hypertension, tachycardia and vasoconstriction, as well as sweating, bradycardia, cardiac arrhythmias, fever, hypotension and hypercarbia.[4,7,15,16] Autonomic dysfunction, irrespective of ventilation requirement or severity of tetanus, predicts a poor outcome.[8] A high-output hyperdynamic circulatory state has been observed in severe uncomplicated tetanus patients,[10] which was postulated to be mainly due to excessive muscular contractions, increased sympathetic tone, and a rise in the core temperature. Increased tissue metabolism and oxygen demand result from frequent convulsive seizures and increased muscle tone.[10] Oxygen supply and consumption are increased through peripheral vasodilatation, increased venous return and an increased cardiac output.

Treatment of autonomic dysfunction

Treatment of autonomic dysfunction entails a treatment plan that will keep the patient comfortable and stabilise the cardiovascular system, while maintaining compensatory mechanisms and avoiding sudden cardiovascular collapse.[9] A combination treatment plan is recommended in the treatment of autonomic dysfunction.

Sedation

Deep analgosedation has been found to be important in overcoming autonomic dysfunction.[17] This should be combined with boluses of sedation before unavoidable stimuli. Sedation on its own does not control sympathetic overdrive and a combination of medication is therefore advised.[9] The drug of choice for sedation may be a benzodiazepine.[9] Benzodiazepines increase gamma amino butyric acid (GABA) via the inhibition of an endogenous inhibitor at the GABAA receptor.[13,15] The two most commonly used benzodiazepines are diazepam and midazolam, and both are also used for the control of spasms.[15] Propofol has also been used as an adjunct to sedation.[4] Propofol has a short duration of action, but it may cause dose-dependent hypotension and bradycardia.[18] With prolonged duration of treatment, severe adverse effects may occur due to accumulation of the drug.[18]

Magnesium sulphate

The use of magnesium in the treatment of tetanus was described in the beginning of the last century.[19-21] Magnesium acts as a muscle relaxant, blocks neuronal and adrenal catecholamine release, and causes antagonism of calcium with subsequent cardiovascular effects such as vasodilatation.[9,15] In a prospective observational study of magnesium sulphate in 40 patients with tetanus, Attygalle and Rodrigo[22] found that spasms were controlled in 38 out of 40 patients, and sympathetic overdrive was controlled without supplementary sedation. Autonomic dysfunction was reported in 6 patients, and in 4 of them, it stabilised on introducing magnesium sulphate. No deaths due to cardiovascular instability occurred. Magnesium levels should be kept at 2 - 4 mmol/L, with the upper limit of safety being lower in elderly patients.[22] Magnesium sulphate in overdose can cause hypotension, arrhythmias and paralysis with respiratory depression. Clinical evidence of magnesium overdose is

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assessed by the loss of patellar reflex, respiratory depression, hypotension and hypocalcaemia.[23] Magnesium has been proven to act as a neuromuscular blocking agent because it leads to the reduction of acetylcholine release and diminishes motor end-plate sensitivity to acetylcholine. It reduces the amplitude of the motor end-plate potential,[9] and also inhibits the release of catecholamines from the adrenal medulla and peripheral adrenergic nerve terminals.[9,15,16] In a randomised, controlled study, Thwaites et al.[24] found that magnesium infusion did not reduce the need for mechanical ventilation, but reduced the requirement for other drugs, such as sedation and neuromuscular blockade to control muscle spasms and verapamil to control cardiovascular instability.[24] Magnesium infusions did not cause substantial respiratory depression and had few cardiovascular side-effects.

Opiates

In 1972, Rie and Wilson[25] reported the successful use of morphine to control autonomic dysfunction in a case of tetanus. It does not appear to act as a peripheral α-adrenergic antagonist but rather attenuates sympathetic efferent discharge within the central nervous system. Buchanan et al.[26] reported in 1979 that morphine had a significant effect on reducing spontaneous sympathetic overactivity in tetanus, though it had little effect on spasms. Morphine sulphate maintains cardiac stability, decreasing blood pressure and heart rate without deleterious effects on cardiac performance.[7,15,27] It replaces endogenous opioids and reduces reflex sympathetic activity and the release of histamine.[7] In commonly used doses, it blocks sympathetically mediated peripheral vasoconstriction,[28] and causes peripheral and arterial vasodilatation by antagonising the sympathetic α-adrenergic tone.[16,29] The effects of morphine are reversible should paroxysmal hypotension arise.[25] Fentanyl has been reported in a case study[30] to have the same effect as morphine in tetanus. Similar to morphine, fentanyl blocks sympathetically mediated constriction of peripheral veins. It induces peripheral arterial dilatation by reflex reduction in sympathetic α-adrenergic tone through alteration of the sympathetic efferent discharge in the central nervous system.[30] Fentanyl has also been shown in animal studies to have a cardioprotective and anti-arrhythmic effect in sympathetic overactivity, independent of its haemodynamic effects.[31] The use of remifentanil in tetanus has also been reported, but was used for spasms only and could cause hypotension and bradycardia in an already cardiovascularly unstable patient.[32]

Epidural blockade

Bhagwanjee et al.[33] assessed the role of epidural blockade with bupivacaine and sufentanil in controlling sympathetic hyperactivity in 11 patients with severe tetanus. Blood pressure fluctuations reduced significantly with a non-significant decrease in heart rate fluctuations.[33]

Clonidine

Clonidine is an α-2 agonist which works centrally in the brain stem.[13] It decreases sympathetic outflow, inducing peripheral vasodilatation, thus reducing arterial pressure. It increases vagal tone, acts as a sedative and also decreases motor activity.[7,9] It also has a peripheral effect by preventing the release of noradrenaline from the pre-junctional nerve endings.[7] Since synthesis, storage, re-uptake and metabolism of adrenergic neurotransmitters are not affected, and adrenergic receptors are not blocked, reflex control of capacitance remains intact.[9] Compensatory changes of blood pressure are preserved,

CASE REPORT

and postural hypotension is less likely than with α- and ß-adrenergic blockers. In the event of hypotension and bradycardia, vasoactive drugs also remain effective. Clonidine was first used by Metz et al.,[34] who demonstrated that it lowers the basal plasma catecholamine levels in healthy adult males. In 1989, Sutton et al.[9] described the first reported use of clonidine to control sympathetic overactivity in tetanus. They reported a decrease in plasma noradrenaline after administration of clonidine, matched by an improvement in cardiovascular stability. In this case it was used in combination with magnesium, sedation and neuromuscular blockade. It should not cause rebound hypertension if withdrawn carefully.[9]

Dexmedetomidine

Dexmedetomidine use has been reported in cases with paroxysmal autonomic instability with dystonia and in tetanus.[35,36] Dexmedetomidine is highly lipophilic and has an affinity for α-2 receptors, with analgesic, anxiolytic, sedative and anti-sympathetic effects.[18,37] It has a α2:α1 adrenoreceptor ratio >7 times greater than that of clonidine.[38] Presynaptic α-2 receptor stimulation blocks noradrenaline release and post-synaptic α-2 stimulation decreases sympathetic activity.[39] It reduces plasma levels of catecholamines, maintaining haemodynamic stability through its anti-sympathetic properties. Dexmedetomidine also reduces the frequency of spasms and may be used as an adjunct with sedation.[37] Due to its vasodilatory effects it may blunt the adrenergic tone and thereby maintain haemodynamic stability.[18,37] Hypotension and bradycardia are not observed with the administration of a maintenance dose (0.2 - 0.7 μg/kg/hour) titrated every 30 minutes instead of using a bolus dose.[18,37] Hypertension is experienced with higher doses.[18] It may be used longer than 24 hours and it has been proven to be safe.[37] In a study of six patients reported by Girgin et al.,[37] dexmedetomidine infusion was started with a loading dose of 1 µg/kg over more than 10 minutes, followed by a maintenance infusion rate of 0.2 - 0.7 µg/kg/hour.

β-blockers

β-blockers such as propranolol were used in the past but can cause hypotension and sudden death; only esmolol is currently recommended.[6] Buchanan et al.[40] described a fatality in tetanus with autonomic instability, apparently due to the use of propranolol. One of the earliest drugs attempted in the treatment of sympathetic overdrive in tetanus was labetalol.[41] This α- and β-blocker reduces blood pressure and tachycardia, but does not improve heart rate and blood pressure variability. Successful use of esmolol has been described in a case report.[42] Because of its short duration of action, the effects are more easily reversible in the event of hypotension and bradycardia.

Atropine infusion

It has been postulated that tetanus is acetylcholine poisoning causing parasympathetic overactivity.[11,43] Dolar[11] suggested that atropine has a sedative effect due to its central depressive action and that acetylcholine accumulation in the CNS causes autonomic instability and anxiety in tetanus. He found in a study of four patients that their anxiety and agitation disappeared with a single dose of atropine and they fell asleep.[11]

Conclusion

Several drugs have been investigated or reported in case studies for the treatment of autonomic instability in tetanus. As yet there is no single drug that will control autonomic instability on its own, therefore combination

therapy is advocated. Dexmedetomidine holds promise for the treatment of autonomic instability, although more studies are needed. Treatment of autonomic instability in tetanus should be individualised. Acknowledgements. Dr Daleen Struwig, Faculty of Health Sciences, University of the Free State, for technical and editorial preparation of the manuscript. Author contributions. Both authors contributed equally. Conflict of interest. None. Funding. None.

1. World Health Organization. World Health Statistics 2015. Part II: Global health indicators. http:// www.who.int/gho/publications/world_health_statistics/2015/en/ (accessed 11 April 2016). 2. World Health Organization. South Africa statistics summary (2002 - present). http://apps.who.int/ gho/data/node.country.country-ZAF (accessed 11 April 2016). 3. Amayeza Information Centre. Disease notification system. http://www.amayeza-info.co.za/?page_ id=428 (accessed 11 April 2016). 4. Taylor AM. Tetanus. Contin Educ Anaesth Crit Care Pain 2006;6(3):101-104. http://dx.doi. org/10.1093/bjaceaccp/mkl014 5. Vincent JL, Abraham E, Cochanek P, Moore FA, Fink MP. Textbook of Critical Care. 6th ed. Philadelphia: Elsevier, 2011. 6. World Health Organization (WHO). Current recommendation for treatment of tetanus during humanitarian emergencies. WHO Technical Note WHO/HSE/GAR/DCE/2010. 2. Geneva: WHO, 2010. 7. Cook TM, Protheroe RT, Handel JM. Tetanus: A review of the literature. Br J Anaesth 2001;87(3):477487. http://dx.doi.org/10.1093/bja/87.3.477 8. Wassay M, Khealani BA, Talati N, Shamsi R, Syed NA, Salahuddin N. Autonomic nervous system dysfunction predicts poor prognosis in patients with mild to moderate tetanus. BMC Neurol 2005;5(1):1-4. http://dx.doi.org/10.1186/1471-2377-5-2 9. Sutton DN, Tremlett MR, Woodcock TE, Nielsen MS. Management of autonomic dysfunction in severe tetanus: the usage of magnesium sulphate and clonidine. Intensive Care Med 1990;16(2):7580. http://dx.doi.org/10.1007/BF02575297 10. Udwadia FE, Sunavala JD, Jain MC, et al. Haemodynamic studies during the management of severe tetanus. Q J Med 1992;83(302):449-460. 11. Dolar D. The use of continuous atropine infusion in the management of severe tetanus. Intensive Care Med 1992;18(1):26-31. http://dx.doi.org/10.1007/BF01706422 12. Bleck TP. Pharmacology of tetanus. Clin Neuropharmacol 1986;9(2):103-120. http://dx.doi. org/10.1097/00002826-198604000-00001 13. Freshwater-Turner D, Udy A, Lipman J, et al. Autonomic dysfunction in tetanus – what lessons can be learnt with specific reference to alpha-2 agonists? Anaesthesia 2007;62(10):1066-1070. http:// dx.doi.org/10.1111/j.1365-2044.2007.05217.x 14. Thwaites CL, Yen LM, Cordon SM, et al. Urinary catecholamine excretion in tetanus. Anaesthesia 2006;61(4):355-359. http://dx.doi.org/10.1111/j.1365-2044.2006.04580.x 15. Farrar JJ, Yen LM, Cook T, et al. Tetanus. J Neurol Neurosurg Psychiatry 2000;69(3):292-301. http:// dx.doi.org/10.1136/jnnp.69.3.292 16. King WW, Cave DR. Use of esmolol to control autonomic instability of tetanus. Am J Med 1991;91(4):425-428. http://dx.doi.org/10.1016/0002-9343(91)90162-Q 17. Duning T, Kraus J, Nabavi DG, Schaebitz WR. Management of autonomic dysfunction in severe tetanus: the importance of deep analgosedation. Intensive Care Med 2007;33(2):380-381. http:// dx.doi.org/10.1007/s00134-006-0481-2 18. Erdman MJ, Doepker BA, Gerlach AT, Phillips GS, Elijovich L, Jones GM. A comparison of severe hemodynamic disturbances between dexmedetomidine and propofol sedation in neurocritical care patients. Crit Care Med 2014;42(7):1696-1702. http://dx.doi.org/10.1097/CCM.0000000000000328 19. Blake JA. The use of magnesium sulphate in the production of anaesthesia and in the treatment of tetanus. Surg Gynaecol Obstet 1906;2:541-550. 20. Meltzer SJ, Auer J. The effects of intraspinal injection of magnesium salts upon tetanus. J Exp Med 1906;8(60):692-706. http://dx.doi.org/10.1084/jem.8.6.692 21. Tidy HL. A case of tetanus treated with intraspinal injections of magnesium sulphate. BMJ 1913;1(2734):1104-1105. http://dx.doi.org/10.1136/bmj.1.2734.1104 22. Attygalle N, Rodrigo N. Magnesium as first line therapy in the management of tetanus: a prospective study of 40 patients. Anaesthesia 2002;57(8):811-817. http://dx.doi.org/10.1046/j.13652044.2002.02698_6.x 23. Rodrigo C, Samarakoon L, Fernando SD, Rajapakse S. A meta-analysis of magnesium for tetanus. Anaesthesia 2012;67(12):1370-1374. http://dx.doi.org/10.1111/anae.12020 24. Thwaites CL, Yen LM, Loan HT, et al. Magnesium sulphate for treatment of severe tetanus: a randomised controlled trial. Lancet 2006;368(9545):1436-1443. http://dx.doi.org/10.1016/S01406736(06)69444-0 25. Rie MA, Wilson RS. Morphine therapy controls autonomic hyperactivity in tetanus. Ann Intern Med 1978;88(5):653-654. http://dx.doi.org/10.7326/0003-4819-88-5-653 26. Buchanan N, Cane RD, Wolfson G, De Andrade M. Autonomic dysfunction in tetanus: the effects of a variety of therapeutic agents, with special reference to morphine. Intensive Care Med 1979;5(2):6568. http://dx.doi.org/10.1007/BF01686048 27. Rocke DA, Wesley AG, Pather M, Calver AD, Hariparsad D. Morphine in tetanus – the management of sympathetic nervous system overactivity. S Afr Med J 1986;70(11):666-668. 28. Ward JM, McGrath RL, Weil JV. Effects of morphine on the peripheral vascular response to sympathetic stimulation. Am J Cardiol 1972;29(5):659-666. http://dx.doi.org/10.1016/00029149(72)90167-1 29. Zelis R, Mansour EJ, Capone RJ, Mason DT. The cardiovascular effects of morphine. The peripheral capacitance and resistance vessels in human subjects. J Clin Invest 1974;54(6):1247-1258. http:// dx.doi.org/10.1172/JCI107869 30. Moughabghab AV, Lefilliatre P, Fenides A, Provot F. Management of autonomic dysfunction in severe tetanus: the use of fentanyl. Can J Anaesth 1995;42(10):955. http://dx.doi.org/10.1007/ BF03011052 31. Lessa MA, Rodrigues E, Tibiriçá E. Cardioprotective action of fentanyl in a model of central sympathetic overactivity in rabbits: antiarrhythmic and anti-ischemic effects. Acta Anaesthesiol Scand 2004;48(9):1115-1122. http://dx.doi.org/10.1111/j.1399-6576.2004.00472.x

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CASE REPORT

32. Beecroft CL, Enright SM, O'Beirne H. Remifentanil in the management of severe tetanus. Br J Anaesth 2005;94(1):46-48. https://dx.doi.org/10.1093/bja/aeh288 33. Bhagwanjee S, Bรถsenberg AT, Muckart DJ. Management of sympathetic overactivity in tetanus with epidural bupivacaine and sufentanil: experience with 11 patients. Crit Care Med 1999;27(9):17211725. http://dx.doi.org/10.1097/00003246-199909000-00004 34. Metz SA, Halter JB, Porte D Jr, Robertson RP. Autonomic epilepsy: Clonidine blockade of paroxysmal catecholamine release and flushing. Ann Intern Med 1978;88(2):189-193. http://dx.doi. org/10.7326/0003-4819-88-2-189 35. Goddeau RP Jr, Silverman SB, Sims JR. Dexmedetomidine for the treatment of paroxysmal autonomic instability with dystonia. Neurocrit Care 2007;7(3):217-220. http://dx.doi.org/10.1007/ s12028-007-0066-0 36. Ozer-Cinar S, Isil CT, Paksoy I. Dexmedetomidine in the management of severe tetanus. Indian J Anaesth 2014;58(1):96-97. http://dx.doi.org/10.4103/0019-5049.126847 37. Girgin NK, Iscimen R, Gurbet A, Kahveci F, Kutlay O. Dexmedetomidine sedation for the treatment of tetanus in the intensive care unit. Br J Anaesth 2007;99(4):599-600. http://dx.doi.org/10.1093/bja/aem251

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38. Kamibayashi T, Maze M. Clinical uses of alpha-2 adrenergic agonists. Anesthesiology 2000;93(5):1345-1349. http://dx.doi.org/10.1097/00000542-200011000-00030 39. Hogue CW Jr, Talke P, Stein PK, Richardson C, Domitrovich PP, Sessler DI. Autonomic nervous system response during sedative infusions of dexmedetomidine. Anesthesiology 2002;97(3):592598. http://dx.doi.org/10.1097/00000542-200209000-00012 40. Buchanan N, Smit L, Cane RD, De Andrade M. Sympathetic overactivity in tetanus: fatality associated with propranalol. BMJ 1978;2(6132):254-255. http://dx.doi.org/10.1136/bmj.2.6132.254-a 41. Dundee JW, Morrow WF. Labetalol in severe tetanus. BMJ 1979;1(6171):1121-1122. http://dx.doi. org/10.1136/bmj.1.6171.1121 42. Beards SC, Lipman J, Bothma PA, Joynt GM. Esmolol in a case of severe tetanus. Adequate haemodynamic control achieved despite markedly elevated catecholamine levels. S Afr J Surg 1994;32(1):33-35. 43. Leonardi G. Acetylcholine poisoning and sympathetic overactivity in tetanus. Lancet 1974;2(7887):1014-1015. http://dx.doi.org/10.1016/S0140-6736(74)92110-2

This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

EDITORIAL

The need for setting standards in critical care transfers M Venter,1 BTech EMC; D Stanton,1 Critical Care Assistant (CCA); N Conradie,2,3 BTech EMC; L Jordaan,4 BTech EMC; C Venter,5 BTech EMC ; M Venter,5 BTech EMC; W Stassen3,5 BTech EMC, MPhil EM Netcare 911, Netcare (Pty) Ltd., Midrand, South Africa Critical Care Transport Unit, Department of Health, Gauteng Provincial Government, South Africa 3 Department of Emergency Medical Care, Faculty of Health Sciences, University of Johannesburg, South Africa 4 Department of Emergency Medical Care, Faculty of Health Sciences, Cape Peninsula University of Technology, Cape Town, South Africa 5 Critical Care Retrieval Services, ER24, Johannesburg, South Africa 1 2

Corresponding author: M Venter (monique.venter@netcare.co.za) South Africa (SA) has a well-described shortage of critical care resources and specialists, often necessitating interfacility transfer to meet the needs of patients requiring further care.[1] Previously published work has reported high rates of adverse events when transfers of critically ill patients (critical care transfers, CCTs) are undertaken by prehospital providers who lack advanced skills and training.[2-4] In our recently published article in SAJCC,[5] we suggested that a remedy for this could be the development postgraduate training curricula for prehospital providers undertaking CCTs, which would allow for an additional scope of practice. Although this is an ideal to strive towards, it is not a realistic solution in the short term. We propose a national standard-setting (board) exam for all prehospital providers undertaking these high-risk transfers. This would enable a standardised level of care, more consistent practice, and significant clinical risk mitigation. Within SA, advanced life support (ALS) practitioners with various qualifications are undertaking CCTs. The training of these providers in critical care has been variable at best.[5] In October 2016, the Health Professions Council of SA released newly proposed scopes of practice for all prehospital providers for commentary.[6] These proposed changes, pending acceptance, would see providers at the technician level, with even less critical care training, undertaking the transfer of ventilated patients, for example. The term ALS would no longer hold its current definition and ALS practitioners of different levels would no longer have the same skill set. The CCT environment would soon be confronted with the new challenge of redefining which practitioners are competent to undertake high-acuity transfers.

Internationally, practitioners who undertake CCTs undergo further training and are required to pass a board exam before becoming certified critical care paramedics.[7,8] This is not the case locally. A concerted effort should be undertaken by critical and prehospital care societies to develop, moderate, and administer the exams to ensure that those involved in CCTs are adequately knowledgeable and skilled to do so safely â&#x20AC;&#x201C; this is in the best interest of patient outcomes.

S Afr J Crit Care 2017;33(1):32. DOI:10.7196/SAJCC.2017.v33i1.319

1. Scribante J, Bhagwanjee S. National audit of critical care resources in South Africa - transfer of critically ill patients. S Afr Med J 2007;97(12.3):1323-1326. 2. Bambi S, Lucchini A, Innocenti D, Mattiussi E. Complications in critically ill adult patientsâ&#x20AC;&#x2122; transportations reported in the recent literature. Emerg Care J 2015;11(1):12-18. https://dx.doi. org/10.4081/ecj.2015.4781 3. Fan E, MacDonald RD, Adhikari NKJ, et al. Outcomes of interfacility critical care adult patient transport: A systematic review. Crit Care 2006;10(1):1-7. https://dx.doi.org/10.1186/cc3924 4. Hatherill M, Waggie Z, Reynolds L, Argent A. Transport of critically ill children in a resourcelimited setting. Intensive Care Med 2003;29(9):1547-1554. https://dx.doi.org/10.1007/s00134003-1888-7 5. Venter M, Stassen W. The capabilities and scope of practice requirements of advanced life support undertaking critical care transfers: A Delphi study. S Afr J Crit Care 2016;32(2):58-61. http://doi. org/10.196/SAJCC.2016.v32i2.275 6. Health Professions Council of South Africa. Revised Clinical Practice Guidelines. http:// www.hpcsa.co.za/uploads/editor/UserFiles/CLINICAL_PRACTICE_GUIDELINES_2016.pdf (accessed 18 January 2017). 7. Paramedic Association of Canada. National Occupational Competency Profile for Paramedics. Ontario: Paramedic Association of Canada; 2011. http://www.paramedic.ca/uploaded/web/ documents/2011-10-31-Approved-NOCP-English-Master.pdf (accessed 12 April 2016). 8. University of Florida. Critical Care Paramedic Certificate. United States: University of Florida; http://www.bcn.ufl.edu/academics/certificates/ccp/ (accessed 12 April 2016).

This journal is sponsored by the Critical Care Society of Southern Africa Join the CCSSA and get free copies of this journal posted to you and pay reduced congress and refresher course fees. To join visit the CCSSA webpage www.criticalcare.org.za Annual Membership R250.00 (incl. VAT) Joining fee R100.00 (incl. VAT) To advertise in this journal contact: Renee Hinze on 012 481 2062 or email: reneeh@hmpg.co.za

SAJCC July 2017, Vol. 33, No. 1

MSD IS COMMITTED TO HELP FIGHT INFECTIOUS DISEASES.

Right Spectrum. Smart Choice.

For full prescribing information refer to the package insert approved by the Medicines Regulatory Authority. S4 INVANZ® Sterile Powder for Injection. Reg. No. 37/20.1.1/0424. Each vial contains ertapenem sodium equivalent to 1 g of ertapenem free acid. S4 TIENAM® 500 Sterile Powder for Injection. Reg. No. S/20.1.1/175. Each vial (20 ml) contains Imipenem equivalent to 500 mg of anhydrous Imipenem and Cilastatin Sodium equivalent to 500 mg of the free acid. S4 CUBICIN® Powder for Solution for Infusion. Reg. No: 43/20.1/0954. Each vial contains 500 mg daptomycin as a sterile, lyophilised powder. S4 CANCIDAS® 50 mg Lyophilised Powder for Solution for Infusion. Reg. No. 37/20.2.2/0544. Each vial contains 50 mg caspofungin anhydrous free base, equivalent to 55,5 mg caspofungin acetate. S4 CANCIDAS® 70 mg Lyophilised Powder for Solution for Infusion. Reg. No. 37/20.2.2/0545. Each vial contains 70 mg caspofungin anhydrous free base, equivalent to 77,7 mg caspofungin acetate. S4 NOXAFIL® 40 mg/ml oral suspension. Reg. No. 41/20.3/0719. Each ml of oral suspension contains 40 mg posaconazole.

MSD (Pty) Ltd (Reg. No. 1996/003791/07), Private Bag 3, Halfway House, 1685, South Africa. Tel: (011) 655-3000. www.msd.co.za. Copyright © 2017. Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, NJ, USA. All rights reserved. Registered applicant for CUBICIN: AstraZeneca Pharmaceuticals (Pty) Ltd. Reg. No. 1992/005854/07. Building 2, Northdowns Office Park, 17 Georgian Crescent West, Bryanston, 2191. Private Bag X23, Bryanston, 2021. Tel: 011 797- 6000. Fax: 011 797-6001. www.astrazeneca.co.za. CUBICIN is a registered trademark of Cubist Pharmaceuticals, Inc., and is used with permission. AINF-1195149-0039 06/2022

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In ICU patients, appropriate antifungal choices are critical in the management of invasive fungal infections. ¹

Help them in the fight of their lives Cancidas®: •

ESCMID 2012 Guidelines for the Diagnosis and Management of Candida Diseases Strongly Recommend CANCIDAS® 2

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Empirical therapy for presumed fungal infections in febrile, neutropaenic patients.

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Treatment of Invasive Candidiasis, including candidaemia.

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Treatment of Oesophageal and Oropharyngeal Candidiasis where IV antifungal therapy is appropriate.

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Treatment of invasive Aspergillosis in patients who are refractory or intolerant of other therapies including amphotericin B, lipid formulations of amphotericin B and itraconazole.

References: 1. Schelenz, S. Management of Candidiasis in the intensive care unit. J Antimicrob Chemoth 2008; 61 ( Suppl 1) i31-i34. 2. Cornely OA, Bassetti M, Calandra T, et al for ESCMID Fungal Infection Study Group(EFISG). ESCMID 2012 Guidelines for the Diagnosis and Management of Candida Diseases: non-neutropaenic adult patients. Clin Microbiol Infect 2012;18(suppl7)19-37. 3. Cancidas Approved Package Insert-12 May 2015. For full prescribing information refer to the package insert approved by the Medicines Regulatory Authority. S4 CANCIDAS® 50 mg Lyophilised Powder for Solution for Infusion. Reg. No. 37/20.2.2/0544. Each vial contains 50 mg caspofungin anhydrous free base, equivalent to 55,5 mg caspofungin acetate. S4 CANCIDAS® 70 mg Lyophilised Powder for Solution for Infusion. Reg. No. 37/20.2.2/0545. Each vial contains 70 mg caspofungin anhydrous free base, equivalent to 77,7 mg caspofungin acetate. MSD (Pty) Ltd (Reg. No. 1996/003791/07), Private Bag 3, Halfway House, 1685. Tel: (011) 655-3000. www.msd.co.za. Copyright © 2017 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Kenilworth, NJ, USA. All rights reserved.MSD. AINF-1099838-0001 01/2018

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