Qatar Medical Journal - 2 - Qatar Critical Care Conference Proceedings, فبراير ٢٠٢٠

Pediatric intensivists are called to patient bedsides in the pediatric cardiac intensive care unit (CICU) after congenital cardiac surgery for low blood pressure (BP) and/or poor perfusion, acute change in heart rate (HR) or rhythm, surgical site bleeding or increased chest tube output, anuria or oliguria, oxygen desaturation less than expected or metabolic acidosis with rising lactic acid and base deficit. Causes of acute circulatory failure after cardiac surgery are divided into four categories which must be considered when approaching the patient in CICU (Table 1).

Assessing cardiac output in CICU remains challenging, hemodynamic parameters are usually monitored, along with physical examination, i.e. HR, BP, right and left atrial pressures. There are surrogate markers i.e., mixed venous saturation, brain and renal NIRS, toe temperature, urine output, and then laboratory workup to determine acidosis due to end-organ dysfunction. Echocardiography can confirm low cardiac output syndrome (LCOS) occurs after cardiac surgery with the following major indicators; abnormal ventricular-vascular interaction after bypass, the functionally univentricular circulation, abnormal diastolic function after surgery to the right heart and residual anatomic lesions.¹

The limited support tools that are available to manage circulatory failure post cardiac surgery in the CICU are the following: Medications: High labile pulmonary vascular tone (PVR) occurs in patients with pulmonary over-circulation i.e., ASD (atrial septal defect), VSD (ventricular septal defect), PDA (patent ductus arteriosus) and AV canal (atrioventricular canal). Pulmonary venous hypertension, i.e. TAPVR with obstruction, HLHS with restrictive atrial communication and in the univentricular heart after Norwood, shunt or PA band has unstable PVR. Functionally univentricular hearts don't tolerate increased SVR and at the same time, decreased SVR may not be desirable for patients who have fixed systemic or pulmonary obstruction. There are a wide variety of medications to use, but essentially two, milrinone^2,3 and epinephrine are very important and widely used. Milrinone is routinely used after cardiac surgery to minimize the LCOS, which works in a receptor independent manner and is synergistic to beta-adrenergic ionotropic effect. Most patients benefit from low dose epinephrine for decreased cardiac function. Nitroprusside is effective where after-load is high, a low dose should always be started titrating to the optimal BP. Generally, there is no role of dopamine in these patients.⁴Ventilation-cardiopulmonary interaction: Ventilation at functional residual capacity needs to be targeted. Managing rhythm: Recognition of rhythm is a crucial aspect of care. It is equally important to pay attention to the appropriate heart rate. Extracorporeal mechanical support: The last resort is to put the patient on extracorporeal membrane oxygenation.

In summary, the past two decades have seen important advances in our understanding of the circulatory physiology of infants and children post cardiac surgery. When approaching the patients with cardiovascular dysfunction, it is essential to approach the cardiopulmonary system in its entirety, rather than consider the heart, lungs, or peripheral circulation as isolated elements. Working towards one common goal of optimizing systemic oxygen delivery and emphasizing anticipatory intensive care tailored to individual patients with the need for early, targeted investigation and intervention is essential when patients are not progressing as expected.

Background: Starting a new extracorporeal membrane oxygenation (ECMO) program requires synergizing different organizational aspects and extensive training of a core team to deliver care safely.^1,2 Sidra Medicine, a newly opened facility in Qatar, started accepting acute inpatients and activated its ECMO program in 2018. The aim of this quality review is to evaluate the training of ECMO Specialists through benchmarking our ECMO program mechanical complications to the Extracorporeal Life Support Organization (ELSO) data. Methods: The hospital trained ECMO Specialists (experts and novices) come from different parts of the world with varying degrees of knowledge and experience and use a comprehensive training program based on the ELSO guidelines for ECMO training and continuous education.³ This program was delivered over a two-year period to all ECMO team members and included: multiple conferences on key ECMO topics; basic wet labs and emergency drills including the change of different components, and; immersive simulation-based training (SBT) on a modified neonatal manikin (Figures 1 and 2). These face to face interactions, in small groups, with different critical scenarios were followed by debriefing.^4,5 SBT sessions started before the opening of the acute unit and continued after the acceptance of the first ECMO patient. Immersive SBT sessions occur monthly and include minor and major troubleshooting, de-airing, priming, circuit change, oxygen failure, pump failure, and other problems that can be encountered during ECMO runs.

All ECMO Specialists, both experts and novices, completed a full ECMO training program and had gone through the Sidra ECMO certification examination before handling ECMO patients. They were evaluated and certified using a checklist assessment tool and with skills having to be demonstrated competently by the candidates. Novice clinicians were initially ECMO bedside nurses and as they became familiar with the ECMO daily routine and learned the protocols and policies, they started caring for patients as ECMO Specialists.

We retrospectively reviewed collected data of technical complications for the 13 patients who have received ECMO therapy since program activation. We analyzed ECMO mechanical complications and benchmarked them with ELSO registry data in corresponding categories to evaluate the training of ECMO specialists and our ECMO program infrastructure. Result: The Sidra ECMO program has now trained a total of 20 ECMO Specialists (experts and novices). Out of the 13 novice clinicians who volunteered to be trained, 8 successfully became ECMO Specialists.

There has been a total of 13 patients on ECMO (Table 1). One of these was the first successful neonatal respiratory ECMO patient in Qatar. Over the 13 cases, minor mechanical complications and usual circuit clots were experienced. There was no pump failure or oxygenator failure encountered. Conclusion: SBT is a valuable ECMO educational approach. It offers the opportunity to practice technical skills repeatedly and to become proficient in high-risk/low frequency events while avoiding harm to patients. Using consistent and continuous training is the key for the success of the ECMO Specialist's model. This is a limited study due to the low number of patients, but as ECMO is a low-volume/high-risk procedure, it still highlights the benefits of simulation in establishing new ECMO programs.

The neonatal circulation is unique due to the presence of fetal shunts. With the advances in biomedical technology, the assessment of sick newborn infants has improved significantly. It allows to collect, store and analyze the complex physiometric data and provides a foundation for advances in diagnosis and management of neonatal cardiovascular compromise. This could allow the clinician to have objective information to compliment the clinical assessment. Additionally, serial assessments and trending of measured parameters provides longitudinal information on disease pathophysiology and the response to treatment.

The advanced hemodynamic monitoring however has to be structured and focussed to get the relevant information to compliment clinical signs and symptoms. It however has an inherent risk of inappropriate or over-treatment leading to a state of confusion. The following questions should thus be addressed at the outset:

1. Objectives of assessment and goal of therapy 2. Available techniques and processing information 3. Point assessment vs continuous assessment 4. Invasive monitoring vs non-invasive monitoring

When utilising these techniques, the limitations of individual devices and the interaction between them should be known. As compared to point-of-care assessment, when non-invasive monitoring devices are used, the trending of data from them with simultaneous single screen longitudinal display of values is helpful for diagnosis of disease and assessing response to treatment (Figure 1).² The examples are continuous cardiac output, blood pressure, central venous pressure, pulse oximetry and near infrared spectroscopy. The trending of heart rate monitoring has already been utilised for early detection of sepsis using HeRO monitor. There has been interest in continuous amplitude integrated EEG but so far it is limited to research trials.

We compared measurement of cardiac output with echocardiography with non-invasive cardiac output monitoring. We observed that absolute values were different but the trend on longitudinal assessment was comparable. This could be due to the fact that non-invasive cardiac output assessment methods utilise indirect techniques such as electric velocimetry, arterial pulse contour analysis etc. Using an example of a baby with septic shock, one can understand how the hemodynamic monitoring can guide initial management.³

BP =  cardiac output (CO) x systemic vascular resistance (SVR) (Figure 2) ⁴

If a patient has low CO, high SVR and normal BP, the choice of treatment is inodilators e.g., milrinone. If CO, SVR and BP are all low, commence treatment with norepinephrine and add epinephrine. If high CO and low BP and SVR, give fluid bolus initially and titrate therapy.

The integration of advanced hemodynamic monitoring in clinical care is akin to whole genome sequencing where a large amount of information is gathered which requires processing. Utilising this information is a challenge at present but it has the potential to open gateways for precision medicine.⁵

Introduction: Delirium is a well-documented problem in the adult population however, its importance in the paediatric population has evolved recently with the development and validation of reliable paediatric delirium (PD) assessment tools. Definition: The key feature of delirium is an alteration in both cognition and arousal. The American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5)¹, defines delirium as a noticeable change in the patient's neurocognitive baseline with an acute disturbance in attention, awareness, and cognition, and is thought to be a direct result of another medical condition rather than due to an established/evolving neurocognitive disorder. Epidemiology: The overall prevalence of delirium in PICU ranges from 4% to 29%, with a recent multi-institutional PD study assessing 994 children for delirium in 25 different PICUs reporting a prevalence of 25%.² Higher rates have been reported in children < 5 years of age.³ A PD prevalence of 49% was found in a paediatric cardiac ICU population. A prevalence rate of 27% was described in a postoperative paediatric population (delirium incidence of 65% within 5 days after surgery).³Pathophysiology: Many hypotheses have been proposed. The neuroinflammatory hypothesis suggests that systemic inflammation leads to endothelial activation, enhanced cytokine activity, and infiltration of leukocytes and cytokines into the central nervous system (CNS), producing local ischemia and neuronal apoptosis. The neurotransmitter hypothesis suggests that dysregulation of neurotransmitters like acetylcholine, dopamine, and gamma aminobutyric acid leads to the development of delirium. The oxidative stress hypothesis suggests that hypoxia coupled with increased cerebral metabolism, leads to the production of reactive oxygen species that cause global CNS dysfunction.³Risk factors: Risk factors are divided into predisposing and precipitating factors many of which are modifiable (Table 1).³Presentation: PD presents in three major subtypes. Hyperactive delirium is characterized by agitation, restlessness, hypervigilance, and combative behaviour, hypoactive delirium is characterized by lethargy, inattention, and decreased responsiveness and mixed type delirium which exhibits aspects of both hyperactive and hypoactive delirium.¹ Hypoactive and mixed type delirium are common presentations in children followed by hyperactive variety. Hypoactive delirium can be easily missed without appropriate screening and diagnostic tools for assessment.³PD screening tools: Various screening tools have been developed to detect PD with their advantages and limitations (Table 2). Treatment: Management of delirium involves a multidisciplinary stepwise approach (Figure 1)³ including the management of the underlying medical illness, minimizing iatrogenic triggers, and optimizing the PICU environment. Pharmacotherapies are indicated if delirium persists and a child's agitated behaviour is distressful or interferes with medical care. Haloperidol, risperidone, and quetiapine have been used safely in children.⁵Outcome and prevention: PD is associated with increased length of mechanical ventilation, increased hospital stay, higher resource utilization, increased healthcare costs, and increased mortality. PD is a hospital acquired complication which can be prevented by using analgosedation approach with the goal to optimize pain and minimize sedation, minimizing iatrogenic factors, early mobilization, and involvement of family members in daily care.³Conclusion: PD is an important underrecognized issue in the PICU which needs to be prevented, detected early using screening tools, and managed using a multidisciplinary team approach.

Neurodevelopmental outcomes are of paramount importance for every clinician as the survival rates of term and preterm babies have continued to improve. We aim to provide a framework for developing a Neuroprotective Neonatal Intensive Care Unit (NICU) by describing five main domains below. We achieve this in our NICU by a multidisciplinary team consisting of neonatologists, respiratory therapist, occupational therapist, physiotherapist, social worker, pharmacist, and a dietician. This approach needs to be individualised for each unit based on the resources and services available.

I. Neuro assessment: clinical neuro assessment remains the most important tool with strong predictive value for long-term outcomes. It is important to develop other tools of assessment like comfort and pain scoring. We use COMFORTneo scale as a standard of care.¹ Neuroimaging is another important factor as part of the assessment. We have a local guideline to decide on the frequency and the timing of the neuroimaging such as cranial ultrasound and MRI.

II. Neuroprotection: antenatal magnesium sulphate and antenatal steroids have become an established treatment in most units.² Interventions like total body cooling have significantly improved the outcomes for babies with hypoxic ischemic injury. One challenge faced in these babies is the ability to provide active cooling during transport when these babies are born outside cooling centres. Optimal nutrition is another important element for the developing brain. We developed neonatal nutritional guidelines in collaboration with the clinical pharmacist and a dietician. Introduction of starter parenteral nutrition bags for out of hours use in line with evidence-based feeding guidelines are known to improve the outcomes. We practice the golden hour protocol for all babies born before 28 weeks gestation and have introduced intraventricular haemorrhage (IVH) prevention bundles³ for the same cohort of babies. Even though individual components of these bundles do not have strong evidence, there is some benefit when these interventions are offered as a bundle. Our care bundle involves midline positioning, using log roll, minimal handling, maintaining normothermia, avoiding IV boluses, and maintaining normal CO2 levels etc.

III. Neuromonitoring: tools like amplitude-integrated electroencephalogram (aEEG), near-infrared spectroscopy (NIRS), and onsite MRI are gaining popularity. eEEG should be routinely used in hypoxic ischemic encephalopathy (HIE) babies when available. All team members should be trained in its application and interpretation. NIRS is a developing modality used by only a few units to monitor the cerebral oxygenation. We have recently started to pilot these machines.

IV. Neurodevelopment: the environment of the NICU has been shown to affect the developing brain. Strategies should be developed to optimise babies sleeping by reducing lighting and noise levels. We use positioning tools like boundaries and midliners as part of their neurodevelopment.

V. Neurointervention: we use therapeutic techniques like auditory, tactile, visual, and vestibular (ATVV) stimulation.⁴ It is an evidence-based technique used to increase alertness in medically stable preterm infants. We use Prechtl's Qualitative Assessment of General Movements observational tool.⁵ It is the most predictive tool (98% sensitivity) for detecting cerebral palsy. This helps provide targeted treatment at an earlier stage.

There is an ongoing debate about the management of the critically ill mother, notably with regards to who should manage this group of patients (the intensivist, the obstetric anaesthetist, or the obstetrician?) and where is the ideal place to manage them (labour ward, obstetric high dependency unit or the intensive care unit?). To make the most appropriate choice, an understanding of how to recognise maternal critical illness is paramount. Using the modified early obstetric warning system score (MEOWS) for obstetric patients is a useful tool ¹. MEOWS looks at additional parameters to the standard early warning systems parameters with modified triggers to suit the altered physiology in the pregnant patient. Other predictors like APACHE and SOFA scores may also be used to predict maternal mortality ². Data from several national audit and surveillance programs such as MBRRACE-UK (Mothers and Babies: Reducing Risk Through Audits and Confidential Enquiries across the UK) ³, UKOSS (The UK Obstetric Surveillance System), and ICNARC (Intensive Care National Audit & Research Centre) are used to aid the understanding of why mothers die in childbirth and up to six weeks postpartum and which critically ill mothers are admitted to the intensive care unit and the reason for their admission ⁴. Audit reports show that a significant number of deaths reported in the maternal mortality reports are associated with suboptimal care. There is a great need for an evidence-based triage system for the critically ill obstetric patient in order to help clinicians direct them to the appropriate level of care and avoid situations of suboptimal care. Regionalizing maternal critical care may help develop this triage system by increasing the exposure to such patients. Deciding on who should manage these patients will depend on the level of training and expertise of the team members involved in the management on how to detect an acutely deteriorating mother. The team members should include obstetricians, anaesthetists, intensivists, intensive care nurses and midwives. The training can be achieved using different educational approaches that are competency-based to improve the knowledge and skills in detecting signs of deterioration in order to take the appropriate actions. Multidisciplinary teams should train together using simulation-based learning focusing on human factors and communication skills ⁵. Deciding on where these patients should be managed will depend on the level of organ support and monitoring available as well as the access to support services such as obstetric and neonatal services, regardless of what the terminology of that location is. The different models of delivering care to the critically ill obstetric patient with the different requirements for these areas are highlighted in Table 1. Taking all the previous factors into consideration will help find the answer to the WHO, WHERE and HOW question.

Introduction: Delirium, the most prevalent form of acute brain dysfunction in the Intensive Care Unit (ICU) is characterized by inattention, changes in cognition and at times thought and perceptual disturbances (e.g., delusions and hallucinations). Recent estimates of delirium prevalence suggest around 70% of patients on mechanical ventilation will experience delirium during their critical illness and almost a third of days in the ICU are days spent with delirium^1,2. There are at least three distinct motor subtypes of delirium: hypoactive (decreased movement), hyperactive (increased movement and at times agitation) and mixed (features of both). The hypoactive form predominates, is under-diagnosed and is associated with worse outcomes. Recent work has suggested that another psychomotor disturbance, catatonia may co-occur in up to a third of patients with delirium in the ICU³. Risk factors: Risk factors for the development of delirium include: pre-existing dementia, advanced age, hypertension, pre-critical illness emergency surgery or trauma, increased severity of illness, mechanical ventilation, metabolic acidosis, prior delirium or coma and use of certain delirium potentiating drugs such as anti-cholinergic and sedative hypnotic medications. Mechanisms: Exact mechanisms leading to the development of delirium are unknown, however early evidence suggests neural disconnectivity of the dorsolateral prefrontal cortex and the posterior cingulate cortex. Reversible reduction of functional connectivity of subcortical regions and neuroinflammation leading to hippocampal and extra-hippocampal dysfunction, may play potential roles. Overall all brain volume loss and disruption in white matter tracts may be associated with new onset dementia in survivors of critical illness. Due to the heterogeneous phenotype of delirium, there may be multiple causative neurobiological mechanisms contributing to its development, instead of one unifying pathway. Morbidity and mortality: Delirium is associated with significant morbidity and mortality. Much of the critical care literature about delirium has focused on the exposure of delirium and its relationship with acquired disabilities, as well as its effect on in-hospital and post-discharge excess mortality. Delirium is known to be predictive of new-onset dementia⁴, depression, excess mortality, longer lengths of stay, institutionalization at discharge, inability to return to work and increased cost of care in the hospital. Prevention and treatment: Despite scant evidence, antipsychotic medications have historically been the treatment of choice for delirium, however recent findings suggest that typical and atypical antipsychotics have no effect on delirium duration in the ICU⁵. As delirium is characterized by alterations in the sleep wake cycle, some studies have explored the role of melatonin or ramelton in the prevention or treatment of delirium, with early promising results. Non-pharmacological interventions such as complete adherence to the ABCDEF (Assess, prevent, and manage pain; Both spontaneous awakening and breathing trials: Choice of analgesia and sedation; Delirium assess, prevent, and manage; Early mobility and exercise; Family engagement/empowerment) bundle have shown benefit in reducing delirium prevalence in the ICU².

Monitoring the health of an injured brain is essential to forewarn neurological worsening and to gain insight into the pathophysiology of a complex disorder.

Clinical examination remains a cornerstone in monitoring patients with brain injury. The Glasgow coma score (GCS) is widely used but lacks information regarding brain stem functions like pupillary reaction and shows moderate inter-observer reliability. However, despite these shortcomings, GCS remains a robust indicator of the need for surgery and prognosis after cardiac arrest, hypoxic brain injury, and posterior circulation stroke. A new scoring system called Full Outline of Unresponsiveness has been proposed and shows excellent inter-observer reliability and includes points concerning brain stem functions.¹

The most commonly used monitoring modality is intracranial pressure (ICP) monitoring. ICP shows threshold physiology where the outcome of the patients changes after a threshold of 20 to 25 mmHg. Refractory ICP is a good predictor of mortality but not of the functional outcome after traumatic brain injury.

Brain injury causes varying degrees of disruption to cerebral blood flow and its autoregulation. Studying autoregulation provides a useful strategy for targeting cerebral perfusion pressure close to the autoregulatory range. Transcranial Doppler and ICMplus (Intensive Care Monitoring) are used to study autoregulation. ICMplus is a software-based tool that studies the correlation between slow changes in mean arterial pressure and ICP to evaluate the state of autoregulation throughout the duration of ICP monitoring.²

Brain tissue oxygen measures the partial pressure of oxygen in the extracellular fluid of the neural tissue. Reduction in brain tissue oxygen is a marker of cellular distress. A phase 2 trial on brain tissue oxygen monitoring demonstrated the safety and feasibility of the protocol-based management of brain tissue oxygenation and ICP, and a trend towards lower mortality and improved functional outcome in patients treated with combined oxygen and ICP protocol.³

Microdialysis is a point of care test that monitors substrate delivery and metabolism at the cellular level. The lactate-pyruvate (LP) ratio is an indicator of the redox state of cells and a high LP ratio is associated with an unfavourable outcome.⁴

The electroencephalogram (EEG) is used in critical care for monitoring sedation and diagnosis of seizure activity. EEG is a complex signal which requires advanced training and skills for interpretation. Novel EEG-based monitors are aimed at simplifying the signal for straightforward interpretation by bedside medical professionals. Cerebral function monitor (CFM) is a compressed single channel amplitude integrated EEG monitor mainly used for the detection of status epilepticus and burst suppression during thiopentone infusion. A novel technique that uses direct electrodes applied on the cortical surface called Electrocorticogram (ECoG) shows spreading depolarisations on the cortical surface that are caused by loss of ionic homeostasis and substrate delivery.⁵ These depolarisations are a sensitive indicator of impending neuronal death and may serve as a target for novel mechanistically oriented therapies.

Detection, prevention, and monitoring of secondary cerebral insults that alter the prognosis from the injury, remains at the centre stage in neurocritical care. In the future, integrated informatics derived from multimodality monitoring will play a pivotal role in clinical decision algorithms.

The use of adrenaline during a cardiac arrest is well-established and supported by international guidelines. However, recent studies^1–2 have questioned the appropriateness of adrenaline administration whereas other papers indicate that any benefit from adrenaline maybe time-sensitive.^3–4

Two recently published studies have both challenged the use of adrenaline during resuscitation and whilst both papers used different methodologies they demonstrated similar results. The Paramedic 2 study¹ was a placebo-based randomised control trial whereas the paper by Loomba et al.,² used a meta-analysis of 14 peer-reviewed publications recruiting 655,853 patients, 7.4% of whom received adrenaline. Neither study was able to demonstrate any meaningful survival benefit associated with adrenaline administration (Table 1 and 2). However, both studies noted poor neurological outcome in post-cardiac survivors. It is noteworthy that both of these studies used different, but validated,⁵ neurological scoring systems (either the Modified Rankin Scale or the Cerebral Performance Category).

Whilst there is an acceptable correlation between the Modified Rankin Scale or the Cerebral Performance Category (Table 3) there is a degree of variation.⁵ This variation is partly due to what the two scales accept as being a good neurological outcome as well as an inbuilt degree of subjectiveness of any assessment of neurological status.⁵

Whilst The Paramedic 2 study¹ and Loomba et al.,² meta-analysis demonstrated no benefit of adrenaline, studies by Goto et al.,³ and Donnino et al., (adults)⁴ have published contradictory findings. Importantly Donnino et al.,⁴ reported improved neurological status in non-shockable cardiac arrest when adrenaline was administered.² However, to date no study has demonstrated a benefit of adrenaline when used to treat shockable cardiac arrest.

Interestingly both Goto et al.,³ and Donnino et al.,⁴ indicated that any benefit from adrenaline administration was time-sensitive. Goto et al.,³ noted that the optimal time for adrenaline administration was < 9 minutes. Whereas, Donnino et al.,⁴ reported on the impact of increasing time delay to the first dose noting that when adrenaline was administered < 1 minute of confirmation of cardiac arrest, 12% of patients survived, but that this dropped to 9% after the fourth minute and was down to 7% after seven minutes (p < 0.001). The findings of Goto et al.,³ and Donnino et al.,⁴ represent a clinical challenge. Notably, during the Paramedic 2 study the average time of administration of adrenaline was approaching 20 minutes (6.6 minutes response time and 13.8 minutes) raising the question would the results of Paramedic 2 have been different if adrenaline was administered faster and whether adrenaline should only be administrated in witnessed cardiac arrest?

The routine use of adrenaline as the mainstay of resuscitation is being challenged, especially with regards to long-term patient survival and its role in the management of shockable cardiac arrest. However, in specific patients, when given early, adrenaline may still have a role to play in resuscitation. The 2020 International Resuscitation Guidelines are eagerly awaited.

Introduction: Hypoxic-ischemic encephalopathy (HIE) is the leading cause of death in comatose patients after cardiac arrest resuscitation.¹ Poor neurological outcome is defined as death from neurological cause, persistent vegetative state, or severe neurological disability which is predicted in these patients by assessing the severity of HIE. Background: The most commonly used indicators of severe HIE include a bilateral absence of corneal and pupillary reflexes, bilateral absence of N2O waves of short-latency somatosensory evoked potentials, high blood concentrations of neuron-specific enolase, unfavorable patterns on electroencephalogram, and signs of diffuse HIE on computed tomography or magnetic resonance imaging of the brain.

Current guidelines recommend performing prognostication no earlier than 72 hours² after return of spontaneous circulation in all comatose patients with an absent or extensor motor response to pain, after having excluded confounders such as residual sedation that may interfere with clinical examination. A multimodal approach combining multiple prognostication tests are recommended so that the risk of a false prediction can be minimized. Materials: Neuroprognostication is vital and yet continues to be one of the most controversial topics in post-resuscitation care. Specifically, concerning HIE, the 2006 practice parameters of the American Academy of Neurology provide specific recommendations for the prognostication of neurologic outcomes for cardiac arrest survivors not treated with therapeutic hypothermia (TH).

To date, there is no adequate paradigm for prognostication in HIE treated with TH.³ Clinical examination including the presence or absence of brainstem reflexes, motor responses and absence of myoclonus were traditionally used to predict a favorable prognosis. Electrophysiologic testing in the form of somatosensory evoked potentials (SSEP), the serum biomarker neuron-specific enolase (NSE), as well as neuroimaging, have been employed as additional tests to attempt to improve the predictive accuracy of neuroprognostication. However, what limited certainty these tests and parameters provided has become even more questionable in the setting of therapeutic hypothermia. The use of sedatives and analgesics adds a degree of uncertainty given unpredictable drug effects on patients’ neurologic status.

EEG, SSEP are the most common electrophysiological modalities utilized in neuroprognostication.⁴ EEG has been evaluated in the prognostication of cardiac arrest survivors and has also led to some essential clinical discoveries. The 2006 American Academy of Neurology (AAN) practice parameters assign EEG a false-positive rate (FPR) of 3% with a CI of 0.9; making it the least predictive method to determine neurologic outcomes. Abend et al., pooled four existing studies on EEG in cardiac arrest (CA) patients who had undergone therapeutic hypothermia and found that 29% of these patients had acute electrographic non-convulsive status epilepticus (NCSE).⁵Conclusion: There is no good evidence from well-designed studies to support substantial accuracy of early prognostication ( < 72 hours post-arrest) in cardiac arrest survivors treated with therapeutic hypothermia.^2,6 Given our lack of understanding of how therapeutic hypothermia improves outcomes, as well as its effects on emergence from the coma and its well-described effects in altering drug metabolism and clearance, it is prudent to be more conservative in approaching prognostication. Patients should be observed for a minimum of 72 hours post-arrest. However, 5-7 or more days of observation may be necessary to fully account for the effects of therapeutic hypothermia.

The incidence of deep vein thrombosis (DVT) in the critically ill ranges from 3.6% to 37%. Despite seemingly adequate prophylaxis the risk for DVT is still between 4 and 15%.

Currently the known risk factors can be divided into inherited and acquired. In addition, the underlying disease and comorbidities play a major role, e.g., history of DVT, malignancy, ongoing infectious disease, cardiovascular disease and pregnancy¹.

DVT prevention is applied in various ways and timings. Principally, the choice is between mechanical, pharmacological and a combination of both.

Regarding the mechanical prophylaxis, recommendations point more to the use of intermittent pneumatic stockings (IPS), which are more effective with less side effects than simple stockings². Whenever pharmacological treatment carries a relatively high risk (e.g., fresh bleeding, traumatic brain injury) mechanical prevention might be started. However, it is still under debate whether the combination of IPS with pharmacological prophylaxis is superior.

Like all anticoagulant therapy, the risk (and consequences) of DVT should be balanced against the risk of bleeding. A variety of scoring systems, like the Well's score, the Caprini score and the Has-Bled score exist to group the risks. In terms of risk assessment, bleeding after peripheral surgery might be less dangerous than after intracranial surgery.

In general, low molecular weight heparins (LMWH) are preferred above unfractionated heparin (UFH). One reason might be the risk of heparin induced thrombocytopenia (HIT), which is higher with UFH than with LMWH. On the other hand, UFH have a shorter half-life necessitating at least two daily injections, while the LMWH schemes apply a once daily injection³. However, the shorter half-life and the ease of reversal might be an argument for UFH use in patients at bleeding risk. In contrast, LMWH's carry a higher risk of bioaccumulation^4,5. The route of application seems to be another point of concern. In the critically ill, peripheral organ perfusion might be disturbed by the disease or the therapy (i.e. vasoconstriction or edema).

It is still a debate if oral anticoagulants should be used in critical care. Mainly concerns are raised from pharmacological considerations. For instance, if enteral feeding is only possible via tubes, grinding of tablets will change the galenic of the drugs and their bioavailability. In addition, it is not clear whether orally applied drugs will be resorbed completely. Excretion of drugs might be altered due to impairment of kidney and/or liver function which could result in their accumulation.

Finally, changes in the coagulation system due to the underlying disease might occur unexpectedly and therefore unanticipated.

In concert with difficulties in laboratory measurement and reversal of the drug benefits of oral anticoagulants do not outweigh risks and disadvantages. Therefore, it seems not recommendable to start any kind of oral anticoagulation before the patient's condition is stable enough which is mostly the moment of discharge from the ICU.

Autoimmune rheumatological disorders are rare but important to consider in Intensive Care Unit (ICU) patients. Overall prevalence of these disorders is approximately 3% in the general population. About 25% of patients presenting with these disorders to the emergency room (ER) require hospital admission and up to one third require ICU admission.¹ Mortality is variable and reported to be around 20% in recent studies.^2,3

The most common rheumatological diseases requiring ICU admission are systemic lupus erythematous (SLE), antineutrophilic cytoplasmic antibody (ANCA)-associated vasculitides, rheumatoid arthritis, scleroderma, and dermatomyositis.^1–3 The most common reasons for admission are infections and exacerbation of an underlying disease. The factors associated with mortality include Acute Physiology and Chronic Health Evaluation (APACHE) - II or Sequential Organ Failure Assessment (SOFA) score, vasopressors support, and prolonged hospital stay.^2,3

In most patients with rheumatological disorders, the underlying disease is known at the time of admission. The diagnostic considerations in these patients include infections, underlying disease exacerbation, iatrogenic toxicity, or a rheumatologically unrelated disorder. The most difficult and challenging problem in these patients is differentiating between sepsis and exacerbation of an underlying disease, and laboratory markers may help in this differentiation. In SLE patients an ESR/CRP ratio >15 is suggestive of disease flare while < 2 is suggestive of infection. CD64, 2’5’-oligoadenylate synthetase (OAS) and soluble triggering receptor expressed on myeloid cell type 1 (sTREM1) are also promising biomarkers in differentiating infection and disease flare in SLE. A “bioscore” combining different biomarkers may be more useful than a single biomarker in differentiating disease flare versus infection.

Some medical conditions should always be on the radar of an ICU physician when patients present with multisystem disease with no clear underlying etiology. These include macrophage activation syndrome which may occur at any stage of rheumatic disease (onset, during active disease, during quiescent disease). A ferritin level of >10,000 microgram/L is pathognomonic, and >5,000 is highly suggestive of this diagnosis. Elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), high CRP with low ESR may also help with this diagnosis.^4,5 In scleroderma, renal crisis should never be missed and initiation of angiotensin converting enzyme inhibitors (ACEI) should be prompt to avoid morbidity. In any patient with livedo reticularis, digital ischemia, splinter hemorrhages, ulceration and superficial gangrene of lower limbs with multi-organ failure and SIRS, catastrophic antiphospholipid (APL) syndrome should be suspected. Any patient on methotrexate (MTX) should be evaluated for pneumonitis and bone marrow toxicity related to MTX. ANCA-associated vasculitis should be considered in any patient with combined respiratory and renal failure.^4,5 Bronchoscopy should be prompt in this situation to rule out diffuse alveolar hemorrhage.

In summary, rheumatological disorders are relevant considerations in any patient with single or multi-organ failure in ICU when the underlying etiology is not obvious. A routine immunological screening may be lifesaving in this setting and prompts further work-up and diagnosis. It is extremely important to involve a rheumatologist early in the management of any patient with known or suspected rheumatological disorder. Frequent collaborative discussions and meetings may go a long way to improve prognosis of these patients in the short and long term.

Background: The World Health Organization acknowledges sepsis as a global priority. Healthcare providers and governments have a critical role to play.¹ National sepsis programs have been established in Qatar and in many other countries.^1,2 Here, we share our pediatric sepsis program development and success. Missing signs of early sepsis in children can result in delayed management, complications, and death. A standardized pediatric sepsis pathway based on creating a “THINK SEPSIS” culture incorporating an electronic early warning system and improving effective communication among healthcare providers using standardized tools can help early sepsis recognition, timely management and proper escalation, and ultimately improve patient outcomes.^3–5Methods: Building on the structure of the adult sepsis program, the pediatric sepsis committee was established in 2017 and a National Pediatric Sepsis Program was created.

It is based on a multifaceted approach of education, governance, awareness campaigns, and utilization of an electronic medical record system. Simulation sessions of pediatric sepsis were delivered to fill knowledge gaps. To further pediatric sepsis care in Qatar the following steps were completed:

• Established a pediatric sepsis clinical pathway and guideline to be followed in all clinical areas at all times whenever a child is suspected or confirmed to have sepsis, hence avoiding variation of practice and saving valuable time. • Introduced sepsis watchers in the daily safety huddle to facilitate continuity of care and alert staff concerning deteriorating patients. • Provided a standardized pediatric sepsis diagnostic kit with all required investigation equipment and IV access to all concerned units to minimise delays and standardize care (Figure 1). • Unified the pediatric sepsis antibiotics kits in all units with a safe first dose preparation protocol based on the most recent antibiogram to ensure the delivery of the first dose within 60 minutes of pathway activation. • Rolled out an e-learning module which is simple, interactive, and evidence-based for staff to be acquainted with the program and to increase awareness. • Developed an electronic pediatric sepsis order set allowing clinicians to initiate all elements of the sepsis bundle within a few minutes, saving time and ensuring consistency and reliability (Figure 1).

1. The proportion of clinical review, Rapid Response Team activation, and sepsis alerts that were appropriately escalated is 91%. This is an important achievement to ensure timely intervention thus saving lives (Figure 2A). 2. 81% of patients received IV antibiotics within 60 minutes of time zero. This is an essential element of sepsis care bundle (Figure 2B). 3. Pediatric sepsis golden-hour order set was initiated in 26% of cases (Figure 2C). 4. Achieved sepsis bundle compliance of 42%.

Sepsis clinically manifests as life-threatening organ dysfunction due to a dysregulated host response to infection.¹ Optimal fluid resuscitation is relevant for all sepsis patients, and perhaps it is most important for those with septic shock. Septic shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greatest risk of mortality, and septic shock is clinically identified as sepsis patients with serum lactate level >2 mmol/L and who require vasopressor infusion to maintain a mean arterial pressure ≥  65 mm Hg in the absence of hypovolemia. Sepsis is among the most common conditions in the intensive care unit (ICU), accounting for up to half of all hospital deaths and being the third leading cause of death overall in the United States.²

Sepsis and septic shock are medical emergencies for which treatment and resuscitation should begin immediately. The goals of fluid resuscitation for these patients are: a) to rapidly replace intravascular volume and restore tissue perfusion, and b) to minimize organ dysfunction through timely interventions that either halt or reverse the physiologic derangements. If hypoperfusion is present, at least 30 mL/kg of IV crystalloid fluid should be given rapidly, and additional fluids should be guided by frequent reassessment of hemodynamic status, preferably using dynamic indices to indicate the likelihood of a beneficial response to fluid administration. Fluid administration should be targeted to achieve a MAP of at least 65 mm Hg, and to normalize lactate in patients with elevated lactate due to hypoperfusion.³

Balanced crystalloids are the fluid of first choice for sepsis resuscitation based on ready availability and taking medication costs into account. Use of 0.9% saline compared to a balanced crystalloid, such as lactated Ringer's or PlasmaLyte, produces more kidney dysfunction and with a greater risk of dying.⁴ The individual side effect profiles may best differentiate the natural and synthetic colloids. Albumin may be considered for administration to sepsis patients with refractory shock or who have received substantial amounts of crystalloid fluids, but should not be administered to patients with severe traumatic brain injury.⁵ Hydroxyethyl starch (HES) products should not be administered to patients with sepsis because of increased risk of acute kidney injury and death. Gelatin solutions are not recommended in sepsis.

Norepinephrine is the vasopressor of first choice for patients with septic shock, and should be administered to achieve a mean arterial pressure of at least 65 mm Hg after excluding hypovolemia as a cause for hypotension. The selection of a second line vasopressor, such as vasopressin, dopamine, phenylephrine, epinephrine or angiotensin-2, depends on patient factors such as underlying cardiac dysfunction, presence of arrhythmias, and current response to vasoconstrictor or inotropic agents. Dopamine should not be used for renal perfusion or protection and it should be avoided in patients with tachyarrhythmias.

Sepsis, a heterogeneous syndrome, is usually associated with uncontrolled body response to a systemic infection leading to dysregulated pro- and anti-inflammatory cascades.¹ This, subsequently, leads to immune suppression, tissue damage, and organ failure. With time, the natural body compensation is lost and a state of shock, characterized by profound hypotension and abnormal cellular metabolism, ensues. Sepsis and septic shock are thus considered major challenges in critical care management due to the high rates of complications, including morbidity and mortality. Successful management of sepsis/septic shock necessitates implementation of urgent treatment measures targeting the underlying infection, as well as improving patient's hemodynamics.² Treatment measures include administration of antimicrobials, vasoactive drugs, sedatives, analgesics, along with others with the aim of achieving effective, yet safe concentrations of different administered medications at the targeted site of action.³ However, this aim of efficient medication dosing attainment can be challenging in critically ill septic patients. The host response to sepsis is usually associated with tremendous changes of different physiological processes.^3,4 Different studies have shown that such pathophysiological alterations were linked to dysregulations in both pharmacokinetic (PK) and pharmacodynamic (PD) properties of different administered medications and thus result in complicated drug dosing.^3,4

Pharmacokinetics of a given therapy is usually linked to the administered dose and the corresponded changes of concentrations inside the body with time, whereas pharmacodynamics describes the resultant relation between the obtained drug concentration and its pharmacological effect. In-vivo efficacy of an administered medication is largely driven by its intrinsic PK and PD properties. Variations in PK/PD are not always universal or easily predictable, and different aspects can affect the overall discrepancies. Those aspects include disease, patient and drug related factors.⁵ For instance, the alterations of PK/PD properties seen with sepsis can be different from those seen with septic shock. A similar thing applies to the drug properties where the therapeutic concentrations of a lipophilic medication might be less prone to changes as compared to a hydrophilic therapy. Likewise, the co-existence of different conditions that influence overall medications' pharmacokinetics can complicate proper prediction of therapeutic concentrations. This is frequently encountered in critically ill patients presenting with sepsis/septic shock and requiring the use of renal replacement therapy (RRT), extracorporeal membrane oxygenation (ECMO), plasmapheresis, or even all in certain individuals.

A deep understanding of various pathophysiologic changes seen in critically ill patients and their effects on the overall drug PK/PD is thus essential. This ensures that personalized dosing regimens are tailored to each patient to achieve an optimized therapy rather than using a “one size fits all” model of drug dosing. The implementation of personalized tailored therapy based on patient specific parameters, along with the utilization of therapeutic drug monitoring can successively give rise not only to improved clinical efficacy but also to decreased toxicity and antimicrobial resistance. Subsequently this would result in improved patient outcomes and survival.

Catecholamines are an integral component of the host stress response and usually increase appropriately at times of need. Unfortunately, in severe and prolonged critical illness, they can contribute to significant harm with unwanted biological effects on cardiac function, inflammatory, immune, metabolic, and coagulation pathways¹. A good example is Takotsubo (‘stress’) cardiomyopathy where heart failure ensues after an emotional stress resulting in extremely high levels of circulating catecholamines, considerably above that seen in a significant myocardial infarction².

Unwittingly, we are likely contributing to catecholamine toxicity in our management of the critically ill septic patient through use of exogenous catecholamine therapies which carry the same detrimental effects as endogenous catecholamines^1,3. Catecholamines are currently recommended first-line agents for septic shock, and are used in an attempt to overcome the vascular hyporeactivity and myocardial depression associated with sepsis. Use of higher doses of catecholamines is however associated with worse outcomes⁴. This is usually ascribed to the patient's underlying illness severity and an iatrogenic contribution is not considered – but perhaps should be.

Beta-blockers have multiple actions, on cardiac function and beyond. They reduce cardiac work through negative inotropic and chronotropic effects. Importantly, through slowing an excessive heart rate, both systolic and diastolic ventricular function are improved. They also act on adrenergic receptor responsiveness, enhancing the activity of catecholamines and allowing reductions in dose to achieve the same haemodynamic effect. Outside the heart, they improve vascular tone, enhance metabolic efficiency, and have anti-inflammatory effects and anti-thrombotic activity.

The first use of beta-blockade in sepsis goes back nearly 50 years with successful use in some patients in refractory shock. In the last decade an increasing number of observational studies and a few single-centre randomised controlled trials have shown both safety and improved outcomes⁵. These reflect findings in animal models of sepsis where various mechanisms were demonstrated including protective effects on the heart, anti-inflammatory actions and preservation of the gut barrier⁵.

Clearly, the patient needs to be adequately fluid-resuscitated and stabilised before commencing beta-blockers. Ideally, the use of a short-acting agent such as esmolol or landiolol allows easy titration, or cessation, of the infusion should hypotension or excess bradycardia occur with the unwanted effects wearing off within minutes. The largest study to date by Morelli et al., randomised 154 septic shock patients to receive either placebo or esmolol to reduce heart rate to 80-95 bpm. This was successfully achieved with no increase in complication rates compared to placebo. Importantly, there were also benefits in terms of earlier recovery of renal function, cessation of norepinephrine infusion, lower troponin levels (indicative of less cardiac damage), and improved survival rates. These encouraging findings need to be repeated in multicentre settings and two studies (one UK-based “STRESS-L”, one in 4 European countries) are currently ongoing.

Debriefing after critical events is a well-known practice in medicine, utilized in both simulated and real-life situations. In addition to reviewing the medical aspects of the care, debriefing allows for examination of team performance and human factors involved in the event. Various methods, locations, and time intervals can be utilized to debrief to meet the team's needs. Some proven methods of debriefing include plus-delta, directive feedback, the Socratic Method, and advocacy and inquiry.¹ Each method has its benefits and limitations and can be applied during various segments of a debriefing to achieve the debriefer's goals. These goals usually include identifying and addressing knowledge gaps, uncovering participants' beliefs and thought processes, reflecting on the team's performance, and synthesizing the information to improve future performance.² Debriefing should be a planned follow-up to every critical event. This standardizes the process and expectation for teams to share their experiences and work towards an improved performance. The debriefing environment should be a safe space for team members to express their emotions while sharing successes and challenges without fear of repercussion or blame. Allowing team members to share their decision-making process and knowledge level lets the debriefer tailor learning points to address appropriate deficits rather than assuming and targeting areas that may not need improvement. In addition, involving team members from all involved disciplines can enhance the outcomes of the debriefing. There is evidence that handoffs with more team members can improve efficiency, documentation, and future patient outcomes.³ The timing of these debriefs can be varied based on the clinical scenario and even the emotional state of the team members. Immediately debriefing after an event, also known as the “hot” debrief, allows most team members to participate and capitalizes on a clear memory of events to identify successes and opportunities for improvement. In addition to performance improvements, these sessions may help team members express their emotions and offer some coping skills to deal with unfortunate outcomes including the death of a patient. However, sometimes the debriefer may assess the emotional state of the team and deem it not appropriate to conduct the debriefing immediately after the event. In these settings a delayed debriefing session, or “warm” or “cold” debrief, may allow team members to process their emotions and reflect on the clinical event prior to coming together as a group to discuss their performance.

Despite the well described benefits of debriefing, there continues to remain a disconnect between knowing to conduct debriefs and their actual implementation. This can be due to various circumstances including, time pressures, patient care, or limited training in how to debrief a team. These failures to debrief can lead to communication breakdowns within the team.⁴ The absence of a debriefing can also lead to improper or inadequate documentation, which can result in clinical error and increased litigation.⁵ Organizations such as the Agency for Healthcare Research and Quality advocate for clinical event debriefing; this attention and effort on research and training can hopefully increase the frequency of and comfort with clinical event debriefing.

There are several questions that need answering regarding mobilization of Intensive Care Unit (ICU) patients. How do we mobilize ICU patients? Is there an internationally agreed definition? Is there an internationally agreed prescription/program for mobilizing the patients? What is considered early? Why should we mobilize our patients, and lastly, why don't we?

Mobilization of ICU patients takes many different forms and views. It includes bed activities such as range of motion, turning, transferring, self-care, breathing exercises, sitting at the edge of the bed, and even stationary cycling. There are also several out of the bed activities such as sitting in a chair, standing, and walking. Although several units have their own protocols, a literature review reveals that definitions are either too broad or too narrow, subsequently challenging to transfer these results.¹

Some trials have started mobilizing patients from as early as the first day, while other trials have waited 48 hrs, 5 days, and even longer before mobilization was started. Most trials which have managed to deliver very early mobilisation have found improved outcomes up to hospital discharge, while trials which intervened later mostly found no significant effect.² The absence of a definition for early, very early, and late initiation of mobilization makes comparing studies very difficult.

Muscle weakness that develops during the ICU stay is called ICU-acquired weakness (ICU-AW). It manifests as generalized muscle weakness that is often severe. It develops in ICU patients who receive mechanical ventilation for 24 hours or more and is associated independently with prolongation of the duration of mechanical ventilation and ICU and hospital stay. ICU-AW is associated with increased mortality in the first year following ICU discharge. Mobilizing patients at an early time point decreases invasive mechanical ventilation (MV) duration, delirium, hospital length of stay, and reduced healthcare costs.^3,4

Reported reasons for not mobilizing patients vary widely and include mechanical ventilation, catecholamine infusion, impaired consciousness, poor functional status, safety considerations, limited staff capacities, or lack of protocols. Absolute contraindications can include acute myocardial infarction, active bleeding, increased intracranial pressure with major instability, unstable pelvic fractures, therapy withdrawal, and lastly patients’ refusal.⁴

Recommendations on safety criteria for early mobilization mention that vasopressor use, endotracheal intubation, renal replacement therapy, or even life support devices like ECMO should not be considered as contraindications for active mobilization. Only one study has explored the safety of very early mobilization in critically ill patients on multiple support systems.⁴

Multiple QI projects have successfully implemented and sustained early mobilization projects within the ICU setting and all identified strong leadership for early mobilization. This along with the multidisciplinary team approach ensured success and sustainability of mobilizing ICU patients.⁵

In conclusion, there is a lack of internationally agreed protocols or guidelines on when and how we should mobilise our patients. There are also several obstacles facing us even once achieving consensus in that. The good thing is that we are clear on why we should mobilise our patients and hopefully this will drive further research to standardize the above unanswered questions.

ICUs in the future will comprise a larger percentage of hospital beds as care of less seriously ill patients shifts to home and other environments. ICUs will need to adapt to increased demand for services and concomitant economic pressures with efficiency and innovation. The future ICU will see changes in form, function, personnel and patients.

The type of patients in ICUs and their medical conditions will be different. Prevention, early detection, and timely treatment of conditions such as infection and respiratory failure should decrease the need for many ICU admissions. Patients needing ICU care will have multiple complex problems that shift the epidemiology of critical care. This shift in patient populations will not change the need for compassionate and empathetic care.

Precision medicine for patient care is the goal of the future ICU—tailoring therapy for conditions based on individual characteristics, risk profile or genetic markers¹. Protocols and guidelines will require the ability to adapt to defined patient groups.

The physical ICU environment of the future must promote a healing environment for patients, families, visitors and ICU staff². Optimal design should reduce noise, maximize work efficiency, minimize potential for errors, decrease infection risk, reduce stress and provide comfort for families and visitors. The environment will address sound, light, temperature, smell, art and entertainment needs. The ICU of the future must be a flexible environment with built-in adaptability for technological advances. Cohorting of critically ill patients in a defined ICU area will continue for efficiency but the flexibility to deliver critical care outside the physical ICU must also be provided. Patient-centered care will continue to drive services in the future.

The ICU of the future continues to require a highly trained collaborative team of professionals but roles and responsibilities as well as composition of the team will change. Intensivists will still oversee these teams but advanced practice providers and non-intensivist physicians may play greater roles in direct patient care. Greater emphasis will be placed on preventing burn out in team members through use of smart technology, optimum work environment and professional support.

Technology will be the most constantly changing variable in future ICUs that will affect the environment, patients, and staff. Sophisticated informatics will interface all hospital systems with the ICU and advance individualized care³. These systems must have characteristics of association, interoperability, integration, security, safety, and real-time synchronization⁴. Artificial intelligence and learning will address the challenges of information overload and integration of data to enable optimum decision making. Electronic “sniffers” will detect and interpret changes in patients’ clinical status and send alerts to clinicians or potentially initiate interventions. In addition, alarm systems will screen out irrelevant signals and decrease the danger of “alarm fatigue” but at the same time provide early alerts to safety issues and provide suggested actions. An outgrowth of advances in information technology will be the use of “big data” to optimize immediate patient care as well as advance research in the ICU⁵.

Background: Improving patient safety and reducing risk is important to a Paediatric Intensive Care Unit (PICU). Simulation-based education has generally focused on the management of clinical diagnoses, whereas the Quality and Safety Team has traditionally focused on collecting and analysing data about adverse events. There is a need to bridge the gap between the two streams - lessons learnt from adverse incidents and their impartation to staff in a targeted format during in-situ simulation training.

Methods: Birmingham Children's Hospital PICU is a 31-bedded tertiary/quaternary unit with approximately 1500 admissions per year in the UK. All adverse incidents are collated (online IR1 with specific forms for incidents involving medications, accidental extubations, buzzer pulls, and extravasations) and analysed by the PICU Safety Group and trends are monitored. The PICU Simulation Team delivers in-situ simulation training for the multidisciplinary PICU staff weekly using interactive, computer-controlled manikins. Each training scenario and debriefing lasts 1 hour. A core team of multidisciplinary simulation facilitators runs the simulation training and the AI (advocacy-inquiry) debriefing model¹ is used for conducting the debriefings. The ‘Simulation Group’ (efferent) and the ‘Risk Group’ (afferent) regularly discuss the priorities for the unit and the lessons learnt based on actual events or near-misses in the unit. It then implements the action points during targeted scenario training sessions. This may be the utilisation of a care bundle or activation of a ‘clinical pathway’. Any practical problem with implementation of these policies is fed back to the Risk Group to close the loop. A concept of ‘Learning from Excellence’ (LfE) has been introduced successfully and both ‘adverse incidents’ and LfE are used together as approaches to improve patient safety in the unit.

Observation/Evaluation: Various simulation scenarios have been run since the start of the project. Examples include accidental extubations, delay in sepsis recognition and antibiotics prescription, ischaemic limb injury due to the indwelling arterial line, emergency chest reopening in post-operative cardiac surgical patients, child protection and safeguarding². The learning gained during each debriefing is generalised to all the participants of the simulation session³ and then subsequently the salient points are shared by email with the entire unit. All staff members have to undergo simulation training. Scenarios are re-run back to back if the team does not achieve the expected outcomes. The anonymous feedback forms completed by the participants of the scenarios have shown they value this targeted training and that it has helped them implement good practice. Anecdotaly, the trend of ‘incident severity’ is believed to have been on the decline over a 7-year period in our PICU but long term monitoring will continue to identify any re-emerging or fresh trends.

Conclusion: ‘Targeted’ simulation-based training is an important approach to enhance the safety culture in PICU. PICU Safety and Simulation Groups should develop a symbiotic relationship for this to succeed. Learning from Excellence can be effectively utilised to embed good practice in a clinical area.