Fran Lockie on Paediatric TBI


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Fran Lockie is a Paediatric Emergency and Retrieval physician currently based in Adelaide. He is quickly becoming a leading expert in paediatric TBI and so was the perfect person to give this talk. The audio that goes with these slides is on Intensive Care Network ( If you like these sorts of presentations, come to Cairns Bedside Critical care this September where we've got a great line up of speakers and we're doing it all again.

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  • Missing: Fluid resus ? Which one Sedatives, NMB Hyperventilation Seizure prophylaxis
  • Remind you all of the recent publication in PCCM earlier this year regarding medical management of TBI in kids Everyone in the room knows we can’t turn back the clock: one of the hardest things about my job is the look in a parents eye who wishes they could have the last 30 mins of their life over again What we can do is prevent secondary insults. This has to happen from the moment the injury is sustained and be sustained with meticulous attention to detail and speed right through from the pre-hospital phase, through the ED and to ICU or definitive surgical care.
  • A lot to talk about Covered a lot of material that are frequent decision making stems in acute emergency, retrieval and PICU environments
  • Clearly what this child needs is definitive care. This raises issues relating to retrieval environment where is that care going to happen Local arrangements need to be thought through. Too often key stake holders in kids care find themselves re-hashing these issues each time a case gets called in
  • Invariably these will be in regional areas given the nature of this vast land.
  • This consensus document was released earlier this year, an update from the last version in 2003 Largely extrapolated from the adult literature. As we’ll see, very hard to do good quality research in this area. Much of it is level C evidence
  • This study from UTAH worried me a lot OBJECTIVES: Traumatic brain injury is a leading cause of death and disability in children. Guidelines have been established to prevent secondary UTAH brain injury caused by hypotension or hypoxia. The purpose of this study was to identify the prevalence, monitoring, and treatment of hypotension and hypoxia during “early” (prehospital and emergency department) care and to evaluate their relationship to vital status and neurologic outcomes at hospital discharge. METHODS: This was a retrospective study of 299 children with moderate- to-severe traumatic brain injury presenting to a level 1 pediatric trauma center. We recorded vital signs and medical provider response to hypotension and/or hypoxia during all portions of early care. RESULTS: Blood pressure (31%) and oxygenation (34%) were not recorded during some portion of “early care.” Documented hypotension occurred in 118 children (39%). An attempt to treat documented hypotension was made in 48% (57 of 118 children). After adjusting for severity of illness, children who did not receive an attempt to treat hypotension had an increased odds of death of 3.4 and were 3.7 times more likely to suffer disability compared with treated hypotensive children. Documented hypoxia occurred in 131 children (44%). An attempt to treat hypoxia was made in 92% (121 of 131 children). Untreated hypoxia was not significantly associated with death or disability, except in the setting of hypotension. CONCLUSIONS: Hypotension and hypoxia are common events in pediatric traumatic brain injury. Approximately one third of children are not properly monitored in the early phases of their management. Attempts to treat hypotension and hypoxia significantly improved outcomes
  • And look at the effect on mortality! Adjusted OR for death and GOS Growing body of evidence that secondary insults occur frequently and exert a powerful, adverse influence on outcomes from severe TBI. Enemies are hypoxaemia and hypotension Trauma Coma Data Bank: hypoxaemia occurred in 22.4% of severe TBI patients: asociated with significantly increased morbidity and mortality. HEMS series 55% of patients were hypoxic prior to intubation. 46% normal BP. In non-hypoxic pts mort 14.3% and 4.8% disability. If SaO2 < 60% mort rate 50% with 100% severely disabled. Hypoxaemia <90% in an inhospital study of 124 TBI patients independent RF for mortality HYPOTENSION. Single pre-hospital obseration of hypotension SBP < 90 was amoung 5 most powerful predictors of outcome. Incr morbidity and doubled mortality Induction of anaesthesia is risky:
  • We need to prevent secondary injury but it’s very lijkely we’ll have to actively manage the airway of patients following TBI and here is a reference table from the London HEMS group Growing body of evidence that secondary insults occur frequently and exert a powerful, adverse influence on outcomes from severe TBI. Enemies are hypoxaemia and hypotension Trauma Coma Data Bank: hypoxaemia occurred in 22.4% of severe TBI patients: asociated with significantly increased morbidity and mortality. HEMS series 55% of patients were hypoxic prior to intubation. 46% normal BP. In non-hypoxic pts mort 14.3% and 4.8% disability. If SaO2 < 60% mort rate 50% with 100% severely disabled. Hypoxaemia <90% in an inhospital study of 124 TBI patients independent RF for mortality HYPOTENSION. Single pre-hospital obseration of hypotension SBP < 90 was amoung 5 most powerful predictors of outcome. Incr morbidity and doubled mortality Induction of anaesthesia is risky:
  • 164 out of theatre intubations 83% had 6 mths anaesthetic experience 41% consultant present Propofol in 76% 96% NMBD 32% DID not use capnography 87% had rescue device 39% suffered at least one adverse event around time of intubation
  • 164 out of theatre intubations 83% had 6 mths anaesthetic experience 41% consultant present Propofol in 76% 96% NMBD 32% DID not use capnography 87% had rescue device 39% suffered at least one adverse event around time of intubation
  • Over 200 patients Complications Hypoxaemia 19.2, hypotension 17.8 arrhythmia 3.4 Usually in adult patients with comorbidities. Only 4.3 % with neuro patients Pts in ED had significantly fewer difficulties!!
  • Concern regarding Ketamine as may raise ICP thought by some authorities to be CI in TBI as it may elevate ICP. Cerebral autoregulation impaired following TBI. Ketamine preserves CBF. Ketamine thought to increase CBF by cerebral vasodilation in spont breathing . Control ventilation and sedate. K reduces cerebral O2 consumption The root of this thinking is a paper published in 1971, which reported increased cerebral blood flow and CSF pressure in 15 unpremedicated dogs following ketamine administration. 4 Subsequent studies in humans reproduced this result. 5,6 However, recent reviews of the evidence have shown that there is no ICP increase where controlled ventilation in used, a GABA g-aminobutyric acid agonist is administered and nitrous oxide is withheld. Ketamine may even be neuroprotective. 7,8 In this prospective clinical trial we intended to study the effects of ketamine on ICP in patients with intracranial hypertension, in light of the long-standing, deeply entrenched opinion that ketamine increases ICP. The major listed contraindication to ketamine, which markedly restricts its use in emergency trauma situations and practically precludes its use in TBI, is its reported effect of increasing ICP. There seems to be a long-standinggeneral consensus in the neurosurgery,19,37 surgery,14,34 anesthesia, pharmacology,16,36 emergency,21,39 and critical care19,24 literature that ketamine is contraindicated in patients who have, or may develop, intracranial hypertension. Both adult9 and pediatric1 guidelines for the treatment of TBI hardly mention ketamine in the chapters dealing with sedation and anesthesia. The notion that ketamine increases ICP stems from several case reports15,17,25,38 and case series11,18,30,33 published mostly between 1970 and 1972, shortly after ketaminewas introduced as an anesthetic agent in the mid-1960s. Increases in ICP were observed following administration of ≥ 2-mg/kg doses of ketamine for short diagnostic or surgical procedures in awake children and adults. Almost allof these ICP elevations were observed in patients with an obstructed ventricular system, mostly due to malfunctioning ventriculoperitoneal shunts or in those with no shunts at all. These elevations were observed in patients who werebreathing spontaneously, although most of the reports stress that the patients continued to breath effectively and that their arterial or end-tidal PCO2 did not increase.11,17,25,33,38 The ICP increased only in patients who had received ketamine as a sole anesthetic agent11,15,17,25,30,33,38 or who were only lightly anesthetized with nitrous oxide.18 The ICP did not increase when thiopental was administered before ketamine, and when thiopental was administered following ketamine-induced ICP elevation, ICP decreased promptly. 33,38 Subsequent clinical and laboratory studies did not support these initial observations. When used for the induction of anesthesia, intravenous administration of ketamine (3 mg/kg) to patients with no intracranial abnormalities resulted in jugular bulb venous pressure elevations of only 1.9 mm Hg (from 7 to 9 mm Hg), whereas MABP and CPP increased by 15.7 and 13.8 mm Hg, respectively.35 Belopavlovic et al.6 used midazolam or diazepam followed by a 1-mg/kg dose of ketamine for the induction of anesthesia in patients with brain tumors or hydrocephalus. The ICP increased by 8 mm Hg after midazolam/ketamine and by 3 mm Hg after diazepam/ ketamine. Much sharper ICP elevations were observed during and after muscle paralysis and tracheal intubation, suggesting suboptimal sedation and anesthesia. Mayberg et al.26 found that ketamine did not elevate ICP or CBF velocity in patients undergoing craniotomy after induction of isoflurane/nitrous oxide anesthesia. In patients with severe TBI who were sedated with propofol, Albanèse et al.5 found that ICP decreased following ketamine administration. In adult patients with severe TBI, Bourgoin et al.8 found no significant differences in the mean daily values of ICP and CPP or in the number of ICP elevations between patients in whom sedation was achieved with a continuous infusion of ketamine/midazolam or with sufentanil/midazolam. Similarly, Kolenda et al.22 compared ketamine/midazolam sedation with fentanyl/midazolam sedation in patients with moderate to severe TBI and found a lower requirement for catecholamines, higher CPP and only nonsignificant 2–mm Hg higher ICP values in the ketamine/ midazolam group. The initial observations of ICP elevations have been related to the cerebral metabolic rate–enhancing effect of ketamine, accompanied by a corresponding increase in CBF,12,20,23,27,35 as autoregulation is maintained during ketamine anesthesia. Other studies, however, have found no changes26,31 or even CBF decreases4,7 following ketamine administration. Measurements of CBF were not obtained in our study, and we do not know whether autoregulation has been fully maintained in our patients, in whom major brain pathological entities were present. Our findings of ICP decreases following ketamine are quite obviously not compatible with concurrent CBF increases. The well-anesthetized, mechanically ventilated patients in this study differed markedly in that respect from the non- or lightly sedated patients described in the early reports.6,11,15,17,18,25,30,33,35,38 Anesthetics such as barbiturates, 12,33,38 benzodiazepines,3,6 isoflurane/nitrous oxide,26 and propofol5 have been shown to blunt or eliminate the cerebral metabolic rate, CBF, and ICP increases associated with ketamine. We assume that this use of additional anesthetics accounts for the absence of ICP elevations following practically all ketamine administrations in our patients. The more unexpected finding of our study is the clinically important and statistically significant decrease in ICP following ketamine. We presume that despite the rather deep sedation and anesthesia, including high-dose thiopental in more than a few instances, ketamine induced an additional potent anesthetic effect. Unfortunately, we performed neither cerebral function monitoring nor CBF measurements. This is a significant limitation of our study, and further research is required to elucidate the mechanism of the ICP-lowering effect of ketamine. Interestingly, deepening sedation is hardly mentioned in the first- or second-tier treatment protocols for intracranial hypertension,1,2,9 although this is rather routinely undertaken in the daily ICU practice. Our findings highlight the efficacy of ketamine in achieving an ICP-lowering effect with practically no undesired side effects such as decreases in blood pressure or CPP. Although our findings were observed in sedated, mechanically ventilated pediatric patients in the PICU setting, we believe that they may be applicable to other patient who respond in a similar manner as their cerebral hemodynamics and pharmacological responses are not different from those of children, and studies in adults5,8,26 support our findings. Ketamine, combined with a benzodiazepine, may be a preferred short-acting anesthetic in emergency situations and in trauma patients, including those with potential intracranial disease. Nevertheless, further laboratory and clinical research is needed before our observations can be generalized and before clear-cut recommendations can be made. Conclusions In patients with intracranial hypertension
  • Certainly part of the MedSTAR SOP We also use the delayed sequence induction for aggitated patients to optimise them pre induction
  • Center; and 3Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel Object. Deepening sedation is often needed in patients with intracranial hypertension. All widely used sedative and anesthetic agents (opioids, benzodiazepines, propofol, and barbiturates) decrease blood pressure and may therefore decrease cerebral perfusion pressure (CPP). Ketamine is a potent, safe, rapid-onset anesthetic agent that does not decrease blood pressure. However, ketamine’s use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure (ICP). Based on anecdotal clinical experience, the authors hypothesized that ketamine does not increase—but may rather decrease—ICP. Methods. The authors conducted a prospective, controlled, clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center. All patients were sedated and mechanically ventilated prior to inclusion in the study. Children with sustained, elevated ICP (> 18 mm Hg) resistant to first-tier therapies received a single ketamine dose (1–1.5 mg/kg) either to prevent further ICP increase during a potentially distressing intervention (Group 1) or as an additional measure to lower ICP (Group 2). Hemodynamic, ICP, and CPP values were recorded before ketamine administration, and repeated-measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration. Results. The results of 82 ketamine administrations in 30 patients were analyzed. Overall, following ketamine administration, ICP decreased by 30% (from 25.8 ± 8.4 to 18.0 ± 8.5 mm Hg) (p < 0.001) and CPP increased from 54.4 ± 11.7 to 58.3 ± 13.4 mm Hg (p < 0.005). In Group 1, ICP decreased significantly following ketamine administration and increased by > 2 mm Hg during the distressing intervention in only 1 of 17 events. In Group 2, when ketamine was administered to lower persistent intracranial hypertension, ICP decreased by 33% (from 26.0 ± 9.1 to 17.5 ± 9.1 mm Hg) (p < 0.0001) following ketamine administration. Conclusions. In ventilation-treated patients with intracranial hypertension, ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions, without lowering blood pressure and CPP. These results refute the notion that ketamine increases ICP. Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension, and it can possibly be used safely in trauma emergency situations. (DOI: 10.3171/2009.1.PEDS08319) Key Words • ketamine • sedation • intracranial pressure • child • intracranial hypertension • traumatic brain injury • cerebral perfusion pressure
  • No mention of GCS <85% TBI so excluded from PCCM paper Many of us like this paper as , despite it’s flaws, it supports what we’re already doing!
  • Mannitol used in 70% of units No placebo controlled trials, other hyperosm therapies or other therapies Mostly extrapolated from adult data 2 mechanisms: reduce bld viscocity via viscosity-mediated reflex vaso-constriction (if autoregulation is intact). Allows CBF to be maintained despite a reduced level of CBV. Transient (<75 mins) Also has osmotic effect: draws water out of the brain parenchyma Hypertonic Saline Less experience but reasonable performance in contemporary clinical trials Class 2 evidence to support use of 3% saline for intracranial HTN and class 2 as a continuous infusion during ICU course. Insuff evidence to support or refute the use of mannitol or >3% NaCl The literature reveals many case reports of hypertonic sodium (HTS) solutions being used as a rescue therapy when mannitol has failed. Further, mannitol can cause renal toxicity with multiple administrations and may accumulate in the brain parenchyma, worsening cerebral oedema. Diuresis may also exacerbate systemic hypotension in polytrauma patients. HTS solutions, on the other hand, have a positive effect on haemodynamics and would seem more appropriate for use in polytrauma patients with TBI. Two of the five papers reviewed here (Oddo and Ware) demonstrate the effectiveness of HTS as a rescue therapy in reducing ICP after mannitol has failed. The remaining papers conclude that HTS solutions are superior to mannitol in both size and duration of ICP reduction, although data regarding long-term outcome either show no difference from mannitol or have not been reported. Further study is needed to determine the optimum concentration and composition of hypertonic sodium solutions for use in this context, ideally in terms of survival and neurological recovery, rather than effect on ICP alone.
  • HS more effective than mannitol in controlling episodes of elevated ICP. Studies had small numbers, methodological differences, lack of rigorous adverse event reporting. Preclude firm recommendation 2/5 reported quantitatic ICP reductions with HS cf mannitol, 1 showed a trend, 1 equivalence and one showed stat signif adv to mannitol Larger, better powered studies are required.
  • If hypothermia induced for any indication, remarming at a rate > 0.5 degrees/hr should be avoided (GRADE B) KOOL KIDS TRIAL OF hypothermia in paediatric TBI was stopped due to futility
  • Brade B
  • PEEP Tapes
  • PEEP Tapes
  • Fran Lockie on Paediatric TBI

    1. 1. Traumatic Brain Injury in Kids: What’s New? Bedside Critical Care Daydream Island September 2012 Dr Francis Lockie, Paediatric Emergency Department, Women’s and Children’s Hospital MedSTAR Emergency Medical Retrieval South Australia
    2. 2. Scope • Case • Recent guideline update • Avoid Secondary Brain Injury – Pre-hospital – ED – Definitive care
    3. 3. 18 month old boy HPC •Dropped 4 times by mum •Cried after first fall, quiet after fourth •Baby left on couch whilst ambulance called •Bradycardia en route
    4. 4. In ED • A – maintained with jaw thrust • B – chest clear, rr 20, SaO2 100% in HF O2 via NRB • C – hr 130, BP 67/55 • D - GCS 15 initially, PERL but sluggish initially, then blown on Rt – Obvious bilat parietal haematomas • VBG: pH 7.17, pCO2 50.6, b/c 18, BE -10, Hb 75
    5. 5. Alternating hypotension / hypertension • 2 x 10ml/kg 0.9% NaCl • 150ml O neg blood • Modified RSI: ketamine and sux • Episode of bradycardia / hypertension – Given 3% saline – Briefly hyperventilated • Taken to CT
    6. 6. Progress • Taken to theatre from CT • Multiple arrests on the table • BP difficult to manage PICU: • Protracted course • Eventually extubated: guarded prognosis
    7. 7. Definitive Care
    8. 8. Pediatric Critical Care Medicine. 13:S1-S82, January 2012 Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents – second edition
    9. 9. Pediatrics 2009;124;56 Early Resuscitation of Children With Moderate-to- Severe Traumatic Brain Injury • 299 kids with mod-severe TBI • 39% became hypotensive – Of these only 48% were treated • 44% became hypoxic – Of these 92% were treated
    10. 10. Pediatrics 2009;124;56
    11. 11. Prevent secondary injury • Hypoxia • Hypotension Emerg Med J 2007;24:139–141
    12. 12. 164 out of theatre intubations 83% had 6 mths anaesthetic experience 41% consultant present Propofol in 76% 96% NMBD 32% DID not use capnography 87% had rescue device 39% suffered at least one adverse event around time of intubation
    13. 13. Anaesthesia 2009, 64(5):532-9 Military Pre-hospital care services Emergency / ICU settings Controversial
    14. 14. • Prospective, controlled trial • 30 ventilated, sedated trauma patients • ICP >18mmHg • Single ketamine bolus
    15. 15. Results • 82 events total (groups 1 &2 • ICP reduced by 30% within 2 minutes of Ketamine administration • P<0.001
    16. 16. “..refutes the notion that ketamine increases ICP..” • In ventilated, anaesthetised patients, with raised ICP, ketamine decreased ICP with no untoward effects on MAP or CPP • Combined with a BDZ, ketamine may be preferred agent for raised ICP
    17. 17. Conclusions • Physician led prehospital trauma teams decrease the length of ICU stay for patients with severe head injury • Trial compromised by highly selective patient cross-over (careflight vs ASNSW)
    18. 18. Steroids?
    19. 19. Steroids? Pediatric Critical Care Medicine. 13:S1-S82, January 2012
    20. 20. C-spine collars may be bad for you
    21. 21. C-spine collars may be bad for you • Tapes • Head up 30 degrees • Judicious use of PEEP
    22. 22. More Issues for the Intensivist • Indications for ICP monitoring • Threshold for treatment of intracranial hypertension • CPP thresholds • Advanced neuromonitoring • Neuroimaging • CSF drainage • DC for treatment of intracranial hypertension Pediatric Critical Care Medicine. 13:S1-S82, January 2012
    23. 23. High quality neuro-intensive care from scene to definitive treatment • Rigorous attention to ABC • Care with RSI, ? Ketamine for all • Crystalloid • Sedation: have a plan! • Deteriorates: – brief hyperventilation – Hypertonic saline over mannitol • Systems: where is definitive care?