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Rapid Sequence Intubation in Traumatic Brain-injured Adults

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Abstract and Figures

Deciding on proper medication administration for the traumatic brain injury (TBI) patient undergoing intubation can be daunting and confusing. Pretreatment with lidocaine and/or vecuronium is no longer recommended; however, high-dose fentanyl can be utilized to help blunt the sympathetic stimulation of intubation. Induction with etomidate is recommended; however, ketamine can be considered in the proper patient population, such as those with hypotension. Paralysis can be performed with either succinylcholine or rocuronium, with the caveat that rocuronium can lead to delays in proper neurological examinations due to prolonged paralysis. Recommendations for post-intubation continuous sedation medications include a combination propofol and fentanyl in the normotensive/hypertensive patient population. A combination midazolam and fentanyl or ketamine alone can be considered in the hypotensive patient.
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Received 04/03/2018
Review began 04/16/2018
Review ended 04/18/2018
Published 04/25/2018
© Copyright 2018
Kramer et al. This is an open access
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Rapid Sequence Intubation in Traumatic
Brain-injured Adults
Nicholas Kramer , David Lebowitz , Michael Walsh , Latha Ganti
1. Emergency Medicine, University of Central Florida 2. University of Central Florida College of Medicine
3. Pharmacy, University of Central Florida 4. Clinical Sciences, University of Central Florida
Corresponding author: Nicholas Kramer, nicholas.kramer@ucf.edu
Disclosures can be found in Additional Information at the end of the article
Abstract
Deciding on proper medication administration for the traumatic brain injury (TBI) patient
undergoing intubation can be daunting and confusing. Pretreatment with lidocaine and/or
vecuronium is no longer recommended; however, high-dose fentanyl can be utilized to help
blunt the sympathetic stimulation of intubation. Induction with etomidate is recommended;
however, ketamine can be considered in the proper patient population, such as those with
hypotension. Paralysis can be performed with either succinylcholine or rocuronium, with the
caveat that rocuronium can lead to delays in proper neurological examinations due to
prolonged paralysis. Recommendations for post-intubation continuous sedation medications
include a combination propofol and fentanyl in the normotensive/hypertensive patient
population. A combination midazolam and fentanyl or ketamine alone can be considered in the
hypotensive patient.
Categories: Anesthesiology, Emergency Medicine
Keywords: rapid sequence intubation, traumatic brain injury (tbi), intubation, ketamine, emergency
medicine, rocuronium, succinylcholine, pretreatment, induction agents, intracranial pressure
Introduction And Background
Rapid sequence intubation (RSI) in the patient with traumatic brain injury (TBI) is a changing
area of research. Airway control is essential for patients with TBI, as hypoxemia and
hypercarbia lead to significant morbidity and mortality. However, we must take into
consideration the fact that RSI also has the potential to worsen brain injury. The simple but
essential act of laryngoscopy and placing of the endotracheal (ET) tube may stimulate the dense
sympathetic and parasympathetic network traversing the pharynx and trachea. In addition to
risks posed directly by the gag and cough reflex, sympathetic stimulation can cause an
increased heart rate (HR), increased blood pressure (BP), and increased intracerebral pressure
(ICP), while parasympathetic stimulation may trigger bronchospasm. It has been shown that
the act of laryngoscopy alone increases systolic blood pressure (SBP) by a mean of 20 mmHg [1-
2]. The effect on ICP has not been studied directly, but endotracheal suctioning has been shown
to increase ICP by a minimum of 5 mmHg [3-4]. The increase in ICP from the sympathetic surge
can cause an increase in cerebral blood volume, cerebral edema, and development of worsening
hemorrhage or hematoma [5-6]. In addition, we must balance this against the risk of
hypotension, as this can also increase both mortality and brain injury. Sedation carries many of
the same concerns in addition to the needs to minimize anxiety, prevent agitation, allow
manipulation of mechanical ventilation, and facilitate neurological assessments [7]. In this
article, the authors explore the latest adult literature and summarize the data regarding agents
for pretreatment, induction, paralysis, and sedation with the goal of preventing secondary
brain injury.
1 2 3 4
Open Access Review
Article DOI: 10.7759/cureus.2530
How to cite this article
Kramer N, Lebowitz D, Walsh M, et al. (April 25, 2018) Rapid Sequence Intubation in Traumatic Brain-
injured Adults. Cureus 10(4): e2530. DOI 10.7759/cureus.2530
Review
Pretreatment
Lidocaine
Lidocaine has historically been used as a pretreatment in TBI as it was believed to lessen the
sympathetic stimulation associated with RSI. However, evidence has been mixed. Two small
studies have shown that lidocaine minimized an increase in ICP during neurosurgical
procedures [8] or ET suctioning [9], while three studies showed no benefit during RSI [10-11] or
ET suctioning [12]. Due to a lack of evidence in blunting ICP, weighed with the risk of potential
side effects including hypotension [13], experts now recommend against using lidocaine for
pretreatment in RSI for TBI [6, 14].
Defasciculating Dose of a Non-Depolarizing Agent
Pretreating with a low dose of a non-depolarizing agent, such as vecuronium, theoretically may
blunt the rise in ICP due to muscle fasciculations when succinylcholine is used for RSI. There is
strong evidence that succinylcholine increases ICP in patients undergoing neurosurgery for
brain tumors (Marsh ML et al.: Succinylcholine-intracranial pressure effects in neurosurgical
patients (Abstract). Anesth Analg 1980; 59: 550-1) and that a defasciculating dose of a non-
depolarizing agent reduced increases in these select patients [15-16]. However, there are
multiple small studies that suggest that succinylcholine does not increase ICP in head-injured
patients and no studies that demonstrate that a non-depolarizing agent would affect ICP in
these patients [17]. The current recommendation is against the use of a defasciculating dose of
a non-depolarizing agent in TBI patients undergoing RSI with succinylcholine [14].
Fentanyl/Remifentanil
Several studies demonstrate that fentanyl attenuates rises in BP and HR in RSI [18-20]. By
decreasing the cardiovascular response of sympathetic stimulation, fentanyl is thought to blunt
increases in ICP related to laryngotracheal stimulation in RSI. One study by Kim et
al. compared remifentanil versus lidocaine for attenuating the hemodynamic response during
RSI. It found that lidocaine (at 1.5 mg/kg) had no effect, whereas remifentanil (at 1 mcg/kg) did
blunt the hemodynamic response associated with RSI [21]. Fentanyl (at 2-3 mcg/kg) is currently
recommended for neuroprotection in patients with increased ICP [14].
Induction
Etomidate
Etomidate is well liked in the RSI world due to its mild hemodynamic profile [22-26]. This is
particularly true during RSI in TBI, as a drop in mean arterial pressure (MAP) will cause a
decrease in the cerebral perfusion pressure (CPP). In addition, etomidate has been shown to
decrease cerebral blood flow and cerebral metabolic demand, all while preserving CPP [26]. One
downside to this drug is that it has no analgesic properties; thus, neuroexcitation can be a
concern if not properly mitigated [27].
Ketamine
Like etomidate, ketamine is exceptionally hemodynamically stable [28-29] but has the added
benefit of possessing analgesic properties. Despite this, ketamine has been generally
contraindicated for use in patients with TBI due to concerns of sympathetic stimulation,
2018 Kramer et al. Cureus 10(4): e2530. DOI 10.7759/cureus.2530 2 of 10
leading to an increase in the ICP. A study by Filanovsky et al. in 2010 examined the origins of
this practice and determined that many of the studies that concluded that ketamine increased
ICP were from the 1970s and were of questionable quality [30]. Additionally, ketamine may, in
fact, be neuroprotective due to an increase in MAP and CPP [30-31], without increasing cerebral
oxygen consumption or reducing regional glucose metabolism [32-33]. In a 2016 retrospective
study of 968 adult trauma patients who underwent RSI with using either etomidate or ketamine,
the authors found no difference in mortality or other patient-centered outcomes between the
two induction agents [34]. In the 2011 Update from American College of Emergency Physicians
(ACEP) Clinical Practice Guidelines for Ketamine Sedation, head trauma is no longer a relative
contraindication, though ketamine remains relatively contraindicated for patients with central
nervous system masses, abnormalities, or hydrocephalus [31]. Ketamine may best be suited for
use in TBI patients with normal to low BP due to its potential for increasing the MAP and CPP
[27].
Paralysis
Succinylcholine
Succinylcholine is a depolarizing neuromuscular blocking agent with rapid onset and offset
properties. The rapid offset is beneficial as it allows for early neurological examinations.
Concerns have been raised over the theory that muscle fasciculations could lead to increased
ICP in these delicate patients; however, a 2001 study summarized the available literature on
this subject and, though limited, concluded that the evidence does not support the hypothesis
that succinylcholine causes an increase in ICP for head-injured patients [17].
Rocuronium
Strong opinions exist when comparing succinylcholine to rocuronium. While a large systematic
review demonstrated superior intubating conditions when using succinylcholine [35], it is likely
the agents are nearly identical in clinical practice [36]. In 2015, the Cochrane database
investigators updated a previous review of RSI medications to include 11 additional studies to
the previous 37 randomized controlled trials (RCT) and controlled clinical trials analyzed in
2008 [35]. Overall, the reviewers found succinylcholine was superior to rocuronium at achieving
both acceptable intubating conditions and excellent intubating conditions when
succinylcholine was dosed at least 1 mg/kg and rocuronium was dosed at least 0.6 mg/kg for
RSI. However, further analysis revealed no statistical difference in intubation conditions when
succinylcholine was compared to rocuronium dosed at 1.2 mg/kg.
While the majority of studies comparing succinylcholine to rocuronium have evaluated their
effect on intubation conditions for RSI, intubation conditions may not necessarily translate into
success of intubation or the number of intubation attempts required. In 2011, a retrospective
study of all RSIs performed using succinylcholine or rocuronium was collected from a tertiary
care emergency department over 15 months [37]. Of the total 327 RSIs performed, the rate of
first attempt intubation success was similar between the succinylcholine and rocuronium
groups (72.6% vs. 72.9%, p = 0.95). While the results of this study found the two paralytic agents
to be equivalent with regard to first attempt intubation, the median dose of rocuronium used
was 1.19 mg/kg (interquartile range (IQR) = 1 - 1.45 mg/ kg). The authors of the study concluded
that higher doses of rocuronium may be necessary to achieve the equivalent effects of
succinylcholine. A 2016 retrospective cohort study of 233 TBI patients requiring intubation in
the emergency department was performed to help fill an important gap in the literature on the
preferred paralytic for RSI in patients with TBI [38]. Patients either received succinylcholine or
rocuronium to facilitate RSI. The two patient groups were similar and shared the same mortality
rate of 23%. For patients with a low head Abbreviated Injury Scale (AIS) severity (AIS 0 to 3),
there was no difference in mortality between the two groups. However, for patients with a high
2018 Kramer et al. Cureus 10(4): e2530. DOI 10.7759/cureus.2530 3 of 10
head AIS score (4 to 6), succinylcholine was associated with increased mortality compared with
rocuronium (44% vs 23%, odds ratio (OR) 4.10, 95% confidence interval (CI) 1.18 - 14.12; p =
0.026). This was the first comparative study between succinylcholine and rocuronium to
evaluate their effects on mortality in TBI patients. While succinylcholine use for RSI in patients
with severe TBI was associated with increased mortality, it may not be possible to discriminate
which patients are likely to benefit from avoiding succinylcholine at the time of presentation.
Prospective clinical trials would help confirm these findings.
Due to its long duration of action, sustained paralysis with rocuronium can prevent repeat
neurologic assessments. Patients receiving rocuronium have also been shown to receive less
sedation and analgesia in the immediate post-intubation phase because the induced paralysis
may make it appear as if they are calm and sedated [39]. A recent study published in 2015 found
the average time to sedation in patients who received rocuronium for RSI was 55 minutes [39].
Considering the elimination half-life of etomidate, ketamine, and propofol are all less than 15
minutes, this reveals an alarmingly high incidence of patients paralyzed after RSI but without
sedation. Additionally, care needs to be taken if opioids are used as remifentanil may delay the
onset of paralysis by 30 - 45 seconds [40]. Currently, there is not enough data to recommend
rocuronium over succinylcholine for RSI in TBI.
Post-intubation sedation/analgesia
Propofol
Propofol is advantageous over other medications in this category in that it as a rapid onset of
action and short duration of action. This allows the effects to be rapidly eliminated from the
patient, allowing for neurological examination, and then quickly titrated back to full effect. Care
must be taken when selecting propofol in the hypotensive patient as it may lower the patient’s
MAP, decreasing the body’s ability to maintain cerebral blood flow. Propofol’s cerebrovascular
effects result in a reduction of episodes of intracranial hypertension (in the continuously
monitored patient), and while there is some evidence that this agent may have neuroprotective
effects in cases of mild TBI, this result has not been demonstrated in moderate to severe cases
[41-42]. Finally, it must be noted that propofol has no analgesic effect, necessitating the use of
additional medications for pain and comfort.
Midazolam
Midazolam boasts a relatively neutral hemodynamic profile, though some have raised concerns
regarding its potential to lower systemic BP and thus, CPP [43]. Midazolam has a relatively fast
onset and offset of action initially (half-life one hour), though tissue accumulation over time
may result in delayed awakening. This effect may be the reason that midazolam has been
associated with prolonged coma, increased ventilator days, and more ICU days when compared
to propofol [7]. Midazolam’s additional benefits to the patient include its anxiolytic and
anticonvulsant properties [41]. In a comparison study by Sandiumenge et al. [44], no significant
difference was noted between midazolam and propofol in regard to a decrease in ICP and both
agents demonstrated similar CPP. Analogous to propofol, midazolam also lacks analgesic
properties and thus, is often paired with an opioid (such as fentanyl).
Fentanyl/Remifentanil
Fentanyl is a commonly utilized medication for analgesia after intubation, though it lacks
appropriate sedation properties. As discussed above, attenuating pain may benefit the patient
by minimizing the sympathetic response of elevated MAP and HR. While the hemodynamic
properties of fentanyl are thought to be relatively neutral compared to other opioids, multiple
2018 Kramer et al. Cureus 10(4): e2530. DOI 10.7759/cureus.2530 4 of 10
studies have shown that bolus doses produce clinically significant increases in ICP, while
decreasing MAP and CCP [45-46]. Thus, care must be taken to utilize the minimal appropriate
dose for these patients. Fentanyl has a short duration of action, when given intravenously (IV),
with the analgesic effect lasting approximately 30 - 60 minutes. Remifentanil is an ultra-short-
acting opioid with analgesic effects lasting five to 10 minutes, which may allow for earlier neuro
checks than fentanyl [47].
Ketamine
As discussed above, ketamine has historically been avoided in TBI patients due to the concern
over raising the ICP. This dogma has been shown to be based on little, poorly conducted
research from the 1970s. More recent studies have countered this data and shown that
ketamine may have beneficial properties when utilized in the appropriate patient population
[30-33, 48]. In a small study of eight TBI patients under propofol sedation, the addition of
ketamine had no effect on HR, MAP, or CPP, while demonstrating the beneficial effect of
lowering ICP [49]. Additionally, ketamine has the unique property of simultaneous sedation
and analgesia, which may minimize the need for additional medications. Ketamine has a
relatively long half-life at 2.5 hours, which limits the ability for neurological checks. As
discussed in the Induction section, ketamine may best be utilized in TBI patients with normal
to low BP as it may increase the patient’s MAP and CPP [27].
Discussion
RSI in the TBI patient is complex. The coordinated stages of pretreatment, induction, paralysis,
sedation, and analgesia each present their own benefits and pitfalls. Much of this information
is based on theoretical risks and benefits, as large randomized case-control studies looking at
specific questions of interest with patient-centered outcomes are scarce, inadequate, or non-
existent at this time.
The fundamental aim of our recommendations is to limit secondary brain injury due to RSI as
measured by neurologic outcomes and mortality. When these indicators are not available, we
focus on the effects on MAP, ICP, and CPP to the best of our current knowledge. A protocol for
RSI in the TBI patient can be broken down into two arms: the hypotensive patients and the
normotensive/hypertensive patients. We believe that the medication choices in these two
groups should differ significantly as the cerebrovascular effects are diverse.
Pretreatment
The authors recommend no pretreatment medications in the hypotensive group. In the
normotensive/hypertensive population, fentanyl IV bolus (2-3 mcg/kg) 3 minutes prior to
induction is recommended. Fentanyl has been shown to blunt the sympathetic response of
elevated MAP and HR during RSI. While fentanyl is relatively hemodynamically neutral, it does
have the potential to decrease MAP and CCP when given at bolus doses [45-46]. This is why we
recommend it as pretreatment only in the patients where hypotension is not a significant
concern. Lidocaine and low-dose non-depolarizing agents are not recommended by current
guidelines as the most recent evidence does not support their use.
Induction
For induction, the authors recommend ketamine in the hypotensive group and etomidate in the
normotensive/hypertensive group. The previously held beliefs that ketamine was
contraindicated in RSI have been successfully dispelled, and the most recent evidence suggests
that it can be neuroprotective without increasing cerebral oxygen consumption or reducing
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regional glucose metabolism [30-31]. Ketamine may have sympathetic stimulation properties
which lead to an increase in MAP and CPP; thus, the authors only recommend it in the
hypotensive patient.
For the normotensive/hypertensive group, we believe the best induction medication is
etomidate. Etomidate’s mild hemodynamic profile, along with evidence that it may decrease
cerebral blood flow and cerebral metabolic demand while preserving CPP [26], makes it a strong
candidate for this patient population.
Paralytic
The authors recommend succinylcholine as the paralytic agent of choice for both categories in
our RSI protocol. Concerns regarding fasciculations and increased ICP with succinylcholine use
have not been shown to be valid in the literature [17]. Succinylcholine’s rapid offset is
exceptionally beneficial as it permits early neurological examinations. Rocuronium is gaining
some traction for RSI in the TBI patient; however, with its prolonged duration of paralysis and
limited data supporting its use over succinylcholine, we cannot yet recommend its use, except
when succinylcholine is contraindicated.
Post-intubation Sedation/Analgesia
A systematic review from 2011 of many of the commonly used agents for sedation in TBI,
including propofol, ketamine, etomidate, and agents from the opioid, benzodiazepine, α-2
agonist, and antipsychotic drug classes, concluded that no drug was superior in terms of
neurological outcomes or mortality in the general traumatic brain injured patient [7].
Regardless, we believe that certain populations may benefit from one medication over another,
though more research is certainly required.
In the hypotensive patient, we suggest a combination of midazolam and fentanyl, as this
pairing has limited hemodynamic effects while simultaneously owning relatively short half-
lives. Ketamine may be considered for this population as well, as its sympathetic effects may
slightly elevate the MAP. However, ketamine has a relatively long duration of action which will
limit neurological checks.
For the normotensive/hypertensive patient, our protocol calls for propofol and fentanyl.
Propofol has the potential to lower the MAP further than other agents in this class, which may
be beneficial in the hypertensive patient. Additionally, propofol may have neuroprotective
effects in cases of mild TBI [42]. Fentanyl is added for comfort and may further benefit the
hypertensive patient by blunting the sympathetic response to pain. Remifentanil may be
substituted for fentanyl as the two medications have similar hemodynamic effects, with
remifentanil allowing for a much more rapid offset of action for neurological checks.
Recommendations
Our recommendations, based on the above evidence, are summarized in Figure 1.
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FIGURE 1: Summary Recommendations
Conclusions
Medication administration for RSI in the patient with TBI is controversial and still not
definitive. Patients with TBI are very sensitive to changes in hemodynamics; hence, adverse
events can occur with improper medication administration. Further research and randomized
control trials are needed to make formal recommendations.
Additional Information
Disclosures
Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors
declare the following: Payment/services info: All authors have declared that no financial
support was received from any organization for the submitted work. Financial relationships:
All authors have declared that they have no financial relationships at present or within the
previous three years with any organizations that might have an interest in the submitted work.
Other relationships: All authors have declared that there are no other relationships or
activities that could appear to have influenced the submitted work.
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... Due to lack of evidence, weighed with the risk of hypotension secondary to lidocaine administration, use of pretreatment agents has fallen out of practice. 12,13 As the body of evidence describing the activity and elimination of RSI medications grows, so too does the understanding that no two disease states are alike. In this article, a thorough update on RSI medications for the EMP is provided. ...
Article
Disclaimer: In an effort to expedite the publication of articles related to the COVID-19 pandemic, AJHP is posting these manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. Purpose: The dosing, potential adverse effects, and clinical outcomes of the most commonly utilized pharmacologic agents for rapid sequence intubation (RSI) are reviewed for the practicing emergency medicine pharmacist (EMP). Summary: RSI is the process of establishing a safe, functional respiratory system in patients unable to effectively breathe on their own. Various medications are chosen to sedate and even paralyze the patient to facilitate an efficient endotracheal intubation. The mechanism of action and pharmacokinetic/pharmacodynamic profiles of these agents were described in a 2011 review. Since then, the role of the EMP as well as the published evidence regarding RSI agents, including dosing, adverse effects, and clinical outcomes, has grown. It is necessary for the practicing EMP to update previous practice patterns in order to continue to provide optimal patient care. Conclusion: While the agents used in RSI have changed little, knowledge regarding optimal dosing, appropriate patient selection, and possible adverse effects continues to be gained. The EMP is a key member of the bedside care team and uniquely positioned to communicate this evolving data.
... In the period immediately preceding injury, cerebral blood flow is understandably decreased, reducing the potential for oxygen utilization (Kawai et al., 2008). The risks of hypoxia are already well-understood and acute mitigation of them is already established as a priority in the emergency treatment of TBIs (Godoy et al., 2018;Kramer et al., 2018). Of greater contention is the utilization of glucose post-TBI. ...
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Full-text available
Metabolic dysfunction is a ubiquitous underlying feature of many neurological conditions including acute traumatic brain injuries and chronic neurodegenerative conditions. A central problem in neurological patients, in particular those with traumatic brain injuries, is an impairment in the utilization of glucose, which is the predominant metabolic substrate in a normally functioning brain. In such patients, alternative substrates including ketone bodies and lactate become important metabolic candidates for maintaining brain function. While the potential neuroprotective benefits of ketosis have been recognized for up to almost a century, the majority of work has focused on the use of ketogenic diets to induce such a state, which is inappropriate in cases of acute disease due to the prolonged periods of time (i.e., weeks to months) required for the effects of a ketogenic diet to be seen. The following review seeks to explore the neuroprotective effects of exogenous ketone and lactate preparations, which have more recently become commercially available and are able to induce a deep ketogenic response in a fraction of the time. The rapid response of exogenous preparations makes their use as a therapeutic adjunct more feasible from a clinical perspective in both acute and chronic neurological conditions. Potentially, their ability to globally moderate long-term, occult brain dysfunction may also be relevant in reducing lifetime risks of certain neurodegenerative conditions. In particular, this review explores the association between traumatic brain injury and contusion-related dementia, assessing metabolic parallels and highlighting the potential role of exogenous ketone and lactate therapies.
... Patients suffering from traumatic brain injury (TBI) need sedation to induce anxiolysis, prevent agitation, and allow mechanical intubation [1][2][3]. Benzodiazepines are the frequently used agents for the sedation of patients with TBI, especially in cases where the standard agent propofol alone does not achieve sufficient sedation depth. These agents generally protect injured brains, especially in comatose patients with severe brain lesions [4], an effect partially attributed to its anticonvulsant properties [5]. ...
Article
Full-text available
Background The benzodiazepine midazolam is a γ-aminobutyric acid (GABA)-A receptor agonist frequently used for sedation or stress control in patients suffering from traumatic brain injury (TBI). However, experimental studies on benzodiazepines have reported divergent results, raising concerns about its widespread use in patients. Some studies indicate that benzodiazepine-mediated potentiation of GABAergic neurotransmission is detrimental in brain-injured animals. However, other experimental investigations demonstrate neuroprotective effects, especially in pretreatment paradigms. This study investigated whether single-bolus midazolam administration influences secondary brain damage post-TBI. Methods Two different midazolam dosages (0.5 and 5 mg/kg BW), a combination of midazolam and its competitive antagonist flumazenil, or vehicle solution (NaCl 0.9%) was injected intravenously to mice 24 h after experimental TBI induced by controlled cortical impact. Mice were evaluated for neurological and motor deficits using a 15-point neuroscore and the rotarod test. Histopathological brain damage and mRNA expression of inflammatory marker genes were analyzed using quantitative polymerase chain reaction three days after insult. Results Histological brain damage was not affected by posttraumatic midazolam administration. Midazolam impaired functional recovery, and this effect could not be counteracted by administering the midazolam antagonist flumazenil. An increase in IL-1β mRNA levels due to postinjury application of midazolam was reversible by flumazenil administration. However, other inflammatory parameters were not affected. Conclusions This study merely reports minor effects of a postinjury midazolam application. Further studies focusing on a time-dependent analysis of posttraumatic benzodiazepine administration are required.
... In recent years, with the development of social industrialization, injuries and deaths caused by traffic and infrastructure have been increasing year by year, among which traumatic brain injury (TBI) is the leading cause of deaths caused by traumatic injury [1][2][3][4]. TBI refers to organic damage on brain tissues caused by external force on the head, mostly from accidents, showing poor prognosis and a very high mortality rate (close to 30%) [5][6][7]. TBI is clinically difficult to treat and has various complications, posing a serious impact on the quality of life in patients as well as an economic and medical burden to the family and the society [8,9]. ...
Article
Objective: To innvestigate the rehabilitation effects of repetitive transcranial magnetic stimulation (rTMS) combined with cognitive training on cognitive impairment in patients with traumatic brain injury (TBI) by using multimodal magnetic resonance imaging. Methods: Clinical data of 166 patients with cognitive impairment after TBI were retrospectively analyzed. The patients were assigned into an observation group and a control group according to different treatment methods, with 83 cases in each group. The observation group was given rTMS + cognitive training, and the control group was given cognitive training only. The changes in GCS score, the Cho/Cr, Cho/NAA and NAA/Cr ratios examined by MRSI, the score of cognitive impairment, the grading of cognitive impairment, and the changes in modified Barthel index were observed and compared between the two groups. Results: The GCS score, and the ratios of Cho/Cr, Cho/NAA and NAA/Cr after treatment were better than those before treatment in both groups and were lower in the observation group compared with the control group (all P<0.05). The score and grading of cognitive impairment as well as modified Barthel index after treatment were all significantly better in the observation group than in the control group (all P<0.05). Conclusion: rTMS can improve the rehabilitation effect on cognitive impairment in patients after TBI and is recommended for clinical use.
Article
Emergency physicians intubate critically ill patients almost daily. Intubation of the critically ill emergency department (ED) patient is a high-risk, high-stress situation, as many have physiologic derangements such as hypotension, hypoxemia, acidosis, and right ventricular dysfunction that markedly increase the risk of peri-intubation cardiovascular collapse and cardiac arrest. This chapter discusses critical pearls and pitfalls to intubate the critically ill ED patient with physiologic derangements. These pearls and pitfalls include appropriate preoxygenation; circulatory resuscitation; proper patient position and room setup; selection of medications for rapid sequence intubation; and intubation of patients with severe acidosis, traumatic brain injury, and pulmonary hypertension.
Chapter
Emergency specialists (ESs) are at the forefront of the scene against secondary injury following traumatic brain injury (TBI). In this sense, management strategies used in the emergency department are very important, particularly those taking the Glasgow Coma Scale score as a reference. TBI management initially uses the same principles as those used for all trauma events and is based on Advanced Trauma Life Support recommendations. Intracranial pressure is the central parameter in the clinical management of especially severe TBI directed by previously established goals. Emergency department care mainly focuses on the prevention of hypoxia, blood pressure optimization, fluid resuscitation, transfusion and coagulation management, and management of specific pharmacotherapy. Although the scientific evidence for the existing recommendations is weak, ESs should still practice a strictly standardized management strategy to limit secondary injury in these patients.
Chapter
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Airway management in trauma is critical and may impact patient outcomes. Particularly in traumatic brain injury (TBI), depressed level of consciousness may be associated with compromised protective airway reflexes or apnea, which can increase the risk of aspiration or result in hypoxemia and worsen the secondary brain damage. Therefore, patients with TBI and Glasgow Coma Scale (GCS) ≤ 8 have been traditionally managed by prehospital or emergency room (ER) endotracheal intubation. However, recent evidence challenged this practice and even suggested that routine intubation may be harmful. This chapter will address the indications and optimal method of securing the airway, prehospital and in the ER, in patients with traumatic brain injury.
Article
Full-text available
The rapid intubation sequence is the method of choice for airway assurance in the emergency department, this procedure in addition to the passage of the orotracheal tube through the glottis consists of different steps which must be done in a thorough and sequential way to ensure the airway in the shortest possible time, with the least number of attempts and ideally without associated complications. Due to the importance of this topic, new recommendations have been given regarding each of the moments of this procedure, starting on indications and contraindications, techniques to the preparation and planning of the approach of the airway such as MACOCHA and HEAVEN mnemotechnics, the early use of vasopressors and crystalloids for patients at risk of hemodynamic deterioration , the use of different techniques for preoxygenation such as non-invasive mechanical ventilation or apneic preoxygenation. In addition, we must individualize each patient when choosing each drug either to premedicate, perform hypnosis or muscle relaxation. Additionally, new techniques such as the use of ultrasonography to corroborate the proper positioning of the orotracheal tube and post-intubation care. All these topics will be addressed in this review.
Chapter
The reference of choice for pediatricians, residents, and medical students, this revised and expanded sixth edition provides clear, practice-oriented guidance on the core knowledge in pediatrics. Edited by a leading primary care authority with more than 100 contributors, this edition provides comprehensive coverage of hundreds of topics ranging from asthma and urinary tract infections to toilet training and adolescent depression. View a message from Dr Berkowitz. Available for purchase at https://shop.aap.org/berkowitzs-pediatrics-6th-edition-paperback/ (NOTE: This book features a full text reading experience. Click a chapter title to access content.)
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Background The benzodiazepine midazolam is a γ-aminobutyric acid (GABA)-A receptor agonist frequently used for sedation or stress control in patients suffering from traumatic brain injury (TBI). However, experimental studies on benzodiazepines have reported divergent results, raising concerns about its widespread use in patients. Some studies indicate that benzodiazepine-mediated potentiation of GABAergic neurotransmission is detrimental in brain-injured animals. However, other experimental investigations demonstrate neuroprotective effects, especially in pretreatment paradigms. This study investigated whether single-bolus midazolam administration influences secondary brain damage post-TBI. Methods Two different midazolam dosages (0.5 and 5 mg/kg BW), a combination of midazolam and its competitive antagonist flumazenil, or vehicle solution (NaCl 0.9%) was injected intravenously to mice 24 h after experimental TBI induced by controlled cortical impact. Mice were evaluated for neurological and motor deficits using a 15-point neuroscore and the rotarod test. Histopathological brain damage and mRNA expression of inflammatory marker genes were analyzed using quantitative polymerase chain reaction three days after insult. Results Histological brain damage was not affected by posttraumatic midazolam administration. Midazolam impaired functional recovery, and this effect could not be counteracted by administering the midazolam antagonist flumazenil. An increase in IL-1β mRNA levels due to postinjury application of midazolam was reversible by flumazenil administration. However, other inflammatory parameters were not affected. Conclusions This study merely reports minor effects of a postinjury midazolam application. Further studies focusing on a time-dependent analysis of posttraumatic benzodiazepine administration are required.
Article
Full-text available
Several different classes of sedative agents are used in the management of patients with traumatic brain injury (TBI). These agents are used at induction of anaesthesia, to maintain sedation, to reduce elevated intracranial pressure, to terminate seizure activity and facilitate ventilation. The intent of their use is to prevent secondary brain injury by facilitating and optimising ventilation, reducing cerebral metabolic rate and reducing intracranial pressure. There is limited evidence available as to the best choice of sedative agents in TBI, with each agent having specific advantages and disadvantages. This review discusses these agents and offers evidence-based guidance as to the appropriate context in which each agent may be used. Propofol, benzodiazepines, narcotics, barbiturates, etomidate, ketamine, and dexmedetomidine are reviewed and compared.
Article
Traumatic brain injury (TBI) is the most common cause of intracranial hypertension. The hallmark of TBI is cerebral edema and raised intracranial pressure with its detrimental effect on the brain. The focus here is on the practical aspects of controlling intracranial pressure, maintaining cerebral perfusion pressure and supporting the patient's hemodynamics and vital functions during the initial critical days. © 2016 Indian Journal of Practical Pediatrics. All rights reserved.
Article
Objective: In neurotrauma care, a better understanding of treatments following traumatic brain injury (TBI) has led to a significant decrease in morbidity and mortality in this population. TBI represents a significant medical problem, and complications following TBI are associated with the initial injury and post-event intracranial processes such as elevated intracranial pressure (ICP) and brain edema. Consequently, appropriate therapeutic interventions are required to reduce brain tissue damage and improve cerebral perfusion. We present a contemporary review of literature on the use of pharmacologic therapies to reduce intracranial pressure following TBI and a comparison of their efficacy. Methods: This review was conducted by PubMed query. Only studies discussing pharmacologic management of patients following TBI were included. This review includes prospective and retrospective studies and includes randomized controlled trials as well as cohort, case-control, observational and database studies. Systematic literature reviews, metanalyses, and studies that considered conditions other than TBI or pediatric populations were not included. Results: Review of the literature describing the current pharmacological treatment for intracranial hypertension following TBI most often discussed the use of hyperosmolar agents such as hypertonic saline (HTS) and mannitol, sedatives such as fentanyl and propofol, benzodiazepines, and barbiturates. Hypertonic saline is associated with faster resolution of intracranial hypertension and restoration of optimal cerebral hemodynamics, although these advantages did not translate into long term benefits in morbidity or mortality. In patients refractory to treatment with hyperosmolar therapy, induction of a barbiturate coma can reduce ICP, although requires close monitoring to prevent adverse events. Conclusion: Current research suggests that the use of hypertonic saline following TBI is the best option for immediate decrease in intracranial pressure. A better understanding of the efficacy of each treatment option can help to direct treatment algorithms during the critical early hours of trauma care and continue to improve morbidity and mortality following TBI.
Article
Study objective: Induction doses of etomidate during rapid sequence intubation cause transient adrenal dysfunction, but its clinical significance on trauma patients is uncertain. Ketamine has emerged as an alternative for rapid sequence intubation induction. Among adult trauma patients intubated in the emergency department, we compare clinical outcomes among those induced with etomidate and ketamine. Methods: The study entailed a retrospective evaluation of a 4-year (January 2011 to December 2014) period spanning an institutional protocol switch from etomidate to ketamine as the standard induction agent for adult trauma patients undergoing rapid sequence intubation in the emergency department of an academic Level I trauma center. The primary outcome was hospital mortality evaluated with multivariable logistic regression, adjusted for age, vital signs, and injury severity and mechanism. Secondary outcomes included ICU-free days and ventilator-free days evaluated with multivariable ordered logistic regression using the same covariates. Results: The analysis included 968 patients, including 526 with etomidate and 442 with ketamine. Hospital mortality was 20.4% among patients induced with ketamine compared with 17.3% among those induced with etomidate (adjusted odds ratio [OR] 1.41; 95% confidence interval [CI] 0.92 to 2.16). Patients induced with ketamine had ICU-free days (adjusted OR 0.80; 95% CI 0.63 to 1.00) and ventilator-free days (adjusted OR 0.96; 95% CI 0.76 to 1.20) similar to those of patients induced with etomidate. Conclusion: In this analysis spanning an institutional protocol switch from etomidate to ketamine as the standard rapid sequence intubation induction agent for adult trauma patients, patient-centered outcomes were similar for patients who received etomidate and ketamine.
Article
Background: Patients often require a rapid sequence induction (RSI) endotracheal intubation technique during emergencies or electively to protect against aspiration, increased intracranial pressure, or to facilitate intubation. Traditionally succinylcholine has been the most commonly used muscle relaxant for this purpose because of its fast onset and short duration; unfortunately, it can have serious side effects. Rocuronium has been suggested as an alternative to succinylcholine for intubation. This is an update of our Cochrane review published first in 2003 and then updated in 2008 and now in 2015. Objectives: To determine whether rocuronium creates intubating conditions comparable to those of succinylcholine during RSI intubation. Search methods: In our initial review we searched all databases until March 2000, followed by an update to June 2007. This latest update included searching the Cochrane Central Register of Controlled Trials (CENTRAL; 2015, Issue 2), MEDLINE (1966 to February Week 2 2015), and EMBASE (1988 to February 14 2015 ) for randomized controlled trials (RCTs) or controlled clinical trials (CCTs) relating to the use of rocuronium and succinylcholine. We included foreign language journals and handsearched the references of identified studies for additional citations. Selection criteria: We included any RCT or CCT that reported intubating conditions in comparing the use of rocuronium and succinylcholine for RSI or modified RSI in any age group or clinical setting. The dose of rocuronium was at least 0.6 mg/kg and succinylcholine was at least 1 mg/kg. Data collection and analysis: Two authors (EN and DT) independently extracted data and assessed methodological quality for the 'Risk of bias' tables. We combined the outcomes in Review Manager 5 using a risk ratio (RR) with a random-effects model. Main results: The previous update (2008) had identified 53 potential studies and included 37 combined for meta-analysis. In this latest update we identified a further 13 studies and included 11, summarizing the results of 50 trials including 4151 participants. Overall, succinylcholine was superior to rocuronium for achieving excellent intubating conditions: RR 0.86 (95% confidence interval (CI) 0.81 to 0.92; n = 4151) and clinically acceptable intubation conditions (RR 0.97, 95% CI 0.95 to 0.99; n = 3992, 48 trials). A high incidence of detection bias amongst the trials coupled with significant heterogeneity provides moderate-quality evidence for these conclusions, which are unchanged from the previous update. Succinylcholine was more likely to produce excellent intubating conditions when using thiopental as the induction agent: RR 0.81 (95% CI: 0.73 to 0.88; n = 2302, 28 trials). In the previous update, we had concluded that propofol was the superior induction agent with succinylcholine. There were no reported incidences of severe adverse outcomes. We found no statistical difference in intubation conditions when succinylcholine was compared to 1.2 mg/kg rocuronium; however, succinylcholine was clinically superior as it has a shorter duration of action. Authors' conclusions: Succinylcholine created superior intubation conditions to rocuronium in achieving excellent and clinically acceptable intubating conditions.
Article
Objective: To compare succinylcholine and rocuronium regarding mortality in patients with traumatic brain injury (TBI) who are intubated in the emergency department (ED). Methods: This was a retrospective cohort study conducted in an academic ED in the United States. Adult patients with TBI who underwent rapid sequence intubation (RSI) in the ED with rocuronium or succinylcholine between October 2010 and October 2014 were included. The main outcome of interest was in-hospital mortality. Subjects were stratified based on severity of injury using head abbreviated injury scores. The high-severity group had a severe or critical head injury (score 4 or higher); the low-severity group had a less than severe head injury (score lower than 4). Main results: The final study cohort included 233 patients who were underwent RSI with succinylcholine (149 patients) or rocuronium (84 patients). In patients who received rocuronium, mortality was 22% (12/54) and 23% (7/30) in the low-severity and high-severity categories, respectively (difference 1%, 95% confidence interval [CI] -18% to 20%). In patients who received succinylcholine, mortality was 14% (14/103) and 44% (20/46) in the low-severity and high-severity categories, respectively (difference 30%, 95% CI 14-46). In the multivariate analysis after adjusting for important confounders, there was no significant association between succinylcholine and mortality in the low-severity category (odds ratio [OR] 0.75, 95% CI 0.29-1.92). However, in patients in the high-severity category, succinylcholine was associated with increased mortality compared with rocuronium (OR 4.10, 95% CI 1.18-14.12). Conclusions: In severely brain-injured patients undergoing RSI in the ED, succinylcholine was associated with increased mortality compared with rocuronium.
Article
Rapid sequence intubation (RSI) involves a rapidly acting sedative plus a neuromuscular blocking agent (NMBA) to facilitate endotracheal intubation. Rocuronium and succinylcholine are NMBAs commonly used in RSI with drastically different durations of action. Evaluate whether patients receiving RSI with a longer-acting NMBA had a greater delay in sedation or analgesia than patients that received a short-acting NMBA. This was a retrospective review of patients presenting to the emergency department requiring endotracheal intubation. Exclusions included age < 18 years, pregnancy, prior intubation, and contraindication to sedation and analgesia. Primary endpoint was time to continuous sedation or analgesia after RSI in patients receiving rocuronium or succinylcholine. Secondary endpoints included hospital length of stay (HLOS), intensive care unit length of stay (ICU LOS), and impact of an emergency medicine pharmacist (EPh). A total 106 patients met inclusion criteria, 76 patients receiving rocuronium and 30 receiving succinylcholine. Mean time to sedation or analgesia was longer in the rocuronium group when compared to the succinylcholine group at 34 ± 36 min vs. 16 ± 21 min (p = 0.002). In the presence of an EPh, the mean time to sedation or analgesia was 20 ± 21 min, vs. 49 ± 45 min (p < 0.001). Time spent on ventilator, HLOS, and ICU LOS were not significantly different between groups. Patients receiving rocuronium in RSI had a significantly longer time to sedation or analgesia when compared to patients receiving succinylcholine. The presence of an EPh significantly decreased the time to administration of sedation or analgesia after RSI. Copyright © 2015 Elsevier Inc. All rights reserved.
Article
Study objective We synthesize the available evidence on the effect of ketamine on intracranial and cerebral perfusion pressures, neurologic outcomes, ICU length of stay, and mortality. Methods We developed a systematic search strategy and applied it to 6 electronic reference databases. We completed a gray literature search and searched medical journals as well as the bibliographies of relevant articles. We included randomized and nonrandomized prospective studies that compared the effect of ketamine with another intravenous sedative in intubated patients and reported at least 1 outcome of interest. Two authors independently performed title, abstract, and full-text reviews, and abstracted data from all studies, using standardized forms. Data from randomized controlled trials and prospective studies were synthesized in a qualitative manner because the study designs, patient populations, reported outcomes, and follow-up periods were heterogeneous. We used the Jadad score and Cochrane Risk of Bias tool to assess study quality. Results We retrieved 4,896 titles, of which 10 studies met our inclusion criteria, reporting data on 953 patients. One study was deemed at low risk of bias in all quality assessment domains. All others were at high risk in at least 1 domain. Two of 8 studies reported small reductions in intracranial pressure within 10 minutes of ketamine administration, and 2 studies reported an increase. None of the studies reported significant differences in cerebral perfusion pressure, neurologic outcomes, ICU length of stay, or mortality. Conclusion According to the available literature, the use of ketamine in critically ill patients does not appear to adversely affect patient outcomes.
Article
Objectives To compare the preventive effects of esmolol and lidocaine on the increase in mean arterial pressure (MAP) and intracranial pressure (ICP) during endotracheal intubation in neurosurgery.