Respiratory Failure in Neurological Disease
Although patients admitted to the NICU can certainly acquire respiratory compromise
by ways not directly related to their neurological disease, there are distinct disease-related
causes to be aware of. These can be grouped into central or peripheral causes of failure.
Central Respiratory Failure
Very different types of severe damage to the central nervous system, that is, supra-
and infratentorial brain or spinal cord lesions due to traumatic, vascular, infectious/inflammatory,
metabolic, neoplastic, or seizure-related disorders, can cause respiratory failure.
The central respiratory centers, that is, those in the cortex and the autonomic centers
in pons and medulla, as well as their connections between each other and to the phrenic
nerve and the upper motor neurons, can be affected at every level. This does not necessarily
only result in loss of respiratory drive or respiratory rhythm but might also cause
loss of protective airway reflexes and airway patency and thus impair ventilation.
Specific patterns of pathologic breathing (e.g., Cheyne–Stokes, Cluster, and Biot)
have been suggested for topographic diagnosis of lesion levels, although that correlation
appears somewhat unreliable in clinical practice.
Mechanisms of respiratory failure depend on types and location of pathology, listed
incompletely in the following. Impaired respiratory drive may be caused by lesions
to pons or medulla, such as after basilar artery occlusion or brain stem intracerebral
hemorrhage (ICH), by brain stem compression via raised intracranial pressure (ICP)
in brain edema, by neurotransmitter imbalance/diffuse brain dysfunction in encephalopathy,
encephalitis, or status epilepticus, or by sympathetic overdrive as in subarachnoid
hemorrhage (SAH) or the early phase of developing brain death. Impaired airway and
ventilatory control may be caused by lesions to the brain stem swallowing centers,
dysphagia, loss of glossopharyngeal muscle tone such as in brain stem stroke or traumatic
brain injury (TBI), by lesions to the reticular formation or bilateral thalami, large
areas hemispheric lesions/hydrocephalus with subsequent coma and loss of protective
airway reflexes in many sorts of etiologies, by vomiting, dysphagia, aspiration, and
by neurogenic pulmonary edema as in SAH. Impaired ventilation mechanics may be caused
by high (above C3–5) spinal cord lesions that reduce the ventilatory force to accessory
neck muscles as in trauma, ischemia, or myelitis.
Peripheral Respiratory Failure
The connections (phrenic nerve, lower motor neurons) to the respiratory muscles, that
is, diaphragm (80% of ventilatory force), intercostal, and accessory muscles, can
be affected by inflammatory, toxic, or degenerative disorders. Inflammatory neuromuscular
diseases and myopathies are other causes of peripheral respiratory failure. It has
to be kept in mind that the control of respiration is intact, while the efferent part
of the system is compromised, which has implications for the type and setting of MV,
as well as for strategies to discontinue it.
Peripherally impaired ventilation mechanics may be caused by lesions to anterior horn
cells as in degenerative anterior horn cell disease, or by lesions to the phrenic
nerve or other lower motor neurons, as in trauma, tumor, motor neuron disease (e.g.,
amyotrophic lateral sclerosis [ALS]), Guillain–Barré's syndrome (GBS), and critical
illness myopathy/polyneuropathy (CIM/CIP).
Principles of General ICU Airway Management to Discontinue Ventilation
General principles for airway management in nonneurological ICU patients have been
presented in several instructive reviews.[10]
[11] Safe extubation can only be tried if intubation even under difficult and ICU conditions
can be mastered. This means that (re)intubation has to be addressed before extubation
is considered or tried.
Managing the (Difficult) Airway in the ICU
Problems of intubation and extubation most often arise if the patient has a difficult
airway. The reader is further directed to reviews on this particular topic,[12] including the recommendations of the American Society of Anesthesiologists[13] and the Difficult Airway Society that contain very helpful algorithms.[14]
[15] Since these guidelines primarily refer to the operation room (OR) situation, they
have to be adapted to fit the ICU scenario. Airway management in the ICU or the emergency
room (ER) is different from the OR situation. Twenty percent of all critical incidents
in the ICU are airway related,[12] and difficult (re)intubation is encountered in the non-OR setting in approximately
10% (about twice as often as in the OR setting).[11] Relevant complications associated with difficult airway management are severe hypoxemia,
severe hypotension, esophageal intubation, aspiration, cardiac arrest, and death,
reported at rates between 5 and 40%.[11] A prospective registry for England and Wales between 2005 and 2007 revealed more
than 1,000 reported airway incidents in the ICU, 18% at intubation, 5% during tracheostomy
placement, and 82% as postprocedural problems.[16] Implementations of difficult airway algorithms were shown to half the number of
intubation-related cardiac arrest[17] or substantially reduce the number of overall complications.[18] If a patient is to be extubated, the treating physician has to strive for information
on whether that particular patient has a known difficult airway and/or presented difficulties
on intubation previously.
Optimally, every airway should be regarded difficult in the ICU setting, and the situation
“can't ventilate, can't intubate” anticipated, avoided, or at least managed adequately.
The following environmental factors can make ICU/ER airway management a particular
challenge: time pressure, a changing team of caregivers that might not have worked
together often before, insufficient lighting, suboptimal patient position in the ICU
bed, limited physiologic reserve of the patient, or an uncooperative patient, for
example, with a reduced level of consciousness. Patient factors predicting a difficult
airway are obesity, small mouth, large tongue, prognathia or dental abnormalities,
mandibular joint dysfunction, facial burns, facial trauma, cervical trauma, cervical
immobility/abnormality, short neck, high/anterior larynx, deep vallecula, or abnormal
epiglottis/subglottis.
There are multiple means, techniques, and devices for securing an airway, the choice
of which depends on the severity of the situation, the setting, the skills of the
team, and on patient factors.[10]
[11] Most importantly, the techniques by which the airway is secured need to be practiced
under supervision, and the care team needs to familiarize itself with the devices
present in the ICU/ER. For extubation and reintubation, this includes bridging devices
such as exchange catheters. Some traditional customs of airway management have recently
been questioned. The so-called sniffing position for (re)intubation that is meant
to align oral, pharyngeal, and laryngeal axes did not appear to be superior to simple
head extension in magnetic resonance imaging and clinical randomized studies. The
“sniffing position” might have advantages in obese and neck-fixed patients, but optimal
positioning has not been clarified for ICU airway management. Among the many techniques
and devices available, noninvasive mask ventilation might be the most important one.
At least one supraglottic airway device should also be present and familiar, in case
(re)intubation fails and has to be bridged by these devices (for instance, a laryngeal
mask) that can later be used as a conduit for endotracheal (re)intubation. Laryngoscope
blades for tube loading, augmented by video-/fiberscopic or patented lens systems
can also be helpful and should be at hand.[11]
Discontinuing Airway Protection
After re-establishment of spontaneous breathing (see later), sufficient swallowing,
and brain stem reflexes, that is, with the patient's regained ability to protect their
own airway unaided, airway protection can be discontinued.[19] Extubation is the procedure to be aimed for as soon as possible, but it can be risky
and its timing is very difficult in the ICU, particularly if the patient had presented
a difficult airway before (see earlier). Between 5 and 10% of extubated general ICU
patients require reintubation.[10]
[12] Reasons comprise dysfunctional airway reflexes, prolonged effects of analgesics
and sedatives, reduced pharyngeal tone, occluded airway, reduced oxygen stores, laryngeal
edema, respiratory exhaustion, etc. Both reintubation after failed extubation and
delayed extubation are associated with a longer ICU length of stay (ICU-LOS), more
infections, and higher mortality.[20] Removal of the orotracheal tube to allow spontaneous breathing and airway protection
requires a successful weaning process and spontaneous breathing trials (SBTs) (see
later), a back-up strategy for reintubation and at best the following parameter targets
([Table 1]).
Table 1
Classical criteria for the general ICU suggesting a successful extubation
|
Patient awake and cooperative, high Glasgow coma scale (> 8)
|
|
Good coughing and swallowing
|
|
Tube intolerance
|
|
Spontaneous breathing (30 minutes) with PaO2 > 60/increase PaCO2 < 15 mm Hg
|
|
Low respiratory rate (RR < 30/min)
|
|
Adequate tidal volume (Vt > 5 mL/kg)
|
|
Rapid shallow breathing index (RSBI < 105)
|
|
Minute volume (MinV ca. 10 L)
|
|
PaO2/FiO2 ratio 150–200
|
Abbreviations: ICU, intensive care unit; MinV, minute volume; RR, respiratory rate;
RSBI, rapid shallow breathing index; Vt, tidal volume.
A cuff-leak test demonstrating the absence of air leak on deflation of the tube cuff
can indicate laryngeal edema and subsequent extubation failure (EF),[21]
[22] although some studies have not confirmed this. It is probably a useful additional
criterion to guide the extubation decision. Laryngeal edema has been subjected to
pre-extubation treatment with steroids. After decades of controversy on this practice,
a recent systematic review and a Cochrane analysis have confirmed that short-term
prophylactic corticosteroids reduce EF in adult critical care patients.[23]
[24] Another safety practice is to apply an exchange catheter and leave it in place for
a while after extubation to allow for easier reintubation.
Principles of Mechanical Ventilation Related to Airway Discontinuation
Few of the basic principles of modern ICU ventilation have a relation to extubation.
Although lifesaving and indispensable in most cases, positive pressure MV is a nonphysiological
procedure that carries risks such as shear stress and barotrauma to the lung, VAP,
atrophy of respiratory muscles, and stress and agitation in the patient. Its duration
should hence be kept as short as possible. The option to discontinue MV has to be
evaluated every day.[19]
No particular mode of ventilation has proven superior over another in studies on patient
outcomes. However, being able to choose from different modes can be helpful in addressing
the individual patient's ventilation needs. One should aim for letting the patient
take part actively in the ventilation process, that is, establish an assisted (as
opposed to a fully controlled) ventilation mode as soon as possible. The reasons are
that on fully controlled ventilation, more sedation and at times neuromuscular blockers
are needed, and respiratory muscle atrophy and CIM/CIP start to develop within the
first day of ventilation.[25]
Noninvasive ventilation can help avoid endotracheal (re)intubation but is largely
reserved for cooperative patients with respiratory compromise by exacerbated chronic
obstructive pulmonary disease (COPD), asthma, or cardiogenic pulmonary edema. It may
well serve to facilitate liberation from MV and stabilization of spontaneous breathing
after extubation,[26] and may hence be planned as a transition phase before permanent spontaneous breathing.
It can be an effective strategy in myasthenia gravis (MG), cautious application provided,
but may be less successful in GBS.[27] Extubation to noninvasive ventilation in chronic neurodegenerative or neuromuscular
disease is beyond the scope of this article.
Weaning
Liberating the patient from the respirator (weaning) can be very challenging, especially
in patients with underlying pulmonary disease and after prolonged ventilation periods.[19]
[28]
[29]
[30]
[31] The weaning period is often exhausting for the patient both physically and mentally,
and is associated with a high incidence of delirium. The optimal method of weaning
has not been clarified. Principally, patients can be put on an assisted ventilation
mode and the support from the respirator be gradually reduced (continuous mode of
weaning), or MV can be interrupted by phases of spontaneous breathing and the intervals
extended over time (discontinuous mode of weaning). Of two randomized trials, one
supported the first[32] and the other the latter;[33] the ventilation mode appearing the least helpful in weaning was the (synchronized)
intermittent mandatory ventilation mode in both trials. The question might have to
be clarified in particular subgroups of patients.[34]
Principles of NICU Airway Management to Discontinue Ventilation
Although many of the general ICU principles described earlier may be adopted for the
neurological or neurosurgical ICU patient, some particularities have to be emphasized.
A lot of patients with centrally caused respiratory failure do not primarily have
a problem with lung mechanics but with respiratory coordination and airway protection,
the latter by way of reduced voluntary clearing of the airways in stupor or coma,
loss of pharyngeal and glossal muscle tone, or dysphagia and/or loss of protective
reflexes. Peripheral, that is, neuronal or neuromuscular disease such as GBS, ALS,
or MG crisis, can cause severe impairment of lung mechanics, but may also cause airway
compromise by way of reduced capacity to cough, swallow, and thus handle saliva and
secretions. In a NICU patient planned for extubation, these compromises have to be
prepared for but may be difficult to predict.
Weaning
Weaning from the respirator should certainly not be delayed in NICU patients, be they
comatose or not, although it seems to be often delayed in the former.[8] The best method of weaning, that is, continuous versus discontinuous, is unclear
(as in general ICU patients). Discontinuous weaning methods, however, involve successive
SBTs and thus wake-up trials. These have been associated with a release of stress
hormones[35] and rises in ICP[36]
[37] in brain-injured patients, particularly those with a higher ICP from the outset.[38] In a small randomized pilot study in ventilated patients with severe stroke, patients
weaned by a gradual (continuous) weaning method had a shorter duration of ventilation.[39] It may be reasonable to try SBTs in patients fulfilling the general criteria allowing
these (see later), but refrain from further SBTs if they are accompanied by ICP crises
or other physiological derangements, and in that case, it might be best to change
to a continuous weaning method. In a subgroup of NICU patients, such as those with
advanced ALS or extensive brain stem injury, weaning will not be successful. In those
cases, tracheostomy and long-term ventilation might be adequate, if this is the patient's
or family's will.
The application of weaning protocols appeared superior compared with unsystematic
weaning in different subgroups of ICU patients over the past 10 years. Predictors
of a successful weaning in the general ICU population have been identified, among
these the rapid shallow breathing index (RSBI, RR/Vt), maximal inspiratory pressure
(Pi max), and minute volume,[40] as well as a passed SBT.[31] These parameters have not been established in the NICU population but may be adapted
and tried for a first orientation. The weaning process has to go hand-in-hand with
de-escalation of sedation, optimally according to a sedation protocol. The steps in
[Table 2] can help successfully wean an ICU patient from the respirator and eventually extubate
or tracheostomize him/her.
Table 2
Suggested steps in discontinuation of (N)ICU ventilation and airway protection
|
Systemic and respiratory criteria for readiness to wean
|
Improvement of underlying disease
|
|
No indication for mechanical ventilation
|
|
No invasive procedure planned in near future
|
|
No fever, no raised ICP
|
|
No or little sedation
|
|
No delirium
|
|
No metabolic/electrolyte derangements
|
|
Application of a weaning protocol
|
Continuous weaning mode OR discontinuous weaning mode (controlled or control/assist
mode + SBTs)
|
|
Criteria for initiating a spontaneous breathing trial
|
Respiratory criteria
|
SatO2 > 90%
|
|
PaO2 > 60 mm Hg on FiO2 < 0.4
(PaO2/FiO2 > 150–200)
|
|
PaCO2 normal or baseline
|
|
PEEP < 8 cm H2O
|
|
P insp < 20 cm H2O
|
|
Pi max > − 20 cm H2O
|
|
RSBI (RR/Vt) < 105
|
|
RR < 35/min
|
|
Vt > 5 mL/kg
|
|
MV < 10 L/min
|
|
Cardiovascular criteria
|
No signs of cardiac ischemia or arrhythmia
|
|
HR < 140 beats/min
|
|
SBP 90–160 mm Hg on no or minimal vasopressors
|
|
Neurological criteria
|
Ideally, patient awake (RASS 0 or −1, GCS > 8)
|
|
Ideally, patient cooperative
|
|
Cough and gag reflexes present
|
|
No excessive saliva/secretions
|
|
Spontaneous breathing trial for 30 min
|
Documentation of events at 5, 10, 20, and 30 min
|
|
Settings on respirator
|
Ventilation mode PSV (or similar)
|
|
PEEP < 8 cm H2O
|
|
No ATC
|
|
Tube diameter > 7 mm
|
|
Flow trigger < 3 L/min
|
|
OR patient off respirator and application of T-piece
|
|
Criteria to abandon SBT
|
Anxiety and/or agitation (RASS > +2), sweating
|
|
Decline in level of consciousness (RASS < − 2)
|
|
Markedly increased work of breathing (use of accessory muscles)
|
|
Rapid breathing with decreasing Vt and without decreasing PaCO2
|
|
Cyanosis
|
|
Hemodynamic instability
|
|
HR 140 beats/min or increase 20% from baseline
|
|
SBP > 180 mm Hg or increase 20% from baseline
|
|
Ventilation and oxygenation
|
|
RSBI (RR/Vt) > 105
|
|
RR < 7/min OR > 35/min or increase 50% from baseline
|
|
SatO2 < 85%
|
|
PaO2 > 50–60 mm Hg on FiO2 >0.5
|
|
PaCO2 >50 mm Hg or increase > 15 mm Hg
|
|
Spontaneous breathing trial for a longer period
|
|
|
Extubation (criteria see above) if SBT was passed
|
|
|
Return to weaning protocol if extubation failed
|
|
|
Another extubation trial OR tracheostomy
|
|
|
Weaning after tracheostomy, applying the previous steps
|
|
|
Criteria for decannulation
|
Same as for extubation
|
|
Ensure intact swallowing, e.g., by endoscopic swallowing test
|
|
Decannulation
|
|
Abbreviations: ATC, automatic tube compensation; FiO2, inspiratory fraction of oxygen; GCS, Glasgow coma scale; HR, heart rate; ICP, intracranial
pressure; MV, minute volume; (N)ICU, (neuroscience)intensive care unit; PaCO2, arterial pressure of carbon dioxide; PaO2, partial arterial pressure of oxygen; PEEP, positive end-expiratory pressure; P insp,
inspiratory pressure; Pi max, maximal inspiratory pressure; PSV, pressure support
ventilation; RASS, Richmond agitation sedation scale; RR, respiratory rate; RSBI,
rapid shallow breathing index; SatO2, arterial saturation of oxygen; SBP, systolic blood pressure; SBT, spontaneous breathing
trial; Vt, tidal volume.
Reintubation
Since extubation in NICU patients fails more often than in general ICU patients (see
later), there has to be a high awareness and adequate preparation for reintubation.
Principally, the general ICU criteria for (re)intubation listed earlier apply to neurocritically
ill patients as well. Details of (re)intubation in these patients have hardly been
studied systematically. Some considerations on certain subgroups, situations, and
pathophysiology deserve mention.
The need to continue invasive MV in the NICU patient with central respiratory failure
may become obvious rapidly, with fast emergence of indicators of respiratory failure.
It may be less obvious, however, in peripheral neuronal or neuromuscular disease,
where respiratory failure can evolve in a more gradual fashion and then suddenly turn
into an emergency situation.[41] Patients with GBS, botulism, MG, Lambert–Eaton myasthenic syndrome, ALS, or CIP/CIM
need to be monitored very closely after extubation. The following are warning signs
of peripheral respiratory failure ([Table 3]).
Table 3
Warning signs of neuromuscular respiratory failure
|
Decreased VC (critical VC < 20 mL/kg)
|
|
Prolonged exhalation time
|
|
Interrupted speech, dyspnea at low levels of exertion
|
|
Attempted compensation by increased RR (RR > 20/min)
|
|
Inability to count to 20 on one breath (approx. 1 L VC)
|
|
Loss of strength in neck flexors and proximal muscles
|
|
Abdominal paradox breathing (abdomen retracts on inspiration)
|
|
Weak cough
|
|
Lost intrinsic sigh
|
|
Decreased maximum inspiratory pressure (< −30 cm H2O)
|
|
Decreased maximum expiratory pressure (< 40 cm H2O)
|
|
Increased work of breathing
|
|
Restlessness
|
|
Tachycardia (> 100 beats/min)
|
|
Forehead sweating
|
|
Use of accessory respiratory muscles (sternomastoid)
|
|
Sitting upright to breath
|
|
Hypoventilation with hypercapnia (late sign of decompensation)
|
|
Hypoxia
|
Abbreviations: RR, respiratory rate; VC, vital capacity.
In these patients, noninvasive ventilation may help compensate a respiratory crisis
and avoid (re)intubation. This has been shown particularly in patients with MG crisis.
Case reports and series on noninvasive ventilation in GBS also exist. However, most
severe GBS cases require long-term invasive ventilation. Noninvasive ventilation is
very time consuming, requires a higher therapist–patient ratio, wakefulness, and cooperation
on the side of the patient, as well as fairly compensated blood gas and acid–base
parameters and the presence of airway protective reflexes. Other than in MG crisis,
it might be applicable in ALS, intoxications, as a support in weaning (see later)
and to treat mild exacerbations of COPD and cardiogenic pulmonary edema. It can also
be used in some less severely afflicted stroke patients, but outside these situations,
it plays a minor role in neurocritically ill patients.[27] In a recent multicenter study on ventilation management in ∼4,968 ICU patients,
noninvasive ventilation was used in only 1% of the 938 neurological patients, compared
with 12% in the others.[8]
(Re)Intubation almost always involves an episode of hypotension, or at least variance
in blood pressure. This can be detrimental in cerebrovascular disease, where cerebral
autoregulation is impaired and systemic hypotension translates directly into decreased
cerebral perfusion pressure. Such hypotension during pharmacological induction for
intubation has been found to be more common in patients with more severe underlying
disease, a baseline MAP < 70 mm Hg, age > 50 years and with the use of propofol or
increasing doses of fentanyl as inductor drugs.[42] Thiopental is another agent often causing hypotension. Therefore, the less vascular-active
etomidate may be more appropriate for induction in cerebrovascular patients; it can
be accompanied by fasciculations that should not be mistaken for seizures. Ketamine
as an alternative induction agent was suggestedly associated with increases in ICP,
but this was not confirmed in several subsequent studies. In fact, it decreased ICP
in many of these. Contrary to other sedatives, ketamine does not have depressing but
rather activating circulatory effects. It can thus cause tachycardia and hypertension
and should not be used in patients already in the upper ranges of these parameters.
(Re)Intubating head trauma patients can be very challenging, not only in the case
of facial trauma with direct airway involvement but because ∼10% have associated cervical
spine injury. Airway management in all trauma patients in which ruling out cervical
injury by imaging has not taken place in the ventilation period (i.e., after inadvertent
or self-extubation) must involve in-line traction and stabilization of the neck (by
hands of an assistant and then by stiff neck device/cervical collar). As conventional
laryngoscopy and intubation might be difficult or impossible in that situation, fiberoptic
intubation, if feasible, should be preferred. Alternatively, one should soon proceed
to cricothyroidotomy, particularly if major facial or airway trauma is present.
Extubation
The question of when a NICU patient is ready to be safely extubated is very difficult
to answer. It is clear that extubation can only be considered in patients who are
respiratorily reconstituted, sufficiently oxygenated, and cardiocirculatorily stable.
One relevant problem, however, is that the above-named classic extubation criteria
from the general ICU apply to an awake and cooperative patient, something rarely encountered
in the NICU where patients might present with aphasia, anarthria, apraxia, agitation,
delirium, or a reduced level of consciousness, depending on their brain lesion. Even
patients with neuromuscular disease or CIP/CIM that should principally have the cerebral
capacity to fulfill these criteria, can develop delirium, psychosis, mutism, cranial
nerve-related communication deficits, agitation, and especially anxiety (at times
a kind of ventilator dependency), making the extubation decision similarly challenging.
Extubation therefore is often delayed in NICU patients.[8] Another problem is the difficulty in predicting neurological compromise of airway
functions.
Classical extubation criteria have not reliably predicted EF in NICU patients in several
studies, and EF occurs far more often than in nonneurological ICU patients, that is,
at a rate of 15 to 35% in patients with brain lesions[8]
[43]
[44]
[45]
[46] and 30 to 40% in patients with neuromuscular disease such as MG.[47] A selection of these studies will be presented in more detail in the following.
Regarding pathologies with predominantly centrally caused respiratory failure, Anderson
et al prospectively studied 285 extubations in 378 NICU patients with predominantly
cerebral pathologies (such as acute ischemic stroke, ICH, SAH, TBI). They found EF
in 17%, associated with patient baseline factors, duration of MV, presence of COPD,
and obstructive sleep apnea. Predictors of extubation success were viscosity of secretions
and the ability to follow four simple commands.[44] An almost identical rate of EF (17.5%) was found in a retrospective study by Ko
et al in 62 mixed, again cerebrally affected, NICU patients. Classical ICU weaning/extubation
criteria did not help predict EF.[43] The subgroup of NICU patients with severe stroke has received particular research
interest. In a retrospective review of 112 NICU stroke patients, Lioutas et al found
that a National Institutes of Health Stroke Scale Score < 15 (milder strokes) and
absence of dysarthria prior to intubation were independently associated with extubation
success, but classic ICU extubation criteria were not.[48]
In another retrospective study in NICU patients with middle cerebral artery infarction,
10 of 47 failed extubation, while the rest was extubated successfully. Extubation
success only trended more likely in patients with a Glasgow coma scale (GCS) ≥ 8,
and other classic extubation criteria were again not helpful.[45] In the only prospective study on extubation prediction in NICU stroke patients to
date, 185 very severely affected patients (80% ischemic, 20% hemorrhagic stroke) were
first triaged for attempting extubation by certain criteria (GCS >8, no elevated ICP,
systolic blood pressure 90–185 mm Hg, heart rate between 60 and 120 bpm, body temperature
36–38.5°C, spontaneous respiratory minute volume [≤ 12 L], positive end-expiratory
pressure [≤ 5 mm Hg], PaO2/FiO2 [>200], and RSBI <105). If these were not met, patients were primarily tracheostomized
(47%). These had more severe strokes, more often of the hemorrhagic type, presented
with a lower level of consciousness, needed neurosurgical intervention more often,
were more often obese, and had been more frequently intubated because of suspicion
of compromised protective reflexes. A subgroup of patients was additionally assessed
by a previously established semiquantitative airway score[49] containing the parameters spontaneous cough, gag, sputum quality, and quantity.
Of 98 patients primarily extubated, 37% failed extubation, that is, had to be reintubated
within 72 hours. EF was independently predicted by prior neurosurgical treatment and
a low airway management score. No differences were found for the ability to follow
simple commands and classic weaning criteria. The authors concluded that criteria
more closely related to extubation success in NICU stroke patients relate to airway
safety and secretion handling, and proposed that specific clinical scoring systems
should be established.[50]
Regarding peripherally caused respiratory compromise, Wu et al retrospectively evaluated
41 episodes of myasthenic crisis in 199 MG patients, 33 of whom needed MV. EF was
as high as 39%, predicted by poor cough and sputum impaction. An independent predictor
of extubation success was a maximal expiratory pressure of > 40 cm H2O.[47] EF rates in similar magnitude and similar predictors (cough or expiration force)
were reported in other studies on airway management in myasthenic crisis.[51]
[52] In a retrospective study on airway management in 44 patients with GBS, 14 were successfully
extubated (associated factors were lower negative inspiratory force [< −50 cm H2O] and higher/improving vital capacity), 20 received tracheostomy, and 10 (23%) failed
extubation. Predictors of the latter were pulmonary comorbidities, autonomic dysfunction,
and NICU-LOS.[53]
In a recent systematic review and meta-analysis involving nine studies on 928 mixed
neurocritical care patients, Wang et al found the following predictors of EF: pneumonia,
atelectasis, duration of MV > 24 hours, thick secretions, and the neurological ones
low GCS, inability to follow commands (especially to close the eyes), and absent gag
reflex. Interestingly, responding to particular commands and coughing were not predictive
in that study.[54] In another very recent prospective study, 140 brain-injured patients were analyzed
for extubation if they first passed a SBT successfully. EF was 31%, and predictors
were upper-airway function (cough, gag reflex, deglutition) and neurological status
(Coma Recovery Scale-revised visual subscale). The authors formed a prediction score
based on the odds ratios and internally validated it by bootstrap methodology. With
a cutoff at sensitivity 92%, specificity 50%, positive predictive value 82%, and negative
predictive value of 70%, the interesting observation was made that extubation was
successful in 85% with a low consciousness level, if at least two airway functions
were operating.[55] It will be very interesting to validate that score externally, preferably in certain
NICU subgroups.
Of note, delaying extubation in NICU patients for not meeting classic extubation criteria,
especially the one regarding consciousness, leads to complications such as more VAPs
and prolonged ICU-LOS, while earlier or later extubated patients do not seem to differ
with regard to the reintubation rate.[49] In a small prospective randomized pilot trial in 16 brain-injured NICU patients,
there was no difference in complications or functional outcome at discharge between
patients extubated immediately after meeting respiratory extubation criteria and those
re-evaluated and extubated later because of coma.[56] Although details and benefits of (early) extubation in NICU patients await further
prospective research, coma should not be the reason to withhold weaning or extubation
from these patients. Rather, particular attention should be paid to presence of dysphagia,
which is much more frequent in the NICU population.[57] Endoscopic swallowing tests that not necessarily require cooperation of the patient
have been successfully applied in stroke patients, and might help guide the extubation
decision in other NICU patients as well.[58]
In summary, nonspecific (i.e., nonneurological) variables such as sputum impaction,
secretion load and viscosity, duration of ventilation, or underlying diseases such
as COPD seem to play a more predictive role for EF. With some controversy, a few disease-specific
positive predictors of extubation success were the ability to follow simple commands
or a higher GCS in the brain-lesioned patients, and a strong cough in the neuromuscular
patients. More and larger prospective studies are clearly and urgently necessary to
clarify safety of extubation in the NICU patient. At present, a stepwise approach
involving a protocol should be applied based on current experience and evidence and
is outlined in [Fig. 1].
Fig. 1 Suggestion for approaching extubation in the neuroscience intensive care unit.
Tracheostomy after Extubation Failure
It is quite customary to proceed to tracheostomy after the first or at the latest
after the second failed extubation in NICU patients. While 10 to 20% of general ICU
patients receive a tracheostomy during their stay, this rate is ∼35 to 45% in NICU
patients.[8]
[59] This may again reflect that neurological ICU patients often are not compromised
with regard to their pulmonary function but rather to their capacity to protect the
airway and handle secretions. Tracheostomy in the NICU, particularly in cerebrovascular
patients, is beyond the scope of this article and has been reviewed.[60]
[61]
Sometimes it becomes apparent within the first week of ventilation that NICU patients
will have to receive a tracheostomy in their clinical course, such as in those with
severe axonal GBS rapidly proceeding to tetraplegia or others with extensive brain
stem damage. If such a situation is not judged overall futile, the patient's and family's
will is in accordance, and if the care team is convinced that tracheostomy is necessary,
there is no reason why this should be delayed, at times not even by an extubation
trial.
