Prospective evaluation of a modified apnea-test without disconnection from the ventilator in brain death candidates

doi:10.21203/rs.3.rs-3411536/v1

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Prospective evaluation of a modified apnea-test without disconnection from the ventilator in brain death candidates

https://doi.org/10.21203/rs.3.rs-3411536/v1

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Background:

The apnea test (AT) is the central clinical component in the diagnosis of brain death (BD) and normally entails disconnecting the patient from the ventilator followed by tracheal oxygen sufflation to ensure adequate oxygenation. Most international guidelines state that a lack of spontaneous breathing must be demonstrated when PaCO₂ ≥ 60mmHg to rate the test as positive. However, the loss of positive end-expiratory pressure (PEEP) that is associated with disconnection from the ventilator may cause rapid desaturation, frequently leading to cardiopulmonary instability (especially in ARDS-patients) and generally putting patients at risk. This prospective study therefore aimed to investigate whether a modified version of the AT (mAT) in which the patient remained connected to the ventilator, is potentially less harmful yet remains a valid test.

Methods:

mAT was performed in all 140 BD candidates registered between January 2019 and December 2022: After 10 min of pre-oxygenation, (i) PEEP was increased by 2mbar, (ii) ventilation mode was switched to CPAP and (iii) apnea back-up mode was turned off (flow trigger 10l/min). mAT was considered positive when spontaneous breathing occurred upon increasing PaCO₂ to ≥ 60 mmHg (baseline 35–45 mmHg). Clinical complications during/after mAT were documented.

Results

mAT was possible in 139/140 patients and had a median duration of 15 min (IQR 13–19). Severe complications did not occur. In n = 51 patients, the post-mAT PaO₂ was lower than that during pre-mAT, while it was equal or higher in n = 88 cases. In ARDS-patients, apneic oxygenation during mAT improved PaO₂. In n = 123 cases, there was a transient post-mAT drop in blood pressure, in n = 12 to a MAP < 60 mmHg.

Conclusions

The mAT is a safe and gentle means for identifying patients in whom the central respiratory drive has not failed.

Irreversible loss of brain function

apnoea test

brain stem areflexia

ventilator-based

apneic oxygenation

The core clinical component of all relevant international guidelines for the diagnosis of irreversible loss of cerebral function (ILBF or "brain death", BD) is the test for the loss of spontaneous respiration (apnea test)(1–4). The consensus of many of these guidelines is that in order to show central respiratory failure, evidence of failure of spontaneous breathing must be obtained at a PaCO₂ of at least 60 mmHg. Some guidelines also allow an increase in PaCO₂ of at least 20 mmHg above a known elevated baseline (and parallel pH drop to values < 7.30) to be considered consistent with failure of spontaneous breathing(1, 3).

The corresponding German guideline prescribes that this hypercapnia, after exclusion of a relevant adaptation to an increase in PaCO₂ (e.g. chronic in the context of COPD or acute in patients with pulmonary contusion) and starting at a baseline PaCO₂ of 35 to 45 mmHg, should be performed by acute hypoventilation until the above-mentioned PaCO₂ of at least 60 mmHg is reached. In parallel, constant clinical monitoring should be performed to detect respiratory excursions or spontaneous respiratory efforts by the patient. Hypoxia must be avoided and sufficient oxygenation of the patient is mandatory, e.g. by intratracheal O₂ insufflation. Disconnection of the patient from the ventilator is usually performed to assess the failure of spontaneous breathing(1, 2).

Because many of the candidates for irreversible loss of brain function have impaired pulmonary function, e.g. due to aspiration pneumonia or neurogenic pulmonary edema with consecutive acute respiratory distress syndrome (ARDS)(5, 6), a relevant proportion of these patients depend on high PEEP values as well as increased fraction of inspired oxygen (FiO₂) for pulmonary stabilization. The loss of PEEP upon disconnection from the ventilator can make the apnea test very difficult or impossible. The risk of hypoxia and associated cardiopulmonary instability, including the need for resuscitation has been described(7). In patients on extracorporeal membrane oxygenation (ECMO), the aforementioned difficulties are particularly frequent(8, 9).

Therefore, various methods have been described to perform the apnea test in a more protective fashion in this patient group(6, 10–12). One of the methods described in retrospective studies and case series/reports is the apnea test under continuous positive airway pressure (CPAP) and sometimes without disconnection from the ventilator(13–16). The aim of this study was to prospectively investigate whether a modified version of such an apnea test on the ventilator (i.e. without disconnection) can be performed safely in everyday life and on a larger number of patients, especially in patients with impaired pulmonary function, and what difficulties may arise.

Ethics check:

This study was approved by our local ethics committee (Nr. 368/19) and registered at the German Clinical Trials Register (DRKS00017803). In all cases, informed consent was obtained from the patient's relatives. No external funding was received.

Study population:

A group of 140 consecutive patients with severe brain damage of various etiology (Table 1) was prospectively examined between January 2019 and December 2022 for the presence of BDBD.

Table 1:

Age [years]	median 56, IQR 44 – 67,5
Sex [female / male]	58 / 82
Included patients	140
Etiology of brain lesion ICH SAH Ischemic Stroke TBI Hypoxia Combined Other	23 12 16 4 40 37 8
Patient on vaECMO/ECLS Relevant levels of analgosedatives Relevant COPD No ARDS ARDS Grade 1 ARDS Grade 2 ARDS Grade 3	16 9 5 45 (32 %) 17 (12 %) 46 (33 %) 31 (22 %)
BD confirmed	114
BD not confirmed	26

Depiction of patient characteristics of all 140 included patients and further details of the BD examinations. BD = “brain death” (irreversible loss of whole brain function), IQR = interquartile range, ICH = intracerebral hemorrhage, SAH = subarachnoid hemorrhage, TBI = traumatic brain injury, Combined = a combination of two or more different etiologies, e.g. SAH and CPR-related hypoxia, vaECMO = veno-arterial extracorporeal membrane oxygenation, COPD = chronic obstructive pulmonary disease, ARDS = acute respiratory distress syndrome

Patients were examined for the presence of BDBD at various intensive care units within the University Medical Center Freiburg. A target sample size of at least 120 patients was calculated based on the number of BDBD candidates examined per annum in previous years.

BD assessment (clinical):

BD testing was performed by two experienced (each with n > 100 BD tests performed) neurointensivist specialists (i.e. board certification both in neurology and intensive care medicine) in accordance with the guidelines published by the GMA and the German Society of Clinical Neurophysiology (DGKN). In most cases, BD testing was required prior to potential organ donation, but in some cases also for the purpose of end-of-life care.

For each patient, a thorough review of the case, including the examination of all available cerebral imaging and laboratory data was initially performed. After ruling out alternative factors that could explain either in whole or in part the patient's comatose state of consciousness (e.g. sedation, shock, etc.), clinical assessment of brainstem reflexes, including apnea testing, was performed. In patients who had received analgosedatives or any other centrally-acting drugs for more than 24 hours, determination of the serum drug levels ensued, if the application end was < 48 hours before BD testing and/or therapeutic hypothermia (which slows metabolism and medication breakdown) had been applied.

Apnea test:

The BD candidates were on various different ventilators (Dräger Evita4®, V500®, V800®, Evita XL®, Maquet Servo-I®, Hamilton C1®). Prior to apnea testing, the ventilators were set on either BiPAP- or SIMV-ventilation with PEEP ≥ 5 mbar. A rising pa PaCO₂ CO₂ causes a drop of the pH which in turn results in vasodilatation and blood pressure loss. In order to prevent this blood pressure loss during or following AT, all patients were started on noradrenaline i.v. (1 or 10 mg/50 ml NaCl 0.9%) if that was not the case already in the context of general circulatory stabilisation. mAT was perfomed according to the following standardized protocol:

After 10 min of preoxygenation at FiO₂ 1.0, arterial blood gas analysis and PaCO₂ measurement (incl. temperature correction) ensued. A target value of 35 to 45 mmHg PaCO₂ was aimed for and ventilation parameters (i.e. respiratory rate, tidal volume) were adjusted, if PaCO₂ was outside these limits.

Next, the PEEP was increased by two points. The flow trigger was set to 10 l/min (to prevent triggering of breaths by artificial air shifts in the intubation tube caused by aortic pulsations) and automatic apnea back-up ventilation was turned off. The apnea alarm time was set to 60s (or higher, if possible). The ventilation mode was then switched to CPAP and a timer started.

The patient’s thorax and abdomen were undressed and closely monitored for breathing attempts and thorax excursions. Furthermore (if available), the machine display was set to show spontaneous vs. ventilator-induced breaths for automatic recording of resumption of spontaneous breathing.

After 8 minutes, blood gas analysis was repeated. If PaCO₂ was ≥ 60 mmHg, the apnea test was deemed positive (i.e. absence of spontaneous breathing) and the ventilator was switched back to the pre-AT settings. If temperature-corrected PaCO₂ was still < 60 mmHg, mAT in CPAP-mode was continued and blood gas analysis repeated until the beforementioned PaCO₂ goal was reached or spontaneous breathing attempts were witnessed. If spontaneous breathing attempts occurred before the aforementioned 8 minutes period had passed, the AT was aborted and the ventilator switched back to the pre-AT settings.

vv and vaECMO-patients:

In vv as well as vaECMO-patients, mAT was performed following the same protocol. ECMO-settings were adapted as previously described(17) in the following way: FiO₂ to the membrane lung was set to 100%, the sweep gas flow was reduced to 0.5–1.0 l/min and the pump flow remained unchanged. In all patients, this was sufficient to achieve a rise in PaCO₂.

Statistical analysis and data presentation:

Statistical analyses (specificity, sensitivity, positive and negative predictive values) were performed using the IBM® SPSS® Statistics 21 software package (IBM Corporation,

Armonk, NY). Data were found to be non-normally distributed and are presented as median and interquartile range (IQR). The performance of the mAT was assessed with regard to the extent of pulmonary affection. The latter was determined by reference to the Horovitz index (PaO₂/FiO₂ post 5 min preoxygenation; PEEP was ≥ 5 mbar in all patients) and all patients were categorized on this basis: No ARDS (Horovitz > 300 mmHg), mild ARDS (201–300 mmHg), moderate ARDS (101–200 mmHg) and severe ARDS (≤ 100 mmHg) [modified Berlin definition].

The patient characteristics are shown in Table 1.

Feasibility:

The mAT could be carried out successfully in 139 of 140 patients. One patient was deemed to be too unstable to initiate the AT (FIO₂ 100%, PEEP 10, SpO₂ 90%, PaO₂ 75 mmHg). In n = 12 patients, spontaneous breathing set in thus yielding a negative AT and incomplete brainstem areflexia. In n = 127 patients, absence of spontaneous breathing was found (i.e. positive AT). The median duration of the mAT was 15 minutes (IQR 13–19).

The absence of spontaneous breathing could not be utilised as indicative of a positive AT in 9 patients due to the detection of relevant levels of analgosedatives (sufentanil, fentanyl, midazolam) upon forensic-pharmacological testing (last application/intake < 48 h prior to mAT). This was also the case in 5 patients with clinically relevant COPD [i.e. adaptation to elevated levels of CO_2, as demonstrated by blood gas analysis: (i) PaCO₂ outside the required 35–45 mmHg range, (ii) simultaneous pH range of 7,35 − 7,45, (iii) altered base excess].

Apneic oxygenation

The PaCO₂ and PaO₂ values pre- and post AT (overall results and PaO₂ categorized according to Horovitz index) are shown in Figs. 1 and 2, respectively. The median body temperature at the time of the mAT was 36.3°C (IQR 35.8–36.75).

Patients on vaECMO

16 patients were on vaECMO-treatment. In all these patients, mAT could be carried out without complications such as a relevant drop in PaO₂ or SO₂. In all patients, a rise to a PaCO₂ of at least 60 mmHg could be achieved solely by reducing sweep gas flow without additionally altering pump flow.

Complications:

a) Deoxygenation:

In none of the 139 patients that underwent the modified AT, the test needed to be interrupted or aborted due to insufficient oxygenation. The PaO₂ values pre and post mAT are displayed in Fig. 2 subdivided according to the different ARDS grades (0 = none to 3 = severe). Figure 3 illustrates the delta between PaO₂ values pre and post mAT. No significant difference was found in patients with no ARDS. The delta was significant in patients with mild (p < 0.05) and highly significant in patients with moderate and severe ARDS (p < 0.01). In n = 51 patients, PaO₂ post mAT was lower and in n = 88 patients, PaO₂ was equal or higher than pre mAT. In none of the patients, PaO₂ post mAT was ≤ 60 mmHg (i.e. no mAT-induced hypoxemia was found).

b) Cardiocirculatory:

In n = 123 patients, the blood pressure post AT was lower than before AT. In n = 12 patients, the MAP transiently dropped below 60 mmHg and the dose of i.v. norepinephrine needed to be increased transiently. Furthermore, no other severe complications during AT were observed.

The apnea test is the central component of international guidelines and the most critical part of clinical testing of BD. Various approaches have been described in the literature on how to perform the AT in a targeted and simultaneously effective manner without endangering the patient. The standard method that is also mentioned in most international guidelines involves disconnection of the patient from the ventilator and insufflation of 100% oxygen (“apneic oxygenation”). The resulting PEEP-loss frequently leads to cardiopulmonary instability particularly in patients with concomitant severe pulmonary diseases like ARDS. The method presented here, which allows the AT to be performed without disconnection and thereby avoiding the critical PEEP-loss is patient-friendly and safe. It is therefore highly relevant to everyday clinical practice.

The main task of the apnea test is to reliably detect a potentially preserved respiratory drive of the patient. Breathing patterns in patients with severe brain damage, which are triggered by the patient when PaCO₂ rises, appear as Biot or Cheyne-Stokes respiration(18, 19), similar to an agonal or sigh respiration (”gasping”). In Biot respiration, deep and vigorous breaths are interrupted by pauses; in Cheyne-Stokes respiration, a crescendo-decrescendo pattern of depth of breaths and additionally regularly changing intervals between breaths occur. Small, fine respiration efforts that are difficult to detect do not occur in this patient cohort. Moreover, as PaCO₂ rises, breathing efforts increase and become more frequent.

Correspondingly, all n = 12 candidates examined in our study, in whom the AT demonstrated preserved spontaneous breathing when PaCO₂ increased, also showed deep breaths, similar to the aforementioned breathing patterns. Additional certainty is provided by the automatic detection of patient-triggered breaths now available on most ventilators. It is important to appreciate patients in whom the rating of a positive apnea test is impossible. In this context, the guidelines often only refer to pulmonary impairment (e.g. caused by COPD or chest contusion) or centrally-acting drugs or medication. However, caution is also warranted in patients with lesions of the upper cervical myelon. It is not possible to distinguish between central failure of spontaneous breathing caused by brainstem areflexia and complete or partial peripheral failure of spontaneous breathing caused by lesions of the anterior horn neurons (C2-C4) or nerve tracts of the phrenic nerve in this cohort.

To solve the central problem of sufficient patient oxygenation (and hereby simultaneously exclude AT-related danger to the patient and at the same time ensure organ protection with potential organ donation in mind), the PEEP was increased by 2 points in each case. This provides sufficient alveolar O₂ circulation and ensured sufficient oxygenation in all patients in our study despite an average of 15 minutes of apneic oxygenation in the absence of ventilation as demonstrated by PaO₂ at the end of mAT. At the same time, the mere increase in PEEP without ventilation does not result in CO₂ washout, which permits the required PaCO₂ increase to ≥ 60 mmHg.

Of note, mAT with apneic oxygenation was not only feasible in patients with various extents of ARDS but proved to be favourable for these patients in our study. After 10 minutes of preoxygenation, the patients were classified into ARDS grades 0–3 (modified Berlin definition(20)). In patients with no ARDS (i.e. grade 0), the delta between PaO₂ pre and post mAT showed no significant difference. By contrast, in patients with mild ARDS, a significant increase in PaO₂ post mAT could be observed (p < 0.05) and in patients with moderate and severe ARDS, this difference was pronounced and highly significant (p < 0.01). This result is in line with current guidelines on the management of patients with ARDS. These suggest low tidal volumes as well as low plateau and driving pressures to reduce work of breathing and lung tissue shear stress in this patient group (i.e. lung-protective ventilation)(21).

The increase in PaCO₂ is known to cause a drop in pH during AT with consecutive vasodilation and a possible drop in blood pressure(22, 23), which was also seen in our collective. Therefore, i.v. norepinephrine was started in all BD candidates in our study prior to initiation of mAT, if this had not already been started as part of general circulatory stabilization. In patients in whom MAP dropped to < 60 mmHg, a transient increase in the dose of norepinephrine i.v. was sufficient to consecutively, none of the patients experienced critical destabilization of blood pressure despite high PaCO₂ values after mAT in some cases. No other cardiocirculatory problems (e.g. arrhythmia, circulatory arrest) occurred. Sixteen of the patients in this study were treated with vaECMO. In this subgroup, mAT was also consistently feasible without complications.

We therefore believe that the following techniques that are currently (or have historically been) used in the context of AT in brain death testing are obsolete: (i) for reasons of patient safety: disconnection from the ventilator with tracheal O₂ insufflation. (ii) for reasons of unambiguity: the use of a fine thread to capture minimal breaths by watching it be pulled into the disconnected intubation tube since respiration in this patient cohort resembles agonal or gasping respiration (i.e. a brain stem reflex) which is always characterised by deep and unambiguous breaths. (iii) again for reasons of unambiguity: holding a mirror in front of the open intubation tube to observe its fogging.

Some ventilators may not allow complete turn-off of apnea ventilation (e.g., 2 mandatory breaths per minute). In these cases, we recommend hypoventilation in combination with (brief) ventilator disconnection after reaching a PaCO₂ of 60 mmHg, as previously suggested(12). In this case, particular care needs to be taken to not confuse machine-generated and patient-generated spontaneous breaths and the disconnection period should be kept as short as possible.

Limitations:

Our study has been conducted without a control group and in a single-center setting which may limit its generalizability. The findings would profit from confirmation in a multi-center setting which is currently being planned on a national level in the IGNITE! Network of the German Society of Neurointensive Care (DGNI). A control group could consist of patients that undergo the standard AT with disconnection from the ventilator.

In summary, the above method of a mAT without disconnection from the ventilator in combination with PEEP increase represents a patient-friendly, safe and easy to perform alternative.

We hereby confirm that the manuscript complies with all instructions to authors.
Authorship requirements have been met and the final manuscript was approved by all authors.
This manuscript has not been published elsewhere and is not under consideration for publication by another journal.
We hereby confirm that the study was performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments. The study was approved by our local ethics committee (IRB Registration number: 368/19) and informed consent from the next of kin was obtained for all patients. Trial registration: DRKS, DRKS00017803, Retrospectively registered 23.11.2020, https://drks.de/search/de/trial/DRKS00017803
None of the authors reports any financial or non-financial interests that are directly or indirectly related to the work submitted.
Not applicable.
No external funding was received for this study.
Authors’ contributions:

JL: study design, acquisition, analysis and interpretation of data, drafting the
manuscript
JB: acquisition, analysis and interpretation of data, manuscript proofreading
CS: acquisition, analysis and interpretation of data, figures, manuscript
proofreading
WN: acquisition, analysis and interpretation of data, manuscript proofreading

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You are reading this latest preprint version

Prospective evaluation of a modified apnea-test without disconnection from the ventilator in brain death candidates

Status:

Version 1

Abstract

Figures

INTRODUCTION

METHODS

Ethics check:

Study population:

BD assessment (clinical):

Apnea test:

vv and vaECMO-patients:

Statistical analysis and data presentation:

RESULTS

Feasibility:

Apneic oxygenation

Patients on vaECMO

a) Deoxygenation:

b) Cardiocirculatory:

DISCUSSION

Limitations:

CONCLUSION

Declarations

References

Status:

Version 1