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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Acknowledgments
- •Contents
- •Contributors
- •1.2 How Is Critical Care Humanized?
- •References
- •2.1 Introduction
- •1.2.2 Communication
- •1.2.5 Post-ICU Syndrome
- •1.2.6 Humanized Infrastructure
- •1.2.7 End-of-Life Care
- •2.2 Which Patients Should Undergo ICP Monitoring?
- •2.5.2.3 CSF Drainage
- •2.5.2.4 Osmotherapy
- •2.5.2.5 Ventilation
- •2.5.2.6 CPP Augmentation
- •2.5.2.7 Metabolic Suppression
- •2.5.2.8 Pharmacologic Suppression
- •2.5.2.9 Temperature Modulation
- •2.5.2.10 Decompressive Craniectomy
- •2.7.1.1 Pressure Reactivity Index (PRx)
- •2.7.1.2 Multimodality Monitoring
- •2.8 Conclusion
- •Algorithm
- •References
- •3.1 Introduction
- •3.2 Intracerebral Hemorrhage (ICH)
- •3.3 ICH: Presenting Symptoms
- •3.5.1 Blood Hypertension
- •3.5.2 Other Risk Factors
- •3.6 ICH: Pathophysiology
- •3.7 ICH: Initial Management
- •3.7.1 Airway: Intubation
- •3.7.3 ICH: Imaging
- •3.7.4 ICH: Grading Scales
- •3.7.5 Fluid Management
- •3.7.6 Follow-Up Imaging
- •3.7.7 Blood Pressure Management
- •3.7.9 ICP Monitoring
- •3.7.10 Surgical Considerations
- •3.7.13 ICH: Venous Thromboembolism Prophylaxis
- •3.7.14 ICH: Seizure Management
- •3.8 ICH: Medical Complications
- •3.8.1 Glycemic Management
- •3.8.3 Disposition
- •3.9 Conclusion
- •Algorithm
- •Appendix: Direct Oral Anticoagulant Reversal
- •Reversal Strategies
- •References
- •4.1 Introduction
- •4.2.1 Hemodynamic Management
- •4.2.2 Hormonal Replacement Therapy
- •4.2.3 Respiratory Management
- •4.3 Cardiopulmonary Resuscitation (CPR)
- •4.4 Conclusion
- •Algorithm
- •References
- •5.1 Introduction
- •5.2.1 Vasoactive Agents
- •5.2.1.1 Vasodilators (Table 5.1)
- •Calcium Channel Blockers
- •Nimodipine
- •Nicardipine
- •Other Vasodilators
- •Magnesium
- •3-Hydroxy-3-Methyl-Glutaryl-CoA (HMG-CoA) Reductase Inhibitors (Statins)
- •Nitroprusside
- •Endothelin-1 Antagonists
- •Hydralazine
- •Phosphodiesterase Inhibitors
- •Papaverine
- •Norepinephrine
- •Epinephrine
- •Dopamine (DA)
- •Phenylephrine
- •Vasopressin
- •Neuromonitoring
- •5.2.2.1 Benzodiazepines
- •5.2.2.2 Barbiturates
- •5.2.2.3 Opioids
- •5.2.2.4 Anticonvulsant Medications
- •5.2.2.5 Other Sedatives/Anesthetics
- •5.2.3 Hemodynamic Agents
- •5.4 Conclusion
- •Algorithm
- •References
- •6.1 Introduction
- •6.2.3 Ultrasound Behaviour at Acoustic Boundaries
- •6.3 Pulse-Echo Principles (B-Mode Techniques)
- •6.4 Transducers
- •6.5 Artefacts
- •6.6 Doppler Principles
- •6.6.1 Pulsed Wave Doppler
- •6.6.2 Duplex Scanning
- •6.6.3 Colour Flow Imaging (CFI)
- •6.7.2 Flow Changes
- •6.7.3 Cerebrovascular Resistance
- •6.8 Transcranial Colour-Coded Duplex Sonography (TCCS)
- •6.9 Ultrasound Safety
- •6.10 Conclusion
- •References
- •7.1 Introduction
- •Mesencephalic Plane
- •7.2.1.2 Diencephalic Plane (Thalamic Plane)
- •6.6.4 Power Doppler Imaging (PDI)
- •6.7 Transcranial Doppler Ultrasound (TCD)
- •6.7.1 Velocity Measurement
- •7.2.1.3 Ventricular Plane (Cella Media)
- •7.2.1.4 Upper Pons Plane
- •7.2.1.5 Lower Pons Plane
- •7.2.2 Transforaminal Window
- •7.3.1.2 Anterior Circulation
- •Carotid System
- •Anterior Cerebral Artery
- •Anterior Communicating Antery
- •7.3.1.3 Posterior Circulation
- •Vertebrobasilar System
- •Posterior Communicating Artery
- •Posterior Cerebral Arteries
- •7.5 Cerebral Circulation: Anatomical Variations
- •7.5.1.1 Anterior Circulation
- •Most Common Variations [28]
- •7.5.1.2 Posterior Circulation
- •Most Common Variants [28]
- •7.6.1.1 Deep Middle Cerebral Vein (DMCV)
- •7.6.1.2 Basal Vein (of Rosenthal)
- •7.6.1.3 Great Cerebral Vein (of Galen)
- •7.6.2.1 Sphenoparietal Sinus
- •7.6.2.2 Superior Petrosal Sinus
- •7.6.2.3 Inferior Petrosal Sinus
- •7.6.2.4 Cavernous Sinus
- •7.6.2.5 Transverse Sinus
- •7.6.2.6 Straight Sinus
- •7.7 Conclusion
- •Algorithm
- •References
- •8.1 Introduction
- •8.2 Cerebral Blood Flow Measures
- •8.3 Transcranial Doppler (TCD/TCCS)
- •8.4.1 Cerebral Autoregulation (CA)
- •8.4.2 CO2 Vasoreactivity
- •8.6.2 TCD/TCCS: Use After Traumatic Brain Injury (TBI)
- •8.7 Conclusion
- •References
- •9.1 Introduction
- •9.3 TCD Hemodynamic Parameters: Variations by Sex
- •9.4 TCD Hemodynamic Parameters: Variations by Age
- •9.5 TCD Hemodynamic Parameters: Variations by Laterally
- •9.7 TCD Normal Values: Latin American Population Sample
- •9.8 TCD Hemodynamic Parameters: Altitude
- •9.10 Conclusion
- •References
- •10.1 Introduction
- •10.2 TCD/TCCS: Acoustic Windows
- •10.2.1.1 Technique
- •10.2.2.1 Technique
- •10.2.3.1 Technique
- •10.2.4.1 Technique
- •10.2.5.1 Technique
- •10.4.1 Decompressive Craniectomy
- •10.4.2 Patient’s Position
- •10.5 TCD/TCCS: Contrast-Enhanced
- •10.6 Conclusion
- •Algorithm
- •References
- •11.1 Introduction
- •11.2 Basic Methods
- •11.2.1 Flow Velocities
- •11.2.2 Pulsatility Index (PI)
- •11.3 Advanced Methods
- •11.3.2 TAU (Cerebrovascular Time Constant)
- •11.3.4 Autoregulation
- •11.4.1 Traumatic Brain Injury
- •11.4.2 Aneurysmal Subarachnoid Hemorrhage
- •11.4.3 Stroke
- •11.4.4 Other Clinical Scenarios
- •11.5 Conclusion
- •Algorithm
- •References
- •12.1 Introduction
- •12.2 TCD: Spectral Wave
- •12.4 TCD: Clinical Utility
- •12.6 TCD: Technique
- •12.6.2 Transtemporal Acoustic Window
- •12.6.2.1 Anterior Circulation
- •Middle Cerebral Artery (MCA)
- •12.6.2.2 Posterior Circulation
- •Posterior Cerebral Artery (PCA)
- •12.6.3 Submandibular Acoustic Window
- •12.6.3.1 Internal Carotid Artery (ICA—Extracranial Portion)
- •12.6.4 Transoccipital Acoustic Window
- •12.6.4.1 Posterior Circulation
- •12.6.5 Transorbital Acoustic Window
- •12.6.6.2 Pulsatility Index
- •12.7.1 High-Velocity Pattern
- •12.7.2 Low-Velocity Pattern
- •12.7.3 High Resistance Pattern
- •12.7.4 Cerebral Circulatory Arrest Pattern
- •12.8 TCD: Other Clinical Uses
- •12.8.1.1 Cerebral Vascular Reactivity
- •12.9 TCD: Limitations
- •12.10 Conclusion
- •Algorithm
- •References
- •13.1 Introduction
- •13.2 Acoustic Windows
- •13.3 2D-Guided TCD Monitoring
- •13.6 Conclusion
- •Algorithm
- •References
- •14.1 Introduction
- •14.2 TCCS: Anatomical Aspects
- •14.3.1 Anterior Circulation
- •14.3.1.1 Carotid System
- •14.3.2 Posterior Circulation
- •14.3.2.1 Vertebro-Basilar System
- •14.5 TCCS: Examiner Considerations
- •14.6 TCCS: Acoustic Windows
- •14.7 TCCS: Examination Protocol
- •14.7.1.1 Considerations
- •Doppler: (Convention)
- •14.7.2 Transtemporal Acoustic Window Examination (Coronal Planes)
- •14.7.3 Transoccipital (Transnuchal/Transforaminal) Acoustic Window Examination
- •14.7.4 Submandibular Acoustic Window Examination
- •14.7.5 Transorbital Acoustic Window Examination
- •14.7.6 Frontal Bone Window Examination
- •14.8 TCCS Protocol: Clinical Applications
- •14.9 TCCS Protocol: Hemodynamic Parameters
- •14.10 TCCS Protocol: Limitations
- •14.10.1 Limitations
- •14.10.1.1 Acoustic Windows
- •Transtemporal Acoustic Window
- •Suboccipital Acoustic Window
- •14.10.1.2 Middle-Line Shift Measurement
- •14.11 Conclusion
- •Algorithm
- •References
- •15.1 Introduction
- •15.2 Clinical Applications
- •15.2.1 Intracranial Stenosis
- •15.2.2 Cerebral Vasospasm
- •15.2.3 Cerebral Veins
- •15.3 Conclusion
- •References
- •16.1 Introduction
- •16.3.1 Autoregulation Index (ARI)
- •16.3.2 Mean Flow Velocity Index (Mx)
- •16.5 Conclusion
- •References
- •17.1 Introduction
- •17.2.1 Cerebrovascular Resistance (CVR)
- •17.2.2 Cerebral Autoregulation
- •17.2.4 Carbon Dioxide Reactivity
- •17.3.2 Collateral Flow
- •17.3.3 Elastic Reservoir (“Windkessel Effect”)
- •17.4 TCD: Waveform Interpretation
- •17.4.1 TCD Waveforms
- •17.5.1 Aneurysmal Subarachnoid Hemorrhage
- •17.5.2 Increased ICP
- •17.6 Conclusion
- •References
- •18.1 Introduction
- •18.3.1 Subarachnoid Hemorrhage (SAH)
- •18.3.1.1 Cerebral Autoregulation (CA)
- •18.3.1.2 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.1.3 Cerebral Blood Flow
- •18.3.1.4 Electrophysiology
- •Seizure Detection
- •18.3.1.5 Cerebral Metabolism
- •18.3.2 Intracerebral Hemorrhage (ICH)
- •18.3.2.1 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.2.3 Electrophysiology
- •18.3.3 Traumatic Brain Injury (TBI)
- •18.3.3.2 Cerebral Autoregulation
- •18.3.3.3 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.3.4 Cerebral Blood Flow
- •18.3.3.5 Electrophysiology
- •18.3.3.6 Cerebral Metabolism
- •18.3.4 Acute Ischemic Stroke (AIS)
- •18.3.4.1 Cerebral Blood Flow
- •18.3.4.2 Electrophysiology
- •18.3.5.1 Cerebral Blood Flow
- •18.4 Conclusion
- •References
- •19.1 Introduction
- •19.2 Cerebral Blood Haemodynamic Measurements
- •19.3 Cerebral Blood Flow (CBF): Physiology Principles
- •19.4 Vasoreactivity Determining: Methods
- •19.6 Technical Tips
- •19.7 Vasoreactivity: Clinical Importance
- •19.8 Conclusion
- •References
- •20.1 Introduction
- •20.5.4.1 Experimental Endotoxemia
- •20.6 Conclusion
- •Appendix
- •Methods
- •Group 1: Graphic Methods
- •“Beat-by-Beat Method”
- •Method Described by Aaslid
- •Group 2: Multiparameter or Impedance Methods [14]
- •References
- •21.1 Introduction
- •21.2.1 Brain Compliance
- •21.2.2 TCD/TCCS: Cerebral Hemodynamics
- •21.4 Pulsatility Index (PI): Intracranial Pressure (ICP)
- •21.5.1 Cardiovascular Factors
- •21.5.2 Cerebrovascular Factors
- •21.5.3 Cardiopulmonary Factors
- •21.5.4 Metabolism Factors
- •21.5.5 Vascular Factors
- •21.5.6 Other Factors
- •21.6 Conclusion
- •Algorithm
- •References
- •22.1 Introduction
- •22.2 Aneurysmal Subarachnoid Hemorrhage (aSAH)
- •22.3 Cerebral Vasospasm After aSAH
- •22.5.1 TCD/TCCS: Examination Protocol
- •22.5.1.1 Transtemporal Window
- •22.5.1.2 Orbital Window
- •22.5.1.3 Suboccipital/Transforaminal Window
- •22.5.1.4 Submandibular Window
- •22.7 Conclusion
- •Algorithm
- •References
- •23.1 Introduction
- •23.3.1 Premise
- •23.3.3 Limitations
- •23.4.1 Technical Requirements
- •23.4.3 Limitations
- •23.6 Future Directions
- •23.7 Conclusion
- •Algorithm
- •References
- •24.1 Introduction
- •24.2.1 Vasospasm
- •24.2.2 Vasospasm Diagnostic Criteria
- •24.3 TCD/TCCS: Cerebral Vasoreactivity
- •24.4 TCD/TCCS: Intraoperative Monitoring
- •24.7 Conclusion
- •References
- •25.1 Introduction
- •25.4 CAD: Diagnosis
- •25.6 Pupil: Ultrasound Examination
- •25.11 Conclusion
- •Algorithm
- •References
- •26.1 Introduction
- •26.2 Optimal Settings
- •26.2.1 Probe Types
- •26.2.2 Frequencies
- •26.2.3 Focus
- •26.2.4 Depth
- •26.2.5 Pulse Repetition Frequency (PRF)
- •26.2.6 Frame Rate
- •26.2.8 Freeze
- •26.2.9 Cine Loop
- •26.2.10 Smoothing (Interpolation), Interlacing, Correlation
- •26.2.11 Postprocessing
- •26.2.12 Resolution
- •26.2.13 Doppler-Technique
- •26.2.14 PW-Doppler (Pulsed-Wave Doppler)
- •26.2.15 Color Duplex
- •26.3 Indications
- •26.4.1.2 Morphological Differences
- •26.4.1.3 Flow Differences
- •26.4.1.4 Compression
- •26.5 B-Mode Examination
- •26.5.1 Dilation
- •26.5.2 Intima-Media Thickness (IMT)
- •26.5.3 Plaque Analysis
- •26.5.3.1 Location
- •26.5.3.3 Maximal Thickness
- •26.5.3.4 Surface
- •26.5.3.5 Echogenicity
- •26.5.4 B-Flow Imaging
- •26.6.1 Color Doppler Imaging (CDI)
- •26.6.2 Power Doppler Imaging (PDI)
- •26.7.1 Stenosis Measurement
- •26.7.1.1 Diameter Stenosis
- •26.7.1.2 Area Stenosis
- •26.7.1.3 Residual Luminal Diameter
- •26.7.2 Occlusion
- •26.7.3 Subtotal Stenosis: (>95% Stenosis)
- •26.7.4 Long Segment Stenosis
- •26.8 Doppler Spectrum
- •26.10 Contrast Enhanced Ultrasound (CEU)
- •26.11.1 Common Carotid Artery
- •26.11.2 Internal Carotid Artery
- •26.11.2.1 Stenosis
- •26.11.2.2 Dissection
- •26.11.2.3 Occlusion
- •26.11.2.4 Subtotal Occlusion: (95–99% Stenosis)
- •26.11.2.5 Multiple (Tandem) Stenosis
- •26.11.2.6 Long Segment Stenosis
- •26.11.3 External Carotid Artery (ECA)
- •26.11.3.1 Occlusion
- •26.13 Negative Report
- •26.14 Conclusion
- •Algorithm
- •References
- •27.1 Introduction
- •27.2 Anatomy: Vertebrobasilar System
- •27.3 Vertebrobasilar Circulation: Ultrasound Examination
- •27.4 TCD: Aneurysmal Subarachnoid Hemorrhage
- •27.4.1 Delayed Cerebral Ischemia
- •27.4.2 Vasospasm
- •27.5 TCD: Vertebrobasilar Dissection
- •27.6 TCD: Intracranial Stenosis
- •27.7 TCD: Microembolus Detection
- •27.9 Subclavian Steal Syndrome
- •27.10 TCD: Multimodal Monitoring
- •27.11 TCD: Traumatic Brain Injury
- •27.12 TCD: Brain Death Determination
- •27.13 Conclusion
- •References
- •28.1 Introduction
- •28.2 Cerebral Venous System: Anatomy
- •28.3 vTCCS: Ultrasound Investigation Technique
- •28.4 CVST: Venous Ultrasound Findings

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69

Chapter 4
Organ Maintenance After Death
byNeurological Criteria (DNC)
inNeuro- ICU: TheImportance
ofDonation
VassoZisimopoulou andPanayiotisN.Varelas
Key Points
1. Many patients with severe brain injury, despite all efforts to save them, die by
neurological death criteria. Many of these brain-dead patients become organ and
tissue donors.
2. The management of these patients before they are declared brain dead may differ
from the management after they are pronounced and may be organ specic.
3. Hemodynamic instability is a common problem in these organ donors and has to
be managed with uid replacement, vasopressors, or inotropes and, if not
responding, hormonal replacement therapy.
4. Aggressive respiratory management with maneuvers aiming at increased alveo-
lar recruitment should be instituted in every organ donor.
5. Cardiopulmonary resuscitation in the brain-dead organ donor is controversial
and should be discussed with the family of the patient.
4.1 Introduction
The advent of modern ventilators and the development of intensive care units have
created a uniquely modern, largely hospital-based phenomenon, the death by neurological criteria (DNC) or brain death (BD). Without mechanical ventilation, the
cessation of brain function leads inevitably to apnea and cardiac arrest, but with it,
V. Zisimopoulou
Air Force General Hospital, Athens, Greece
P. N. Varelas (
Department of Neurology, Albany Medical Center, Albany, NY, USA
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_4
*)
71© Springer Nature Switzerland AG 2022

72
V. Zisimopoulou and P. N. Varelas
patients continue to have heartbeat and circulation for a period of time that usually
spans few days to a week.
Since the seminal paper by Mollaret and Goulon almost 60years ago [1], the
concept of BD was gradually adopted by clinical, ethical, and legal authorities as an
alternative to cardiorespiratory death in every country. The determination of BD,
however, is not uniform and has led to variability across borders [2] or even within
countries such as the USA [3]. The rst systematic attempt to address this problem
and establish standard practice parameters for the determination of BD was not
made until the American Academy of Neurology’s 1995 guidelines were issued [4],
with an update published in mid-2010 [5]. Therefore, following these clear and succinct guidelines, the vast majority of health practitioners worldwide recognize that
declaration of BD is a complex process that requires familiarity and includes
six stages:
1. Detection of an irreversible coma.
2. Prerequisites that have to be met before a patient is evaluated for BD.
3. Thorough clinical examination by a physician who has expertise on assessing
brain function.
4. Apnea testing to exclude any spontaneous respirations.
5. Ancillary testing in specic situations, where parts of 3 and 4 are not certain or
cannot completely be assessed.
6. Precise documentation of all the above and the time of death of the individual.
Because details about the BD declaration process and the role of transcranial
Doppler have been discussed in another chapter of this book, our aim here is different. But before we delve into details, let us clarify here the three periods that these
very seriously ill patients pass through during their stay in the intensive care
unit (ICU):
1. The patient is admitted to the ICU with a severe brain injury, but brain function
is detected and is not BD.All the efforts by the treating team are aiming at preserving life, despite the fact that in many situations futility is obvious and it is a
matter of time until all brain activity ceases.
2. There is no detectable brain activity, the BD process is initiated and is completed
later on, with the patient declared BD.
3. If the patient is an organ donor, all efforts aim at optimizing organ function to
allow safe transplantation to a living recipient.
Although it is obvious that the ICU team manages the patient during periods 1
and 2, it is not clear who manages the dead patient during period 3. In the USA, this
is usually accomplished by a coordination of care between the local intensivists who
were managing the patient before and during the declaration and the Organ
Procurement Organization (OPO) team, which takes over after the patient is conrmed an organ donor. These health professionals (usually nurses and a physician
medical director) have been already notied as soon as the, still alive, patient meets

4 Organ Maintenance After Death by Neurological Criteria (DNC) in Neuro-ICU…
clinical triggers (usually deep coma, on a ventilator, without sedation, or paralytics
masking the presence or absence of clinical function). After the patient is declared
BD, this same team discusses with the family, conrms consent for donation, starts
histocompatibility matching, decides which organs are potentially transplantable,
and orders additional procedures, tests, or biopsies. However, who really manages
the dead patient in the ICU during the third period is variable, with the intensivists
or the OPO team providing care until the patient reaches the operating room. There
are emerging data, however, that an intensivist-led management of brain-dead
donors increases the number of organs recovered for transplantation, more specically lungs and kidneys [6].
Independently of whoever is the leader, the goal should be common and the
cooperation between the various teams imperative. This is our aim in this chapter:
to provide information on how to manage the BD patient in the ICU, maximize
organ recovery, and optimize posttransplant organ function.
73
4.2 ICU Management oftheBrain-Dead Organ Donor
The majority of transplanted organs come from donors who meet Death by
Neurological Criteria (DNC). Once these criteria are met, the neurointensivist’s
goal shift from optimizing cerebral perfusion to maximizing organ preservation by
compensating the physiologic deterioration leading to and following brain death.
The care of the potential organ donor aims at stabilizing hemodynamic changes and
endocrine abnormalities resulting from a complex interplay of neurohumoral, hormonal, proinammatory phenomena, and other not yet fully understood mechanisms [7, 8]. The Society of Critical Care Medicine, the American College of Chest
Physicians, and the Association of Organ Procurement Organizations have published guidelines for donor management [7], which should be used as a framework
in these situations.
4.2.1 Hemodynamic Management
Monitoring is essential for balancing interventions needed for optimal organ preservation. Routine monitoring with parameters such as temperature, blood pressure,
heart rate and rhythm, pulse oxygen saturation, and urine output should be combined with serial or continuous measurements of central venous pressure (CVP),
pulmonary artery occlusion pressure (PAOP), stroke volume, cardiac output (CO),
cardiac index, and mixed venous oxygen saturation. The latter are measured by
placement of central venous and pulmonary artery catheters, but noninvasive methods have gained grounds, although with fewer data in this situation.

74
V. Zisimopoulou and P. N. Varelas
Intense monitoring, based on serial assessments of the aforementioned parameters, is crucial to achieve normovolemia and control extremes of blood pressure.
General guidelines for adequate IV uid resuscitation are as follows:
1. Mean arterial pressure (MAP)>60mmHg.
2. Urine output >1ml/kg/hr.
3. Left ventricle ejection fraction >45%.
4. Lower vasopressor dose (e.g., dopamine ≤10μg/kg/min).
These goals are essential since the rostrocaudal brain herniation, which eventually leads to brain death, is associated with a massive sympathetic discharge also
known as autonomic storm. Autonomic storm includes physiologic changes such as
catecholamine-induced increased heart rate, increased myocardial oxygen consumption, and hypertension. B-adrenergic agents such as esmolol have been traditionally used to treat this phase in an effort to preserve cardiac function. This phase
is later followed by an abrupt hypotensive period attributed to vasodilation or cardiac dysfunction as the cardiorespiratory medullary centers collapse, usually in the
context of hypovolemia [9].
Hypovolemia according to guidelines is initially treated with replacement of
intravascular volume with crystalloids or colloids. The optimal choice of uid therapy has not yet been nalized since studies addressing the issue are missing.
Lactated Ringer solution and 0.9% saline are traditionally used, but in case of
hypernatremia that needs to be treated, hypotonic uids such as dextrose 5% or
saline 0.45% are also utilized. Colloids such as albumin 5% and hydroxyethyl starch
(HES) in bolus solutions are commonly available in ICUs to treat acute hypotension. Nevertheless, HES should be used with caution and is not recommended for
infusions especially above 500–1000mL since it has been associated with acute
kidney injury, coagulopathy, delayed graft function, and graft failure. Packed RBCs
can also serve as colloidal solutions in cases of bleeding or hematologic conditions
with hemoglobin levels <7g/dL but the optimal hemoglobin level for organ preservation is not known.
Vasodilation with hypotension has been traditionally treated with pressors or
inotropes in parallel with uid administration or when uid correction fails to
quickly achieve hemodynamic stability. Dopamine is the preferred vasoactive agent
in these situation. In addition to having renal vasodilatory properties, and inotropic
and vasoconstrictive effects as the dose increases, it also has immunomodulatory
properties that may counterbalance the proinammatory cascade of cytokines by
induction of enzymes like heme oxygenase-1. Nevertheless, there are no studies to
strongly support dopamine over other vasopressor agents such as vasopressin, but
most intensivists prefer to use the latter as rst or second agent. Generally, there is
a desirable dopamine goal of ≤10μg/kg/min and vasopressin can be added if this
dose is exceeded. Norepinephrine, phenylephrine, dobutamine, and epinephrine are
more commonly considered and used for severe shock. Use of norepinephrine and
phenylephrine should be done with caution in brain-dead patients and only as tertiary agents when dopamine dose is above 10μg/kg/min or there is no adequate

4 Organ Maintenance After Death by Neurological Criteria (DNC) in Neuro-ICU…
75
response to vasopressin, as they exhibit more potent α-receptor agonist activity
leading to increased pulmonary capillary permeability causing increased extravascular lung water and coronary and mesenteric vasoconstriction [7].
Transthoracic echocardiography (TTE) is used to access myocardial function but
it should be delayed after the early course of brain death and after the patient is
weaned off catecholamines or repeated following aggressive donor management.
Myocardial dysfunction may be due to underlying cardiac disease, cardiac injury
from chest trauma, or stress cardiomyopathy. Guidelines suggest that if hemodynamic goals are not met and/or left ventricular ejection fraction remains less than
45%, then hormonal replacement therapy (HRT) may be undertaken [7].
4.2.2 Hormonal Replacement Therapy
Up to 80% of brain-dead patients develop signs of central diabetes insipidus (DI)
due to ischemic—or other—injury of the hypothalamic-pituitary axis.
Hypothyroidism and hypocortisolism also occur but in lower rates.
High, dilute urine output (>3–4L/d or 2.5–3.0mL/kg/hr) associated with hypovolemia, serum hyperosmolality, and rising hypernatremia (Na+ > 145mmol/L)
may indicate the presence of DI due to arginine vasopressin (AVP or antidiuretic
hormone) deciency in the absence of other causes (e.g., hyperglycemia and mannitol administration). Treatment with AVP as a replacement therapy should be considered when hypotension persists despite high rate uid resuscitation since it
improves vasodilatory shock and reduces the need for catecholamines. A typical
dosing regimen is an initial bolus infusion of 1 unit, followed by a continuous infusion of 0.01 to 0.1units/minute (typical doses are 0.01 to 0.04units/minute), titrating to a systemic vascular resistance of 800 to 1200 dynes-sec/cm5. Desmopressin
(DDAVP, a vasopressin analogue) is a more reasonable option in the presence of DI
without hypotension due to greater afnity for V2 receptors (in the distal nephron)
than V1 (on vascular smooth muscles) compared to AVP.Initial dose of 1–4μg is
given intravenously and then the dose is adjusted to achieve a urine volume <4mL/
kg/hour (typical required dose of 1–2 μg intravenously every 6–12 hours).
Desmopressin can be used concurrently with AVP in patients with severe hypernatremia and hypotension. When DI occurs, electrolytes should be closely monitored
(at least every 4hours) and replenished to avoid hypokalemia, hypophosphatemia,
and hypomagnesemia.
Corticosteroid therapy is used to reduce brain death-induced inammation and
more specically to optimize donor lung quality, as it is associated with reduced
extravascular lung water accumulation. The typical dose of methylprednisolone is
15mg/kg as an intravenous infusion or 250mg as an intravenous bolus followed by
an infusion of 100mg/hour, but it should be administered after blood has been collected for tissue typing.

76
Routine administration of thyroid hormone therapy has been controversial since
the potential benet has not been clearly shown in all studies. Guidelines suggest
use of thyroid replacement therapy alone or in combination with AVP, corticosteroids, and insulin in hemodynamically unstable donors or with decreased left ventricular ejection fraction (<45%). Suggested dose is T4 as a 20μg bolus IV, followed
by an infusion at 10μg/hr., or administration of T3 as a 4.0μg bolus IV, followed by
an infusion at 3μg/hr.
Hyperglycemia is common in deceased organ donors and it should be treated
even though target glucose levels are in debate. Most ICUs aim for glucose level
less than 180mg/dL while routine use of dextrose IV uids is generally avoided,
unless the water decit from DI aquaresis cannot be easily corrected with 0.45%
saline and AVP or DDAVP.
V. Zisimopoulou and P. N. Varelas
4.2.3 Respiratory Management
Brain-dead patients may have signicant lung dysfunction from trauma (pulmonary
contusions), pulmonary edema (either cardiogenic or neurogenic), infection (pneumonia), or V/Q mismatch (pulmonary embolism or atelectasis). The goal of the
managing team is to optimize the function of lungs, by inducing diuresis, and
achieve euvolemia, treat the infection, recruit more alveoli, and decrease the oxygen
and positive end expiratory pressure (PEEP) requirements. The goal should be to
reach a PaO2/FiO2 ratio ≥ 300 mm Hg on high oxygen and low PEEP (i.e.,
PaO2>300mm Hg with 100% FiO2 and 5cm PEEP). Survivability of recipients,
however, has not been different in recipients with lower compared to higher than
300 ratio in large studies with over 10,000 patients [10].
There is abundance of lung donor management protocols. A combination of therapeutic bronchoscopy, chest physiotherapy, and lung recruitment maneuvers usually
improve oxygenation even in donors who initially fail to meet these goals. Lung protective protocol, similar to acute respiratory distress syndrome (ARDS) ventilation
settings, using tidal volumes of 6–8mL/kg, 8–10cm PEEP, a closed circuit for suctioning, and continuous positive airway pressure equal to previous PEEP for apnea
test led to increased lung recovery rates compared to conventional ventilator protocol
with 10–12ml/kg tidal volume [11]. Increased alveolar recruitment may also explain
the increased lung recovery found with airway pressure release ventilation (APRV)
compared with traditional assist control ventilation in a small retrospective study [12].
4.3 Cardiopulmonary Resuscitation (CPR)
Brain-dead patients can sustain a cardiac arrest (CAA). In a large study from
NewYork, 12% of patients sustained a CAA between the two brain death examinations or after the second examination [13]. Physicians should be prepared since

4 Organ Maintenance After Death by Neurological Criteria (DNC) in Neuro-ICU…
77
these patients are critically ill, with several comorbidities, including previous CAA
that contributed to BD declaration.
There are many philosophical and ethical issues regarding any attempt to resuscitate a brain-dead patient, who has been declared ofcially and legally dead. Who
will lead the efforts, the ICU team or the OPO? What is the purpose of doing cardiopulmonary resuscitation (CPR) in a dead patient? For how long these efforts should
continue? If a second CAA happens in a different but alive patient, how the triage
of resources should be done? There are also several periods during the process of
BD declaration and after and for each a clear response plan regarding resuscitation
or not (the Code Status) should be implemented:
1. Period between the two brain death exams. Although the patient may seem BD
during the rst exam, but is not ofcially declared BD.The Code Status remains
the same.
2. Period after patient is declared BD and before discussion with family. Should the
patient be resuscitated if a CAA occurs to allow the family to have the option of
organ donation? What if the patient is already a registered donor and his/her
wishes are already clear?
3. Period during discussion with family. As above. However, a decision to resusci-
tate can be made quickly and in real time.
4. Period after the patient became a donor and before the operating room for organ
procurement. Does the Code Status automatically change from pre-brain death
to do resuscitate in every case because the patient became a donor? Is a separate
consent from the family required or is it implied when consent for donation
is signed?
4.4 Conclusion
There are no data about national, state, or hospital policies on these issues. The
meager literature available is revealing. Ethicists, however, have developed the
notion of organ preserving cardiopulmonary resuscitation (OP-CPR), which is
dened as the use of CPR in cases of cardiac arrest to preserve organs for transplantation, rather than to revive the patient [14]. They conclude that although successful
resuscitation may benet the society by saving recipients lives, CPR in the braindead patient can cause physical damage and may provoke psychological harm to
families and healthcare professionals. What is certain is that without clear and predened plans on how to react in a not so rare situation, confusion among ICU health
providers will ensue. Therefore, we recommend this issue to be addressed in the
hospital or National policies of Organ Donation and families to be questioned on
their preferences during the process of consent for donation.
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