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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

3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
57
a humanized monoclonal antibody fragment against dabigatran) and, for the others,
there is no high-quality evidence for drug removal from the circulation, prohemostatic therapies like desmopressin (DDAVP) or antibrinolytic agents, or the administration of prothrombin complex concentrates [54]. Andexanet alfa is a factor Xa
inhibitor antidote intended for patients presenting with major bleeds who are taking
FXa-Is. Most hospital protocols include the administration of PCC for the reversal
of FXa-Is, while there is currently no randomized prospective data to base this decision on, there are case series and some animal experiments [55–58]. Please see the
algorithm at the end of this chapter for specic doses.
The management of patients on antiplatelet agents is currently a matter of debate.
In the recent past, several reports described worse clinical outcomes and increased
hematoma expansion in these patients [59, 60]. Recent studies show that rates of
hematoma expansion and outcome are independent of antiplatelet use [61, 62]. A
number of recent observational studies suggested that platelet transfusion could be
of benet in ICH, so a randomized phase 3 trial (the PATCH trial) was recently
completed in Europe looking at whether platelet transfusion in ICH patients
improved outcomes [63, 64]. Patients who received platelets were actually more
likely to have poor outcomes at 3months than those who did not (OR 2.5, 95% CI
1.18–3.56, p = 0.0114). Further, 42% of patients who got platelets have serious
adverse events compared to 29% in the control group. Platelet transfusion is not
currently indicated in ICH patients pending further clinical trials and can only be
considered as a risk reduction measure in patients planned for urgent neurosurgical
intervention [65, 66].
3.7.9 ICP Monitoring
The recommendations for ICP monitoring in ICH is largely borrowed from the traumatic brain injury literature, where ICP monitor placement is recommended in
patients with a GCS of 8 or less, with a goal of maintaining ICP <20 and CPP at
50–70mmHg [67]. The use of ICP monitoring would seem to make intuitive sense
in patients with an ICH, but ICP monitoring exposes patients to nonnegligible risk
for hemorrhage and infection and the present literature is limited in the setting of
ICH [68]. In a cohort study of 243 ICH patients, 57 (23%) underwent ICP monitoring and of those 70% had at least one episode of elevated intracranial pressure but
this did not negatively impact mRS scores (OR 0.8, 95% CI 0.3–2.3) [69].
In analysis of 100 patients from two prospective multicenter trials of patients
with intraventricular hemorrhage (IVH), who underwent placement of external ventricular drain (EVD) for injection of intraventricular alteplase or saline, most
(91.5%) of the transduced ICP readings were within normal range, demonstrating
the effectiveness of cerebral spinal uid (CSF) drainage for controlling ICP [70].
ICP readings >30mmHg in this analysis were an independent predictor of 30-day
mortality after adjustment for other outcome predictors. External ventriculostomy
should be performed only in a select group of ICH patients with evidence of herniation, signicant hydrocephalus, and GCS<8.

58
T. J. Cusack and W. Ziai
3.7.10 Surgical Considerations
Presently, the evidence does not show open surgical evacuation Intracerebral hemorrhage (ICH) does to hold signicant advantage over medical therapy. The Surgical
Treatment of Intracerebral Hemorrhage (STICH) trial compared early surgical
evacuation of ICH to medical therapy [71]. The trial did not show a survival advantage in patients with early surgery. STICH II investigated the subgroup of patients
from STICH I who appeared to have improved outcomes: those with supercial
hematomas with no IVH present and with GCS between 8 and 15. STICH II randomized patients to receive either craniotomy within 12h or best medical care with
the goal of improved functional outcome. Despite the demonstration of noninferiority in STICH II, the surgical technique did not demonstrate statistically signicant
clinical improvement using existing surgical techniques employing open craniotomy with resection of the hemorrhagic tissue. At present, the evidence shows craniotomy to remove clots may only be effective in a select subset of patients and
generally has clinical equipoise with medical management.
A number of studies have compared standard craniotomy versus conservative
treatment. A recent meta-analysis of ten randomized controlled trials (2059 participants) showed that craniotomy reduced the odds of death or disability at nal follow- up (OR 0.74) [72]. In clinical practice, craniotomy is offered to patients who
are having rapid neurological decline, but none of the included trials specically
considered these patients, so this continues to be at the discretion of the consulting
neurosurgeon. Newer minimally invasive techniques are currently being tested,
which aim to decrease the damage to cortex and cortical tracts while at the same
time offering increased access to the region of ICH.These will not be considered
here, as it remains to be seen whether the successful volumetric reduction in clot is
matched with improvement in patient outcomes, but as techniques with increasingly
low morbidity emerge it is hoped that appropriately selected patients will increasingly benet from such treatment.
3.7.11 ICH: Surgical Option forCerebellar
Hemorrhage Patients
Patients with cerebellar hemorrhage causing brainstem compression and rapid neurologic deterioration should undergo surgical removal of the hemorrhage if aggressive management is pursued [9]. Treatment of cerebellar ICH patients with
ventricular drainage alone is not recommended. Evacuation of a supratentorial
hematoma or decompressive hemicraniectomy can be considered lifesaving for
deteriorating patients, but early hematoma evacuation is not clearly benecial for
otherwise stable patients. The effectiveness of minimally invasive techniques for
clot evacuation has not been proven with a randomized controlled trial, and surgical
evacuation has been associated with excellent clinical outcomes. Moreover, posterior fossa hemorrhage is often quickly followed by decompensation in 25–75% of

3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
patients [73]. Retrospective series have suggested that suboccipital decompression
signicantly lowers mortality [73, 74]. Patients with cerebellar hemorrhage >3cm3,
those with brainstem compression or symptomatic hydrocephalus have better outcomes with surgical decompression. Treatment with ventricular drainage alone is
ineffective [74].
59
3.7.12 ICH: Patients withIntraventricular Extension
Intraventricular extension of ICH (IVH) is seen in almost half of the patients with
ICH [75]. The presence of IVH doubles the likelihood or poor outcomes in spontaneous ICH [76]. Meta-analysis has shown that ICH with IVH increases the risk of
mortality from 20% to 51% [77]. Removing the blood from the ventricles via catheter alone is difcult as blood tends to occlude the catheter and the speed of drainage is slow [78]. The use of adjunctive thrombolytic agents makes catheter-assisted
drainage a viable treatment option and has been demonstrated to be safe and effective in the large, randomized, double-blind, placebo controlled CLEAR-III trial
[79]. The CLEAR-III protocol involves administering 12 doses of alteplase 1mg or
0.9% saline through an extraventricular drain every 8h. At present, this protocol is
the only one demonstrated via a large, multicenter, randomized, controlled trial to
be safe. Intraventricular alteplase is not currently recommended for the routine
management of IVH, although ongoing studies are evaluating conditions under
which this treatment may have long-term functional benet which may be related to
more complete reduction in ventricular clot burden.
3.7.13 ICH: Venous Thromboembolism Prophylaxis
The priority of stopping the bleeding in ICH and avoiding triggering further bleeding must be balanced against the need to prevent deep venous thromboembolism
(DVT). The incidence of symptomatic DVT in patients with ICH has been reported
in retrospective case series to be on the order of 1–2% [80, 81], with symptomatic
pulmonary embolism in 0.5–1% of ICH patients [82]. The CLOTS3 trial showed an
absolute risk reduction of 3.6% (95% condence interval 1.4–5.8) of DVT in
patients with the use of IPC [83]. It is, therefore, recommended that patients receive
DVT prophylaxis with pneumatic compression devices (with or without compression stockings) immediately upon hospital admission and continuing until discharge
[84]. The evidence for the use of DVT prophylaxis with subcutaneous unfractionated (UFH) or low molecular weight (LMWH) heparin in ICH relies on two small
prospective randomized trials, which were limited by their small size on low frequency of hemorrhagic or thromboembolic events [85, 86]. A comprehensive meta-
analysis of these and two other observational studies showed the use of UFH or
LMWH to be effective in reducing pulmonary embolism (PE) (RR 0.37, 95% CI
0.17–0.80) but no effect on the incidence of DVT, expansion of hematoma, or death

60
[87]. Current guidelines recommend the use of subcutaneous UFH or LMWH only
in those ICH patients who have had stable hematomas for 48h and who have no
coagulopathy [84].
T. J. Cusack and W. Ziai
3.7.14 ICH: Seizure Management
Most patients with ICH do not experience seizures, but in the rst 7days up to 16%
experience clinical seizures and up to 31% have electrographic seizures [87–89].
Current guidelines support continuous EEG monitoring in patients with clinical seizures or patients with mental status out of proportion to their ICH [9]. Seizures are
the product of cortical irritation, and are most likely in patients with cortical extension of their ICH [90, 91]. Of note, while a large single-center study has shown that
prophylaxis decreases the risk of seizures in ICH, prospective studies report that
seizures do not seem to effect mortality or neurologic outcome [92–94]. In fact, the
available data seem to suggest that antiepileptic prophylaxis is associated with
worse outcomes and increased mortality in particular with phenytoin [95, 96]. In
response, levetiracetam use for seizure prophylaxis has been on the rise despite
limited knowledge about its potential effects on outcomes [97]. Present guidelines
do not support the use of antiseizure medications for prophylaxis in ICH but do
recommend treating patients who have seizures accompanied by a change in mental status.
3.8 ICH: Medical Complications
ICH is associated with a number of medical complications that must be managed
along with the primary insult. In the 607 patients Cerebral Hematoma and NXY-059
Treatment trial, 88% of patients have at least one adverse event [98]. These included,
in order of frequency, pneumonia, pulmonary embolism, respiratory failure, aspiration pneumonia, sepsis, and urinary tract infection. Given that medical complications of stroke cause up to 50% of mortality in this context, aggressive management
of these complications is imperative. Dysphagia is a risk factor for aspiration and
consequent aspiration pneumonia or chemical pneumonitis, but formal bedside
swallow screening for all stroke patients has been shown in a prospective multicenter study to reduce the absolute risk of pneumonia from roughly 5% to 2% [99].
A Cochrane meta-analysis of 33 studies looking at nutrition and swallowing in
stroke showed that avoiding malnutrition is possible with placement of an orogastric or nasogastric feeding tube and that PEG placement reduces treatment failures
and gastrointestinal bleeding while increasing food delivery [100]. Up to 21% of
patients with ICH require mechanical ventilation for inability to protect their airway

3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
[101]. Ventilated patients are at risk for in-hospital mortality as high as 48%, and
should be surveilled for ventilator-associated pneumonia and acute respiratory distress syndrome [102]. To minimize risk of aspiration pneumonia, the head of the
bed should be kept at 30°, frequent oral care should be instituted, and the duration
of intubation should be minimized inasmuch as it is possible.
61
3.8.1 Glycemic Management
Hyperglycemia is an independent risk factor for death and poor outcomes in patients
with ICH, regardless of whether there is underlying diabetes mellitus [103].
Intensive control of glucose to 80–110mg/dL has been shown to both increase incidence of hypoglycemia and intracranial hypertension in one study [104] and to
decrease it in another [105]. At present, there is no large, randomized, controlled
trial demonstrating the effectiveness of strict normoglycemia in ICH and it is not
recommended [106]. ICH patients should have frequent monitoring of glucose to
avoid extreme hypo- and hyperglycemia, but normoglycemia should not be an
aggressively pursued goal.
3.8.2 Avoiding Hyperthermia andHypothermia
Fever is common after ICH, and has an established relationship with worse outcomes and growth of hematoma [107]. While a causal relationship has not been
established between the complex inammatory, neurohormonal, and metabolic cascades involved in temperature management and their derangement in the context of
ICH, it seems intuitive that targeting normothermia could improve outcomes.
However, maintenance of normothermia has not been shown to have an impact on
improving outcomes [108]. There have been no trials of targeted hypothermia in
ICH, so cooling is currently only for investigational use and per the current guidelines and management of fever “may be reasonable” [5]. The authors in their own
practice treat fever >38.5°C and try to maintain normothermia in ICH patients.
3.8.3 Disposition
Upon stabilization, patients with ICH should be dispositioned to dedicated neurological intensive care or stroke units, especially in the initial 24h of care [109].
Patients requiring ventriculostomy drainage or mechanical ventilation will necessarily require ICU care, ideally in a dedicated neurological unit.

62
T. J. Cusack and W. Ziai
3.9 Conclusion
By adhering to present evidence and guidelines for clinical practice, practitioners
caring for ICH can decrease mortality, minimize harm, and increase the likelihood
of functional outcome.
Algorithm
MONITORING KEY HISTORY
Vital Signs Last Known Normal
GCS / NIHSS
SBP > 180 mmHg
TARGET SBP < 160 mmHg
(Tolerate range 140–160)
Within 1 h of presentation
LOCATION
Supratentorial ?
Infratentorial? Hematoma Volume (ABC/2)
INFRATENTORIAL
ICH > 3 cm in diameter with
deteriorating mental status?
Compression of the Brainstem?
Hydrocephalus?
Intraventricular Hemorrhage (IVH) YES
YES NO
Consider EVD and
Clear-III Protocol
NO YES
ETIOLOGY
DISCERNABLE ?
NO
CONSIDER
Brain MRI
MRA
MRV or Angiography
Sign of Herniation or
Mass Effect ?
INTENSIVE CARE UNIT (ICU)
EMERGENCY DEPARTMENT (ED)
Clinical Status of the Patient
ABCD
Oxygenation (SpO
Normocapnia (PaCO2 35–45 mmHg)?
Hemodynamic Stability?
YES
> 94%)?
2
IMAGING
Non-contrast Brain CT-Scan
CT-Angiogram Head Coagulopathy Present ?
MEASUREMENT
SUPRATENTORIAL
Ongoing Clinical deterioration?
Mass effect / Cortical location?
Persistent elevated ICP refractory
to medical management?
Treat clinical Seizures
Not role for Seizure prophylaxis
Early Enteral nutrition
Avoid Hyponatremia (Serum Na+ < 135 )
Avoid Hypoglycemia and Hyperglycemia
Maintain Normothermia
Prevention of VTE (Pharmacological prophylaxis if
Bleed stable on day 2–3)
Hemoglobin > 7 g/dL
Drugs
Recent Surgery
Advanced Health directives
Allergies
LABORATORY
CBC / Glucose
Electrolytes / Creatinine
PTT / INR / Troponin
Toxicology Screen
Correction of Coagulopathy
VKAs (FFP and IV Vitamin K)
DOAC (Oral charcoal and PCC)
Heparin / LMWH (IV Protamine)
Antiplatelets (Platelet
Transfusion only NCx intervention)
Thrombocytopenia (transfuse
To >100.000 and/or Desmopressin)
Fibrinolytics (PCC and FFP)
Consider Surgical Intervention
1. Neurosurgical consult for evacuation or
decompression.
2. Consider external ventricular drain (EVD) if
Hydrocephalus present.
Prevention of Secondary Brain Injury
ABCD airway-breathing-circulation-disability, PCC prothrombin complex concentrate, VKAs
vitamin K antagonist, MRA magnetic resonance angiography, MRV magnetic resonance venography, NCx neurosurgery, FFP fresh frozen plasma, SBP systolic blood pressure

3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
63
Appendix: Direct Oral Anticoagulant Reversal
After ve half-lives, anticoagulation can be considered fully resolved.
Apixaban: 8–15h; 5 half-lives: 24–75h after last dose (day 1.5–3)
Betrixaban: 19–27h; 5 half-lives: 95–135h after last dose (day 4–5.5)
Dabigatran: 12–17h; 5 half-lives: 60–85h after last dose (day 2.5–3.5)
Edoxaban: 6–11h; 5 half-lives: 30–55h after last dose (day 1.3–2)
Rivaroxaban: 5–9h; 5 half-lives: 30–45h after last dose (day 1–2)
Activated charcoal to absorb drug if taken in prior:
Apixaban: up to 6h
Edoxaban: up to 2h
Rivaroxaban: up to 8h
Reversal Strategies
Dabigatran: Idarucizumab (Praxbind) 5g IV; if unavailable, FEIBA 50–80μ/kg; if
unavailable, use a three- or four-factor PCC at 25–50 μ/kg. If using three-factor
PCC, consider supplementation with FFP for factor VII.Tranexamic acid (TXA)
may be considered. Hemodialysis has been shown to remove active dabigatran from
circulation.
Apixaban, betrixaban, edoxaban, and rivaroxaban: If emergent surgery is
required, andexanet alfa may be given. Low dose (for those who received rivaroxaban <10mg, apixaban <5mg, or >8 h since last dose of factor Xa inhibitor) is a
bolus 400mg at rate of 30mg/min followed by infusion of 480mg at rate of 4mg/
min. High dose (for those who are on rivaroxaban >10mg, apixaban >5mg, or dose
unknown or <8h since last dose of factor Xa inhibitor) is bolus of 800mg at 30mg/
min followed by infusion of 960mg at a rate of 8 mg/min. If andexanet alfa not
available, four-factor PCC.
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