Edema Cerebral y SX HIC

Edema cerebral y
Síndrome de Hipertensión Endocraneal

LARA BAHENA LUIS ALFREDO R5NC
ASESOR: DR. BAYRON SANDOVAL MBNC

 
Estructura
• Craneo: protección fisica rigida
• LCR: absorción de choque hidráulico
• Vascular y BHE: aporte de sustratos, homeostasis celular, recambio de fluido extracelular,
protección de sustancias nocivas
Andrew Beaumont. (2022). Physiology of the Cerebrospinal Fluid and Intracranial Pressure. En Youmans & Winn Neurological Surgery(472e1-472e18). EUA: Elsevier.

Doctrina de Monro-Kellie
• V1LCR + V1sangre+ V1cerebro + V1otros = V Espacio intracraneal = V2LCR + V2sangre + V3otros
• Parenquima 1250-1500mL
• LCR 125-150mL
• Sangre 125-150mL
• Normal
• LCR: Presión de senos venosos
• Sangre: parametros cardiacos y autoregulación cerebral.

Historia
• Quinke describe la punción lumbar para mejorar la “presión cerebral” en 1911
• Guillaume and Janny en 1951 monitoreo continuo de la PIC
• Lundberg: ondas A,B C
• Actualmente: Enfermedad, respuesta al tratamiento y monitoreo de la perfusión cerebral.

Fisiología de Presión intracranial

• Limite superior 15-20mmHg
• Supino 7-15mmHg
• Vertical: negativa hasta -15mmHg
• Tos/estornudo 30-50mmHg
• Actividad cardiaca y respiratoria -> Componente pulsátil por cambios en el volumen de sangre
cerebral
• Transmisión del pulso (Plexo coroideo, arterias piales, venas de alta compliansa)
• Cambios en abdomen y tórax: inspiración caída de presión arterial y disminución del gradiente
de presión de venas cerebrales a vasos centrales venosos,

SF
us
I formation P
c
CHAPTER 69 Physio
T
de I absorbed PRESSURE-VOLUME CURVE PRESSURE-VOLUME INDEX (PVI)
L
Normal adult Normal adult
id
R (ICP vs. ∆V) (ICP vs. ∆V) S
ar C 80
us I storage
90 S
ic 60
a P
id 80 40 M
es C
70
es I (t) Compliance = .14 C
Pd 20
Log ICP (mm Hg)

32 Storage b
60 B
ICP (mm Hg)

es Formation Absorption A
ve b 50 10 O
a, 8 p
40
nd Figure 69.4. Equivalent electrical circuit showing the principal
se 30 6 D
factors that govern intracranial pressure. Formation of cerebrospinal PVI = 25 mL
fluid (CSF), denoted by I, is represented as a current source, I (t), and 20 4 (Calculated volume
CSF storage as a capacitive element (C). Resistance to CSF outflow is to raise ICP = 10)
represented by a resistive element (R), and dural sinus pressure is Pd. 10 Compliance = .62
a
This framework has allowed accurate description of CSF dynamics.
0 0 C
(From Marmarou A, Shulman K, Rosende RM. A nonlinear analysis of
of the cerebrospinal fluid system and intracranial pressure dynamics. J
–8 0 8 16 24 –8 0 8 16 24
i- Neurosurg. 1978;48[3]:332–344.) ∆V (mL)
ull A B
e-
al single resistive element (Ro). This component represents the total Figure 69.3. The pressure-volume curve and the pressure-volume app
to resistance to the outflow of CSF, which under normal conditions index (PVI) describe the response of intracranial pressure (ICP) sid
ue remains fixed and independent of ICP.
Andrew Beaumont. The final
(2022). Physiology element
of the Cerebrospinal ofIntracranialto
Fluid and theEnaddition
Pressure. ofNeurological
Youmans & Winn volume (V). (A) The
Surgery(472e1-472e18). normal
EUA: Elsevier. curve shows how
472.e6 SECTION 3 Basic and Clinical Sciences

NORMAL ADULT AFTER TBI EFFECTS OF ELEVATED INTRACRANIAL PRE
PVI = 25 mL PVI = 10 mL
Under non–steady-state conditions, failure of co
50
50 mechanisms ultimately results in elevated ICP, the
• #1consequences
TCE of which can be severe. First, continue
40
40 of the brain relies on a cerebral arteriovenous pressure
• maintain
Edema circulation. ICP is transmitted to the compli
ICP (mm Hg)

ICP (mm Hg)
30 veins, and therefore the CPP is defined as arterial infl

30
• minus
Sangre ICP. (extradural,
If ICP increases, subdural,
then CPP decreases, and
20
subaracnoidea
limit of autoregulation o intraparenquimatosa/
is exhausted, CBF will begin
20
autorregulación
ing ischemia, which ewill hiperemia)
in turn propagate more swe
efforts at managing pathologic elevations in ICP ha
10
Po
10 • Velocidad
either an de mecanismos
ICP-targeted approach or a CPP-targeted
Po
is likely that neither is accurate, but rather ideal tre
0 0 need to address maintenance of appropriately regu
–2 0 2 4 6 8 10 12 14 16 –2 0 2 4 6 8 blood flow in the context of disordered ICP, CPP, an
∆V (mL) ∆V (mL) lation. However, for this to be used clinically, a real-ti
of autoregulation must be available.
Figure 69.5. Pressure-volume curves. Left, From a normal adult. Right, The autoregulatory reserve may be defined as th
From an adult with cerebral edema. In the pathologic state, the curve is between the CPP at a given moment and the low
steeper and the pressure-volume index (PVI) is greatly reduced as a result autoregulation. Considering that the lower limit of aut
of VOTHER (the abnormal component of the skull). ICP, Intracranial pressure; is within the range of 50 to 70 mm Hg, the autoregula
Po, steady state; TBI, traumatic brain injury; V, volume.

Flujo cerebral CHAPTER 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure 472.e7
CEREBRAL BLOOD FLOW IN RESPONSE TO

CHANGES IN CEREBRAL PERFUSION PRESSURE
• Presión de perfusión cerebral
• Limite menor de regulación 50-70mmHg 125 No autoregulation
CBF (mL/100 g/min)

• Mantener >70mmHg 100
• Mecanismos Disturbed
75 autoregulation
• Disminución de FSC 6h posterior a TCE ECG<8 22.4 + 5.2mL/
100g por min
50
• Hiperemia 45-65% TCE en 12-24h Autoregulation
• Estabiliza en 36-48h posterior a TCE
25
• Mediciones de FSC 0
• Método Kety-Schmidt Todo el cerebro 0 25 50 75 100 125 150 175
• Xenon Xw 133 sin sustancia blanca CPP (mm Hg)
• IRM variación anatómica
Figure 69.7. Cerebral autoregulatory curves. Normal autoregulation
5 min Time
maintains cerebral blood flow across a range of mean arterial pressure
(MAP). Disturbed autoregulation causes a shift of the curve to the right
and introduces a more linear component (i.e., cerebral blood flow [CBF]

Hipertensión intracraneal
• 40-60% de TCE severo
• Factor de mortalidad en 50% muertes
• >20mmHg predictor deal pronostico en TCE severo
• Aumento de 10mmHg en primeras 48h OR 3.12 en mortalidad

Efecto Cushing (hipertensión arterial, bradicardia, alteración respiratoria)

(en el niño aumento de tensión fontanela, aumento del perimetro craneal)
Cuadro clínico
• Cefalea
• Vomito (sin nausea)
• Papiledema
• Alteración del estado de
consciencia
• Triada de Cushing

Hernia
• Transtentorial descendente (central y uncal)
• Subfalcina
• Transtentorial ascendente
• Transforaminal
• Extracranial

Monitoreo de la presión intracraneal

• Guías actuales • ECG 3-8 con TC anormal
• No hay consenso en • TC normal con >2:
• Selección de pacientes • Edad >40 años
• Tiempo
• Postura motora unilateral/bilateral
• Duración
• TA sistólica <90mmHg
• Sin mejoría en la sobrevida
• Beneficio en ECG>8 + TC alteraciones
• Gold Standard ventriculostomia (masas o lesiones asociadas que requieran
• Intraventricular, intraparenquimatoso, manejo)
subdural y epidural.

69 Physiology of the Cerebros

Monitoreo de la presión intracraneal Intracranial Pressure
Andrew Beaumont
This chapter includes an accompanying lecture presentation that

has been prepared by the authors: Video 69.1.
• Guías actuales:
SECTION 3 Basic and Clinical Sciences
• Manejo PIC >22mmHg NORMAL INTRACRANIAL PRESSURE 20

INTRACRANIAL PRESSURE WAVEFORMS
INTRACRANIAL PRESSURE WAVEFORMS WAVEFORM AT RAPID CHART SPEED
mm Hg
• PPC meta >60-70mmHg 10 10
8 0
• Tratar HAS cuando PPC 6
W1 Respiratory pulse
>120mmHg
Respiratory pulse
4
W2
Cardiac pulse
W3
2 Baseline
Cardiac pulse
0
0
Baseline Figure 69.2. Normal intracranial pressure waveform at rapid chart
speed. Several small components can be seen, the most constant
of which are the percussion wave (W1), the tidal wave (W2), and the A wide variety of neurological and neurosurgical conditions are
0 associated with disordered physiology of the cerebrospinal fluid
dicrotic wave (W3). (CSF) and intracranial pressure (ICP). The position of the brain
within a rigid structure, namely the skull, creates a unique physi-
1. Normal intracranial pressure (ICP) waveform. The ologic environment in which changes in absolute intracranial
that can alter intrathoracic pressure during the respiratory cycle
essure level is affected by rhythmic components caused by volume (VINTRACRANIAL SPACE) are limited, and thus create patho-
of resuscitation. The impedance threshold device limits inflow of
atory activity. Fluctuation of mean arterial pressure with heart logic elevations in ICP or shifts in the relative volumetric propor-
respiratory gas and therefore creates greater and longer negative tion of intracranial contents.
small amplitude rapid pulsation, and respiration causes larger- 10
intrathoracic pressure. The device has been shown to improve The basic physiologic tenets of this concept were put forward
uctuations of lower frequency. ICP is completely described only
cerebral
Andrew Beaumont. (2022). Physiology of theand coronary
Cerebrospinal Fluid perfusion
and Intracranialand to En
Pressure. reduce
YoumansICP inNeurological
& Winn cardiac Surgery(472e1-472e18).
arrest
in the Monro-Kellie
EUA: Elsevier. doctrine, or hypothesis, which can be
on about both the baseline level and the pulsatile components.


• Ventriculostomia + transductor
• 2-22% complicaciones hemorrágicas
• Aumento de riesgo >5 días 3-22% infecciones
• Cambio profiláctico no reduce la taza de infecciones y no se
recomienda
• Monitoreo parenquimatoso
• Infecciones <1%
• Alta variabilidad anatómica
• Microtransductores
• Diafragmas con sensibilidad a la luz, galgas extensométricas
neumáticas en un catéter con punta de balón y piezoelectricas


• Menos invasivas
• Medición sonográfica del diámetro de la vaina nerviosa del nervio óptico
• Medición 3mm del polo posterior del globo ocular
• 4.5-5.5mm es indicativo de aumento de PIC
• Otras tecnologías desplazamiento de la membrana timpánica, IRM, TC, el EEG, la
espectroscopia de infrarrojo cercano y los potenciales evocados visuales

Edema
Cerebral
Definición
• Aumento en el contenido de agua en tejido cerebral.
• Intra/extracelular
• Multifactorial
• Tumores, infección, falla hepática, envenenamiento, hidrocefalia, TCE, hipertensión,
hemorragia parenquimatosa, cambios de altitud, desordenes metabólicos e infarto cerebral.
Douglas A. Hardesty, Russell R. Lonser. (2022). Cerebral Edema. En Youmans & Winn Neurological Surgery(473e1-473e13). EUA: Elsevier.

Barrera hemato-encefalica 473.e2 SECTION 3 Basic and Clinical Sciences
• Cerebro 2-3% masa total

• 20% del volumen sanguíneo total para funcionar
• Área capilar total de 12-20m2
• Distancia entre vasos de 40microns
Neuron
• BHE: uniones estrechas de células endoteliales

• >180 Da Figure 70.1. Illustration of the normal
blood-brain barrier. Endothelial cells
and their tight junctions are wrapped Astrocyte
Tight junction
• Hidrofilicas
by the basement membrane and
Endothelial cell
astrocyte foot processes, separating
Basement membrane
the intravascular space from the Pericyte
brain interstitial space. A perivascular Astrocyte foot plate
• Moléculas cargadas space filled with small amounts of

cerebrospinal fluid is found between
these layers. (© The Ohio State
University, reproduced with permission.) ©The Ohio State University
transcytosis, active adenosine triphosphate-driven transcellular complexes. There cerebrospinal fluid movement into the brain
transport, or efflux pumps.8-12 Notable molecules and compounds interstitial space is facilitated by the aquaporin-4 water channels
that can move across the blood-brain barrier include gases expressed on astrocyte foot processes that envelop the cerebral
Douglas A. Hardesty, Russell R. Lonser. (2022). Cerebral Edema. En Youmans & Winn Neurological Surgery(473e1-473e13).microvasculature.
EUA: Elsevier. 20 Specifically, cerebrospinal fluid flows through
(e.g., oxygen, carbon dioxide), small lipophilic structures (e.g.,

Barrera hemato-encefalica 473.e2 SECTION 3 Basic and Clinical Sciences
• Mecanismos de transporte
• Proteinas de transporte selectivo
• Difusión lipofílica
• Transcitosis adsortiva
• Transcitosis mediada por receptores
• Transporte transcelular ATP-dependiente Neuron
• Bombas de Eflujo.
• Paso libre Figure 70.1. Illustration of the normal
blood-brain barrier. Endothelial cells
• Gases (O, CO2) and their tight junctions are wrapped
by the basement membrane and
Astrocyte
Tight junction
Endothelial cell
astrocyte foot processes, separating
• Estructuras lipofílicas pequeñas (metanol, etanol) the intravascular space from the
Basement membrane
Pericyte
brain interstitial space. A perivascular Astrocyte foot plate
space filled with small amounts of
• Nutrientes (Glucosa, acido ascorbico) cerebrospinal fluid is found between
these layers. (© The Ohio State
transcytosis, active adenosine triphosphate-driven transcellular complexes. There cerebrospinal fluid movement into the brain
transport, or efflux pumps.8-12 Notable molecules and compounds interstitial space is facilitated by the aquaporin-4 water channels
that can move across the blood-brain barrier include gases expressed on astrocyte foot processes that envelop the cerebral
Douglas A. Hardesty, Russell R. Lonser. (2022). Cerebral Edema. En Youmans & Winn Neurological Surgery(473e1-473e13).microvasculature.
EUA: Elsevier. 20 Specifically, cerebrospinal fluid flows through
(e.g., oxygen, carbon dioxide), small lipophilic structures (e.g.,

the pia mater at the brain surface, leaving the perivascular space, perivascular spaces and the surrounding interstitium. Whe
the subpial space, and the Virchow-Robin space surrounding large molecular tracers were used (>500 kD), the tracer could no
the vein in communication (see Fig. 71.3C). In this way, the exit the perivascular spaces and followed the vascular basemen
anatomy of perivascular spaces surrounding arteries and veins at membrane to the level of the basal lamina in the terminal capillar
Sistema Glifático
the brain surface differs in an important manner. Recent in vivo bed, demonstrating continuous communication between cisterna
measurements have demonstrated that the perivascular spaces are CSF, perivascular spaces, and the vascular basement membrane
10 times larger than what has been measured in postmortem fixed Thus these perivascular pathways are key routes by which CSF
CSF influx ISF efflux

Paraarterial CSF influx Paravenous ISF efflux
CSF
To cervical
• Sistema glial-linfático Glial limitans Glial

limitans
lymphatics
Bloodstream
• A través del espacio periarterial A B
CSF
(Virchow-Robin) por pulsación

arterial, gradiente de presión,
Paravacular influx
in the mouse brain Brainwide perivascular pathway for CSF-ISF exchange
respiración y motilidad vasomotora.

CSF A
Pia PVS
SAS
End-foot Pia mater
Surface Convective bulk flow
AQP4
artery
Astrocyte
Cortex Cortical surface
PAS
A Synapse Convective bulk flow

Vein
Penetrating
Capillary
Artery arterioles
End-foot
AQP4 PF
PVS
AQP4 Paraarterial influx Interstitial solutes
Below cortical surface Water flux Paravenous efflux Solute clearance
CAPS
B C
C D
Figure 71.3. Apposition of astrocytic end-foot processes with perivascular and perivascular spaces. (A) Astrocyte end-feet form the glial
limitans facing the subpial spaces and express high levels of the water channel aquaporin 4 (AQP4). (B) Perivascular astrocytic end-feet ensheath the Figure 71.4. Perivascular pathways of cerebrospinal fluid (CSF) influx imaged in the mouse brain. (A–B) Schematic depicts periarterial
cerebral microcirculation and express AQP4 at high levels in the vessel-facing perivascular membrane. (C) Diagram showing relationships between
pia mater and penetrating cerebral blood vessels. Leptomeningeal vessels are ensheathed by a layer of the pia mater, forming a perivascular space
pathways of CSF movement into and through the brain interstitium and the clearance of interstitial fluid (ISF) along perivascular spaces surrounding
(PVS) between the pial sheath and the vessel wall that runs through the subarachnoid space (SAS). In penetrating arteries, this PVS follows the large-caliber draining veins. (C) Imaging of intracisternally infused fluorescent CSF tracer into the living mouse brain. At the cortical surface, CSF
vessel into the brain, becoming perforated and fusing with the basement membrane of the distal arteriole, before the terminal capillary bed (CAPS).
The PVS surrounding veins do not enter the brain, but rather reflect back on the pia mater, Douglas
rending theA.
tracer moves through the perivascular space (PVS) surrounding cerebral surface arteries (upper panel). Below the cortical surface, CSF tracer move
PVSHardesty,
surroundingRussell R. Lonser.
veins continuous (2022).
with the Cerebral Edema. En Youmans & Winn Neurological Surgery(473e1-473e13). EUA: Elsevier.
subpial space. A, Arachnoid membrane; CSF, cerebrospinal fluid; PAS, periarterial space; PF, pial fenestrations. (A and B, Modified from Nagelhus into the parenchyma along the PVS surrounding penetrating arterioles and then exchanges with the surrounding ISF (lower panel). (D) Schematic

Clasificación
• Vasogénico
• Alteración en la integridad de la BHE
• Citotoxico
• Falla energética de las bombas
• Intersticial
• Aumento de presión LCR, flujo transependimario
• Osmótico
• Estados sistémicos hipo-osmolares

Edema Vasogenico 473.e4 SECTION 3 Basic and Clinical Sciences
• Permeabilidad anormal de la BHE

• Uniones estrechas y relación astrocitica-celula endotelial Plasma
ultrafiltrate
• Causas:
• Neoplasias (primarias/secundarias), Daño cerebral,
Infección, Inflamación
• Edema por Ultrafiltrado del plasma Plasma
ultrafiltrate
Figure 70.2. Illustration of blood-
• Fluido, proteinas sericas, solutos tônicos y otros productos brain barrier derangements found
in vasogenic edema. Breakdown Plasma
del plasma of the tight junctions and opening

of the normal blood-brain barrier
ultrafiltrate
via abnormal vascular endothelial

growth factor expression and other
• Acumulación en el espacio extracelular (intersticial) del mechanisms allows for pericellular flow
and accumulation of plasma ultrafiltrate
parenquima into the brain interstitial spaces. (© The
Ohio State University, reproduced with
©The Ohio State University
permission.)
With increasing tumor vessel surface area (via neovascu- Cytotoxic Edema
larization and/or tumor progression) and/or increased tumor
vascular
Douglas A. Hardesty, Russell R. Lonser. (2022). Cerebral permeability,
Edema. the Neurological
En Youmans & Winn amount ofSurgery(473e1-473e13).
plasma ultrafiltrate Pathophysiology
EUA: Elsevier.

Edema Vasogenico
• Edema peritumoral
• Secresión de factores angiogenicos VEGF (aumenta permeabilidad, disfunción de uniones
estrechas)
• Glucocorticoides (dexametasona) inhibición de producción y acción de VEGF
• Bevacizumab en glioblastoma reduce edema y reforzamiento de gadolinio
• Expansión de espacio extracelular -> Reabsorbido por tejido nervioso y sistema linfático hasta
alcanzar homeostasis
• Formación de quistes al vencer la resistencia de tejido sólido

70
Initial Imaging
24 months after
initial imaging
47 months after
initial imaging
B D F
C E G
Figure 70.7. Axial CT and MR images of right frontal metastasis-associated vasogenic edema. (A) Non–contrast-enhanced CT scan
demonstrates right frontal white matter hypodensity consistent with peritumoral edema. (B) Non–contrast-enhanced T1-weighted MR image
Edema Citotoxico
• Daño temporal o permanente a tejido cerebral
(glia, neuronas, endotelio)
• Alteración en fisiologia que mantiene la
integridad y homeostasis de la membrana
celular
• Causas:
• Isquemia cerebral, trauma, hemorragia
Figure 70.4. Illustration of the
blood-brain barrier in the setting
intracerebral, falla hepática, toxinas,
of cytotoxic edema. Loss of normal
cellular homeostasis due to ischemia
Extracellular
síndrome de Reye e intoxicación por agua.

ADP+P
results in failure of Na /K adenosine + +

Na+
triphosphatase (inset) and results in the
accumulation of intracellular sodium. Na+ Na+
Free water flows into the cell along the ATP
osmotic gradient that is induced by Na+
Na+
the accumulation of sodium causing Na+
intracellular swelling. (© The Ohio State ©The Ohio State University Intracellular Na+
University, reproduced with permission.)

70
A B
C D
Figure 70.8. Axial CT and MR images in cytotoxic

cerebral edema due to right middle cerebral artery
ischemic stroke. (A) Non–contrast-enhanced CT scan
obtained 8 hours after the ischemic event demonstrates
hypodense changes of the right frontal white matter
(yellow arrow). (B) Non–contrast-enhanced head CT scan
approximately 36 hours post-stroke demonstrates diffuse
swelling of the right frontal lobe with increasing hypodensity
in region. (C) Fluid-attenuated inversion recovery MR image
demonstrates region of edema (hyperintensity). (D) T2-
weighted MR image shows increased fluid (hyperintensity)
content in the region of edema. (E) Apparent diffusion
coefficient MR image reveals region of cerebral ischemia/
cytotoxic edema (hypointensity). (F) Diffusion-weighted MR
image demonstrates restriction (hyperintensity) in cytotoxic
edema that anatomically correlates with the hypointensity E F
seen in apparent diffusion coefficient imaging.
Figure 70.4. Illustration of the
blood-brain barrier in the setting
of cytotoxic edema. Loss of normal Extracellular
Edema intersticial/hidrostatico
cellular homeostasis due to ischemia ADP+P
results in failure of Na+/K+ adenosine Na+

triphosphatase (inset) and results in the
accumulation of intracellular sodium. Na+ Na+
Free water flows into the cell along the ATP
osmotic gradient that is induced by Na+
Na+
the accumulation of sodium causing Na+
intracellular swelling. (© The Ohio State ©The Ohio State University Intracellular Na+
• Flujo de LCR através del ependimo de las
paredes ventriculares.
• Aumento de líquido en espacio
periventricular Gap region
• La eliminación de este edema es por el

Figure 70.5. Illustration of interstitial
Ventricle
sistema glifático edema. The ventricular ependyma

(inset) in interstitial edema as seen on
coronal brain imaging (transependymal
• Causas flow). Hydrostatic pressure from the
ventricular space pushes cerebrospinal
fluid into the surrounding brain tissue Ependymal layer
• Hidrocefalias via bulk flow (inset). (© The Ohio State
in animal models of hydrocephalus/increased ventricular fluid

perfusion.53 Based on emerging data,54,55 clearance of cerebral
Osmotic Edema
edema due to transependymal flow of cerebrospinal fluid in
interstitial hydrocephalus appears to potentially be driven by
Pathophysiology
the glymphatic system. Additional insights into the interplay Osmotic cerebral edema arises from a mismatch in osmolarity
between pressure-driven transependymal flow and the glym- between the brain parenchyma and circulating blood (Fig. 70.6). A
phatic clearance
Douglas of excess
A. Hardesty, Russell R. Lonser. fluid are being
(2022). Cerebral Edema. Endefined. The
Youmans & Winn relatively hypo-osmotic
most Surgery(473e1-473e13).
Neurological EUA: Elsevier. plasma leads to passive free water influx into

al
ve
an
ry
ellow A B
us.
Edema Osmótico CHAPTER 70 Cerebral Edema 473.e7
70
• Gradiente osmotico por hipo-osmolaridad

plasmatica relativa a SNC
Na+
Na+
• Causas Plasma
ultrafiltrate
Na+
• Reposición rápida de hipernatremia

• Hemodiálisis
• Alteraciones en el metabolismo relacionado a
Figure 70.6. Illustration of the Na+
glucosa osmotic cerebral edema. Osmotic

pressure results from a mismatch Na+
Plasma
between osmolarity in the brain (relative Na+ ultrafiltrate
• SIAD
hyperosmolarity) interstitial and cellular Na+
compartments relative to plasma Na+
(hypo-osmolar), such as overly rapid Na+ Plasma Na+

correction of hypernatremia. Under ultrafiltrate
• Toma excesiva de agua these conditions, free water flows along

an osmotic gradient from the plasma
into the brain. (© The Ohio State ©The Ohio State University
cerebral edema includes the too-rapid treatment of hypernatremia the type of cerebral edema. Tumor-associated edema (Fig. 70.7)
via infusion of isotonic or hypotonic infusion fluids. 56,57 The initial will often relatively spare gray matter and demonstrate hypoden-
underlying
Douglas A. Hardesty, Russell R. Lonser. (2022). hypernatremia
Cerebral in these
Edema. En Youmans cases
& Winn raises theSurgery(473e1-473e13).
Neurological relative osmotic sity in
EUA: the white matter adjacent to a mass lesion. Cytotoxic edema
Elsevier.
content of the brain as sodium enters the brain from plasma across associated with infarction will typically follows a vascular distribu-

Manejo Hipertensión intracraneal

• No farmacologico • Hipotermia 32-34˚C
• Hiperventilación 1-torrPaCO2=3%FSC • Recalentar <24h
• Meta PaCO2 30-35mmHg • Aumento de riesgo de infección,
desbalance hidroelectrolitico, alteración
• Eliminación en 24-48h para evitar de coagulación, arritmias cardiacas,
elevación abrupta PIC depresión de función miocardio.
• Límite 1-24h
• Elevación de la cabeza 30˚
• Neutra
Edward R Smith, MDSepideh Amin-Hanjani, MD. (2019). Evaluation and management of elevated intracranial pressure in adults. 11 abril 2022, de UpToDate Sitio web: https://www.uptodate.com/contents/evaluation-and-management-of-elevated-intracranial-pressure-in-adults
Jan Drappatz, MD. (2021). Management of vasogenic edema in patients with primary and metastatic brain tumors. 11 abril 2022, de UpToDate Sitio web: https://www.uptodate.com/contents/management-of-vasogenic-edema-in-patients-with-primary-and-metastatic-brain-tumors
Cook, A.M., Morgan Jones, G., Hawryluk, G.W.J. et al. Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients. Neurocrit Care 32, 647–666 (2020). https://doi.org/10.1007/s12028-020-00959-7


• Farmacologico • Na 155-160mEq/L Cl 110-115mEq/L
• Acetazolamida
• Manitol (20%) 1-1.5g/kg inicial y
• 500mg c/12h Máximo 2-4g por día 0.25-0.5g/kg en bolo c/6-8h
• Disminución de LCR 16-66% • Límite 320mOsm/kg, Na >150mEq
• Presión ocular, electrolitos séricos, BH • Pico 1h, duración 4-24h
con diferencial
• Furosemida 0.5-1.0mg/kg
• Agentes osmóticos
• Hipokalemia
• Salina hipertónica 3%

 
• Farmacologico • Infusión 4mg/kg/h hasta 8mg/kg/h
• Barbitúricos • Hipokalemia en inducción e hiperkalemia al retiro
• Fenobarbital carga 5-20mg/kg en 30min seguido de • PAM <80mmHg detener infusión
infusión de 1-4mg/kg/h
• Profilaxis Anticomicial
• Meta sérica 3.5-4.5mg/100mL o 10-20 seg de
supresión en EEG. • Alto riesgo MAV con hemorragia parenquimatosa y
absceso cerebral, falta de cierre dural
• 50% hipotensión arterial que requiera dopamina,
hiponatremia, neumonía, depresión cardiaca • Tumores 15-50% (temporal 86%, frontal 82%)
• Tiopental • Niños 12%
• 1.5-3.5mg/kg/dosis • Fenitoina / Levetiracetam
• Carga 250mg en 10mL IV en 5 min (Max 5g) • 1 semana (sin beneficio después de la primer
semana)


• Farmacologico • Reducción 50% cada 4 dias
• Corticosteroides • Complicaciones:
• Dexametasona • Gastrointestinales: Profilaxis de ulceras en dexa
>8mg al dia
• Severo:
• Miopatía: 2-20%, semana 9-12, recuperación 2-3
• Carga de 10mg meses
• Mantenimiento 16mg(dividido 2-4dosis) • Neumonía: Profilaxis con TMP/SMX en pacientes
con >4 semanas de glucocorticoide
• Leve-moderado
• Supresión HPA dexa 3mg por 3 semanas
• Sin carga
• Infecciones de sitio qx 3%
• 4-8mg (dividido 1-2 dosis)
• Uso prequirurgico mortalidad HR 3.0
• Beneficio clínico de 24-72h
Medikonda, R., Patel, K., Jackson, C., Saleh, L., Srivastava, S., Feghali, J., Mohan, A., Pant, A., Jackson, C. M., Weingart, J., Mukherjee, D., Bettegowda, C., Gallia, G. L., Brem, H., & Lim, M. (2022). The safety and ef cacy of dexamethasone in the perioperative management of glioma patients, Journal of Neurosurgery, 136(4), 1062-1069.

fi
• Quirúrgico • 15% por hueso y 70% por dura
• Drenaje ventricular externo/interno • Infarto de ACM bien definido
• 1-2mL/min por 2-3min con intervalos de
2-3min hasta lograr PIC <20mmHg o
hasta no obtener LCR
• Evacuación quirúrgica
• Craniectomia
• Reducción de PIC y estancia en UCI

Caracteristica Vasogenico Citotoxico Intersticial Osmotico

El cerebro es
Falla metabolica de la bomba Na/K
Aumento permeabilidad Flujo transependimario de hiperosmolar con
ATPasa y otros energía-dependiente
vascular en la BHH con LCR a espacio respecto al plasma,
Fisiopatologia balance ionice metabolismo con
acumulación de fluido periventricular extracelular agua entra por
hinchazón celular (neuronas, glia, células
extracelular q gradiente osmótico al
endoteliales)
cerebro
Composición Temprano: LCR perivascular Plasma relativamente
Ultrafiltrado del plasma LCR
del edema Tardio: plasma hipo-osmotico
Localización Preferencialmente sustancia Sustancia blanca
Sustancia gris y blanca Sustancia gris y blanca
del edema blanca periventricular
Volumen
Aumentado Disminuido Aumentado Aumentado
extracelular
Anoxia, cetoacidosis diabetica,
Tumores, intoxicación por Hemodiálisis,
encefalopatia hepatica, hipotermia,
plomo, necrosis por radiación, corrección rapida de
Etiiología típica infarto/isquemia, trauma, infección, Hidrocefalia
trauma, absceso, encefalitis y hypernatremia, crisis
meningitis, Síndrome Reye, Intoxicación
etapas tardías de infarto hipertensiva, SSIHA
por agua, necrosis por radiación
Respuesta a Tx Si Depende de etiologia Si Depende de Etiologia
Esteroide Efectivo No efectivo No efectivo No efectivo
Diuréticos Minimo o no efectivo Transitoriamente efectivo Transitoriamente efectivo No efectivo
Tx hiperosmolar Transitoriamente efectivo Transitoriamente efectivo Minimo o no efectivo No efectivo
Remover origen, inhibición Remover origen Remover origen,
Otros Remover origen, craniectomia
VEGR, otras terapias (obstrucción, derivación o restaurar gradiente
tratamientos descompreita
especificas 3er ventriculostomia osmotico

Idioma

Edema Cerebral y SX HIC

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Edema Cerebral y SX HIC

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Edema cerebral y

Síndrome de Hipertensión Endocraneal

Fisiología de Presión intracranial

Log ICP (mm Hg)

ICP (mm Hg)

Fisiología de Presión intracranial

ICP (mm Hg)

30 veins, and therefore the CPP is defined as arterial infl

CEREBRAL BLOOD FLOW IN RESPONSE TO

CBF (mL/100 g/min)

Efecto Cushing (hipertensión arterial, bradicardia, alteración respiratoria)

Monitoreo de la presión intracraneal

69 Physiology of the Cerebros

This chapter includes an accompanying lecture presentation that

• Manejo PIC >22mmHg NORMAL INTRACRANIAL PRESSURE 20

INTRACRANIAL PRESSURE WAVEFORMS WAVEFORM AT RAPID CHART SPEED

Monitoreo de la presión intracraneal

Monitoreo de la presión intracraneal

Barrera hemato-encefalica 473.e2 SECTION 3 Basic and Clinical Sciences

• Cerebro 2-3% masa total

• BHE: uniones estrechas de células endoteliales

• Moléculas cargadas space filled with small amounts of

Barrera hemato-encefalica 473.e2 SECTION 3 Basic and Clinical Sciences

CSF influx ISF efflux

• Sistema glial-linfático Glial limitans Glial

(Virchow-Robin) por pulsación

respiración y motilidad vasomotora.

A Synapse Convective bulk flow

Edema Vasogenico 473.e4 SECTION 3 Basic and Clinical Sciences

• Permeabilidad anormal de la BHE

del plasma of the tight junctions and opening

via abnormal vascular endothelial

síndrome de Reye e intoxicación por agua.

results in failure of Na /K adenosine + +

Figure 70.8. Axial CT and MR images in cytotoxic

results in failure of Na+/K+ adenosine Na+

• La eliminación de este edema es por el

sistema glifático edema. The ventricular ependyma

in animal models of hydrocephalus/increased ventricular fluid

• Gradiente osmotico por hipo-osmolaridad

• Reposición rápida de hipernatremia

glucosa osmotic cerebral edema. Osmotic

(hypo-osmolar), such as overly rapid Na+ Plasma Na+

• Toma excesiva de agua these conditions, free water flows along

Manejo Hipertensión intracraneal

Manejo Hipertensión intracraneal

• Tiopental • Niños 12%

• 1.5-3.5mg/kg/dosis • Fenitoina / Levetiracetam

Manejo Hipertensión intracraneal

Caracteristica Vasogenico Citotoxico Intersticial Osmotico

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