come 1 2015

Terapia intensiva a starilor de coma

Elena Copaciu

Clinica ATI Spitalul Universitar de Urgenta Bucuresti

Diplome Universitaire en Neuroreanimation

Univ Paris Sud Ouest, 2011

* LB. GREAC- STARE DE SOMN- KOMA* Hippocrate- descrie nivelul cel mai redus al

activitii cerebrale* n limba englez-

"the state of sleep is a sleep-like state

Ce este coma?

TIME IS BRAIN!

PPC= MAP- PIC

PPC- presiunea de perfuzie cerebrala

MAP- presiunea arteriala sistemica medie

PIC- presiunea intracraniana

Obiectiv terapeutic principal in urgetne

neurologice

Mentinerea PPC

Mentinerea presiunii arteriale sistemice

Reducerea presiunii intracraniene

Figure 1

FIGURE 1. The immediate and delayed

pathways that are activated after an

ischaemic insult to the brain. The pathways

lead to cell death by necrosis or apoptosis.

Copyright 2013 Current Opinion in Anesthesiology. Published by Lippincott Williams & Wilkins. 10

Protecting the brain during neurosurgical procedures:

strategies that can work

El Beheiry, Hossam

Current Opinion in Anesthesiology. 25(5):548-555, October

2012.

doi: 10.1097/ACO.0b013e3283579622

Barone & Feuerstein 1999

EVALUAREA BOLNAVULUI COMATOS

EXAMEN CLINIC COMPLET

EXAMEN NEUROLOGIC AMNUNIT

GCS

+ scor de trunchi cerebral

teste paraclinice

EX.NEUROLOGIC BLS EX. rapid de orientare: senzorial, motor, semne de lateralitate, refl. oculare de trunchiCerebral, BabinskiPostur de decorticare- sugereaz leziune sever de trunchi cerebralPostur de decerebrare- sugereaz leziune TC sau diencefalMicri involuntare asimetrice- leziuni structuraleClonii persistente ale extremitior- status epilepticus

GLASGOW COMA SCALEE : Eye OpeningV : Best Verbal ResponseM : Best Motor Response

total scoring

IMAGISTICA- DECISIVA

PENTRU DIAGNOSTIC SI

TRATAMENT IN PATOLOGIA

INTRACRANIANA ACUTAObligatorie in leziuni cu semne de focar

Suferinta neurologica acut instalata

Cu semne de focar

CT urgent

1. AVC ischemic- neurologie-protocol stroke

2. AVC hemoragic- protocol hemoragii cerebrale

3. Anevrism, malformatierupta- neurochirurgie

4. TCC

5. Tumora- risc herniere

Fara semne de focar

Protocol encefalopatiimetabolice

Come diabetice

Uremica, hepatica, hipercapnica, hipoxica,

diselectrolitemii

PROTOCOL STROKE

1. Terapie acuta si optimizarea status/ului neurologic

2. Diagnostic etiologic in vederea preventiei secundare

3. Preventia deteriorarii neurologice si a complicatiilormedicale

4. Recuperare si reabilitare functionala.

1. Terapia acuta si optimizarea status-

ului neurologic

- Repermeabilizarea arterei cu restabilirea fluxului sanguin in zonele de ischemie

- Tromboliza

- TIME IS BRAIN!!!

LEZIUNE OCLUZIV DE A. CAROTID DR. I CEREBRAL MEDIE DR.

TROMBOLIZ INEFICIENT

TROMBOLIZ INTRAARTERIAL- rtPA

TROMBOLIZ INTRAARTERIAL- PROUROKINAZA

Teste diagnostice/ stabilirea etiologiei Tromboza

Embolie

Stenoza

CT cerebral

Doppler transcranian

angioCT cerebral

Angio RMN

angiografie

Mentinerea presiunii de perfuzie cerebrala Mentinerea volemiei/ solutie salina/ coloid

Sustinerea presiunii arteriale sistemice

Tratament hipotensor:

Atentie:

Tromboliza

ICC, IMA, disectie de aorta, encefalopatie HTA

Modalitati de tratament

Tratament antiagregant/ anticoagulant la bolnavul cu stroke

Aspirina

Incarcare cu clopidogrel

Dipiridamol

Anticoagulare- la recomandarea specialistului neurolog/ cardiolog eficacitate discutabila

Obligatoriu control imagistic inainte de initierea terapiei

Algoritm investigatii etiologice Ateromatoza

Cardioembolic

Vase mici- lacune

Disectii, tromboza venoasa, medicamentoasa

Evaluare cardiaca> Ecg, echocord transtoracic, transesofagian

Identificare factori de risc: fumat, TA, diabet, screening trombofilii

URGENTA IN TERAPIE INTENSIVA

SINDROAMELE DE HERNIERE CEREBRALA

UNCALA- LA NIV STINCII TEMPORALULUI

CENTRALA TRANSTENTORIALA

TERAPIA SD DE HIPERTENSIUNE INTRACRANIANA

EDEM CEREBRAL- HIPERTENSIUNE

INTRACRANIAN

Extremitatea cefalic la 30

Analgezie/ control agitaie motorie

Controlul alterrilor de homeostazie extracranian

PPC= PAM- PIC

Redus PIC Osmoterapie: Manitol, sol. saline hipertone

Bolus barbituric- monitorizare hemodinamic invaziv, EEG

THAM

Drenaj ventricular

Meninere PPC- cretere PAM: ncrcare volemic + vasopresor

( STI, monitorizare invaziv, inclusiv PIC)

CRANIECTOMIA DECOMPRESIV

Permite expansiunea esutului edemaiat, scade PIC, crete PPC

n infarctele de emisfer pot reduce rata mortalitii : 80 30%, fr a crete % supravieuitori cu sechele invalidante

Decompresiune precoce( < 24 de ore)- poate crete mai mult % supravieuitori

Studii n derulare

ACSOS ( AGRESIUNI CEREBRALE SECUNDARE DE ORIGINE SISTEMICA)

ACSOS INTRACRANIENE

hipertensiunea intracraniana

convulsii

vasospasm

hiperemie

edem peritumoral

ACSOS EXTRACRANIENE

hipotensiunea arteriala hipoxemie, hipercapnie hipertensiunea arteriala bradicardie/ tahicardie anemie hipertermie hiperglicemie variatii de osmolaritate plasmatica

ACSOS DE ORIGINE CIRCULATORIE

HIPOTENSIUNEA ARTERIALA

Incidenta: 11- 33% la internare

72% la marii politraumatizati

81% din bolnavii cu TCC + hta la internare - prognostic nefavorabil 82%- mortalitatea la TCC+ hta intraoperator

! Elementul independent cel mai deteriorant pentru prognosticul TCC

!! Hipotensiunea arteriala severa la bolnavul cu TCC multiplica de doua ori rata mortalitatii!!

ACSOS DE ORIGINE RESPIRATORIE

HIPERCAPNIA

Miller si col- 4% din bolnavii cu Tcc severe prezinta hipercapnie la internare

Exista o relatie lineara intre GCS- paCO2

HIPOCAPNIA

1992- Sheiberg si col- 1/3 din episoadele de desaturare a singelui din vena jugulara ( SjO2< 50%)- atribuite unei hipocapnii profunde ( PaCO2< 20

mmHg)-

ACSOS DE ORIGINE RESPIRATORIE

HIPOXEMIA

1980- Miller si col- > 30% TCC severe au hipoxemie la internare

1990- TCDB- cca 15% Tcc severe au hipoxemie la internare! In principal prin neprotejarea cailor aeriene pe durata transportului de la locul accidentului

! Cca 39% TCC - cel putin un episod de hipoxemie prelungita in STI ( > 15 minute)!

! Nivelul mortalitatii la bolnavul cu TCC este dublat de un episod de hipoxemie izolata!

ACSOS DE ORIGINE CIRCULATORIE

HIPERTENSIUNEA ARTERIALA

20%- pe durata transportului intraspitalicesc

peste 90% din episoade apar in sectiile de Terapie Intensiva

ANEMIA

scaderea de Ht este compensata prin reducerea viscozitatii sanguine, cu vasodilatatie cerebrala si cresterea DSC- in TCC grave - creste PIC

Ht> 30%

ALTE ACSOS

GLICEMIA

HIPOGLICEMIA

( episoadele prelungite> 10-20 minute - crestere

de DSC, necroza celulara, convulsii)

HIPERGLICEMIA

(> 180 mg/dl agraveaza ischemia cerebrala si

prognosticul vital ; creste talia infarctului

cerebral)

OSMOLARITATE PL

Obiectiv terapeutic Osm pl< 315- 320 mOsm/ kg

Hiponatremie ( Na seric< 120 mEq/l)-SIADH, cerebral salt wasting

Diabet insipid

STRATEGIA TERAPEUTICA LA BOLNAVUL CU SUFERINTA NEUROLOGICA ACUTA

MONITORIZARE MULTIMODALA A FUNCTIEI CEREBRALE!

PREVENIREA ACSOS

TRATAMENTUL HIPERTENSIUNII INTRACRANIENE

PROTECTIE CEREBRALA

PREVENIREA ACSOS

STABILIZAREA FUNCTIILOR VITALE LA LOCUL ACCIDENTULUI

BOLNAVUL CU SUFERINTA NEUROLOGICA NECESITA STABILITATE HEMODINAMICA+ NORMOVOLEMIE

Selectarea atenta a terapiilor hipotensoare

MENTINEREA SCHIMBURILOR GAZOASE ALVEOLARE

HIPOCAPNIE TERAPEUITCA NUMAI PENTRU EPISOADE DE AGRAVARE ACUTA CU RISC DE ANGAJARE ( si unele cazuri de hiperemie documentata de SjO2)

normoglicemie/ controlul osmolaritatii plasmatice/ corectarea diselectrolitemiilor

normo/ HIPOTERMIE( STI- la nivelul extremitatii cefalice)

Prognosticul stroke ischemic

Fc de severitate, dimensiuni, mecanism, virsta, status functional premorbid, tromboliza

Mortalitate 30% in primul an, 40- 50% in primii 5 ani

AIT- 15% mortalitate la 1 an, 50% la 5 ani!

Grad de dizabilitate

10% TBI patients, More common in devastating TBI leading to brain death ( Bhardwaj, Mirski, 2011)

Elevated cardiac enzymes

LVWM abnormalities on echocardiography exam

Main mechanism: cathecolamine release, inflammatory cascade

139 patients, studied for 2 wks after head trauma

Neurogenic pulmonary edema in TBI patients( Bhardwaj, Mirski, 2011)

Up to 40% all head injury subtypes, combat victims with isolated TBI higher incidence

Mechanism- extravasation of proteinaceous fluid due to secondary lesion to the alveolar membrane from the catecholamine storm associated with the severe neurologic injury.

Different from pulmonary edema and ALI

PWP- ussually not elevated, LVEF- normal

Rapid onset- at the time of neurological injury

Often involves one lung field

Limited duration

Response to PEEP ++++

TBI- AC

Incidence < 1% mild TBI, av 60% in severe TBI( Gomez et al, 1996)

Highly associated with increased injury severity

Independent risk factor for increased mortality( Wafaisade A et al, 2010)

Harhangi 2008- metaanalysis of 34 studies Overall incidence- 32.7%

Increased the odds of mortality ratio x 9

Increased the likelihood of poor outcome by a factor of 36

Prothrombin time- PT

IMPACT positive linear relationship between PT and poor prognosis( Van Beek, J Neurotrauma, 2007)

PT prolonged on admission in 26% patients

64% increased mortality rate

46% increased risk of unfavourable outcome at 6 mo GOS

aPTT- less often affected

Kumar 2013

Platelets

Decreased in< 10% TBI patients on admission

Nadir at 48- 72 hrs

Normalised in 1 week( Kumar, 2013)

35% risk of death at 6 mo( Van Beek, 2007)

Higher platelet transfusion thresholds in neurotrauma patients

Kumar 2013

DIC in TBI patients?

ISTH DIC definition

1/3 TBI patients with DIC at 6 hrs

Higher DIC scores correlated with increased progression of hemorrhagic injuries( PHI), increased mortality, longer ICU and hospital stay( Sun, 2009,

Taylor J et al, 2001)

Not associated with dramatic decrease in PLT nb- more localized process

Kumar 2013

TBI- AC & PHI

Reduced PLT- associated with 10x increased PHI risk

Abnormal INR- 3 x( Allary et, J Neurotrauma, 2009)

Duration PT increased at 6 hrs, normalized at 12- 18 hrs( Halpern et al, J Neurotrauma, 2008)

Pathopsysiology: Massive release of tissue factor from the damaged brain parenchima

Microparticles

Platelet hyperactivity

Activated protein C- maladaptive response to trauma induced shock.( Kumar, 2013)

Kumar 2013

Is there a brain induced MODS?

BRAIN

LUNG

COAGULATION

GUT

HEART

AVC HEMORAGIC

Unitate de urgente neurovasculare

CT/ RMN/ angiograf/ neurochirugie/ neurologie

Hemoragie intracerebrala

Hemoragie subarahnoidiana

Protocoale distincte

HEMORAGIILE CEREBRALE

SPONTANE 10- 15% AVC 38% supravieuiesc la un an

Incidena: 10-20/ 100000 locuitori, 50/ 100000 rasa neagr, 55/ 100000 loc.- Japonia

Cauze: 78-88% - hemoragii cerebrale rupturi spontane vase mici:

angiopatie amiloid sau HTA cronic

Malformaii vasculare arteriovenoase, anevrisme

Tumori cerebrale, coagulopatii, alcoolism, cocainomanie

AVC ischemic transformat hemoragic

Hematom cu angiopatie amiloid

Malformaie arteriovenoas

profund, comprim

corpul calos

HEMORAGIILE

CEREBRALE SPONTANE

HEMORAGIILE CEREBRALE

SPONTANE

Expansiunea hematomului primar continu Brott i col: la 1 or- la 16% bolnavi, la 36% continu expandarea la 20 de ore

- Kazui i col. la 20% din bolnavi hemoragia continu 3-36 ore de la debut

leziuni neurologice deteriorare climic secundar edem perihematom: 5- 14 zile dup > 6 ore: edem vasogen i citotoxic, cu alterarea barierei hematoencefalice

moartea neuronal n parenchim perihematom: tip necroz, exist i component apoptotic

Hematom cerebral cu expansiune rapid

Hemoragii cerebrale-

tratament chirurgical

Hemoragie ventricular- risc major de mortalitate! Drenaj ventricular- risc colmatare, infecii

Tromboliz intraventricular

TERAPIE CHIRURGICAL CRANIECTOMIE DESCHIS- rata mare a mortalitii, dependen>, resngerare

Hematoame cerebeloase- intervenie rapid

Aspiraie stereotactic, lichefiere hematom prin instilare de trombolitice

PERIOPERATIVE CARE OF

THE TRAUMATIC BRAIN

INJURY PATIENT

ELENA COPACIU

ANESTHESIA & ICU DEPARTMENT

UNIVERSITY HOSPITAL BUCHAREST, ROMANIA

DIPLOME UNIVERSITAIRE EN NEUROREANIMATION, FRANCE

Case report

46 yrs old male patient, victim of a car crash, passenger,

First medical evaluation on field

GCS- 8

Motor GCS- 4

Anisocoria,

Epistaxis, facial bones fractures with with active bleeding

SaO2- 90%, systolic AP- 85 mmHg, HR- 130/min

TBI - DEFINITION

Nondegenerative, noncongenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical and psychosocial function, with..and associated with diminished or altered state of consciousness

Head injury may not be associated with neurological deficit

Clasification- GCS Mild- 14- 15

Moderate- 9- 13

Severe < 9

EPIDEMIOLOGY

the burden of TBI( traumatic brain injury)

Leading cause of death for pts 1-45 yrs old in USA

Europe: 235 TBI/ 100000 inhabitants- 15 deaths/ 100000 people.

Cause of severe long term disability in survivors

Main causes: motor vehicle accidents/falls/violence

Sex ratio: male/female: 2- 2.8/1, for severe TBI: male/ female ratio: 3.5/1

( Langlois 1997, Kraus 1996, Feigin, 2012).

Severe TBI- outcome

Av. 52000 deaths annualy in USA 6/100000 patients deaths during hospitalization

17/100000 deaths outside hospital

40% of all deaths of acute causes!

80- 90000 pts experience long term disability( Langlois, CDC< 2006)

Mortality rate after severe TBI decreased by late 20th century Severity of primary brain lesions/hemorrhage from extracranial trauma

First year survivors die are more likely to die of seizures, septic shock, pneumonia, digestive complications than people of the same age, sex and race( Harrison- Felix C., 2006).

Costs: 4 billion USD/year

CEREBRAL

CONTUSION

TBI OUTCOME UPON POSTRESUSCITATION

GCS

MORTALITY RATE AND TIME OF DEATH IN

THE PTS WITH SEVERE TBI AND POLITRAUMA

Acute( < 48 h) Early ( 48 h- 7

days)

late ( > 7 days)

Brain damage 40% 64% 39%

Blood loss 55% 9% 0

MOFS 1% 18% 61%

0

2

4

6

8

10

12

14

1 2 3 4 5 6 7 8 9 10 11 12

Day upon

admission

when death

occuredPersonal data

Cerebral Blood Flow

Cell death

10mls/100gms/min

Cell membranes become dysfunctional

15-20mls/100gms/min

EEG flat

15-20mls/100gms/min

Evoked Potentials change

20mls/100gms/min

Loss of function (awake patient)

25mls/100gms/min

Ischaemia

54mls/100gms/m (average grey > white)

Normothermic persons with a normal brain

CB

F

Pathophysiology of TBI

temporal events

Primary brain lesions- mechanical forces- lesions of neurons, glial cells, vessels, axons

Necrotic cellular death

Long term outcome

Secondary brain lesions: cerebral edema/ cerebral ischemia/delayed cellular death Penumbra- tissue at risk!

Cellular apoptosis- starting at 2 hrs- lasts for 14 days- 1 year!

Significant contribution to final neurologic deficit( Tweedie, 2007)

Time window of opportunity for prevention

Figure 1. Schematic drawing of hyperacute stroke in the left middle cerebral artery territory.

Bandera E et al. Stroke 2006;37:1334-1339

Copyright American Heart Association

Table 1

Table 1 Prehospital clinical practice guidelines to be used by first medical responders for victims suspected of having suffered a traumatic brain injury


Traumatic brain injury in modern war

Ling, Geoffrey SF; Ecklund, James M

Current Opinion in Anesthesiology. 24(2):124-130, April 2011.

doi: 10.1097/ACO.0b013e32834458da

Secondary insults to the brain

INTRACRANIAL

Intracranial hypertension

convulsions

vasospasm

Hyperemia

EXTRACRANIAL

Arterial hypotension

Hypoxemia/ hypercapnia

Arterial hypertension

bradycardia/ tachycardia

anemia

hypertermia

hyperglycemia

Shifts in plasma osmolarity ( natriumion homeostasis)

Table 2

Table 2 Guidelines for treatment of moderate to severe TBI


Traumatic brain injury in modern war

Ling, Geoffrey SF; Ecklund, James M

Current Opinion in Anesthesiology. 24(2):124-

130, April 2011.

doi: 10.1097/ACO.0b013e32834458da

Changes in the management of severe traumatic brain

injury: 1991-1997Marion, CCM, Jan. 2000

Ghajar,

1991(%)

1997

ICP monitoring 40 83

Ventriculostomy 72 50

Prophylactic

hyperventilation

83 36

Corticoides 64 19

- anonymous enquiry in 3256 US neurosurgeons , before (Ghajar 1991),

and after the release of Brain Trauma Foundation guidelines for severe

TBI management

-1262 responders (40 %)

Box 1


Transcranial doppler and near infrared spectroscopy

in the perioperative period

Kampf, Stephanie; Schramm, Patrick; Klein, Klaus Ulrich

Current Opinion in Anesthesiology. 26(5):543-548,

October 2013.

doi: 10.1097/01.aco.0000432517.70844.a6

Timining of surgery

Neurosurgical emergencies in TBI( Bullock, Chesnut, 2006)

Extradural hematoma

Volume > 30 cm

Median line shift > 5 mm

CT thickness > 15 mm

Secondary neurological worsening

Anisocoria

Subdural hematoma Thickness > 10 mm

Median line shift> 5 mm, no matter GCS

Any severe TBI worsening 2 GCS points during transport

Pupillary anomalies- bilateral midriasis, anisocoria

Neurosurgical emergencies in TBI( Bullock, Chesnut, 2006)

Intraparenchimatous

contusions/hematoma

CT volume > 50 cm

Volume > 20 with median line shift and/or

Basal cisternae compression with GCS 6- 8

Posterior fossa lesions

Mass effect- brain stem compression

Fourth ventricle obstruction

Noncomunicans hydrocephalia

DECOMPRESSIVE CRANIECTOMY

Hippocrates

Modern era- H. Cushing, 1905

To prevent brain damage in diffuse TBI or after evacuation of a hematoma

Technique- controversial

DECRA trial- final results showing no benefit, but many decisions debatable

Can be life saving in severe TBI/ best moment? Outcome? No standardization

Decompressive craniectomy

Table 3

Table 3 Current status of perioperative

neuroprotection during neurosurgery


Protecting the brain during neurosurgical procedures: strategies that can work

El Beheiry, Hossam

Current Opinion in Anesthesiology. 25(5):548-555, October 2012.

doi: 10.1097/ACO.0b013e3283579622

Key elements in TBI perioperative management

EARLY RESUSCITATION

HEMODYNAMIC OPTIMISATION/ AVOID HYPOTENSION

MAINTAIN ARTERIAL BLOOD GASES HOMEOSTASIS

EMERGENT SURGICAL EVACUATION OF MASS LESIONS

ICP CONTROL

CPP SUPPORT

OPTIMISATION OF EXTRACRANIAL HOMEOSTASIS

KEY ELEMENTS IN TBI

PERIOPERATIVE MANAGEMENT CONTINUE AND REFINE ONGOING RESUSCITATION

CORRECT PREEXISTING SECONDARY INSULTS

SURGERY AND ANESTHESIA MAY PREDISPOSE TO NEW ONSET LESIONS

RAPID EVALUATION

CONTINUE CEREBRAL & SYSTEMIC RESUSCITATION

EARLY SURGICAL INTERVENTION

INTENSIVE MONITORING

ANESTHETIC PLANNING

Major stepforwards

Highly specialized trauma centers with neurotrauma team and logistis

Highly specialized neurointensive care unit

Neuroanesthesia & neurointensive care as subspecialties

Guidelines for neurointensive care

International networks - IMPACT

Take home messages

Dont forget: Time is brain

Beside sophisticated technology- simple but rapid clinical exam and BTF management guidelines to be applied

Simple therapeutic gestures: maintaining normal homeostasis

AVOID HYPOXEMIA AND HYPOTENSION- deadly combination at any moment!!

MULTIMODAL MONITORING OF THE 3RD MILLENIUM COMES AFTER!

Thank you for your atention!

come 1 2015

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