Terapia intensiva a starilor de coma

TIME IS BRAIN!
PPC= MAP-PIC
PPC presiunea de perfuzie cerebrala
MAP presiunea arteriala sistemica medie
PIC presiunea intracraniana
Obiectiv terapeutic principal in urgentele neurologice
Mentinerea PPC
Mentinerea presiunii arteriale sistemice
Reducerea presiunii intracraniene

Evaluarea bolnavului comatos

- examen clinic complet

- examen neurologic amanuntit
- GCS
- + scor de trunchi cerebral
- teste paraclinice
Examen neurologic
BLS
Examen rapid de orientare: senzorial, motor, semne de lateralitate, refl. oculare de trunchi
cerebral, Babinski
Postur de decorticare: sugereaz leziune sever de trunchi cerebral
Postur de decerebrare: sugereaz leziune TC sau diencefal
Micri involuntare asimetrice: leziuni structurale
Clonii persistente ale extremitior: status epilepticus
GLASGOW COMA SCALE
E : Eye Opening
V : Best Verbal Response
M : Best Motor Response
total scoring

Imagistica decisiva pentru diagnostic si tratament in patologia intracraniana acuta

- obligatorie in leziuni cu semne de focar
- suferinta neurologica acut instalata
Cu semnede focar CT urgent
Farasemnede focar
1. AVC ischemic-neurologie-protocol
Protocol encefalopatiimetabolice
stroke
Come diabetice
2. AVC hemoragic-protocol
Uremica, hepatica, hipercapnica, hipoxica,
hemoragiicerebrale
diselectrolitemii
3. Anevrism, malformatieruptaneurochirurgie
4. TCC
5. Tumora-rischerniere
Protocol stroke
1. Terapie acuta si optimizarea status-ului neurologic
- repermeabilizarea arterei cu restabilirea fluxului sanguin in zonelede ischemie
- tromboliza
- TIME IS BRAIN!!!
2. Diagnostic etiologic in vederea preventiei secundare
- etiologie: tromboza . embolie / stenoza
- teste: CT cerebral, Doppler transcranian, angioCT cerebral, angioRMN, angiografie
3. Preventia deteriorarii neurologice si a complicatiilor medicale

4. Recuperare si reabilitare functionala.

Mentinerea presiunii de perfuzie cerebrala
Mentinerea volemiei/ solutie salina / coloid
Sustinerea presiunii arteriale sistemice
Tratament hipotensor:
- atentie: - tromboliza
- ICC, IMA, disectie de aorta, encefalopatieHTA
- 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
Algoritminvestigatiietiologice
Ateromatoza
Cardioembolic
Vase mici-lacune
Disectii, trombozavenoasa, medicamentoasa
Evaluare cardiaca ECG, echo cordtranstoracic, transesofagian

 Identificare factoride 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)
1. ACSOS intracraniene
hipertensiunea intracraniana
convulsii
vasospasm
hiperemie
edem peritumoral
2. ACSOS extracraniene
de origine circulatorie: hipotensiunea arteriala, hipertensiunea arteriala, bradicardie / tahicardie,
anemie
de origine respiratorie: hipoxemie, hipercapnie
hipertermie
hiperglicemie
variatii de osmolaritate plasmatica
ACSOS de origine circulatorie
hipotensiunea arteriala: 11-33% la internare, 72% la marii politraumatizati
- 81% din bolnavii cu TCC + hta la internare prognostic nefavorabil; mortalitatea la TCC+ hta
intraoperator = 82%
! Elementul independent cel mai deteriorant pentru prognosticul TCC
!! Hipotensiunea arteriala severa la bolnavul cu TCC multiplica de doua ori rata mortalitatii!!
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%
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)
hipoxemia
- 1980-Miller si col: 30% TCC severe au hipoxemie lainternare

- 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!
ASCOS de origine glicemica
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
ASCOS de origine osmolara
obiectiv terapeutic osmolaritate plasmatica < 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 terapeutica 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
in functie 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
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
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
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

Tramuatic Brain Injury

Case report
Definition
46 yrsold male patient, victim of a car
- nondegenerative, noncongenital insult to the brain
crash, passenger,
from an external mechanical force, possibly leading to
First medical evaluation on field
permanent or temporary impairment of cognitive,
GCS-8
physical and psychosocial function, with..and associated
Motor GCS-4
with diminished or altered state of consciousness
Anisocoria,
- head injury may not be associated with neurological
Epistaxis, facial bones fractures with
deficit
withactive bleeding
- clasification-GCS
SaO2-90%, systolic AP-85mmHg,
Mild-14-15
HR-130/min
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
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 ptsexperience long term disability( Langlois, CDC< 2006)
- mortality rate after severe TBI decreased by late 20thcentury
- severity of primary brain lesions/hemorrhage from extracranialtrauma
- 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
TBI outcome upon postresuscitation
GCS

Mortality rate and time of death in the PTS with severe TBI and
politrauma
Acute( <
Early (48 h- 7
Late (> 7
48 h)
days)
days)
Brain
40%
64%
39%
damage
Blood loss
55%
9%
0
MOFS
1%
18%
61%

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 hrslasts for 14 days-1 year!
- significant contribution to final
neurologic deficit( Tweedie, 2007)
- time window of opportunity for
prevention

Figure 1. Schematic drawing of hyperacutestroke in the left middle cerebral artery

territory.

Pathophysiology of secondary cerebral damage after TBI

- cerebral blood flow: impaired autoregulation, brain edema, increased ICP
- oxygen: hypoxia / ischemia, impaired O2 regulation, impaired microcirculation
brain damage
- energy flow: glucose utilization, glucose availability, mitochondrial failure

secondary

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

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

Table 1
Secondary insults to the brain
Intracranial
Extracranial
intracranial
arterial hypotension
hypertension
hypoxemia/
convulsions
hypercapnia
vasospasm
arterial hypertension
hyperemia
bradycardia/
tachycardia

anemia
hypertermia
hyperglycemia
shifts in plasma osmolarity( natriumion
homeostasis)

Preliminary report on cardiac dysfunction after isolated traumatic brain injury

- 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 ++++
Coagulopathy associated with TBI
- incidence < 1% mild TBI, av60% in severe TBI
- highly associated with increased injury severity
- independent risk factor for increased mortality
- 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

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

Disseminated intravascular coagulation in TBI

patients?
Prothrombintime-PT
- ISTH DIC definition (International Society on
- IMPACT positive linear relationship between
Thrombosis and Haemostasis)
PT and poor prognosis
- 1/3 TBI patients with DIC at 6 hrs
- PT prolonged on admission in 26% patients
- higher DIC scores correlated with increased
- 64% increased mortality rate
progression of hemorrhagic injuries( PHI),
- 46% increased risk of unfavourableoutcome at 6
increased mortality, longer ICU and hospital
moGOS
stay( Sun, 2009, Taylor J et al, 2001)
- aPTT-less often affected
- not associated with dramatic decrease in PLT
nb-more localized process
TBI-AC & PHI (progressive hemorrhagic injury)
- reduced PLT-associated with 10x increased PHI risk
- abnormal INR-3 x( Allaryet, 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)

Guidelines for treatment of moderate to severe TBI

Transcranial Doppler and near infrared spectroscopy in the perioperative period

Neurosurgical emergencies in TBI

Extradural hematoma
- volume > 30 cm
- median line shift > 5 mm
- CT thickness > 15 mm
- secondary neurological worsening
- anisocoria
Intraparenchimatous contusions /
hematoma
- CT volume > 50 cm
- volume > 20 with median line shift
and/or
- basal cisternae compression with GCS
6-8

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
Posterior fossa lesions
- mass effect-brain stem compression
- fourth ventricle obstruction
- noncomunicans hydrocephalia

Decompressive craniectomy
- 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

Protecting the brain during neurosurgical procedures: strategies that can work

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
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 neurotraumateam and logistis
Highly specialized neurointensivecare unit
Neuroanesthesia& neurointensivecare as subspecialties
Guidelines for neurointensivecare
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!