PACIENTE NEUROCRITICO

GUSTAVO JEMIO ARNEZ ; Ph. D. neurocirujano

El cerebro la expresion evolutiva del universo para ser consciente

Gustavo Jemio

 Las afecciones que agreden de forma

grave el S.N.C. a menudo comprometen la vida y generan un elevado numero de secuelas permanente. El abordaje integral , permite minimizar el dao cerebral y por lo tanto preservar la vida y lo que es mas importante , su calidad .

 Avanzar en el conocimiento de los

eventos fisiopatologicos , de los procedimientos y tecnicas terapeuticas , nos permite un abordaje de excelencia del enfermo neurologico grave y mejorar los resultados.

Tipos de dao cerebral primario

Trauma

: concusion , contusion , Isquemia : global- paro/anoxia regional vasoespasmo, infarto , embolia Inflamatorio : meningitis Compresion : tumor, edema cerebral, Metabolicos : encefalopatia

Mecanismos de lesion secundaria

Hipoperfusion : global , HTEC, Hipoxia : hipoxemia sistemica Dao por perfusion: formacion de

radicales libres Liberacion de aminoacidos excitatorios Cambios electroliticos o del equilibrio acido base, Edema cerebral

EDEMA CEREBRAL

Klatzo I. 1967

Es un acumulo anormal de fluido en el parnquima cerebral asociado a un aumento volumtrico del mismo.

EDEMA CEREBRAL
ES UNA RESPUESTA INESPECIFICA A UNA GRAN VARIEDAD DE INSULTOS CEREBRALES.

Edema citotxico
Fundamentalmente intracelular, debido a

la produccin de txicos por hipoxia / isquemia. Se produce una alteracin tanto estructural como funcional de la membrana celular. La permeabilidad de la BHE esta intacta. Predomina en la sustancia gris. Lquido pobre en protenas.

Edema vasognico
Es fundamentalmente extracelular.

Se produce una disrupcin de la BHE.

El lquido es rico en protenas. Se puede influenciar por la presin

hidrosttica. Predomina en la sustancia blanca aunque afecta tambin a la sustancia gris.

Edema hidrosttico
Es extracelular, de composicin distinta

al vasognico. Se produce tras la evacuacin de hematomas intracraneales, por perdida de la autorregulacin vascular cerebral. La BHE esta intacta.

Edema osmtico
Se produce por disminucin de la

osmolaridad plasmtica (secrecin inadecuada de ADH). La BHE esta intacta.

Mecanismos de resolucin
Drenaje hacia el sistema ventricular, el

mas importante y efectivo. Fagocitosis del contenido proteinaceo por astrocitos y neuronas. Mecanismos poco conocidos de pinocitosis por parte de clulas endoteliales con paso al torrente circulatorio.

MECANISMOS LESIVOS DEL EDEMA CEREBRAL

La principal es la hipertensin intracraneal. Provoca desplazamientos, herniaciones del

encfalo o potenciar el efecto de masa. En E.Vasognico separacin progresiva de los capilares de las clulas a nutrir. Permite paso de sustancias: cascadas metablicas, y lesin a la membrana. El cido Araquidnico y metabolitos, prostaglandinas y leucotrienos, que tiene su papel en la gnesis del edema citotxico.

Edema cerebral postraumtico

Representa la lesin secundaria. Lesin que contribuye a la mortalidad y

morbilidad. Potencialmente evitable, con tratamiento precoz.

Presin intracraneal
El crneo es un compartimiento cerrado

en el que la suma de los siguientes volmenes ha de ser constante: -volumen cerebral - volumen sanguneo cerebral -volumen de LCR - volumen de otros

 Si la compliance disminuye cualquier volumen

adicional elevara la PIC. El FSC se vera comprometido y se producir isquemia regional o general. Los efectos deletreos de la HIC se deben al desarrollo de isquemia cerebral.

Complicaciones

Alteraciones en la microcirculacin -compresin, isquemia, estasis, rotura. Desplazamientos y herniaciones. Alteraciones en la perfusin cerebral. -disminucin de la presin de perfusin cerebral, isquemia cerebral.

HERNIAS CEREBRALES
A Supratentoriales 1. Hernia del cingulo o subfalcial 2. Hernia central o transtentorial 3. Hernia uncal o temporal B Infratentoriales 1. Hernia de las amigdalas cerebelosas 2. Hernia transtentorial hacia arriba

Emergencias Neuroquirurgicas

Trauma Craneo Encefalico

Lesion cerebro-vascular
Coma

COMA

Y los hombres debieran saber que del cerebro y de ninguna parte mas , tienen la dicha , el deleite ,la risa , y las bromas , as como las penas , aflicciones, abatimiento, y lamentaciones,. Y por el , en forma especial adquirimos sabidura y conocimiento y ver y escuchar y saber lo que es sucio y lo que es agradable, lo que es dulce y lo que no tiene sabor. Escritos hipocrticos

CONCIENCIA

El conocimiento que uno tiene de si

mismo y del medio que lo rodea

Fisiologa
El contenido de la conciencia

representa la suma de las funciones mentales afectivas y cognoscitivas . ( cortex cerebral). El despertar relacionado con la apariencia de estar completamente despierto (S.A.R.A)

COMA
Es un estado de falta de respuesta

psicologica sin fenomeno de despertar y en el cual el sujeto permanece con los ojos cerrados Las lesiones estructurales bilaterales del SARA o el cerebro medio , o los disturbios funcionales de las areas cerebrales pueden empeorar la conciencia y producir coma.

LESIONES ANATOMICAS
Afectacion difusa de la corteza cerebral ya sea

de causa estructural , toxica, o metabolica . (lesiones supratentoriales) Lesion combinada de la corteza-tronco cerebral agravamiento de las causas citadas o secundaria a lesiones hemisfericas (herniaciones cerebrales) Lesion primaria del tronco encefalico, secundaria a lesiones infratentoriales. (herniaciones)

Causes of structural or surgical coma

Trauma
Subdural injury Epidural injury Diffuse axonal injury Brain contusions Penetrating head injury

Intracranial hemorrhage
Subarachnoid hemorrhage Intracerebral hemorrhage Posterior fossa (pontine, cerebellar) Supratentorial (basal ganglia, lobar)

Ischemic stroke
Large middle cerebral artery infarction with brain herniation Brainstem stroke involving bilateral rostral pons or midbrain "Top of the basilar" syndrome with bilateral infarction

Causes of structural or surgical coma

Diffuse microvascular abnormality
Thrombotic thrombocytopenic purpura Rocky Mountain spotted fever Cerebral malaria

Tumor
Glioblastoma multiforme with herniation Multiple metastatic lesions

Other disorders Osmotic demyelination syndrome (central pontine myelinolysis)

Causes of metabolic or medical coma

Drug overdose
Benzodiazepines, barbiturates, opioids, tricyclic agents

Infectious disease
Sepsis Bacterial meningitis Encephalitis (eg, herpes simplex, arboviral infection)

Endocrine disorders
Hypoglycemic reaction Diabetic ketoacidosis Hyperosmolar coma Myxedema Hyperthyroidism

Causes of metabolic or medical coma

Metabolic abnormalities
Hyponatremia Hypernatremia Uremia Hepatic encephalopathy Hypertensive encephalopathy Hypomagnesemic pseudocoma

Toxic reactions
Carbon monoxide poisoning Alcohol poisoning Acetaminophen overdose Ethylene glycol poisoning

Causes of metabolic or medical coma

Medication side effects
Reye's syndrome Neuroleptic malignant syndrome Central anticholinergic syndrome Serotonin syndrome Isoniazid intoxication

Deficiency states
Thiamine deficiency (Wernicke's encephalopathy) Niacin deficiency (pellagra)

Hypothermia
Psychogenic coma

PRIMARY SURVEY
Airway maintenance with cervical spine control Breathing and Ventilation Circulation with haemorrhage control Disability: Neurological status Exposure/Environmental control: completely undress patient but prevent hypothermia

Physical examination - Vital signs Central Nervous System (CNS)

neck pupils corneal reflex fundi gag occulovestibular reflex motor withdrawal pain deep tendon reflexes planter responses document full GCS spontaneous and induced movement

Approaches to Diagnosis - Clues

purpuric rash battle sign meningococcemia base of skull fracture

bilateral large fixed pupils unilateral large sluggish pupils

mid position pupils no light response nuchal rigidity gynaecomastia/spider naevi bilateral pinpoint reactive pupils Horner's syndrome myoclonus hyperventilation Cheynes Stokes breathing Apneustic breathing

atropine poisoning III nerve lesion temporal cone

midbrain lesion meningitis hepatic encephalopathy narcotic overdose medullary lesion hypoxic encephalopathy brainstem (usually pulmonary) deep bilateral subcortical lesion pontine lesion

Table 3. Selected Key Findings from General Physical Examination for Altered Level of Consciousness System or region Vital signs Finding Hypertension Suggested cause(s) Cerebral hemorrhage, hypertensive encephalopathy, increased intracranial pressure, renal or endocrine disorder Ethanol or sedative drug toxicity, blood loss, diabetic coma Systemic infection, heat stroke, withdrawal from alcohol or drugs Ethanol or barbiturate toxicity, shock, extracellular fluid deficit Heart block, Stokes-Adams syndrome, increased intracranial pressure, hypothyroidism

Hypotension Hyperthermia Hypothermia Bradycardia

Tachycardia

Arrhythmia associated hypoxemia; atrial fibrillation associated with cerebral embolism

Alcohol ingestion, hepatic failure, ketoacidosis, or uremia Hepatic disorder Toxic disorder Infectious disease, drug reaction, autoimmune disease, pellagra, thrombotic thrombocytopenic purpura Hemorrhage (internal or external)

Breath Skin

Peculiar odor Jaundice Needle-tracks Rashes

Pallor

Table 3. Selected Key Findings from General Physical Examination for Altered Level of Consciousness Head Localized tenderness, hematoma, crepitus Skull fracture

Hemorrhage from ears or nostrils; hematoma, tenderness, or crepitus over mastoid process

Basilar skull fracture

Face and conjunctiva hyperemic

Tongue bitten or scarred

Alcohol intoxication

Epilepsy

Neck

Stiffness

Suggests meningitis/encephalitis, trauma, or subarachnoid hemorrhage (exam contraindicated if cervical spine fracture suspected)

Table 4. Key Eye Examination Findings in Patients with Altered Level of Consciousness Finding Position Eyes and head deviated to one side Hemispheric lesion on that side or pontine lesion on opposite side; typically associated with hemiparesis Comments/common causes

Visual fields

Blink response

If patient partially responsive, threatening movements can be used to test visual fields; asymmetry of blink response suggests hemianopia, blindness, or optic nerve damage

Funduscopy Papilledema Exudates, hemorrhages, vesselcrossing changes Increased intracranial pressure Hypertensive encephalopathy

Subhyaloid hemorrhage

Subarachnoid hemorrhage

Table 4. Key Eye Examination Findings in Patients with Altered Level of Consciousness Pupils Symmetrically reactive, round, 3-5 mm Usually excludes midbrain damage; if extraocular movements and cornea reflexes absent, suggests metabolic disorder or drug toxicity

One enlarged (>5 mm), unreactive or poorly reactive

Secondary to mass affecting CN III; sometimes due to intrinsic midbrain lesion on same side

Oval and slightly eccentric

Bilateral dilated and unreactive

Early midbrain/CN III compression

Severe midbrain damage (e.g., transtentorial herniation); rule out anticholinergic drugs May require magnifying glass to verify; characteristic of narcotic or barbiturate overdose; possible pontine hemorrhage Brainstem lesion Thalamic hemorrhage; usually associated with pinpoint nonreactive pupils

Bilateral pinpoint but reactive

Skew deviation (one up, one down) Forced downward deviation

Table 4. Key Eye Examination Findings in Patients with Altered Level of Consciousness Extraocular movements (elevate lids to examine) s-head reflex (passive head rotation) Full and conjugate eye movements rule out brainstem lesion; if suspected cervical spine injury, do oculovestibular reflex testing instead Bilateral pontine damage

Ocular bobbing (brisk downward and slow upward movements with loss of horizontal movements) Ocular dipping (slower arrhythmic downward and faster upward movements with normal reflex horizontal gaze) Oculovestibular reflex (instill 10-30 cc ice water into 1 external auditory canal; opposite ear in 3-5 min)

Diffuse anoxic damage to cerebral cortex

Bilateral deviation toward and nystagmus (fast phases) away from the stimulated side (normal response) excludes a structural brainstem lesion; abnormal slow phases in one or both directions suggest brainstem damage; abnormal fast phases in either direction with normal slow phases suggest bilateral cerebral hemisphere disorder

Table 5. Tests to Order for Patients with Unexplained Altered Level of Consciousness Test Laboratory Blood glucose Complete blood count Electrolytes (include Ca, PO4) Routine/emergent Routine/emergent Routine/emergent Hypoglycemia is a major cause of reversible (treatable) coma Indications Comments

BUN/creatinine Urinalysis Arterial blood gases Coagulation studies Blood and/or urine toxicologic screen Liver function tests Thyroid function tests Drug levels Carboxyhemoglobin

Routine/emergent Routine/emergent Suspected metabolic disorder or hypoxemia Suspected bleeding or hypercoagulation disorder Routine/emergent or specific indication Routine/emergent Suspected hypothyroidism Specific drug implicated Suspected carbon monoxide toxicity Coarse facies, dry hair, bradycardia Ethanol >300 mg/dL causes stupor Urosepsis causes ALC in elderly Helps differentiate among metabolic encephalopathies

Ammonia
Selected cultures

Suspected hepatic failure

Suspected infection Bacterial meningitis is a cause of ALC that requires immediate antibiotic treatment

Table 5. Tests to Order for Patients with Unexplained Altered Level of Consciousness Radiologic/imaging Chest film Cranial CT Cranial MRI Invasive Lumbar puncture If meningitis or subarachnoid hemorrhage suspected If increased intracranial pressure is suspected, start antibiotics and obtain CT before doing LP Routine/emergent If focal intracranial lesion suspected (almost routine) Usually the first test after initial stabilization More difficult to do than CT in ALC

Other Electrocardiogram Routine/emergent Arrhythmia or myocardial infarction may present as ALC without obvious cardiac symptoms Hypoxemia requires respiratory support

Pulse oximetry Electroencephalography

Routine/emergent Suspected nonconvulsive status epilepticus

Diagnostico
Historia clnica
Examen neurolgico

1. Conciencia 2. Respiracin 3. Tamao pupilar y reaccion 4. Movimientos oculares 5. Motora

Coma Glasgow coma scale recommended for age 4 yrs)

Points 6 5

Best eye opening -

Best verbal Oriented

Best motor Obeys Localizes pain

4
3 2

Spontaneous
To speech To pain

Confused
Inappropriate Incomprehensible

Withdraws to pain
Flexion (decordicate) Extensor (decerebrate)

None

None

None

Childrens coma scale (for age<4 yrs)

Points+ 6 5 Best eye Best verbal Smiles, oriented to sound, follows objects, interacts Crying Interaction Best motor Obeys Localizes pain

Spontaneous

Consolable

Inappropriate

Withdraws to pain Flexion (decorticate)

To speech

Inconsistently consolable

Moaning

To pain

Inconsolable

Restiess

Extensor (decerebrate ) None

None

None

None

Effect of lateral shift on level of consciouness

Amount of midline shift Level of consciousness

0-3 mm

alert

3-4 mm

drowsy

6-8.5 mm

Stuporous

8-13 mm

comatose

Central herniation
DIENCEPHALIC STAGE
Consciousness Altered alertness is first sign; usually lethargy, agitation in some. Later: stupor > coma. Sighs, yawns, occasional pauses. Later: Cheyne-Stokes. Small (1 - 3 mm), small range of contraction. Conjugate or slightly divergent roving eyes; it conjugate then brain stem intact. Usually positive DQLLS EYES and conjugate ipsilateral response to cold water calorics (CWC). Impaired upgaze due to compression of superior colliculi and diencephalic pretectum (Parinauds syndrome see page 87)

Respiration Pupils Oculomotor

Motor

Early: appropriate response to noxious stimuli, bilateral Babinski, gegenhalten (paratonic resistance). It previously hemiparetic contralateral to lesion: may worsen. Later: motionlessness & grasp reflexes, then DECQRTICATE (initially contralateral to lesion in most cases).

MIDBRAIN - UPPER PONS STAGE

Respiration

Cheyne-Stokes > sustained tachypnea.

Pupils

Moderately dilated midposition (3-5 mm), tixed*.

Oculomotor

Dolls eyes & CWC impaired, may be dysconjugate. MLFs lesion > intenuclear ophthalmoplegia (when dolls or CWC elicited and dysconjugate, medially moving eye moves less than laterally moving eye).

Motor

Decorticate > bilaterally DECEREBRATE (occasionally spontaneously).

LOWER PONS - UPPER MEDULLARY STAGE

Respiration

Regular, shallow and rapid (20-40/min)

Pupils

Midposition (3-5 mm), fixed

Oculomotor

Dolls eyes and CWC unelicitable

Motor

Flaccid. Bilateral Babinski. Occasionally LE flexion to plain

MEDULLARY STAGE (TERMINAL STAGE)

Respiration

Slow, irregular rate and depth, sighs/gasps. Occasionally hyperpnea altemating with apnea

Pupils

Dilate widely with hypoxia.

Uncal herniation
EARLY THIRD NERVE STAGE
(NOT A BRAIN STEM FINDING, DUE TO 3RD NERVE COMPRESSION)

Unilaterally dilating pupil (may be sluggish); 85% ipsilateral fo lesion Pupils

Oculomotor

Dolls = normal or dysconjugate. CWC = slow ipsilateral deviation, impaired nystagmus, may be dysconjugate if exlernal oculomotor ophthalmoplegia (EOO).

Respirations

Normal.

Motor

Appropriate response to nociceptive stimulus. Contralateral Babinski.

LATE THRID NERVE STAGE

Pupils

Pupil fully dilates.

Oculomotor Consciousness Respirations Motor

Once pupil biown, then external oculomotor ophthalmoplegia (EOO). Once EOO, stuporous > comatose. Sustained hyperventilation, rarely Cheyne-Stokes. Usually produces contralateral weakness. However, the contralateral cerebral peduncle may be compressed against the tentorial edge causing ipsilateral hemiplegia (Kemohans phenomenon, a false localizing sign). Then bilateral decerebration (decortication unusual).

MIDBRAIN - UPPER PONS STAGE

Pupils Contralateral pupil fixes in midposition or full dilation. Eventualty, both midposition (5.6 mm) and fixed. Impaired or absent.

Oculomotor

Respirations Motor

Sustained hyperpnea. Bilateral decerebrate rigidity

Signs of herniation syndrome or posterior fossa lesion

HERNIATION SYNDROMES (Also see Herniation syndromes, page 123) unilateral sensory or motor deficit progressive obtundation -> coma unilateral 3rd nerve palsy decorticate or decerebrate posturing (especially if unilateral) SIGNS OF P-FOSSA LESION also see Posterior fossa (infratentorial) tumors, page 391) initial symptoms of diplopia, vertigo, bilateral limb weakness, ataxia, occipital H/A rapid onset of deterioration/coma bilateral motor signs at onset miosis absent calones to horizontal movement, possibly with preserved vertical movements ocular bobbing ophthalmoplegia multiple cranial nerve abnormaiities with long tract signs apneustic, cluster or ataxic respirations

Cortico Subcortical stage (stage 1)

LEVEL OF LESION CONSCIOUSNESS MOTOR SYSTEM RESPIRATION, AUTONOMIC S. EYE MOVEMENTS PUPILLARY SIZE REFLEXES

CORTICAL OR

NORMAL OR

NORMAL OR

NORMAL

NORMAL OR ROVING

ORBIC. OCULI

SUBCORTICAL

SOMNOLENT

APPROPRIATE TO

EYE-MOVEMENTS

PUPILLARY

PAIN STIMULUS

PUPILS NORMAL

CORNEAL

MASSETER CILIO-SPINAL OCIJLOCEPHALIC vertical horizontal OCULOVESTIBULAR OCULOCARDIAL

+ +

+ + + +

PALMOMENTAL

-/+

Diencephalic stage
LEVEL OF LESION CONSCIOUSNESS MOTOR SYSTEM RESPIRATION, AUTONOMIC S. EYE MOVEMENTS PUPILLARY SIZE REFLEXES

DIENCEPHALIC upper/early

SOMNOLENT RESTLESS OR

APPROPRIATE TO NOXIOUS STIMULI

NORMAL OR

ROVING EYE MOVEMENTS

Lower/late

COMA

MUSCULAR TONE RAISED, begin-ning FLEXION RICIDITY

CHEYNESTOKES RESPIRATION

possible DOWNWARD GAZE SMALL PUPILS

ORBLC. OCULI PUPILLARY CORNEAL MASSETER CILIOSPINAL OCULOCEPHALIC vertical horizontal OCULOVESTIBULAR OCULOCARDIAL PALMOMENTAL CORNEOMANDIBULAR BABINSKI PHENOM.

(+) + + + (+) +/++ +/++ +

+/+

Diencephalo-mesencephalic stage
LEVEL OF LESION CONSCIOUSNESS MOTOR SYSTEM RESPIRATION, AUTONOMIC S. EYE MOVEMENTS PUPILLARY SIZE REFLEXES

DIENCEPHALIC MESENCEPHALIC upper early lower/late

SOPOR OR COMA COMA

MUSC .TONE, REFLEXES INCREASED FLEXOR RESPONSE (pref. arms) EXTENSOR RESP.= DECERBRATE RIGIDITY (pref. legs)

CHEYNE STOKES OR HYPERVENTILATION BP INCREASED TACHYCARDIA HYPERTHERMIA

ROVING EYE MOVEMENTS possible GAZE DEVIATION DOWNWARD FUPILS MIDDLE SIZE, INTERNUCLEAR GAZE PALSY

ORBIC. OCULI PUPILLARY CORNEAL MASSETER CILIOSFINAL OCULOCEPHALIC vertical horizontal OCULOVESTIBULAR OCULOCARDIAL PALMOMENTAL CORNEOMANDIBULAR BABINSKI PHENOM.

(+) + +/++ (+) (+) + + +

Mesencepahlic stage

LEVEL OF LESION

CONSCIOUSNESS

MOTOR SYSTEM

RESPIRATION, AUTONOMIC S.

EYE MOVEMENTS PUPILLARY SIZE

REFLEXES

MESENCEPHALIC

COMA

MUSC TONE, REFLEXES INCREASEO DECEREBRATE RIGIDITY

HYPERVENTILATION BP INCREASED TACHYCARDIA HYPERTHERMIA

NO EYE MOVEMENTS PUPILS of MIDDLE SIZE

ORBIC. OCULE PUPILLARY R. CORNEAL MASSETER CILIOSPINAL OCULOCEPHALIC vertical horizontal OCULOVESTIBULAR OCULOCARDIAL PALMOMENTAL CORNEOMANDIBULAR BABINSKI PHENOM.

(+) ++ (+) (+) + + +

Mesenphalo-pontine stage

LEVEL OF LESION

CONSCIOUSNESS

MOTOR SYSTEM

RESPIRATION, AUTONOMIC S.

EYE MOVEMENTS PUPILLARY SIZE

REFLEXES

MESENCEPHALO PONTINE

COMA

MUSC. TONE, REF LEXES INCREASED DECEREBRATE REGIDITY

HYPERVENTILATION OR APNEUSIS Bp INCREASED TACHYCARDIA HYPERTERMIA

NO EYE MOVEMENTS PUPILS SMALL PINPOINT

ORBIC. OCULI PUPILLARY CORNEAL MASSETER CILIOSPINAL OCULOCEPHALIC vertical horizontal OCULOVESTIBULAR OCULOCARDIAL. PALMOMENTAL. CORNEOMANDIBULAR BABINSKI PHENOM

-/+ ++ -/+ -/+ + -/+ +

Ponto-medullary stage

LEVEL OF LESION

CONSCIOUSNESS

MOTOR SYSTEM

RESPIRATION, AUTONOMIC S.

EYE MOVEMENTS PUPILLARY SIZE

REFLEXES

PONTO MEDULLARY

COMA

MUSC. TONE FLACCID NO REFLEXES NO MOTIONS possible FLEXOR RESPONSE

MACHINE TYPE OR PERIODIC OR ATAXIC RESPIRATION HYPOTERMIA BP UNIFORM HR UNIFORM

NO EYEMOVEEMENTS PUPIL WIDE

ORBIC. OCULT PUPILLARY CORNEAL. MASSETER CILIOPINAL OCULOCEPHALIC vertical horizontal OCULOVESTIBULAR OCULOCARDIAL PALMOEENTAL CORNEOMANDIBULAR BABISKI PHENOM.

-/+ -

Medullary stage (brain death) (stage 6)

LEVEL OF LESION

CONSCIOUSNESS

MOTOR SYSTEM

RESPIRATION, AUTONOMIC S.

EYE MOVEMENTS PUPILLARY SIZE

REFLEXES

PONTO MEDULLARY

COMA

MUSC. TONE FLACCID NO REFLEXES NO MOTIONS possible FLEXOR RESPONSE

MACHINE TYPE OR PERIODIC OR ATAXIC RESPIRATION HYPOTERMIA BP UNIFORM HR UNIFORM

NO EYEMOVEEMENTS PUPIL WIDE

ORBIC. OCULT PUPILLARY CORNEAL. MASSETER CILIOPINAL OCULOCEPHALIC vertical horizontal OCULOVESTIBULAR OCULOCARDIAL PALMOEENTAL CORNEOMANDIBULAR BABISKI PHENOM.

 Necesita REANIMACIN RESPIRATORIA/CIRCULATORIA Y/O

HEMOSTASIA?
Requiere inmovilizacin inicial y/o prevencin de dao medular

secundario por edema o liberacin de sustancias lticas?. Precisa atencin priorizada por otras especialidades? Tiene dolor, globo vesical o vmitos con peligro de broncoaspiracin?. Necesita operacin de emergencia (en menos de 1-2 horas)?. Necesita tratamiento clnico inmediato de neurointensivismo (uci)? Requiere operacin de urgencia (en menos de 24 horas)?. Requerir operacin electiva (despus de 24 horas)?. Necesitar atencin en sala de pacientes con traumas moderados (cuidados intermedios), o de lesionados no graves?