gangguan kesadaran

Al Rasyid, MDNeurology DepartmentFKUI/RSCM

Gangguan Kesadaran

ObjektifDefinisi dan komponen kesadaran, menentukan tingkat kesadaran secara kualitatif dan kuantitatifMengetahui tentang koma struktural dan metabolik Pendekatan diagnosis, differential diagnosis dan managemen komaMemeriksa refleks pupil dan herniasiMemeriksa dan menginterpretasikan tanda rangsang meningeal

Definisi

Kesadaran adalah keadaan sadar terhadap diri sendiri dan lingkungan. Koma adalah suatu keadaan tidak sadar total terhadap diri sendiri dan lingkungan meskipun distimulasi dengan kuat. Diantara keadaan sadar dan koma terdapat berbagai variasi keadaan/status gangguan kesadaran.Secara klinis derajat kesadaran dapat ditentukan dengan pemeriksaan bedside.

Derajat kesadaran secara kualitatifNormal waking state ( compos mentis): sensorik utuh sepenuhnya. Orientasi waktu, tempat dan orang baik dan dapat berkomunikasi penuh.Somnolen: pasien sadar bila di stimulasi normal akan tetapi akan kembali tertidur bila stimulus dihilangkan. Fungsi sensorik adekuat saat bangun

contSopor (Stupor): Pasien tertidur tetapi akan terbangun dengan stumulus lebih kuat. Dapat terbangun spontan tetapi respon sensorik berkabut. Dapat bergerak spontan dan dapat mengikuti beberapa perintah sederhana. Koma dangkal (semi-koma): Tidak ada respon terhadap stumulus verbal. Gerakan hanya bila dengan stimulus nyeri. Refleks korne dan pupil utuh. Bernafas adekuat.Koma dalam atau komplit: Tidak ada gerakan atau siklus bangun secara spontan. Refleks-refleks negatif. Nafas terganggu atau tidak ada usaha nafas

Anatomi Kesadaran Keadaan sadar ditentukan oleh 2 komponen yaitu formasio retikularis dan hemisfer serebral. Formasio retikularis terletak di rostral midpons, midbrain (mesencephalon) dan thalamus ke korteks serebri. Ini dinamakan ascending reticular activating system (ARAS).

Content (isi kesadaran) ditentukan oleh korteks serebri.

ARAS

The ARAS and Essential NeurotransmittersLocus Coeruleus: Epinephrine Raphe Nucleus: SerotoninBasal Nucleus: Acetylcholine

Etiologi gangguan kesadaran (koma).

1.Proses difus dan multifokal. Metabolik : hipo atau hiperglicemia, hepatic failure, renal failure, toxin induced (drugs,alcohol), infectious, concussion etc.2 Lesi Supratentorial: Haemorrhage: extradural(epidural),subdural, intracerebral. Infarction : embolic, thrombotic. Tumours : primary, secondary, abscess.3. Lesi Infratentorial. Haemorrhage : cerebellar, pontine. Infarction : brainstem. Tumours : cerebellum. Abscess : cerebellum.

Koma

Diagnosis KomaDefinisiSuatu keadaan tidak ada respon terhadap stumulus kuat.Gambaran klinisTidak ada gerakan spontanTidak ada respon terhadap stumulasi dalam berbagai tingkatan.Penyebab utama Stroke Anoksia Intoksikasi-obat-obatan. Trauma kepala Locked in syndrome Pseudokoma (psychological unresponsiveness)Tes Diagnostik Laboratorium : GD, LFT, RFT, elektrolit dll. Imaging CT atau MRI

Respiratory patterns yields information regarding the activity of different cerebral areas

Cheyne stokes respiration This respiration pattern is associated with periods hyperpnoe alternating with period apnoe, usually from 10-20 seconds.Bilateral cerebral hemisphere dysfunction (diencephalic level).Maybe seen in some patient during sleep, due to increased inhibitory influences may create this pattern, because sleep induced further cerebral depressing mechanism.

contBilateral forebrain impairment, due either to a diffuse metabolic process such as uremia, hepatic failure, or bilateral infarct or a forebrain mass lesion with diencephalic displacement, this breathing may emerge.

Mechanism : relates to an abnormal response of CO2-sensitive respiratory brain centre.

After the concentration of CO2 drop the below the level at which the centers a stimulated, the apneu phase appears an continous until the CO2 reaccumulates and the cycle repeats itself.

Central neurogenic hyperventilation Appears and its noted dysfunction midbrain or upper pons.Rapid respiration up to 40-50x/mntPO2 must be greater than 70-80 mmHg.If the PO2 level isnt above the level hipoxemiaCardiac, pulmonary, and metabolic problem must be ruled out as possible causes of the hiperventilation.

Apneustic respiration noted in lower pontine lesions,consist of prolong inspiratory phase with a pause at full inspiration. Cluster breathing also signifying lower pontine damage, is characterized for by disorderly sequence of closely grouped respirations followed by apnoe

Ataxic respirations signify a lower pontine or medullary respiratory center problem.The pattern is chaotic and haphazard with irregular pauses its lead to gasping and eventual cessation of breathing.

The other type of breath Obstructive sleep apnea disorder the cross section of the upper airway is anatomicaly narrow.The only clues is excessive drowsiness during the day and loud snoring at nightObese patients because deposition of fat in neck tissue reduces airway diameterMen the increased ratio of the length oh the airway to its diameter predisposed colapsMiddle age/older patients reduce muscle tone

Ondines curseFailure of automatic breathing ondines curse In adults its seen after lesions of the ventrolateral medullary chemosensory areas or bilateral damage to the descending pathways that control automatic respiration in the lateral colums of the spinal cord

In children most frequently congenital condition ( infant) associated with Hirschprungs disease, neuroblastoma, pheochromocytoma, mutation in the PHOX2B gene.

Coordinating Respiratory related BehaviorsLocated in Vento lateral medulla close proximity nucleus ambiguous.Yawning a motor pattern that involves deep inspiration associated with wide opening of the jaw and generalized muscle stretching.Yawning sometimes also seen in complex partial seizures ( medial temporal lobe)

Hiccups occur patients with abdominal or subphrenic pathology ( e.g. pancreatic cancer) impinges upon the vagus nerve.Dexamethasone induce hiccups but the mechanism is unknownOccasionally occur with lesion in the medullary tegmentum,

Vomiting is a reflex response involving coordinated somatomotor (posture, abdominal muscle contraction) and gastrointestinal( reversal of peristaltic), respiratory (retching, breath holding) components that are coordinated by neuron in the ventrolateral medullary tegmentum near the compact portion of the nucleus ambiguus.

Quantitative level of conc.Glasgow Coma Scale (GCS)Estimate : Eye response ( E ) Motor response ( M ) Verbal response ( V ) A GCS score 13 15 mild 9 12 moderate 3 - 9 severe

Eye responseEyes open spontaneously = 4Eye opening to verbal command = 3Eye opening to pain = 2No eye open = 1

Motor responseObeys command = 6Localizing pain = 5Withdrawal from pain = 4Flexien response to pain = 3Extension response to pain = 2No motor response = 1

Verbal responseOriented = 5Confuse = 4Inappropriate word = 3 Incomprehensible sound = 2No verbal response = 1

Approach to the diagnosis of the unconscious patientDetermine rapidly the cause of the impairment the structural or metabolic and what treatment The key component of the examine include the level of conc, the pattern of breathing, the size and the reactivity of the pupils, the eye movement and oculovestibular response

Differential Diagnosis of ComaDisorderDistinguishing clinical featureMaking the diagnosisStroke Acute onset Neurological deficitClinical diagnosis of coma and sign of severe brain damage in focal distribution approriate to the comaImaging : infarct or haemorrhageAnoxia Coma following episode of anoxia Myoclonus and/or seizure are often seen Multifocal sign with unequal region of anoxic History of cardiac arrest or other cause of anoxiaClinical feature of coma with or without myoclonusIntixication Coma with lost of brainstem reflexes without other focal sign History of substance ingestion Clinical feature are nonspecific. Suspicion is key Drug screen is critical

Differential Diagnosis of ComaDisorderDistinguishing clinical featureMaking the diagnosisHead injury Coma following head injury with or without focal sign Mental status fluctuate with cerebral edema and other factor Overts sign of injury are present Clinical feature History of head injury Imaging : normal, contusion, edema, haemorrhageMetabolic derangements Metabolic derangements are uncommon cause of coma, more often encephalopathy Coma with preserved brainstem function can be seen. Seizure can occur Lab results show abnormality : electrolytes, etc. Imaging and lab result do not show other cause consider another causes Locked in syndrome in brainstem infarction Patient imobile, on casual observation appear to be comatose Patient retain vertical eye movement and communication is possible with this condition Able to communicate with eye movement Brainstem infarction may see in MRI or CT

Differential Diagnosis of ComaDisorderDistinguishing clinical featureMaking the diagnosisPseudocoma Clinical appearance of coma with preservation of brain function Patient may be unaware of the pseudocoma or be intentionally unresponsiveness Evidence of exam of preserved response : Hold arm over head and let it fall-with pseudocoma the arms fall so that the face is not hit Normal EEG Persistence vegetative state State of unconsciousness with preserved reflexe responsiveness Differentiated from coma by the ability to make elementary responses to stimuli Patient may appear awake or a sleep, but exam show that they are unable to appreciate their environment, commands, and situation Clinical exam Finding of maintained brainstem response to stimuli Imaging and lab results show causes for the unresponsiveness

Unconcious PatientHow to manage and what to do

N NeckA AirwayB - BreathingC - CirculationD - Diabetes Drug

E EpilepsyF - FeverG GCSH HerniationI investigate

Resuscitation, use the neurological ABC

B. Pupil (size in mm) in ambient light, and in reaction to direct/consensual light.

1. Equal and reactive pupils Toxic/metabolic cause2. Unequal.Fixed and dilated pupil three oculomotor palsy. Herniation : if larger pupil associated with ipsilateral 3rd nerve extra ocular muscle palsy.Possible horner syndrome,consider carotid occlusion/dissection.3. Bilateral pupil abnormalities.Pinpoint- pontine lesionBilateral fixed and dilated(7-10 mm): sub total damage to medulla or immediate post anoxia or hypothermia.Midposition ( 4 6 mm ) and fixed: more extensive md brain lesion.

Pupillary Responses in Various Lesions

Signs of increased ICP/HerniationPupilsUnilateral dilated pupil Bilateral small poorly reactive pupils

Eye movementsThird nerve palsySixth nerve palsyCan be assessed by cold caloric

FundoscopySigns of papilledema?

Respiratory pattern?

Herniation syndromes.

The most common causes of herniations of the brain are :The mass effect increases the intracranial pressure and causes internal shifts or herniations of the brain that compress the normal tissue, in particular the diencephalons and brainstem.This compression impairs consciousness and the life-sustaining functions of breathing, blood pressure control, and temperatur regulation. Herniations also compress cerebral arteries resulting in infarctions.

Etiology :Cerebral contusions, hematomas, abscesses, neoplasms, cerebral edema.

Trans facial herniation.The part of the hemisphere that shifts under the falx is called the cingulate gyrus.It may compress the artery against the free edge of the falx, causing infarction of medial hemispheric wall dorsal to the corpus callosum. This infarction would cause UMN paralysis of the leg.

Uncal herniation (trans tentorial herniation )Occurs in rapidly expanding traumatic hematomasFrequently in the lateral middle fossa or temporal lobe pushing medial uncus and hippocampal gyrus(uncal herniation) over edge of tentorium (tentorial herniation), entrapping third nerve and directly compressing midbrain.Impaired conscousness is not a reliable early sign. Earliest consistent sign : unilateraly dilating pupil

Trans foraminal herniation.Herniation of the intracranial contents caudally, the cerebellum and medulla into the foramen magnum.May result from expanding supratentorial lesions or from expanding infatentorial lesions, such as cerebellar hemorrhage or neoplasm. Infratentorial masses also may cause upward transtentorial herniation, causing midbrain compression and midbrain sign.

Clinical syndrome of transforaminal herniation :Quadriplegia.Apnea compression of reticulospinal tracts that stop automatic breathing.

Meningeal signNeck stiffness

Not to be performed if the could be cervical instability e.g following traumaWhat to do :The patient should be lying downPlace your hands behind the patient headGently rotate the head moving the head as the patient was indicating no. Fell the stiffness.

Gently lift the head off the bed, feel the tone in the neckWatch the legs for hip and knee flexion

What you find and what it meansNeck moves easily in both planes, with the chin easily reaching the chest, or neck flexion : normal

Neck rigid on movement - neck stiffnessIndicates meningeal irritation common causes bacterial, viral, subarachnoid hemorrhage, rare causes meningeal carcinomatosis

Brudzinski neck sign (1)What to do Moving until the chin easily reaching the chestWhat you find (+) when response both flexed on lower extremities

Kernig signWhat to do The patient is lying flat on the bed -flex the leg at the hip with the knee flexed -then try to extend the knee -repeat on the other side. What you find -knee straigten without difficulty normal -resistance to knee straightening indicates meningeal irritation, if unilateral , may occur root irritation on HNP

Brudzinski contralateral leg sign(2) What to doThe patient lying flat on the bed, flex the leg at the hip,with the knee flexed What you findFlex the knee at contralateral

Lasegue sign

What to doLifting the right sign lower extremity

What you find More than 70 positive lasegue sign

MENINGEAL SIGN

1. NECK STIFFNESS 2. BRUDZINSKI I 3. KERNIG SIGN ( N > 1350 )

MENINGEAL SIGN4. BRUDZINSKI II 5. LASEQUE SIGN (N > 60 - 700)

Sagital section through the cervical spinal cord and vertebrae

A. Head flexion B. Head extension Spinal cord and nerve roots are stretched and lengthened in A and relaxed and pleated in B

Sagital section of the head to show the effect of a head extension and flexion in streching and relaxing the spinal cord

POSITIVE Meningeal signResistance to neck flexion causes of the nuchal rigidity most commonly

Inflammation (Meningitis ) Subarachnoid hemorrhage

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