Dr.Yuwono, Sp.S, FINSFK. UNTAR

Royal Taruma

Altered Mental StatusCentral nervous system dysfunction can be due to a primary neurological condition or secondary to a medical condition

Coma =an eyes-closed, unresponsive state,no verbal response, & a failure to localize noxious stimuli

Delirium= abnormally excessive motor and verbal activity, including agitation &hallucinations

bilateral cerebral hemisphere dysfunction, unilateral hemisphere dysfunction with impaired brainstem function (usually due to compression), or primary brainstem dysfunction Coma & Delirium

EvaluationAbnormal vital signs are noted

HR : atrial fibrillation ,ventricular tachycardias, Cushing’s syndrome of bradycardia, hypertension(brainstem autonomic dysfunction due to increased ICP)

BP : Hypertension (diastolic > 120 mm Hg) can cause coma in hypertensive encephalopathy, commonly seen in ICH&ischemic stroke

T : Fever (sepsis, meningitis, heat stroke, neuroleptic malignant syndrome, & intoxications), Hypothermia (sepsis, intoxications, and hypoglycemia)

R : Cheyne-Stokes respiration (bi-hemispheric dysfunction due to ischemic or metabolic causes), Hyperventilation(metabolic disturbance), Apneustic breathing(midcaudal pontine injury), Ataxic breathing(medullary dysfunction)

Abnormal respiratory patterns in coma and cerebral localization

a) Cheyne-Stokes respiration

b) Central neurogenic hyperventilation

c) Apneustic breathing

d) Cluster breathing (low pontine or medullary damage)

e) Ataxic breathing

Focal neurologic findings

Pupillary reflexocular reflexes (oculocephalic and oculovestibular)

Motor response (Decorticate & Decerebrate)

Pupils in comatose patients

DD/ of Coma, Stupor, and Delirium (focal neurological sign (-))

Trauma(Multifocal/multiorgan trauma,)Isolated cranial trauma

Metabolic encephalopathiesElectrolyte abN(Hypo/hyperglycemia/ diabetic ketoacidosis/ nonketotic hyperosmalor coma,Hypo/hypernatremia,Hypercalcemia)

Organ system dysfunction(Hepatic/ hyperammonemia,Renal/ uremia ,Endocrine/ myxedema coma/ Addison’s disease (hyperthyroidism can cause delirium)

Hypertensive encephalopathy

Toxic encephalopathy(Sedative medication/ alcohol/ tricyclics/ opioids,Carbon monoxide/ inhalants,Neuroleptic malignant syndrome)

Environmental causes(Hyper/Hypothermia)

Nutritional(Wernicke’s syndrome)

Anoxic/hypoxic encephalopathy

Seizures/postictal statePsychiatric causes

Differential Diagnosis of Comaor Delirium with Focal Neurological SignsStroke

Ischemic/ hemorrhagicSubarachnoid hemorrhageSubdural/epidural hematomasVenous sinus occlusion

SeizurePostictal stateSubclinical status epilepticus

Intracranial traumaMeningitis/encephalitisIntoxications

Ancillary TestsComputerized tomography(CT)magnetic resonance imaging (MRI) Lumbar punctureElectroencephalogram (EEG)Electrocardiogram (ECG)

Traumatic Head InjuryEpidemiology (US)1.5 million/year Americans230,000 hospitalized50,000 die80-90 thousand significant long-term disability.

MECHANISMS OF INJURYScalp Injury

internal carotid artery anteriorexternal carotid artery posterior & lateral

scalp laceration/avulsion hemorrhage profusely hypovolemic shock

Skull FracturesLinear Skull Fractures

risk factor for the development of delayed epidural hematoma

Depressed Skull FractureBasal Skull Fractures

Skull Fracture

Focal Brain Injury• Epidural Hemorrhage

– 1.5% of head injuries– Etiology: trauma to the skull & underlying vessels

– meningeal artery (50–85%) & Venous (diploic, meningeal veins) or venous sinus (<10%)

• Subdural Hematoma– 0.5–5% of head injuries– Acceleration of the brain sagittally

stretching & tearing of the surface bridging veins drain into the dural venous sinuses

– no history of trauma : anticoagulation therapy or bleeding dyscrasias

– aneurysm rupture

Focal Brain Injury(Cont.)• Intraparenchymal/Intracerebral Hemorrhage

– 4–23% in TBI– Acceleration of the brain– 80–90% occur in the white matter of the temporal and frontal lobes

– often accompanied by other pathologies of TBI– Signs and symptoms: unconscious(>50%), lucid interval (19%), never lose consciousness (30%)

– Delayed ICH a= delayed EDH a CT initially negative for hemorrhage and subsequently found to have ICH/EDH (80%in the first 48 h after injury&may be delayed for longer than 1 wk)

ICH

Focal Brain Injury(Cont.)• Contusion

– large percentage of TBI (89%)– Head CT scans are less sensitive than pathologic studies & MRI is more sensitive

– sudden deceleration impacts the brain with the bony prominences of the inner table

– countercoup (distant from impact) ischemia, necrosis, edema, and hemorrhage predominantly appear in the frontal and temporal poles

– increased ICP (temporal lobe)herniation

Contussion

Diffuse Brain Injury• Concussion

– A transient alteration in consciousness, with confusion and amnesia.

• Diffuse Axonal Injury– disruption of intracerebral axons a differential of force between gray and white matter and subsequent shear injury

– differentiated from concussion by a loss of consciousness> 6 h, significant amnesia > a few hours & a 3-mo good outcome (15% to 65%) x concussion ( 100% )

EARLY EVALUATION AND MANAGEMENTABCs (airway, breathing, and circulation)

Glasgow Coma Scale (GCS)Fluid resuscitation with isotonic saline

Immobilization of the spine

• Low risk patients : asymptomatic or have predominantly scalp lacerations, abrasions, or contusions with no moderate- or high-risk criteria. Nonprogressive headache and nonvertiginous dizziness may occur.

• Moderate risk : a change in the level of consciousness at any time during or since the injury, post traumatic seizure or amnesia, vomiting, signs of skull fracture or depressed skull fracture, basilar fracture, multiple trauma, serious facial trauma, alcohol or drug intoxication, unreliable or inadequate history, younger than 2 yr old children/infants with more than very trivial history and presentation and/or suspected child abuse

• High-risk : depressed level of consciousness not attributable

• to alcohol or drug exposure or metabolic derangement or postictal state, focal neurologic signs, palpable depressed skull fracture, or penetrating skull injury

PREVENTION OF SECONDARY INJURY• Hypoxia• Hypotension• Elevated Intracranial Pressure

– Head Position 30–45° (reverse Trendelenberg)– Mannitol Therapy– Hypertonic Saline Therapy– Hyperventilation– Craniectomy

• Hyperglycemia (90–150 mg/dL)• Seizures• Hyperthermia (temperature < 37.5°C)• Infection• Deep Venous Thrombosis and Pulmonary Embolism• Nutrition• Vasospasm Prophylaxis

Spinal cord injury (SCI)often results in permanent neurological deficit

Delayed ot missed diagnosis, poot initial management, comorbidity, and age can significantly affect outcome

Early diagnosis, early stabilization of spinal fractures, aggressive management of comorbid disease, and multidisciplinary rehabilitation have increased survival rates and quality of life for these patients

ASIA/IMSOP impairment scaleGrade A Complete No motor or sensory function is

preserved in the sacral segmentsS4-S5.

Grade B Incomplete

Sensory but not motor function ispreserved below the neurologicallevel and extends through thesacral segments S4—S5.

Grade C Incomplete

Motor function is preserved belowthe neurological level, and themajority of key muscles below theneurological level have a musclegrade <3.

Grade D Incomplete

Motor function is preserved belowthe neurological level, and themajority of key muscles below theneurological level have a musclegrade >3.

Grade E Normal Minor and sensory functions arenormal,

ManagementIMMOBILIZATION/SPINE STABILITYMETHYLPREDNISOLONE

intravenousbolus (30 mg/kg) over 15 minutes, followed by a 45-minute pause, then a continuous drip (5.4 mg/kg/hr)for 23 hours.

NEUROLOGIC ASSESSMENT (American Spinal Injury Association (ASIA))

Management (Contd.)RESPIRATORY DYSFUNCTION

complete SCI above C3 ventilator dependent

Below C3 ventilator independent, but many require temporary ventilator support

cervical and high thoracic injuries airway hyper-reactivity and increased secretion production bronchodilators, mucolytic agents (i.e.,guaifenesin), chest physiotherapy, and assisted coughing

Management (Contd.)DEEP VEIN THROMBOSIS PROPHYLAXISCARDIOVASCULAR COMPLICATIONS (vagal episodes—bradycardia, transient third-degree heart block, asystole atropine)

NEUROGENIC BOWEL AND BLADDER DYSFUNCTIONstool softenerStress ulcer prophylaxiscatheter & urine output monitoring

PRESSURE ULCER PREVENTION (mattress, reposition 2 hrs, Adequate nutrition/albumin