133068088 kegawat daruratan medik kesadaran menurun dan trauma
TRANSCRIPT
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Dr.Yuwono, Sp.S, FINSFK. UNTAR
Royal Taruma
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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
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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)
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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
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Focal neurologic findings
Pupillary reflexocular reflexes (oculocephalic and oculovestibular)
Motor response (Decorticate & Decerebrate)
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Pupils in comatose patients
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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
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Differential Diagnosis of Comaor Delirium with Focal Neurological SignsStroke
Ischemic/ hemorrhagicSubarachnoid hemorrhageSubdural/epidural hematomasVenous sinus occlusion
SeizurePostictal stateSubclinical status epilepticus
Intracranial traumaMeningitis/encephalitisIntoxications
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Ancillary TestsComputerized tomography(CT)magnetic resonance imaging (MRI) Lumbar punctureElectroencephalogram (EEG)Electrocardiogram (ECG)
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Traumatic Head InjuryEpidemiology (US)1.5 million/year Americans230,000 hospitalized50,000 die80-90 thousand significant long-term disability.
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MECHANISMS OF INJURYScalp Injury
internal carotid artery anteriorexternal carotid artery posterior & lateral
scalp laceration/avulsion hemorrhage profusely hypovolemic shock
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Skull FracturesLinear Skull Fractures
risk factor for the development of delayed epidural hematoma
Depressed Skull FractureBasal Skull Fractures
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Skull Fracture
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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
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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)
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ICH
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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
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Contussion
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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% )
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EARLY EVALUATION AND MANAGEMENTABCs (airway, breathing, and circulation)
Glasgow Coma Scale (GCS)Fluid resuscitation with isotonic saline
Immobilization of the spine
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• 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
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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
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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
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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,
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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))
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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
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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
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