Transcript Neurologic and neurosurgical emergencies in the ICU
CRANIO-CEREBRAL AND SPINAL CORD INJURIES
CDR JOHN P WEI, USN MC MD 4th Medical Batallion, 4th MLG BSRF-12
INTRODUCTION
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Current military actions with high risk for neurologic trauma to head and spinal cord Isolated blunt force trauma Penetrating trauma Combination of blunt and penetrating injuries
TRAUMATIC BRAIN INJURY
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Closed head injury: an object or an external force has sufficient energy to damage brain tissue Open head injury: an object pierces the skull and enters the brain or when blunt force fractures the bony skull with soft tissue disruption
TYPES OF BRAIN INJURIES
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Closed head injury
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Contusion / concussion Coup / Contre-Coup Cerebral edema Diffuse axonal injury Open head injury
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Gunshot wound Stab wound Compound skull fracture
COMPLEX HEAD TRAUMA
MANAGEMENT IN FIELD
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Airway Breathing Circulation Disposition
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Cervical spine
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immobilization Stop on going
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bleeding Splint or bandage extremity injuries
EPIDURAL HEMATOMA
Guidelines for Prehospital Management of TBI
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Aggressive airway management, hyperventilation (but not mannitol) only if signs of
ICP or herniation
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Fluid resuscitation / glucose to achieve euvolemia / glycemia
MANAGEMENT OF SEVERE BRAIN INJURY
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Maintain MAP>90.
Hyperventilate only if neurologic deterioration Mannitol (0.25-1gm/kg) if neurologic deterioration No glucocorticoids
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While awaiting surgery, Propofol vs LA NMB depending on MAP
CONTUSION AND IPARENCHYMAL HEMMORHAGE
TRANSCRANIAL GUNSHOT WOUND
INCREASED INTRACRANIAL PRESSURE The volume of the skull is a constant and contains:
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Brain
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Blood CSF An increase in the volume of any of these will raise intracranial pressue.
INCREASED INTRACRANIAL PRESSURE
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Initial ICP rises as volume is added (CSF and then blood exits the skull)
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As volume increases, compliance worsens and ICP rises rapidly:
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Arterial blood flow is impaired, producing ischemia
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Focal increases in volume also cause herniation from high pressure compartments to lower pressure ones
HERNIATION
INCREASED INTRACRANIAL PRESSURE
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Management
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Correct the underlying pathology with surgery if possible
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Airway control and prevention of hypercapnea
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When intubating patients with elevated ICP use thiopental, etomidate, or intravenous lidocaine to blunt the increase in ICP associated with laryngoscopy and tube passage
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ICP monitoring needed to guide therapy
INCREASED INTRACRANIAL PRESSURE
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Avoid jugular vein compression
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Head should be in neutral position
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Cervical collars should not be too tight
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Elevate head and trunk to improve jugular venous return
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Zero the arterial pressure transducer at the ear to measure the true cerebral perfusion pressure when the head is above the heart
INCREASED INTRACRANIAL PRESSURE
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Hyperventilation (PaCO 2 < 35 mmHg) works by decreasing blood flow and reserved for emergency treatment and for brief periods
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The major determinant of arteriolar caliber is the extracellular pH not measured PaCO 2
INCREASED INTRACRANIAL PRESSURE
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Pharmacologic options
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Mannitol 0.25 gm/kg q4h (may need to increase dose over time)
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Hypertonic saline (requires central line)
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3% 7.5% 23.4% (30 mL over 10 min)
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Steroids not for use in trauma
INCREASED INTRACRANIAL PRESSURE Sedation to decrease cerebral metabolic rate
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Benzodiazepines
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Propofol Requires autoregulation, which often fails in patients with elevated ICP Often causes drop in MAP, impairing cerebral perfusion and thus requiring vasopressors (e.g., norepinephrine)
INCREASED INTRACRANIAL PRESSURE
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Neuromuscular junction blockade
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titrate with train-of-four stimulator to 1 or 2 twitches
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High-dose barbiturates
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pentobarbital 5 – 12 mg/kg load followed by infusion to control ICP
INCREASED INTRACRANIAL PRESSURE
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Surgical options
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Evacuate hematoma Ventriculostomy to drain CSF Resection of brain tissue, i.e. temporal lobectomy
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Craniectomy
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Lateral for focal lesions Bifrontal for diffuse swelling
CRANIOTOMY
Secondary Injury in Head Trauma
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Hypoxia and hypotension are the 2 major causes of secondary CNS injury following head trauma
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Even in intensive care these complications occur frequently
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Preventing hypoxia and hypotension could have the greatest effect of any available treatment for head trauma
DIFFUSE AXONAL SHEAR
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Process triggered by the injury that takes about 24 hours to develop May occur without any radiographic abnormality Seen in areas of radiographically apparent “shear injury”, usually occurs at the grey white junction Often with negative CAT scan, and will require MRI
DIFFUSE AXONAL SHEAR
TREATMENT OF BRAIN INJURY
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Antiseizure drugs
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phenytoin 20 mg/kg Keppra 1000 mg/day
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Nutrition and GI bleeding prophylaxis
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Thromboembolism prophylaxis
SPINAL CORD INJURIES
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ABCs
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If intubation needed, use in-line stabilization Maintain blood pressure with volume, packed RBCs, vasopressors as needed
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Prevent secondary injury
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C-spine immobilization with C-collar
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Log-rolling
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Consider concomitant head injury
SPINAL CORD INJURIES
SPINAL CORD INJURIES
COMPLETE SPINAL CORD INJURY
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Loss of all function below level of the lesion
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Typically associated with spinal shock
INCOMPLETE SPINAL CORD INJURY
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Central cord syndrome
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Anterior cord syndrome
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Brown-Sequard syndrome
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Spinal cord injury without radiologic abnormality (SCIWORA)
SECONDARY INJURY TO SPINAL CORD
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After the initial macroscopic injury, secondary injuries are an important cause of disability:
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Movement of unstable spine
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Vascular insufficiency
SPINAL CORD INJURIES AND THE CARDIOVASCULAR SYSTEM
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“Spinal” shock
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Acute loss of tendon reflexes and muscle tone below the level of spinal cord lesion
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Neurogenic hypotension is very common and can be profound with spinal cord lesions above T1
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Hypotension in spinal shock accompanied by bradycardia
SPINAL CORD INJURIES AND THE CARDIOVASCULAR SYSTEM
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Treat hypotension with volume expansion
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If conscious, making urine, and lactate is decreasing, MAP is adequate
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Neurogenic pulmonary edema common in cervical spinal cord injuries
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May develop pulmonary vascular redistribution and interstitial edema
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SPINAL CORD INJURIES AND THE CARDIOVASCULAR SYSTEM Suspect associated injuries:
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symptoms and physical findings absent due to the spinal cord injury
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Resuscitation cannot be guided by physical findings:
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Hypotension and bradycardia persist regardless of the volume of administered
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Replace the missing adrenergic tone with
agonists (phenylephrine or norepinephrine depending on heart rate)
SUMMARY
Trauma to head and spinal structures common in current military actions Combination of blunt and penetrating injuries Consideration for early medical intervention from field to definitive treatment center Surgical intervention at earliest time