Epidemiology Injury is leading cause of death for children 40% of those are from TBI Mortality between 17 – 33% Most common cause of death & disability in childhood in developed countries 3000 children die each year from TBI in the US Krug EG et al. Am J Public Health. 2000. Langlois JA et al. Centers for Disease Control & Prevention. 2006. White JR et al. CCM. 2001. Krug EG et al. Langlois JA et al.
GCS Severity of TBI is defined by the GCS Score Mild GCS 13-15 Moderate GCS 9-12 Severe GCS <9
GCS Motor Response Follows commands6 Localizes pain5 Withdraws to pain4 Abnormal flexion to pain (decorticate posturing) 3 Abnormal extension to pain (decerebrate posturing) 2 No response1 Verbal Response Oriented (age appropriate vocalization, smiling, cooing, tracks objects) 5 Confused, disoriented (cries, irritable) 4 Inappropriate words (cries to pain) 3 Incomprehensible sounds (moans to pain) 2 No response1 Eye Opening Spontaneous4 To command3 To pain2 No eye opening1 Total score ranges from 3 - 15
Effects of Trauma Increase in volume of any or all intracranial components Uncoupling of cerebral blood flow & metabolic activity (loss of autoregulation) can lead to excessive CBF Increased CSF production in response to increased CBF Hypercapnia or hypoxia (cause vasodilation & increased CBF) Herniation, brain swelling, subarachnoid hemorrhage may obstruct flow of CSF Hematomas, contusions, edema may increase intracranial volume
Definition of ICP ICP = ICP vascular + ICP CSF Used to estimate cerebral perfusion pressure CPP = MAP – mean ICP CPP: Cerebral Perfusion Pressure ICP: Intracranial Pressure MAP: Mean Arterial blood Pressure
Normal Values ICP is typically ≤ 15 mmHg in adults and lower in children & newborns ICP ≥ 20 mmHg is pathologic in adults Physiologic events such as sneezing, coughing, Valsalva will transiently raise ICP as well CPP normals for adults range from 50 – 70 mmHg Not well established in children, likely 40 – 60 mmHg depending on age When CPP falls below a critical level, brain receives inadequate blood flow
Intracranial Pressure The intracranial compartment has a fixed internal volume Brain parenchyma – 80% CSF – 10% Blood – 10% ICP is a function of the volume & compliance of each component The Monroe-Kellie Doctrine
Monroe-Kellie Principle Intracranial compensation for an expanding mass lesion Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd ed, Rogers, MC (Ed), Williams and Wilkins 1996. p. 646; figure 18.1.
The relationship between intracranial volume and pressure is nonlinear An initial increase in volume results in a small increase in pressure because of intracranial compensation (blue line). Once intracranial compensation is exhausted, additional increases in intracranial volume result in a dramatic rise in intracranial pressure (red line).
Cerebral Edema Diffuse swelling more common among infants and children compared to adults Infant skull is more compliant, tolerates significant deformation without fracture Brain atrophy begins in young adulthood and allows for more room in the adult skull for brain to expand Lang DA. J Neurosurg 1994 Coats B. J Neurotrauma 2006 Kochanek PM. Dev Neurosci 2006
Cerebral Edema Worsened with hypoxia & hypoperfusion Types of edema: Vasogenic- breakdown of the blood-brain barrier Cytotoxic- cellular swelling Interstitial- periventricular exudation of cerebrospinal fluid through the ependymal lining Osmotic- movement of water into the interstitial spaces induced by osmotically active products of tissue injury and blood clot
Cerebral Autoregulation Often impaired in children with TBI Impaired autoregulation is associated with worse outcome Cerebral autoregulation in hypertension Kaplan, NM, Lancet 1994
2 Insults Primary Injury Direct injury to brain parenchyma Blunt force: Contusions, hematomas Acceleration-deceleration: physical shearing or tearing of axons http://www.tbilawyers.com/diffuse-axonal-injury.html
Secondary Injury: Potentially avoidable or treatable Hypoxemia Hypotension Elevated ICP Hypercarbia Hyper- & Hypoglycemia Electrolyte abnormalities Enlarging hematomas Coagulopathy Seizures Hyperthermia Endogenous cascade of cellular & biochemical events Occurs within minutes and continues for months after initial injury Leads to neuronal cell death
Diffuse Axonal Injury Widespread damage to axons in the white matter Corpus callosum Basal ganglia Periventricular white matter Caused by Hypoxic-ischemic injury Calcium & ion flux Mitochondrial & cytoskeletal dysfunction A major cause of morbidity in pediatric TBI More extensive DAI associated with worse outcome
History Mechanism of injury Loss of consciousness + duration Vomiting Headache One of the earliest symptoms of increased ICP Progression of symptoms
Physical Exam—General Hypoxia & hypotension should be immediately identified and treated Respiratory depression, bradycardia, and/or hypertension may indicate impending herniation and also requires prompt treatment Maintain C-spine immobilization
Neuro exam Assign a GCS Level of consciousness Pupils Extraocular movements Funduscopic exam Brainstem reflexes DTRs Response to pain
Setting-Sun Sign Late sign of increased intracranial pressure. Pressure on cranial nerves III, IV, and VI forces the eyes downward, revealing a rim of sclera above the irises.
Funduscopic Exam www.dontshake.org http://cloud.med.nyu.edu/modul es/pub/neurosurgery/cranials.ht ml
Types of Herniation a)Subfalcine : uneven, one-sided expansion of a cerebral hemisphere that pushes a portion of the brain tissue (cingulate gyrus) under the falx cerebri b)Uncal: medial temporal lobe is pushed against the tentorium. Can compress brainstem in severe cases c)Central transtentoral : downward pressure centrally, can cause bilateral uncal herniation. d)Extracranial : brain tissue pushes through an opening in the cranial cavity either surgically or by trauma e)Tonsillar : swelling or bleeding in the cerebellum pushes the cerebellar tonsils downward into the foramen magnum. Life threatening b/c can compress the brainstem
Signs of herniation Uncal herniation: Third cranial nerve palsy Hemiplegia Progressive changes in respiratory pattern, pupil size, vestibuloocular reflexes, posturing Cushing’s Triad Hypertension Bradycardia Slow, irregular respirations OCCURS LATE!!
Mydriasis Can be associated with CN III injury Uncal herniation can cause unilateral mydriasis & ptosis
Labs Depends on type & extent of injury Minimum: hct, T&S, UA Useful in TBI: Glucose Hyperglycemia is a poor prognostic indicator Electrolytes w/ osmolarity Coags DIC is associated with poor outcomes Chiaretti A. Childs Nerv Syst 2002.
Imaging CT is preferred initial imaging Following initial stabilization Focal injuries are readily diagnosed by CT Patients with DAI may have normal CT scans Most common finding is diffuse cerebral swelling
Goals Minimize ICP elevation Maintain adequate CPP to prevent secondary ischemic injury CPP goal for adults should be 60 – 70 mmHg Minimum acceptable for children is not defined, but recommended 40 – 65 mmHg depending on age. Studies show that CPP from 40 – 65 improves outcome CPP < 40 associated with poor outcome ICP goal typically < 20 mmHg Adelson PD. PCCM. 2003
Initial Decisions Immediate NSGY consultation Quickly identify focal injuries that require neurosurgical intervention GCS ≤ 8 or GCS 9-12 and deteriorating/not protecting airway require intubation Recognize signs of herniation & treat if present Assure adequate oxygenation, breathing, BP Give hyperosmolar therapy Provide mild hyperventilation Immediate NSGY evaluation
Airway & Breathing Advanced airway management necessary if Decreasing level of consciousness (GCS ≤ 8) Marked respiratory distress Hemodynamic instability Other considerations C-spine immobilization must be maintained Nasotracheal intubation contraindicated with midface trauma or basilar skull fracture Cuffed tubes to protect from aspiration
Rapid Sequence Intubation Pretreat with lidocaine to minimize increase in ICP Preoxygenation Etomidate & Thiopental have neuroprotective properties ? Risk of increased ICP with succinylcholine Rocuronium may be preferred Avoid high PEEP and PIP because they will increase intrathoracic pressure and may impede cerebral venous drainage.
Monitoring Standard VS: HR, BP, Pulse Ox Capnography To monitor ventilation & avoid excessive hyperventilation ICP monitoring recommended for abnormal head CT & initial GCS 3 – 8 Interventions used to decrease ICP require accurate and continuous ICP monitoring!!
ICP Monitoring Indications Traumatic brain injury (GCS < 8 with focal findings on CT) Obstructive intracranial lesion Post operative edema Contraindications Coagulopathy: i.e. high risk of hemorrhage Relative Indications Metabolic cerebral edema
ICP Monitoring Options External Ventricular Device (EVD) both diagnostic and therapeutic Intra-parenchymal device: Diagnostic guide to therapy Others: diagnostic
Management of ICP First tier therapies Maintain CPP Sedation & analgesia HOB at 30 degrees Ventriculostomy drain Neuromuscular blockade Hyperosmolar therapy (mannitol & hypertonic saline) Mild hyperventilation Second tier therapies Hyperventilation Decompressive craniectomy High dose barbiturates Hypothermia (32 – 34 degrees)
Hyperventilation Reduces ICP May be harmful with routine use Results in hypocapnia Vasoconstriction Decreased cerebral blood flow Associated with poor outcomes among children with TBI  PCO2 < 30 mmHg associated with increased mortality Maintain PaCO 2 between 35 – 38 mmHg unless signs of impending herniation Curry R. PCCM 2008. Adelson PD. Pediatr Neurosurg 1997. Skippen P. CCM 1997.
Initial Fluid Management Restore volume—Isotonic fluids preferred Blood products as indicated Outcomes are poor for children who are hypotensive at initial evaluation Systolic blood pressure should be maintained above the 5 th percentile for age and sex at the minimum Improved outcomes for patients with initially higher blood pressure White JR. CCM 2001 Vavilala MS. J Trauma 2003 Luerssen TG. J Neurosurg 1988 Pigula FA. J Pediatr Surg 1993 Adelson PD. PCCM. 2003
Head Positioning As head-up position is increased, ICP may be reduced, but beyond 30 o heads-up CPP is likely compromised. Second source: Durward, QJ, Amadner, AL, Del Maestro, RF, et al: Cerebral and vascular responses to changes in head elevation in patients with intracranial hypertension, J Neurosurg 59: 938, 1983. Maintain head in neutral position to avoid jugular venous obstruction
Sedation and Neuromuscular Blockade Maintain adequate analgesia to blunt response to noxious stimuli Maintain sedation to permit controlled ventilation Cerebral oxygen consumption may be decreased in patients receiving neuromuscular blockade Vernon DD. CCM 2000
Antiseizure Prophylaxis Reduces the incidence of early posttraumatic seizures among children with severe TBI Seizures increase metabolic demand and increase ICP Leads to secondary brain injury Retrospective studies demonstrate improved outcomes among children with TBI treated with anticonvulsants Recommend anticonvulsants during the first week following TBI if high risk Penetrating skull fractures, hematomas, masses, bleeds Schierhout G. Cochrane Database Syst Rev 2001 Tilford JM. CCM 2001 Adelson PD et al. PCCM 2003
Temperature control Aggressively prevent & treat hyperthermia Raises metabolic demand & ICP Hypothermia decreases cerebral metabolism and may reduce CBF & ICP Controversial One multicenter trial showed harm Control shivering with muscle relaxants (Considered second tier therapy)
Hyperosmolar Therapy Establishes an osmotic gradient between plasma and parenchymal tissue Reduces brain water content Extensive research shows that it effectively decreases ICP in children with TBI
Mannitol Decreases ICP effectively based on extensive clinical experience Dose 0.25 – 1 g/kg IV Adverse effects: hyperosmolarity, hypovolemia, electrolyte imbalance Nephrotoxicity can occur, especially if patients are hypovolemic Don’t typically use if serum osmolarity >320 Adelson PD et al. PCCM 2003.
Hypertonic Saline Can be administered as a bolus or as an infusion Optimal dosing not clear 3% saline commonly used as bolus of 2-6 ml/kg Continuous infusion of 0.1 – 1 ml/kg/hr also described Effective at reducing ICP in small randomized trials & observational reports Does not cause profound osmotic diuresis, so decreased risk of hypovolemia Adverse effects: Rebound intracranial hypertension Central pontine myelinolysis (theoretical, not reported) Qureshi AI. CCM 2000. Huang SJ. Surg Neurol 2006.
Glucose Control Hyperglycemia associated with poor outcomes Marker for severity of injury Worsens brain tissue lactic acidosis Recommend to keep glucose level at least less than 200 Adelson PD. PCCM 2003.
Corticosteroids No benefit in trauma Large, prospective multicenter trial demonstrated increased mortality among patients with acute TBI who received steroids Useful only for vasogenic edema from tumors because they stabilize the BBB
Barbiturate coma—second tier therapy Used if ICP refractory to other modalities Pentobarbital typically used Decreases cerebral metabolic rate and thus cerebral blood flow May have protective effects during periods of hypoxia and/or hypoperfusion Cardiac suppression, hypotension Treat with fluids & inotropic support No evidence for prophylactic use
Other second tier therapies Aggressive hyperventilation (PaCO2 < 30) Recommend brain tissue oxygenation monitoring or jugular venous O2 saturation or CBF monitoring Decompressive craniectomy Ideal patient has had no episodes of ICP > 40 before surgery, have had a GCS > 3 at some point Evolving herniation syndrome within 48 hrs of injury Lumbar CSF drainage Not common Must have a functioning EVD in place, open basal cisterns, no mass effect or shift on CT (to avoid herniation) Hypothermia Core temp 32 – 34 degrees More studies needed
Management Algorithm Adelson PD et al. PCCM 2003
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