UTHSCSA

Pediatric Resident Curriculum for the PICU

HEAD INJURY AND INTRACRANIAL HYPERTENSIO

Pediatric Resident Curriculum for the PICU

HEAD INJURY
Major cause of morbidity and mortality in children Leading cause of death in children > 1 yr is trauma Head injuries responsible for most trauma deaths Adverse outcomes result from Primary injury Result of mechanical forces producing tissue deformation at the moment of injury Secondary ischemic injury Associated with post injury hypotension, hypoxemia, and intracranial hypertension

UTHSCSA

Pediatric Resident Curriculum for the PICU

ETIOLOGIES
Motor vehicle accidents Responsible for most severe head injuries Falls Usually in children < 4 yrs and usually mild Recreational activities Half of these are bicycle accidents Assault or nonaccidental trauma Most head injuries in kids < 1 yr are from NAT and falls

UTHSCSA

Pediatric Resident Curriculum for the PICU

ANATOMY
Uniquely susceptible to injury Brain Inelastic and noncompressible Has no internal support Cranium Rigid and unyielding after sutures fused Bony buttresses at anterior poles and temporal poles Membranous slings Falx cerebri compartmentalizes R and L hemispheres Tentorium separates infra- and supratentorial regions

UTHSCSA

Pediatric Resident Curriculum for the PICU

MECHANISM OF BRAIN INJURY

Brain is thrown against bony irregularities or membranous slings or compressed against these surfaces by Contact injury Head strikes or is struck by an object Acceleration/deceleration injury Violent head motion causes compressive, tensile, and shear strain in brain tissue

UTHSCSA

Pediatric Resident Curriculum for the PICU

COUP - CONTRECOUP INJURY

UTHSCSA

LifeArt: Williams & Wilkins http://www.lifeart.com

Pediatric Resident Curriculum for the PICU

TYPES OF PRIMARY INJURIES

Focal injuries Diffuse injuries Skull fracture Diffuse axonal Parenchymal injury contusion Diffuse vascular Parenchymal injury laceration Vascular injury resulting in hematoma (subdural, extradural, or parenchymal)

UTHSCSA

Pediatric Resident Curriculum for the PICU

SKULL FRACTURES
Most are uncomplicated Basilar skull fractures
Battles sign, raccoon eyes CSF rhinorrhea, CSF otorrhea possible Cranial nerve injury possible

Depressed skull fractures represent more severe injury

1/3 are associated with dural laceration 1/3 are associated with cortical laceration May require surgical elevation

UTHSCSA

Fracture crossing path of major vascular structure increases risk for significant bleeding
Middle meningeal artery Large dural sinus

Pediatric Resident Curriculum for the PICU

CONTUSION
Usually frontal or temporal lobe Small cortical vessels and neural tissue damaged Damaged vessels may thombose, leading to ischemia

UTHSCSA

WebPath: University of Utah http://www-medlib.med.utah.edu/WebPath/webpath.html

Pediatric Resident Curriculum for the PICU

INTRACEREBRAL HEMORRHAGE
Usually frontal or temporal lobe Can be bilateral (contracoup injury) Can act as mass lesions and cause intracranial hypertension

UTHSCSA

Pediatric Resident Curriculum for the PICU

EPIDURAL HEMATOMA
Usually arterial in origin Between skull and dura, limited by suture lines Often from tear in middle meningeal artery Initial injury may seem minor, followed by lucid interval, then neurologic deterioration May expand rapidly and require emergency craniotomy
WebPath: University of Utah http://www-medlib.med.utah.edu/WebPath/webpath.html

UTHSCSA

Pediatric Resident Curriculum for the PICU

SUBDURAL HEMATOMA
Usually venous bleeding (bridging veins) On surface of cortex, beneath dura and outside arachnoid, not limited by suture lines. Typically requires greater force to produce than epidural hematoma Usually associated with severe parenchymal injury
WebPath: University of Utah http://www-medlib.med.utah.edu/WebPath/webpath.html

UTHSCSA

Pediatric Resident Curriculum for the PICU

. ...... . ..

DIFFUSE BRAIN INJURY

Diffuse axonal injury Usually from rapid acceleration/deceleration Shear forces disrupt small axonal pathways
After disruption, axons degenerate, fragment, then disappear The neurons then undergo Wallerian degeneration

Spectrum from mild to severe Diffuse vascular injury Microvasculature more resistant to shear than axons Results in multiple small hemorrhages throughout brain Usually seen in fatal head injuries

UTHSCSA

Pediatric Resident Curriculum for the PICU

SECONDARY ISCHEMIC BRAIN INJURY

Compounds the potential for adverse neurologic outcome Caused by: Post injury hypotension Hypoxemia Intracranial hypertension which impairs cerebral blood flow

UTHSCSA

Pediatric Resident Curriculum for the PICU

INTRACRANIAL HYPERTENSION
Vascular etiologies Vasogenic edema
BBB impaired, protein rich fluid leaks to ECF

Nonvascular etiologies Cytotoxic edema

Ionic gradients impaired and cells swell

Hyperemia
Occurs days 1 to 3 after injury

UTHSCSA

Obstructed venous drainage

Hydrostatic pressure increased, protein poor fluid leaks into ECF

Obstruction to CSF outflow Hematoma Osmotic brain edema

Decreased osmolality from iatrogenic hemodilution or SIADH

Pediatric Resident Curriculum for the PICU

INTRACRANIAL HYPERTENSION
Normal intracranial pressure:
Adults: < 10 mm Hg Infants/children: somewhat lower, depending on age

Elevated ICP impairs cerebral perfusion Risk for herniation with ICP > 40 mm Hg Herniation can occur at lower ICPs when mass lesion is present

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF HEAD INJURY

Goals of resuscitation and treatment is to minimize secondary ischemic brain injury by promoting and preserving cerebral perfusion
Prevent or treat post injury hypotension Prevent or treat hypoxemia and reduce oxygen demand of the brain Prevent or treat intracranial hypertension Avoid measures that decrease cerebral perfusion

UTHSCSA

Pediatric Resident Curriculum for the PICU

RESUSCITATION
A, B,Cs Major early risk is hypotension
Adequate fluid resuscitation to restore normal BP does NOT worsen neurologic outcome Avoid hypotonic fluids

Emergent airway control for

GCS 8 or less GSC 10 or less with abnormal head CT Rapid neurologic deterioration If needed for other injuries

UTHSCSA

Pediatric Resident Curriculum for the PICU

INTUBATION OF PATIENT WITH HEAD INJURY

Preserve cerebral oxygenation Maintain cerebral perfusion
Adequate analgesia and anxiolysis Avoid meds that increase ICP Avoid meds that cause hypotension Avoid Trendelenburg position

Avoid aggravating C spine injury

C-spine injuries in as many as 10% of head injury patients In-line axial stabilization by an assistant recommended

UTHSCSA

Pediatric Resident Curriculum for the PICU

DRUGS FOR RAPID SEQUENCE INTUBATION

Analgesia/sedation Neuromuscular blockade Fentanyl, etomidate Succinyl choline little effect on BP short acting Thiopental muscle fasciculations can decreases ICP but increase ICP can drop BP use with Anxiolysis defasciculating Midazolam dose of little effect on BP nondepolarizing Lidocaine IV Non depolarizing blunts vecuronium sympathetic longer acting and response to no increase in ICP intubation

UTHSCSA

Pediatric Resident Curriculum for the PICU

RULE OUT & PREVENT NEUROSURGICAL EMERGENCIES

Head CT as soon as possible Initial CT may be normal in severe head injury Repeat CT in 12 to 24 hours Moderate hyperventilation advisable during transport and initial evaluation If signs of impending herniation develop (lateralizing signs, pupil asymmetry) Hyperventilate Give mannitol

UTHSCSA

Pediatric Resident Curriculum for the PICU

MONITORING OF INTRACRANIAL PRESSURE

Ventriculostomy catheter Catheter tip in frontal horn of lateral ventricle Can drain CSF Can be recalibrated as necessary Transducer tipped catheter Intraparenchymal or subdural Cannot drain CSF Cannot be recalibrated Exhibits drift in values measured over time

UTHSCSA

Pediatric Resident Curriculum for the PICU

MONITORING OF INTRACRANIAL PRESSURE

Indications
GCS < 8 after resuscitation Abnormal head CT Rapid neurologic deterioration

UTHSCSA

ICP monitoring is continued for as long as treatment of intracranial hypertension is required

Pediatric Resident Curriculum for the PICU

CEREBRAL PERFUSION PRESSURE

Can be determined from ICP and mean arterial pressure: CPP = MAP - ICP Calculated CPP does not reflect perfusion of entire brain CPP further decreased in areas of injury Factors that cause cerebral vasoconstriction without lowering MAP result in a falsely low calculated CPP

UTHSCSA

Pediatric Resident Curriculum for the PICU

CEREBRAL PERFUSION PRESSURE

Goal of therapy
CPP > 60 mm Hg if ICP < 22 mm Hg or CPP > 70 mm Hg if ICP > 22 mm Hg Lowering ICP while maintaining MAP will increase CPP Increasing MAP will increase CPP

UTHSCSA

Pediatric Resident Curriculum for the PICU

FACTORS AFFECTING INTRACRANIAL PRESSURE

Increases ICP hypercarbia hypoxia (pO2 < 50) seizures or shivering hyperthermia arousal pain, anxiety venous congestion fluid overload intrathoracic Decreases ICP hyperoxia hypothermia barbiturates hypocapnia via cerebral vasoconstrictio n lowers CPP and is undesirable

UTHSCSA

Pediatric Resident Curriculum for the PICU

EFFECT OF pCO2 and pO2 ON CBF AND CPP

Hypoxia increases CBF by vasodilation Hypercapnia increases CBF Hyperventilation and resulting hypocapnia decrease CBF Hyperventilation is useful to prevent impending herniation but will worsen secondary ischemic injury

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Head position Head elevated 30 degrees and midline Sedation and pain control Analgesic + anxiolytic Fentanyl, morphine, or propofol plus a benzodiazepine Continuous infusions or scheduled doses to maintain sedation Watch for and treat hypotension Seizure prophylaxis Phenytoin or phosphenytoin

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Neuromuscular blockade Facilitates mechanical ventilation and control of pCO2 Prevents shivering Use if movement increases ICP Temperature control A rise in temp of 1o C increases cerebral metabolic rate by 10%, increasing ICP by several mm Hg Maintain temp < 37.5 o C
Scheduled acetaminophen, body exposure, cooling blanket

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Osmotherapy with mannitol Decreases extracellular fluid in brain Intermittent doses for ICP spikes or scheduled if elevated ICP is persistent Adverse effects:
Hypernatremia, hypokalemia Hyperosmolality Hemodilution and drop in hematocrit Hypotension

UTHSCSA

Follow serum osmolality and Na Hold mannitol if serum osm > 320 mOsm/l

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Drainage of CSF
Possible if ventricular catheter is in place CSF drainage pressure usually set at 20 cm H2O CSF drains when ICP exceeds drainage pressure Ventricular catheters cannot be placed if cerebral edema has obliterated or significantly compressed ventricles

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Second tier therapies for intracranial hypertension refractory to sedation, muscle relaxation, osmotherapy, and moderate hypothermia:
barbiturate coma induced hypertension decompressive craniotomy hypothermia

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Barbiturate coma ICP control is the principal endpoint EEG burst suppression is a useful guide to optimal barbiturate dosage
Pentobarbital 10mg/kg followed by infusion at 1 mg/kg/hr, titrated to effect May give additional boluses during infusion for acute spikes in ICP Moderate doses cause sluggishly reactive pupils while large doses may cause mid position to 5 mm nonreacting pupils Watch for hypotension

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Induced hypertension Inotropes to increase MAP, even beyond normal for age, to achieve an optimal CPP
Dopamine Norepineprine

Rise in ICP in tandem with a rise in MAP implies total loss of autoregulation and is a poor prognostic sign Decompressive craniotomy Large portion of cranium removed to allow room for brain to swell and minimize ischemia Dura must be opened as well

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF INCREASED ICP

Hypothermia Core body temp of 32o to 33o C Reduced cerebral metabolic activity, reducing ICP Also has cytoprotective effects Adverse effects Arrythmias Coagulopathies Hypokalemia Increased risk of infection

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF OTHER SYSTEMS

Respiratory
Maintain normocapnia
Hyperventilation only appropriate during early diagnosis and management or if herniation is impending

Maintain oxygenation PEEP to maintain alveolar recruitment

ARDS, neurogenic pulmonary edema frequent complications Hypoxemia has more deleterious effects on brain than modest venous congestion caused by PEEP PEEP of 5 to 10 cm H2O not shown to have detrimental effect on neurologic outcome pO2 > 100 is optimal

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF OTHER SYSTEMS

Cardiovascular Maintain normal blood pressure Hypotension significantly reduces CPP Inotropes if necessary to maintain normal BP Induced hypertension if necessary Gastrointestinal Stress gastritis prophylaxis with H2 blocker Jejunal feeds to maintain healthy intestinal mucosa and prevent bacterial translocation from gut

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF OTHER SYSTEMS

Fluids, Electrolytes, Nutrition
Goal is NORMOVOLEMIA Total fluid intake should be @ 100% maintenance Bolus as necessary to achieve normal CVP Avoid hypotonic fluids Lactated Ringers and 0.9% saline w/ 20 mEq KCl/l are good choices for maintenance fluids Follow electrolytes closely Avoid hyponatremia Mannitol can cause electrolyte abnormalities Watch for SIADH, diabetes insipidus,

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF OTHER SYSTEMS

Fluids, electrolytes, nutrition
Provide calories to meet metabolic demands of patient Increased metabolic demands during acute phase of injury Heavily sedated, relaxed, cooled patient has decreased metabolic demands Enteral feedings via nasojejunal catheter preferable to TPN if gut deemed to be healthy Avoid hyperglycemia Associated with poor neurologic outcome Watch serum glucose closely if dextrose containing fluids used

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF OTHER SYSTEMS

Renal
Place foley for strict Is and Os

Hematologic
Coagulopathy common with head injuries Brain derived thromboplastin activator substances released Follow PT/PTT or DIC screens Blood component replacement if evidence of active bleeding or if surgical intervention anticipated Maintain normal hematocrit to optimize oxygen delivery

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF OTHER SYSTEMS

Endocrine
DIABETES INSIPIDUS Complete or partial failure of ADH secretion from shearing of pituitary stalk Polyuria, hypernatremia, urine osm < plasma osm Treatment: Run maintenance fluids @ 100% Replace urine output cc for cc with dextrosecontaining fluids Continuous vasopressin infusion or DDAVP (subQ or intranasal) q 12 to 24 hrs

UTHSCSA

Pediatric Resident Curriculum for the PICU

MANAGEMENT OF OTHER SYSTEMS

Endocrine
CEREBRAL SALT-WASTING ANP-like substance released from brain, inducing natriuresis and diuresis SIADH Elevated level of ADH inappropriate for prevailing osmotic or volume stimuli Hyponatremia, hypo-osmolality, urine osm > plasma osm, high urine Na Treatment is water restriction

UTHSCSA

Pediatric Resident Curriculum for the PICU

SUMMARY
Identify and treat primary brain injury
Rule out neurosurgical emergency

Minimize secondary ischemic brain injury by promoting cerebral perfusion

Maintain normovolemia and adequate BP Maintain normal electrolytes and euglycemia Maintain normocapnia and adequate oxygenation Avoid factors that increase ICP Treat intracranial hypertension

UTHSCSA