HEAD INJURY AND INTRACRANIAL HYPERTENSION

1. HEAD INJURY AND INTRACRANIAL HYPERTENSION

2. 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

3. 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

4. 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

5. 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

6. COUP - CONTRECOUP INJURY LifeArt: Williams & Wilkins http://www.lifeart.com

7. Diffuse injuries Diffuse axonal injury Diffuse vascular injury Focal injuries Skull fracture Parenchymal contusion Parenchymal laceration Vascular injury resulting in hematoma (subdural, extradural, or parenchymal) TYPES OF PRIMARY INJURIES

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

9. CONTUSION • Usually frontal or temporal lobe • Small cortical vessels and neural tissue damaged • Damaged vessels may thombose, leading to ischemia WebPath: University of Utah http://www-medlib.med.utah.edu/WebPath/webpath.html

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

11. 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

12. 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

13. . ...... . .. 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

14. SECONDARY ISCHEMIC BRAIN INJURY • Compounds the potential for adverse neurologic outcome • Caused by: • Post injury hypotension • Hypoxemia • Intracranial hypertension which impairs cerebral bloodflow

15. Vascular etiologies Vasogenic edema BBB impaired, protein rich fluid leaks to ECF Hyperemia Occurs days 1 to 3 after injury Obstructed venous drainage Hydrostatic pressure increased, protein poor fluid leaks into ECF Nonvascular etiologies Cytotoxic edema Ionic gradients impaired and cells swell Obstruction to CSF outflow Hematoma Osmotic brain edema Decreased osmolality from iatrogenic hemodilution or SIADH INTRACRANIAL HYPERTENSION

16. 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 ICP’s when mass lesion is present

17. 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

18. RESUSCITATION • A, B,C’s • 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

19. 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

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

21. 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

22. 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

23. MONITORING OF INTRACRANIAL PRESSURE • Indications • GCS < 8 after resuscitation • Abnormal head CT • Rapid neurologic deterioration • ICP monitoring is continued for as long as treatment of intracranial hypertension is required

24. 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

25. 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

26. Increases ICP hypercarbia hypoxia (pO2 < 50) seizures or shivering hyperthermia arousal pain, anxiety venous congestion fluid overload intrathoracic pressure Decreases ICP hyperoxia hypothermia barbiturates hypocapnia via cerebral vasoconstriction lowers CPP and is undesirable FACTORS AFFECTING INTRACRANIAL PRESSURE

27. 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

28. 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

29. 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

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

31. 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

32. 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

33. 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

34. 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

35. 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

36. MANAGEMENT OF OTHER SYSTEMS • Respiratory • Maintain normocapnia • Hyperventilation only appropriate during early diagnosis and management or if herniation is impending • Maintain oxygenation • pO2 > 100 is optimal • 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

37. 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

38. 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 Ringer’s 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, cerebral salt wasting

39. 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

40. MANAGEMENT OF OTHER SYSTEMS • Renal • Place foley for strict I’s and O’s • 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

41. 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 dextrose-containing fluids Continuous vasopressin infusion or DDAVP (subQ or intranasal) q 12 to 24 hrs

42. 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

43. 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