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ICP & Head Trauma Sophia R. Smith, MD WRAMC November 2, 2005.

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Presentation on theme: "ICP & Head Trauma Sophia R. Smith, MD WRAMC November 2, 2005."— Presentation transcript:

1 ICP & Head Trauma Sophia R. Smith, MD WRAMC November 2, 2005

2 Introduction Head injuries are one of the most common causes of disability and death in children. Head injuries are one of the most common causes of disability and death in children. The Centers for Disease Control and Prevention (CDC) estimates that more than 10,000 children become disabled from a brain injury each year. The Centers for Disease Control and Prevention (CDC) estimates that more than 10,000 children become disabled from a brain injury each year. Head injuries can be defined as mild as a bump to severe in nature. Head injuries can be defined as mild as a bump to severe in nature.

3 Prevalence of Pediatric Trauma Trauma is the leading cause of death in infants and children Trauma is the leading cause of death in infants and children Trauma is the cause of 50% of deaths in people between 5 and 34 years of age Trauma is the cause of 50% of deaths in people between 5 and 34 years of age Motor vehicle related accidents account for 50% of pediatric trauma cases Motor vehicle related accidents account for 50% of pediatric trauma cases $16 billion is spent annually caring for injuries to children less than 16 years of age $16 billion is spent annually caring for injuries to children less than 16 years of age

4 Traumatic Brain Injury Primary Brain Injury Results from what has occurred to the brain at the time of the injury Secondary Brain Injury Physiologic and biochemical events which follow the primary injury Physiologic and biochemical events which follow the primary injury

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6 Examples of Primary Brain Injuries

7 Factors that Effect Secondary Brain Injuries Blood Pressure Blood Pressure Oxygenation Oxygenation Temperature Temperature Control of Blood Glucose Control of Blood Glucose Fluid Volume Status Fluid Volume Status Increased Intracranial Pressure Increased Intracranial Pressure

8 Brain trauma BBB disruption diffuse axonal injury edema formation Eicosanoids endocannabinoids necrosis energy failure cytokines SOME of the SECONDARY EVENTS IN TRAUMATIC BRAIN INJURY apoptosis inflammation ROS polyamines Calcium Acetyl Choline ischemia Shohami, 2000 Green – pathophysiological processes; Yellow – various mediators

9 Anatomy of the cranium There are various brain contents that are localized within a rigid structure. There are various brain contents that are localized within a rigid structure. –Cranium The cranial vault contents include: The cranial vault contents include: –The brain –The cerebral spinal fluid –The cerebral blood

10 Cerebral Spinal Fluid CSF CSF –150 cc in adults at all times Children slightly less Children slightly less –Produced by choroid plexus – 20 cc/hr –CSF is absorbed into venous system at the subarachnoid villi

11 Cerebral blood and brain Cerebral blood Cerebral blood –Sum of blood in capillaries, veins, and arteries Brain Brain –80% of the total intracranial volume All of these contents are maintained @ a balanced pressure referred to as intracranial pressure (ICP) All of these contents are maintained @ a balanced pressure referred to as intracranial pressure (ICP)

12 Monro-Kellie Doctrine The ICP within the skull is directly related to the volume of the contents. The ICP within the skull is directly related to the volume of the contents. –Defined as the Monro-Kellie Doctrine –This doctrine states that any increase in volume of the contents within the brain must be met with a decrease in the other cranial contents.

13 Monro-Kellie Doctrine V intracranial vault =V brain +V blood + V csf

14 Increased Intracranial Pressure

15 Cerebral Blood Flow CBF is directly linked to the metabolic requirements of the brain. CBF is directly linked to the metabolic requirements of the brain. As the brain metabolic activity increases, CBF increases As the brain metabolic activity increases, CBF increases –Vasodilatation of cerebral vessels –Increase in cerebral blood volume –Consequent increase in ICP

16 Cerebral blood flow CBF maintained when MAP range is 50mmHg to 150mmHg CBF maintained when MAP range is 50mmHg to 150mmHg –Cerebral auto regulation As BP increase  baroreceptors sense event and cerebral arteries vasoconstrict  CBF maintained with a CBV decrease As BP increase  baroreceptors sense event and cerebral arteries vasoconstrict  CBF maintained with a CBV decrease As BP decrease  cerebral arteries dilate to increase flow  CBV increase As BP decrease  cerebral arteries dilate to increase flow  CBV increase

17 Auto regulation This process is lost in pathological states This process is lost in pathological states –Esp. Head trauma –CBF decreases linearly to MAP below range Results is ischemia (strokes) to brain regions Results is ischemia (strokes) to brain regions –CBF increases linearly to MAP above auto regulation range HTN encephalopathy as CBV and ICP increase HTN encephalopathy as CBV and ICP increase

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19 Mediators of CBF Local and global mediators of CBF and metabolism are important. Local and global mediators of CBF and metabolism are important. –Hypoxia and pH are most important –As local paO2 decreases, CBF increases –CBF is affected by pH (and its surrogate pCO2)

20 u The brain has the ability to control its blood supply to match its metabolic requirements u Chemical or metabolic byproducts of cerebral metabolism can alter blood vessel caliber and behavior Blood: Cerebral Blood Flow

21 Studies of hyperventilation & ICP This relationship has been well studied as a therapeutic option in particular intentional hyperventilation to lower cerebral blood flow and thus intracranial pressure. This relationship has been well studied as a therapeutic option in particular intentional hyperventilation to lower cerebral blood flow and thus intracranial pressure. No longer a practice No longer a practice –Modest hyperventilation

22 On call So, you are in the ER on your first night of call and the next thing you know you get your very first trauma patient. So, you are in the ER on your first night of call and the next thing you know you get your very first trauma patient. How do you evaluate? How do you evaluate?

23 Trauma

24 Traumatic Brain Injury

25 Glascow Coma Scale Eye Opening Spontaneous 4 To Voice 3 To Pain 2 None 1 Best Verbal Oriented 5 Confused 4 Inappropriate Words 3 Incomprehensible Sounds 2 None 1 Best Motor Obeys Commands 6 Localizes Pain 5 Withdraws to Pain 4 Flexion to Pain 3 Extension to Pain 2 None 1

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27 Severe TBI Indications for Intubation Indications for Intubation –GCS< 8 –Fall in GCS of 3 –Unequal pupils –Inadequate respiratory effort or significant lung/chest injury –Loss of gag –apnea

28 Treatment Intubation. Intubation. – Pretreatment with lidocaine 1 mg/kg IV may prevent rise in intracranial pressure (ICP).

29 Treatment Hyperventilation Hyperventilation – to maintain PO2 >90 torrs, PCO2 30 to 32 torrs. –Hyperventilation may actually increase ischemia in at risk brain tissue if PCO2 <25 torr by causing excessive vasoconstriction and has fallen out of favor. Prophylactic hyperventilation for those without increased ICP is contraindicated and worsens outcomes. PEEP relatively contraindicated because reduces cerebral blood flow. PEEP relatively contraindicated because reduces cerebral blood flow.

30 Maintain normal cardiac output. If hypotensive from other cause such as multi-trauma, treat shock as usual. If hypotensive from other cause such as multi-trauma, treat shock as usual. Normal saline is preferred over LR since LR is slightly hypotonic. Normal saline is preferred over LR since LR is slightly hypotonic. Hypertonic saline (3% or 7.5%) can be used. Especially if you see ICP changes. Hypertonic saline (3% or 7.5%) can be used. Especially if you see ICP changes.

31 Maintain normal cardiac output. If markedly hypertensive, consider labetalol or nitroprusside. If markedly hypertensive, consider labetalol or nitroprusside. Avoid lowering the blood pressure unless diastolic blood pressure is >120 mm Hg. Avoid lowering the blood pressure unless diastolic blood pressure is >120 mm Hg.

32 Diuresis Mannitol 1 g/kg IV over 20 minutes induces osmotic diuresis. Mannitol 1 g/kg IV over 20 minutes induces osmotic diuresis. –Avoid if hypotensive or have CHF/renal failure. Some suggest furosemide (Lasix and others). Some suggest furosemide (Lasix and others). –Avoid if hypotensive.

33 ICP Precautions Elevate head of bed 30 degrees. Elevate head of bed 30 degrees. Seizure prophylaxis: Phenytoin will reduce seizures in the first week after injury but does not change the overall outcome. Seizure prophylaxis: Phenytoin will reduce seizures in the first week after injury but does not change the overall outcome. Steroids are ineffective in controlling ICP in the trauma setting. Steroids are ineffective in controlling ICP in the trauma setting.

34 Positioning II

35 Manipulation of CPP Maintain adequate intravascular volume Maintain adequate intravascular volume –CVP Increase MAP Increase MAP –Utilize alpha agonist--dopamine, phenylephrine, norepinephrine What is appropriate goal for children? What is appropriate goal for children? CPP = MAP - ICP

36 CPP for children Aim for a CPP of >60 mmHg Aim for a CPP of >60 mmHg –by maintaining an adequate MAP and control of ICP MAP – ICP = CPP MAP – ICP = CPP –Minimizing the morbidity of TBI in children

37 Additional therapies Prevent hyperglycemia: exacerbates ischemic cerebral damage Prevent hyperglycemia: exacerbates ischemic cerebral damage Attention to electrolyte status. These patients are prone to electrolyte abnormalities due to osmotic diuresis, cerebral salt losing states, SIADH and diabetes insipidus Attention to electrolyte status. These patients are prone to electrolyte abnormalities due to osmotic diuresis, cerebral salt losing states, SIADH and diabetes insipidus

38 Manipulation of ICP Decrease cerebral metabolic demand Decrease cerebral metabolic demand –sedation, analgesia, barbiturates –avoid hyperthermia –avoid seizures Hyperventilation Hyperventilation –decreases blood flow to brain –only acutely for impending herniation Mannitol Mannitol Blood

39 Manipulation of ICP Mannitol Mannitol –dehydrate the brain, not the patient! –monitor osmolality Hypertonic saline Hypertonic saline Decompressive craniectomy Decompressive craniectomy Brain

40 ICP Monitoring ICU patients who have sustained head trauma, brain hemorrhage, brain surgery, or conditions in which the brain may swell might require intracranial pressure monitoring. ICU patients who have sustained head trauma, brain hemorrhage, brain surgery, or conditions in which the brain may swell might require intracranial pressure monitoring. The purpose of ICP monitoring is to continuously measure the pressure surrounding the brain. The purpose of ICP monitoring is to continuously measure the pressure surrounding the brain.

41 Why Monitor? Detect “events” Detect “events” Manage intracranial pressure Manage intracranial pressure Manage cerebral perfusion pressure Manage cerebral perfusion pressure

42 How? Ventriculostomy Ventriculostomy Intraparenchymal fiberoptic catheter Intraparenchymal fiberoptic catheter Subarachnoid monitor Subarachnoid monitor Useful adjuncts: Useful adjuncts: –Arterial line –Central venous line –Foley catheter

43 Manipulation of ICP External drainage External drainage –therapeutic as well as diagnostic –technical issues –infectious issues CSF

44 What to do with the information... Goal: adequate oxygen delivery to maintain the metabolic needs of the brain. Goal: adequate oxygen delivery to maintain the metabolic needs of the brain. Intracranial pressure <20 Intracranial pressure <20 Cerebral perfusion pressure >50-70 mm Hg CPP=MAP-ICP Cerebral perfusion pressure >50-70 mm Hg CPP=MAP-ICP

45 Indications for ICP monitoring Glasgow coma scale <8 Glasgow coma scale <8 Clinical or radiographic evidence of increased ICP Clinical or radiographic evidence of increased ICP Post-surgical removal of intracranial hematoma Post-surgical removal of intracranial hematoma Less severe brain injury in the setting which requires deep sedation or anesthesia Less severe brain injury in the setting which requires deep sedation or anesthesia

46 Other monitoring devices CT Scan CT Scan MRI MRI PET Scan PET Scan Jugular Venous Oxygen Saturation Jugular Venous Oxygen Saturation

47 Near-infrared Spectroscopy Uses absorption characteristics of oxy Hgb, deoxy Hgb, and [o] cyt aa3 Uses absorption characteristics of oxy Hgb, deoxy Hgb, and [o] cyt aa3 Uses the ability to penetrate the superficial brain Uses the ability to penetrate the superficial brain Therefore the state of oxygenation can be determined. Therefore the state of oxygenation can be determined. Good assessment of cerebral oxygenation Good assessment of cerebral oxygenation

48 Transcranial Doppler US TCD is a noninvasive technique used to determine cerebral blood velocity in large intracranial arteries. TCD is a noninvasive technique used to determine cerebral blood velocity in large intracranial arteries. Assessment of Assessment of –Brain death –Reperfusion injury –Identify regions S/P TBI that are adversely effected

49 Cerebral Microdialysis Measuring the partial pressure of oxygen of brain parenchyma and metabolites using microdialysis Measuring the partial pressure of oxygen of brain parenchyma and metabolites using microdialysis Electrode in vulnerable brain region measures O2 concentration Electrode in vulnerable brain region measures O2 concentration Measures also local brain metabolism Measures also local brain metabolism


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