TBI talk Uganda

EVIDENCE BASED MANAGEMENT OF TRAUMATIC BRAIN INJURY IN CHILDREN:

EVIDENCE BASED MANAGEMENT OF TRAUMATIC BRAIN INJURY IN CHILDREN Craig D. McClain, MD, MPH Children’s Hospital, Boston

BASICS:

Lam HW, et al. Pediatric Anesthesia 1999; 9:377-85. BASICS Worldwide - trauma is most common reason for hospital admission in children 75% of all children admitted to hospitals with trauma have an associated head injury 70% of deaths from trauma as a result of head injury

EPIDEMIOLOGY:

Berney et al. CHILD'S NERVOUS SYST 1994; 10:509. EPIDEMIOLOGY Per Year in the US (children) 500,000 ER visits 95,000 Hospital admissions 7,000 deaths 29,000 permanent disabilities > $1 billion in hospital costs

HOW THEY DIE:

Lam HW, et al. Pediatric Anesthesia 1999, 9:377-85. HOW THEY DIE Approx 50% within minutes of impact from an overwhelming injury incompatible with life 20% die within hours due to respiratory failure, increased ICP or circulatory collapse 30% die in days to weeks secondary to infection and organ failure

PRIMARY AND SECONDARY INJURY:

PRIMARY AND SECONDARY INJURY Primary direct mechanical injury disruption of vascular or neuronal elements initiation of cytotoxic cascades

PRIMARY AND SECONDARY INJURY:

PRIMARY AND SECONDARY INJURY Secondary Systemic: hypoxia (Pa O2 < 60), hypotension (SBP< 90), hyperthermia, hypoglycemia, anemia, SIRS Cerebral: edema, vasospasm, seizures, infection, ischemia Cellular: excitotoxicity, membrane transport failure, fluid shifts, free-radical oxidation injury, apoptosis

CONTROL OF ICP:

CONTROL OF ICP

INTRACRANIAL PRESSURE:

INTRACRANIAL PRESSURE Infant = 1.5-5.9 mm Hg Children = 3-7.4 mm Hg

ICP:

ICP The effect of elevated ICP appears to be related to both the absolute peak as well as the duration of elevation All current recommendations based on Class III data

ICP:

ICP 2 retrospective reviews in early 80s by Pfenninger et al. and Esparza et al. Found outcome better if ICP kept <20 Poor outcome if ICP allowed to stay 20-40 and ICP>40 assoc. with death Suggests that ICP<20 a reasonable treatment goal in patients with TBI from a variety of etiologies (MVA, fall, abuse)

ICP:

Sharples et al. J NEUROL NEUROSURG PSYCH 1995; 58:145-52. ICP Sharples et al. looked prospectively at 21 pediatric patients with severe TBI (GCS <8 on presentation) Showed an inverse relationship between elevations in ICP>20 for >10minutes and CBF 66 measurements of CBF/ICP found mean CBF of 57 ml/100g/min when ICP<20 56 measurements of CBF/ICP showed mean CBF of 47 ml/100g/min when ICP>20

ICP:

Shapiro et al. J NEUROSURGERY 1982; 56:819-25. ICP Shapiro et al. Performed a prospective nonrandom case series of 22 pediatric patients with TBI Looked at ICP and measured cerebral compliance with a pressure-volume index Intracranial hypertension defined as ICP>20 for >10 minutes OR plateau waves or spikes >30 with noxious stimulation

ICP:

Shapiro et al. J NEUROSURGERY 1982; 56:819-25. ICP Shapiro et al. found that ICP>20 was inversely correlated with the PVI suggesting impaired cerebral compliance

SURVIVAL and ICP:

Michaud IJ, et al. NEUROSURGERY 31:254-64 SURVIVAL and ICP

ICP: TREATMENT RECOMMENDATIONS:

ICP: TREATMENT RECOMMENDATIONS Current pediatric data support defining intracranial hypertension in patients with TBI as ICP>20 The data suggest treatment of ICP to maintain <20

ICP: TREATMENT RECOMMENDATIONS:

ICP: TREATMENT RECOMMENDATIONS Intracranial hypertension in TBI patients results in increased morbidity and mortality No prospective, randomized clinical trials that look at ICP thresholds and outcome (No Class I or II studies)

HYPERVENTILATION IN TBI:

HYPERVENTILATION IN TBI

HYPERVENTILATION:

Bruce et al. CHILD'S BRAIN 1979; 5:174-91. HYPERVENTILATION Aggressive hyperventilation has been used in treatment of TBI in children since the mid 1970s Bruce et al. (in 1979) showed good outcomes with a protocol that included aggressive hyperventilation (uncontrolled study)

HYPERVENTILATION:

HYPERVENTILATION Historic thinking Hyperemia is the cause of elevated ICP Decreased PaCO2 leads to decreased ICP CBF is normally elevated in children with head injuries

HYPERVENTILATION:

HYPERVENTILATION Hyperventilation leads to vasoconstriction and a consequent reduction in CBV and CBF and a decrease in ICP Several recent studies indicate that routine hyperventialtion, even mild, may decrease cerebral oxygenation and lead to brain ischemia

HYPERVENTILATION:

Bruce et al. CHILD'S BRAIN 1979; 5:174-91. HYPERVENTILATION Bruce et al. looked at 76 children with severe TBI and found that 36 had diffuse cerebral swelling on CT The thinking was that the cerebral swelling was due to hyperemia and therefore aggressive hyperventialtion (PaCO2 23-25 mm Hg) was recommended

HYPERVENTILATION:

Sharples et al. J NEUROL NEUROSUR PSYCH 1995; 58:145-52. HYPERVENTILATION Sharples et al. looked at 151 CBF measurements in 21 children with severe TBI (kept normocapnic unless evidence of acute herniation) Only 7% of the measurements were above normal for age Showed that absolute cerebral hyperemia was uncommon

HYPERVENTILATION:

Sharples et al. J NEUROL NEUROSUR PSYCH 1995; 58:145-52. HYPERVENTILATION Sharples found that elevated ICP was associated with decreased CBF rather than increased CBF as was previously thought Thus, this study concluded that elevated ICP was not the result of excessive CBF in children with TBI

HYPERVENTILATION:

Skippen et al. CRIT CARE MEDICINE 1997; 25:1402-09. HYPERVENTILATION Skippen et al. looked prospectively at 23 children with severe TBI, GCS<8, and looked at CBF in relation to varying levels of PaCO2 Found that absolute CBF and cerebral O2 consumption both decreased below normal after TBI

HYPERVENTILATION:

Skippen et al. CRIT CARE MEDICINE 1997; 25: 1402-09. HYPERVENTILATION Skippen further demonstrated that 28.9% of the subjects had one or more regions of cerebral ischemia (defined as CBF <18ml/100g/min) during normocapnia This increased to 73.1% with PaCO2<25 mm Hg

HYPERVENTILATION:

Coles et al. CRIT CARE MEDICINE 2002; 30:1950-59. HYPERVENTILATION Coles et al. looked at the effect of hyperventilation on the volumes of hyper and hypoperfused tissues in healthy volunteers and patients with closed head injuries

HYPERVENTILATION IN TBI:

Coles JP, et al. CRIT CARE MEDICINE 2002; 30:1950-59. HYPERVENTILATION IN TBI

HYPERVENTILATION Summary:

HYPERVENTILATION Summary Hyperemia may not be as common in children with severe TBI as originally thought Hyperventilation (even mild) can reduce CBF to ischemic levels in injured as well as normal tissue

HYPERVENTILATION Summary:

HYPERVENTILATION Summary Hyperventilation is clearly effective for reducing ICP - should probably be reserved for impending herniation and not routinely used in TBI management No studies comparing hyperventilation to other forms of ICP management (barbituate coma, etc.) No studies defining the precise relationship between hyperventilation and outcome

OSMOTIC THERAPY:

OSMOTIC THERAPY Traditional teaching of TBI management dictates use of mannitol for suspected or documented elevated ICP

MANNITOL:

MANNITOL How does mannitol work? Osmotic diuretic - develops slowly over 15-30 minutes; movement of water from parenchyma to systemic intravascular space; this effect persists up to 6 hours Excreted unchanged in the urine Free radical scavenger

MANNITOL:

MANNITOL Also has an immediate effect of reducing blood viscosity resulting in decreased blood vessel diameter; CBF is maintained while CBV and consequently ICP are decreased Effect lasts approx 75 minutes Effective dose of 0.25 to 1 g/kg body weight

OSMOTIC THERAPY: MANNITOL:

James HE. ACTA NEUROCHIR 1980; 51:161-72. OSMOTIC THERAPY: MANNITOL James looked retrospectively at 60 patients (aged 1-73 yrs) treated with mannitol (0.18-2.5 g/kg/dose) for ICP>25 Found that ICP decreased >10% after 116 of 120 doses and bolus doses of >0.5g/kg produced a reduction in ICP 97% of the time

OSMOTIC THERAPY: MANNITOL:

McManus and Soriano ANESTHESIOLOGY 1998; 88:1586-91. OSMOTIC THERAPY: MANNITOL McManus and Soriano looked at astroglial cells in culture exposed to mannitol and found initial cellular shrinkage followed by rebound swelling Hypertonic saline does not exhibit a similar phenomenon The rebound swelling can be attenuated with furosemide

HYPERTONIC SALINE:

HYPERTONIC SALINE Hypertonic saline is a very old agent (first described in 1919) that has seen a renewed clinical interest

HYPERTONIC SALINE:

Worthley LI, et al. J NEUROSURG 1988; 68:478-81. HYPERTONIC SALINE Worthley et al. reported two cases of refractory intracranial hypertension successfully treated with small volumes of 29% saline

HYPERTONIC SALINE:

Khanna S, et al. CRIT CARE MED 2000; 28:1144-1151. HYPERTONIC SALINE Khanna et al. looked at the prospective administration of 3% saline with a treatment goal of keeping ICP<20 (in ten children) Found significant reduction in ICP spikes as well as an increase in CPP (mean peaks for serum Na and Osm were 170.7 meq/L and 364.8 mOsm/L) Reversible renal failure occurred in 2 patients Hypernatremia and hyperosmolarity were tolerated well

OSMOTIC THERAPY:

Fisher B, et al. J NEUROSURG ANES 1992; 4:4-10. OSMOTIC THERAPY Fisher et al., in a double-blind crossover study, compared mannitol to 3% saline in 18 children with TBI Over the 2 hour trial, 3% saline found to be superior to mannitol in reducing ICP and also displayed a reduction in necessity for additional measures to control ICP (serum Na increased approx 7 meq/L)

MANNITOL VS. HYPERTONIC SALINE:

MANNITOL VS. HYPERTONIC SALINE Mannitol Limited clinical evidence in children (two class III) studies Long standing acceptance and safety record In adults the data are more supportive - two class I and one class II

MANNITOL VS. HYPERTONIC SALINE:

MANNITOL VS. HYPERTONIC SALINE Hypertonic Saline Limited clinical experience Better record in clinical trials (three class II and one class III study for reduction of intracranial hypertension)

OSMOTIC THERAPY:

OSMOTIC THERAPY In summary - there is class II and III evidence to support the use of both mannitol and hypertonic saline to control ICP in children with TBI Bolus mannitol or continuous infusion of 3% saline is supported Physician preference should dictate which therapy is utilized

ROLE OF SURGICAL MANAGEMENT IN TBI:

ROLE OF SURGICAL MANAGEMENT IN TBI

DECOMPRESSIVE CRANIECTOMY:

DECOMPRESSIVE CRANIECTOMY Objective of the surgery is to control intractable intracranial hypertension in order to maintain cerebral blood flow and perfusion pressure Second tier therapy for intractable intracranial hypertension

DECOMPRESSIVE BIFRONTAL CRANIECTOMY:

Polin et al. NEUROSURGERY 1997; 41:84-94. DECOMPRESSIVE BIFRONTAL CRANIECTOMY Comparison of medical mgmt. to surgery matched for age, sex, maximum preoperative ICP and preoperative GCS. 35 Bifrontal craniectomies, 92 controls

PREDICTORS OF GOOD OUTCOME WITH CRANIECTOMY:

Polin et al. NEUROSURG 1997; 41:84-94. PREDICTORS OF GOOD OUTCOME WITH CRANIECTOMY ICP < 40 preop Operation within 48hr of presentation Patients meeting both of these criteria were far more likely to have a favorable outcome Younger patients do better than older ones.

DECOMPRESSIVE CRANIECTOMY:

Cho et al. PEDIATRIC NEUROSUR 1995; 23:192-8. DECOMPRESSIVE CRANIECTOMY Cho et al. reported outcomes in 23 children <2 yrs old with severe TBI from abuse Prospective, case controlled study looking at Child Outcome Scores in 10 patients with ICP>30 medically managed plus decompressive craniectomy vs. 13 patients with elevated ICP (>20) treated with medical therapy alone

DECOMPRESSIVE CRANIECTOMY:

Cho et al. PEDIATRIC NEUROSUR 1995; 23:192-8. DECOMPRESSIVE CRANIECTOMY Subjects with severe intracranial hypertension (ICP>30) that underwent medical and surgical intervention had improved survival and neurologic outcomes compared to those who received medical therapy alone

DECOMPRESSIVE CRANIECTOMY:

Taylor et al. CHILD'S NERVOUS SYST 2001; 17: 154-62. DECOMPRESSIVE CRANIECTOMY Taylor et al. prospectively randomized 27 children with severe TBI and intracranial hypertension to medical management plus bitemporal decompressive craniectomy or medical management alone

DECOMPRESSIVE CRANIECTOMY:

Taylor et al. CHILD'S NERVOUS SYST 2001; 17:154-62. DECOMPRESSIVE CRANIECTOMY Patients who were in the surgery arm showed a trend at 6 months follow up toward a better clinical outcome (using the modified Glasgow Outcome Scale) 2/14 children in the control group vs 7/13 in the surgery group were “normal” or had mild disability

DECOMPRESSIVE CRANIECTOMY:

DECOMPRESSIVE CRANIECTOMY In the past, small craniectomies have been used with some poor outcomes (from inadequate relief of intracranial hypertension, cerebral incarceration Most centers now will perform larger craniectomies, most often either a bifrontal or two separate bilateral procedures There are no studies looking at the efficacy of the various techniques that are currently in practice

DECOMPRESSIVE CRANIECTOMY:

DECOMPRESSIVE CRANIECTOMY Who is a candidate? Cerebral swelling on CT Within 48 hours of injury No sustained ICP>40 prior to surgery GCS>3 at some point subsequent to injury Secondary clinical deterioration

DECOMPRESSIVE CRANIECTOMY:

DECOMPRESSIVE CRANIECTOMY The available evidence supports the contention that decompressive craniectomy lowers refractory elevated ICP in children and MAY improve outcome in selected patients.

SUMMARY RECOMMENDATIONS:

SUMMARY RECOMMENDATIONS ICP should be kept <20 mm Hg Administration of mannitol or hypertonic saline can be useful in the management of intracranial hypertension

SUMMARY RECOMMENDATIONS:

SUMMARY RECOMMENDATIONS Routine hyperventilation should be avoided, rather, hyperventilation should be reserved for impending herniation Decompressive craniectomy should be considered as an option for intracranial hypertension refractory to aggressive medical management (if the patient meets criteria outlined)