Severe traumatic brain injury. Fellowship Training Intensive Care Radboud University Nijmegen Medical Centre

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1 Severe traumatic brain injury Fellowship Training Intensive Care Radboud University Nijmegen Medical Centre

2 Primary focus of care Prevent ischemia, hypoxia and hypoglycemia Nutrient & oxygen supply Limited capacity for substrate storage High metabolic rate

3 Surrogates for brain ischemia and hypoxia GCS or FOUR score ICP Cerebral blood flow PbtO 2 Cerebral metabolism (microdialysis) EEG Biomarkers

4 Focal (subdural- and epidural hematoma, contusion) Diffuse (DAI) Combination Primary injury Catecholamine surge Systemic effects Depolarization and disturbance of ionic homeostasis Neurotransmitter release Apoptosis Lipid degradation Mitochondrial dysfunction Inflammatory and immune responses Dysautoregulation of brain vessels BBB disruption Organ dysfunction Hypoxia Hyperoxia Hypocapnia Hypercapnia Hyperthermia Hypotension ICP increase CPP decrease with ischemia Secondary injury

5 Primary Injury Secondary Injury Contusions Haematomas Diffuse injury ICP Ischaemia Receptor mediated Calcium damage mediated Inflammation damage Oxidative damage Secondary insults Hypoxia, Hyper- & Hypocapnia, Hypotension, Hyperthermia, Hyper- & hypoglycemia

6 Epidural hematoma Subdural hematoma Hemorrhagic contusion Diffuse axonal injury

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8 Cerebral edema Minutes Immediately thereafter Hours Primary injury Cytotoxic edema Ionic edema Vasogenic edema = Cellular swelling = Extracellular swelling with intact BBB = Extracellular swelling with damaged BBB

9 Fluid compartments Brain Vasculature 100 ml CSF 100 ml Brain interstitial space 100 ml Intracellulair space 1.1 L Brain edema is an increase in the brain interstitial space Cerebral edema requires perfusion

10 ICP ICP > 20 mmhg is considered ICH - worse outcome Classic indications: GCS 3-8 with abnormal CT-scan GCS 3-8 with normal CT-scan and at least 2 of the following: age 40, unilateral or bilateral motor posturing, SBP < 90 mmhg

11 ICP monitoring Multicenter (N = 6) stratified RCT comparing ICT monitoring clinical examination/imaging Patients with TBI, aged > 13 and with a GCS 8 within 48 hours All patients had CT scan at 0 and 48 hrs and at 5-7 days Chesnut RM. N Engl J Med 2012;367:

12 N = ICP group Clinical group P = 0.49 P = 0.60 P = M Primary composite outcome 6 M Mortality (%) 6 M Favourable outcome (%) Pressure monitoring group received more barbiturates while clinical group received more hyperventilation and hypertonic saline Chesnut RM. N Engl J Med 2012;367:

13 Pressure and time burden of raised ICP Lower pressures with a longer duration also correlate with a bad outcome 6-M GOS) (red) In children lower pressure for a shorter amount of time have the same damage Güiza F. Intensive Care Med 2015;41:

14 Pressure and time burden of raised ICP Curve is shifted to the left if autoregulation (PRx) is absent (blue all patients, green normal autoregulation, red absent autoregulation) Güiza F. Intensive Care Med 2015;41:

15 Pressure and time burden of raised ICP CPP 50 mmhg CPP > 50 mmhg Güiza F. Intensive Care Med 2015;41:

16 Severe TBI For patients with age 65 the safe CPP zone is between CPP mmhg when autoregulation is active Deficient autoregulation reduces the tolerability for low CPP Episodes with ICP > 25 were associated with a worse outcome independent of CPP Güiza F. J Neurotrauma 2017

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18 RescueICP trial Decompressive craniectomy for refractory ICP Hutchinson PJ. N Engl J Med 2016

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20 Electrophysiological changes Cortical spreading depolarizations and nonconvullive seizures / periodic discharges Definite link between these electrophysiological changes and metabolic crises: L/P Microdialysis Tau levels correlate with MRI (DTI)- based measurements of reduced brain white matter integrity (sign of diffuse axonal injury)

21 Autoregulation - old and new Old New Slope 0.21 Slope 0.81 Buffering capacity against hypertension is certainly better

22 Bhatia A. Intensive Care Med 2007;33:

23 PRx

24 CPPOPT and PbrO2 CPPOPT range between and mm Hg Jaeger M. Crit Care Med 2010;38:

25 Global and regional CBF are nicely correlated Severe TBI, N = Regional CBF Regional (around triple-lumen bold) compared to 2 other regions of interest (supraventricular white matter supplied by ACM and ACA) Global CBF Bouzat P. Crit Care Med 2015;43:

26 Prediction of low CBF by multimodal monitoring < 35 ml/100g/min ROC variable AUC 95% CI ICP ICP + CMD ICP + PbtO ICP + PbtO2 + CMD Bouzat P. Crit Care Med 2015;43:

27 Paroxysmal sympathetic hyperactivity Fever Hypertension Tachycardia Tachypnea Diaphoresis Dystonic posturing Incidence: 15-33% in severe TBI From 24 hrs to weeks after TBI Differential diagnosis Sepsis Seizures Hydrocephalus / intracranial hypertension Agitation, pain, central fever, withdrawal

28 Pathophysiology Excitatory-Inhibitory model Inhibitory centers brainstem diencephalon Afferent stimuli Sympathetic output +++

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30 Cardiac effects of severe TBI Overall 20% of als severe TBI patients show early systolic dysfunction within first week (risk factors lower age and lower admission GCS) Krishnamoorthy V. Crit Care Med 2017

31 Hyponatremia CSW SIADH BNP Inhibits: sympathetic outflow RAAS vasoconstrictor peptides Normal renal function No volume expansion Normal adrenal function Inappropriate sodium loss High Una, high urine output, hypotension, low CVP Correction of volume depletion Hypertonic saline Fludrocortisone ADH Inappropriate water retention Lower Una, lower urine output, normotension, normal CVP Fluid restriction

32 Acute spinal cord trauma Combination of fractured and retropulsed bone fragments, disk herniation and subluxation of vertebral bodies (sometimes spinal epidural hematoma) Overall 20% affect more than 1 level Cervical spine especially vulnerable

33 Symptoms Relatively symmetric paralysis of the limbs Urinary retention or incontinence Localized pain and sensory level In acute phase hyperreflexia and Babinski often absent Systemic hypotension

34 Classification - prognosis

35 Central cord syndrome (Typically cervical spine from trauma) Weakness and reflex loss in arms (less in legs) Reduced pain and thermal sense in arms often with hyperesthesia (vibration and proprioception often normal) Variable hyperreflexia in legs

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38 Treatment No corticosteroids Immediate treatment of hypotension with fluid and NE to maintain a MAP of mmhg (1 week) Surgical decompression and stabilization within 24 hrs (complications: infection, hardware failure, pseudoarthrosis, degenerative changes at adjacent spinal levels)