PACT module. Traumatic Brain Injury. Intensive Care Training Program Radboud University Medical Centre Nijmegen

Transcription

1 PACT module Traumatic Brain Injury Intensive Care Training Program Radboud University Medical Centre Nijmegen

2 Severe traumatic brain injury Leading cause of morbidity/mortality among young individuals Mild (GCS 13-15), Moderate (GCS 9-12) or Severe (GCS 8) Focal (extra-axial hematomas - subdural/epidural, intraparenchymal hematomas and hemorrhagic contusions or diffuse (diffuse axonal injury)

3 Epidural hematoma Subdural hematoma Hemorrhagic contusion Diffuse axonal injury

4

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

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

8 Wijdicks EFM. Ann Neurol 2005;58:

9 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

10 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:

11 N = ICP group Clinical group P = 0.49 P = 0.60 P = M Primary composite outcome 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:

12 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:

13 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:

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

15 Brain tissue Space-occupying mass Tumor Abscess Hematoma Infarction Cerebral edema Vasogenic Cytotoxic Skull CSF CSF CSF outflow obstruction Noncommunicating HC Decreased CSF absorption Venous outflow obstruction CSF overproduction Choroid plexus papilloma Blood Hyperemia Impaired autoregulation Hypercarbia Cerebral metabolism Brain parenchyma Blood

16

17

18 Stabiel lage ICP Stabiel hoge ICP B golven tot 20 mmhg boven basis iedere 30 sec - 2 min verandering vaattonus tegelijk Fv ACM A - plateau golven stijle toename > 40 duur 5-20 min altijd pathologisch intacte autoregulatie compliance Hoge ICP pieken door acute RR toename Toename ICO door lange RR afname Hyperaemische ICP Refractaire IC HT

19

20 Consequences Herniation syndromes Subfalcine (= cingulate) Small reactive pupils Contralateral leg weakness Transtentorial descending bilateral (= central) Transtentorial descending unilateral (= uncal) Medium-sized fixed pupils Cheyne-Stokes respiration Decorticate posturing Coma precedes pupil changes Diabetes insipidus Mass Ipsilateral pupil dilation Hemiparesis (contra- or ipsilateral) Decerebrate posturing Varying levels impaired arousal Transtentorial ascending Nausea, vomiting hiccups Dysconjugate gaze/ophtalmoplegia Progressive stupor Sudden respiratory arrest Mass Tonsillar Hypertension, bradycardia Bradypnea Coma Respiratory arrest

21 In general... Measured ICP may be normal with a focal mass effect Expanding mass compresses and damages surrounding tissue or major cerebral arteries Global mass effect (edema) usually without lateral or vertical structural shift

22 19 patients with large hemispheric infarction and edema Frank JI. Neurology 1995;45:

23 Brain tissue Space-occupying mass Tumor Abscess Hematoma Infarction Cerebral edema Vasogenic Cytotoxic Skull CSF CSF CSF outflow obstruction Noncommunicating HC Decreased CSF absorption Venous outflow obstruction CSF overproduction Choroid plexus papilloma Blood Hyperemia Impaired autoregulation Hypercarbia Cerebral metabolism Brain parenchyma Blood

24 Treatment options Remove extra space occupying mass Surgery, osmotic therapy Decrease cerebral blood volume Sedation, hyperventilation, hypothermia, hemoglobin, head elevation Decrease amount of CSF Ventricular drainage Remove part of skull / dura

25 Lund concept Maintain normal colloid osmotic pressure (normal sodium and normal albumin) Reduce hydrostatic capillary pressure (CPP as low as 50 mmhg with metoprolol and clonidine) Normoventilation Epoprostonol to improve microcirculation and reduce capillary permeability If ICP > 20 than thiopental - CSF drainage - dihydroergotamine - decompression

26

27 CT shift and symptoms

28 Pressure autoregulation

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

30 Bhatia A. Intensive Care Med 2007;33:

31 PRx

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

33 Non-convulsive seizures Up to 40% of patients with severe TBI Worsening secondary brain injury

34 Biomarkers

35 General treatment Normothermia (?) for 5-7 days Seizures treatment (and prevention? - 50% after penetrating brain injury) - levetiracetam Treat obvious coagulopathy Glycemic control (8-10 mmol/l) without hypoglycemia Early enteral nutrition based on indirect calorimetry Treat endocrine derangements

36 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

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

38