PATHOPHYSIOLOGY OF ACUTE TRAUMATIC BRAIN INJURY. Dr Nick Taylor MBBS FACEM

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1 PATHOPHYSIOLOGY OF ACUTE TRAUMATIC BRAIN INJURY Dr Nick Taylor MBBS FACEM

2

3 The Monro Kellie Doctrine

4 CPP= MAP-ICP

5

6

7 PRIMARY DAMAGE TBI is a heterogeneous disorder Brain damage results from external forces, as a consequence of direct impact, rapid acceleration or deceleration, penetration or blast waves The nature, intensity, direction, and duration of these forces determine the pattern and extent of damage.

8 MACROSCOPIC DAMAGE On the macroscopic level, damage includes shearing of white-matter tracts, focal contusions, haematomas and diffuse swelling

9 DAI DAI is characterised by multiple small lesions in white-matter tracts. Patients with DAI are usually in profound coma as a result of the injury, do not manifest high ICP, and often have a poor outcome.

10 BLEEDING Focal cerebral contusions are the most common traumatic lesion, are more frequent in older patients, and usually arise from contact impact. Traumatic intracranial haematomas occur in 25 35% of patients with severe TBI and in 5 10% of moderate injuries

11 CELLULAR LEVEL Early neurotrauma events include microporation of membranes, leaky ion channels, and stearic conformational changes in proteins. At higher shear rates, blood vessels can be torn, causing (micro)haemorrhages.

12 ISCHAEMIA Ischaemic brain damage is often superimposed on the primary damage and can be widespread or, more commonly, perilesional. Impaired cerebral perfusion and oxygenation, excitotoxic injury, and focal microvascular occlusion can be contributing factors.

13 ISCHAEMIA Although the total ischaemic brain volume may be less than 10% on average, the presence of cerebral ischaemia is associated with poor ultimate neurological outcome, that is, dead or vegetative state

14

15 SECONDARY INJURY Each type of head injury initiates different pathophysiological mechanisms, with variable extent and duration Secondary processes develop over hours and days, and include neurotransmitter release, freeradical generation, calcium-mediated damage, gene activation, mitochondrial dysfunction, and inflammatory responses.

16 EARLY SECONDARY INJURY The first stages of cerebral injury after TBI are characterized by direct tissue damage and impaired regulation of CBF and metabolism. This ischaemia-like pattern leads to accumulation of lactic acid due to anaerobic glycolysis, increased membrane permeability, and consecutive oedema formation. Since the anaerobic metabolism is inadequate to maintain cellular energy states, the ATP-stores deplete and failure of energy-dependent membrane ion pumps occurs.

17 LATER INJURY Glutamate and other excitatory neurotransmitters exacerbate ionchannel leakage, worsen astrocytic swelling, and contribute to brain swelling and raised ICP. Neurotransmitter release continues for many days, paralleling the course of high ICP, and, with free-radical and calcium-mediated damage, is a major cause of early necrotic cell death

18

19 INFLAMMATION: 2 EDGED SWORD Inflammatory response is an important component of TBI, particularly around contusions and (micro) haemorrhages. The maximum response occurs within a few days, but cytokines are released within hours after TBI, leading to opening of the BBB, activation of cell death and apoptosis. Although the inflammatory response can be deleterious in excess, it is necessary in order to clean up cellular debris after injury

20 MITOCHONDRIA Recent research has raised new insights that challenge existing concepts of pathophysiology. Mitochondrial dysfunction can cause energy failure after TBI, with a decrease in production of ATP and consumption of oxygen by 40 50%. This can trigger apoptosis and necrosis.

21 MITOCHONDRIA Mitochondrial dysfunction might also lead to axonal disruption. The classical concept that DAI is due to mechanical rupture of axons, incompatible with regeneration or repair, has now been abandoned. Neurons can at least partially regenerate their axonal anatomy. This accords with clinical observations Lab work has shown that DAI can take up to 48 hours to become fully established and is thus amenable to therapeutic interventions.

22 CEREBRAL BLOOD FLOW Whether decreased cerebral blood flow (CBF) after trauma is indicative of ischaemia or is secondary to metabolic depression remains the subject of debate. Cerebral hemodynamics change significantly post injury,and the pattern of these changes depends upon the type of injury and its severity

23 CBF The critical threshold of CBF for the development of irreversible tissue damage is 15 ml 100 g 1 min 1 in patients with TBI compared with ml 100 g 1 min 1 in patients with ischaemic stroke. This is likely because of the other brain damage occurring in TBI vs CVA

24 CBF Patients with TBI may develop cerebral hyperperfusion (CBF >55 ml 100 g 1 min 1) in the early stages of injury. Likewise, hyperaemia may follow immediate posttraumatic ischaemia. This pathology seems as detrimental as ischaemia because increases in CBF beyond matching metabolic demand relate to vasoparalysis leading to increases in cerebral blood volume and in turn intracranial pressure (ICP).

25 CBF AUTOREGULATION After TBI, CBF autoregulation is impaired or abolished in most patients. Defective CBF autoregulation may be present immediately after trauma or may develop over time, and is transient or persistent in nature irrespective of the presence of mild, moderate, or severe damage. Also, autoregulatory vasoconstriction seems to be more resistant compared with autoregulatory vasodilation which indicates that patients are more sensitive to damage from low rather than high CPPs

26

27

28 CO2 RESPONSIVENESS Compared with CBF autoregulation, cerebrovascular CO2-reactivity seems to be a more robust phenomenon. In patients with severe brain injury and poor outcome, CO2-reactivity is impaired in the early stages after trauma. In contrast, CO2-reactivity was intact or even enhanced in most other patients offering this physiological principle as a target for ICP management in hyperaemic state

29 PRINCIPLES OF MX Trauma renders the brain more vulnerable to insults, and hypoxia and hypotension are strongly associated with poor outcome (hypoxia: odds ratio [OR] 2 1, 95% CI ; hypotension: OR 2 7, 95% CI Treat the patient (but consider the impact this will have on their brain)

30 PRINCIPLES Protect the brain from secondary injury Maintain CPP (by maintaining MAP and reducing ICP) Maintain oxygenation Prevent complications Arrange timely interventions

31

32 HOW DO WE SAFELY INTUBATE Protect the C-spine Avoid hypotension IVF load first Judicious induction drug doses based on patient characteristics Eg Propofol/Thio low dose (0.5-1mg/kg) Fentanyl 3-5 mcg/kg Ketamine (Theoretical raised ICP vs absolute risk hypotension) Combinations Have metaraminol drawn up and ready

33 HOW DO WE SAFELY INTUBATE Avoid hypertensive spikes Avoid prolonged, multiple attempts (experience) Consider fentanyl Paralyse for transport Avoid hypoxaemia Pre O2 Maximise your first attempt success Have a back up plan and rapidly use it

34 WHAT ELSE SHOULD WE DO

35 TREATING RAISED ICP Reduce the CMR Drain the extra blood Reduce brain water Crack the box Assist venous outflow Control arterial inflow

36 DRAIN THE BLOOD, CRACK THE BOX Urgent CT scan is used to stratify patients who need emergency neurosurgery Surgically drainable blood is a priority for OT Decompressive craniectomy is controversial, (DECRA inconclusive) but used with high ICP and no drainable blood

37 CONTROL THE INFLOW Keep MAP >80 (ideally with ICP monitor in, keep CPP>60) Avoid SBP <90 Keep PaCO2 low normal CO2 is a cerebral vasodilator Reducing CO2 below normal ranges causes vasoconstriction and worsens secondary ischaemia Can acutely hyperventilate to a lower number if herniation suspected

38 ASSIST VENOUS OUTFLOW Head up 30 degrees (incline whole bed) Avoid tight hard collars Avoid tight tube ties

39 REDUCE BRAIN WATER Avoid free water: N/Saline only (NOT dextrose, NOT albumin) Osmotherapy agents Mannitol: Exact mechanism unknown; multiple studies showing efficacy Rebound phenomena exist Hypotension may be worsened Eg 0.5-1g/kg Hypertonic Saline: Mobilises water across intact BBB via osmotic effect; may increase local blood flow, may have anti inflammatory effect Good theory, used widely, solid evidence lacking Eg 100mL 3% saline, esp if hypotension

40 REDUCE THE CMR Hypothermia Evidence for prophylactic hypothermia has failed to find a mortality benefit despite early promise but may increase infection. The jury is still out Barbituate coma Recommended for refractory ICP Mx in ICU Assoc with signif increased VAP and K+ morbidity

41 OTHER STUFF Steroids Unsurprisingly the CRASH study showed patients did worse Glutamate / Lipids/ anti free radicals Maybe Mg2+ the magic elixir No Antifibrinolytic drugs Need more info

42 THANKYOU

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