Raised ICP in Traumatic Brain Injury

Raised ICP in Traumatic Brain Injury Mortality from Head Injury Over Four Decades in Scotland • 1974-2012 • Decreased from 503 annually to 339 • Decreased from 9.6 to 6.4 per 100,000 population • 100,000 A&E attendances a year 15% require admission • 4% of those GCS 3-8 Causes of Head Injury Monro-Kellie Hypothesis To keep the intracranial pressure within normal limits, any change in volume of one of the intracranial contents must be accompanied by a change in one or two of the other components. The ability of the brain to adjust to changes in volume is called COMPLIANCE. Normal ICP 7-15mmHg in the horizontal position Cerebral Perfusion Pressure • This is the CPP is Mean arterial pressure - ICP • Normal CPP is 80 to 100 mmHg in most adults • Cerebral blood flow is maintained by autoregulation Cerebral Perfusion Pressure • Outside 60 to 150 mmHg autoregulation has failed • Below 60 mmHg cerebral ischaemia will occur • Below 30-40 mmHg cell death will occur Items beginning with C that raise ICP • Clot • Contusion • Cells (tumour, abscess) • CSF • Cytotoxic Oedema • Cerebral Oedema • Cerebral vasospasm • Clonic Activity • Care Case Study • 19 year old boy fell off his friends’ shoulders. • His friend was driving a quad bike in a quarry at the time • Patient was GCS 9 at the scene • GCS 14 in A/E • Then deteriorated to <8 Avoidance of Secondary Brain Injury • The brain needs blood flow, oxygen and nutrients to survive. There are key things beginning with H that make ICP worse following trauma: • Hypoxaemia • Hypotension • Hypoglycaemia • Hypercapnia • Hypocapnia • Haemoglobin • Hyperthermia?? Tier 1 treatment Intubation and Ventilation • Advantages – – – – – – Secure and protect the airway Avenue for suction Maintain ABGs through ventilation Deliver high FiO2 End TIDAL CO2 monitoring Allows paralysis • Disadvantages – – – – Coughing against tube VAP Requires Sedation Hypotension during procedure Tier 1 treatment Ventilation • Secure airway • Avoid hypoxia aim for PaO2 ≥ 13kPa • Avoid hypoxia aim for SpO2 95% • Maintain PaCO2 at 4.5-5.0kPa (34-38mmHg) • Use end tidal CO2 monitoring • Use with high respiratory rate and moderate breaths as an emergency treatment in the setting of a fixed and dilated pupil Tier 1 treatment Sedation and Pain Relief • Sedation will reduce cerebral metabolic requirement and will reduce blood flow Propofol (fast/short) Midazolam (long term) Alfentanil (opiate) • Sedation will prevent coughing and gagging against the ET tube • Sedation might prevent seizures • Allows procedures to be carried out • Beware hypotension as this will reduce CPP !! NMB’s /Muscle relaxants reserved for; Transport of patients Unstable ICP Tier 1 treatment Basic care • Head and Neck in alignment with a straight torso • Avoid excessive flexion at the hips • Maintain head up at 30o but some patients like a higher position 45o • Use of bed tilt • Tape the ET tube. Do not use ties • Regular oral care. Did Nigel have a good B/P • Initially the MAP was over 90mmHg • Edinburgh would aim for this figure • The BTF say > 100mmHg for 50-69 years • > 110mmHg systolic 15-49hyrs • Hb always above 90g/l • Platelets never <75x109 Nigel’s ICP going • Up to 30mmHg • Tier 2 therapy • However a good CPP was always maintained by the use of fluid and noradrenaline. • The noradrenaline dose was the equivalent of 24mg% running at 10-15mls per hour on some occasions. Tier 2 treatment Mannitol • Guidelines suggest 0.25-1gm per kg bolus • Edinburgh use 200mls of 20% • 0.5gm per kg for 80kg patient • With 250mls of Plasmalyte 148 Mannitol • Meaningful entries in the literature appear around 1961 • Transient hypervolaemia • Transient haemodilution • Dehydrates brain tissue • Administer over 15minutes-30minutes • Effects may last 3-6hours • Beware fluid overload and rebound hypertension. Excessive use may cause renal failure • Check pupils frequently • If no ICP response after 15-20 minutes get a medical review • What do we measure every 12 hours? Hypertonic saline • 1919 Weed and McKibben reduced brain volume by injection of 30% Normal Saline • • • • • • 10% 29% 20% 23.4% 5% 3% Tier 2 treatment Hypertonic Saline • 125 mls of 5% over 15 minutes • Via a central line Mannitol versus HTS • Which is better at lowering ICP? • Which avoids hypotension? • Which is best at improving overall outcome. ‘’insufficient evidence about effects on clinical outcomes to support a specific recommendation, or to support use of any specific hyperosmolar agent” Carney et al (2017) Hypertonic Saline infusion • Some small recent studies have investigated the use of continuous infusions of hypertonic saline to reduce ICP. • Asehnoune et al 2017 Nigel’s ICP • Still up to 30mmHg and a new scan revealed a small temporal haematoma. • This was surgically evacuated. • However the ICP was still rising to 30mmg and 35mmHg during nursing care so he received boluses of neuromuscular blocker Hyperventilation • Prophylactic hyperventilation is not recommended as although it transiently reduces ICP it does not improve final outcome in patients with TBI. • • • • Should be avoided in the first 24hours Used in conjunction with PbtO2 from Licox catheter Sjo2 • Transient use for high ICP Licox Tier 3 treatment Thiopentone infusion • Reduces metabolic brain requirement and therefore blood flow. • ICP reduction should follow • Often the infusion is titrated to the EEG brain activity. • The aim is usually 3-5 bursts of brain activity a minute or 75% suppression of activity. EEG Burst Suppression Problems with Thiopentone • May cause , hypotension, drop in temperature, dilated pupils, immuno-suppression • May take 96 hours to wash out of the system. • Rebound hyperkalaemia up to 48 hours after infusion has stopped so 2-3 hourly potassium levels • Levels need to be checked before brain stem tests can be carried out. Tier 3 treatment Therapeutic Hypothermia Eurotherm Trial • Hypothermia for Intracranial Hypertension after Traumatic Brain Injury • The primary outcome measure was the extended Glasgow Outcome Score at 6 months Favourable Outcome Hypothermia Favourable outcome control 37% 26% Conclusions • Titrated hypothermia to reduce raised intracranial pressure in addition to standard care did not achieve better outcomes than standard care alone. • Hypothermia resulted in higher mortality and poorer outcomes and should not be used to reduce ICP after TBI Normothermia Instead • Aim 36o C- 38.3C • Achieved by anti pyretics, fan, sponging or a cooling blanket. Tier 3 treatment Craniectomy Craniectomy RESCUEicp • Removal of a bone flap to relieve intracranial pressure. • Study to compare craniectomy as a third tier treatment for high ICP with medical management including barbiturate coma. • Primary outcome was GOSe at 6 months Results • Deaths in the craniectomy group 26.9% • Deaths in medical group 48.9% • Vegetative state in craneictomy group 8.5% • Vegetative state in medical group 2.1% • Favourable outcome in craniectomy group 42.8% • Favourable outcome in medical group 34.6% • Good recovery in the craniectomy group 4% • Good recovery in the medical group 6.9% DVT Prophylaxis • Graduated compression stockings • Flowtron boots • Reassess heparin at one week. Glucose control • Nigel’s blood glucose was always around 510mmls/l • Edinburgh would try to keep this at 4.510mmols/l Seizure Activity • Seizure activity increases metabolic activity and cerebral blood flow. • ICP will rise • Phenytoin is given if there are confirmed seizures. Loading followed by 100mg evry 8 hours with levels checked the following day. Outcome for Nigel • Home after 1 month • At outpatients he complained of some visual disturbance of peripheral vision on the side of his injury and sore heals. • Nigel’s mother said he was a bit louder than usual and was not great with numbers and maths • He could no longer go into the army as planned Neuropoly Antibiotics Intubation Hyperventi lation Nursing Care Sedation Pressure Anti convulsant Barbiturates an ni to l H yp Sa erto lin ni e c HTS M Cooling Mannitol EVD Ba r T bi t h er urat ap e y s tic s id lo l Co re Ca Nursing Care Nimodipine Hyperventi lation Anti convulsant Mannitol Neuropoly Intubation Nursing Care Pressure C g sin ur Sedation NMB ce n ha N tio n Sedation yp e g in ol o C H r v en til a Colloids io tib An EVD n tio ba tu In Cooling Neuropoly e in ip od im Chance Neuropoly Mannitol An tic on vu lsa nt N d an n io esia t da lg Se Ana HTS EV D Colloids r la cu s u m de ro k a eu lo c N B re t s u en es em Pr n ag a M Intubation Lose 5 mins Ch an ce ce an Ch Admission References • • Carney, N. M., Totten, A. S., OʼReilly, C. W., Ullman, J. J., Hawryluk, G. L., Bell, M. A., . . . Ghajar, J. (2017). Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery, vol 80, no.1, pp.6-15 https://braintrauma.org/guidelines/guidelines-for-the-management-of-severe-tbi-4th-ed#/Fourth Edition • Asehnoune ,K et al 2017 Association between continuous hyperosmolar therapy and survival in patients with traumatic brain injury- a multicentre prospective study and systemic review, Critical Care, vol 21, no328. • Godoy,D.A., Seifi,A., Garza,D., Lubillo-Montenegro, S., Morilloa-Cabezas, F. 2017 Hyperventilation Therapy for Posttraumatic Intracranial Hypertension, Frontiers in Neurology, vol 8, Article 250. • Hutchinson,P.J et al 2016 Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension, The New England Journal of Medicine, vol 375, no.12, pp.1119-1130 • Mortazavi, M.M., Romeo, A.K., Deep A. 2012. Hypertonic saline for treating raised intracranial pressure: literature review with meta-analysis. Journal of Neurosurgery, vol 116, pp.210–21. • Mangat,H.S. 2018 Hypertonic Saline Infusion for Treating Intracranial Hypertension after Severe Traumatic Brain Injury, Critical Care, vol 22, no.37, 3 pages. References • Bader,M.K., Arbour,R., Palmer,S. 2005 Barbiturate Coma and Bispectral Index Monitoring, AACN Clinical Issues, vol 16, no.4, pp.526-541 • Heliwell,R. 2009 Advances in brain tissue oxygen monitoring: Using the Licox system in neurointensive care, British Journal of Neuroscience Nursing, vol5, no.1, pp.22-24. • Kamel,H., Navi,B,B., Nakagawa,K., Hemphill,J,C., Ko, N,U. 2011 Hypertonic Saline versus mannitol for the treatment of elevated intrcranial pressure: A meta-analysis of randomized clinical trials, Critical Care Medicine, vol 39, pp.554-559. • Marko,N.F. 2012 Hyperosmolar Therapy for Intracranial Hypertension: Time to Dispel Antiquated Myths, American Journal of Respiratory Critical Care Medicine, vol 185, no.5, pp. 467-478. • Todd,M,M. 2013 Hyperosmolar Therapy and the Brain; A Hundred Years of Hard –earned Lessons, Anesthesiology, vol 118, no.4, pp.777-779. • Wang,L,C., Papangelou,A., Lin,C., Mirski,M,A., Goottschalk,A., Toung,T,J,K. Commparison of equivolume, equiosmolar solutions of mannitol and hypertonic saline with or without furosemide on brain water content in rats, Anesthesiology, vol 118, no.4, pp.903-913 • Hamill,V., Barry,S.J.E., McConnachie,A., McMillan,T.M., Teasdale,G.M. 2015 Mortality from Head InjuryOver Four Decades in Scotland, Journal of Neurotrauma, vol 32, no.10, pp.689-703. • • NHS Lothian Neurological Guidelines available at: http://intranet.lothian.scot.nhs.uk/Directory/CriticalCare/Pages/Default.aspx?RootFolder=%2FDirectory%2FCritical Care%2FCritical%20Care%20Guidelines%2FNeurological&FolderCTID=0x012000788B35528E417F40AC7B36A A74550EE9&View=%7B358BA3D2%2D95A0%2D4C4E%2D98D0%2D8CF3EF13C93C%7D • Qureshi A.I, Suarez J.I. 2000 Use of hypertonic saline solutions in treatmentof cerebral edema and intracranial hypertension. 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