27
BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATA G. Hallaert, Neurochirurg UZ Gent / UGent, 22 oktober 2016 VAKGROEP HEELKUNDE - NEUROCHIRURGIE

BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

  • Upload
    others

  • View
    6

  • Download
    0

Embed Size (px)

Citation preview

Page 1: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATA

G. Hallaert, Neurochirurg UZ Gent / UGent, 22 oktober 2016

VAKGROEP HEELKUNDE - NEUROCHIRURGIE

Page 2: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Studiedag Verzekeringsgeneeskundige aspecten bij neurotrauma

Basis Pathofysiologie bij Hersentraumata

G. Hallaert, neurochirurg

UZ Gent / UGent

OLV Aalst, 22/10/2016

Page 3: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Inhoud❖ Korte inleiding❖ De centrale rol van de Monro-

Kellie hypothese❖ Pathofysiologie:

❖ ICP❖ CPP❖ intracraniële hypertensie

❖ Behandeling❖ Prognose

Page 4: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Inleiding❖ Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1 in

USA voor leeftijdsgroep 1 - 45 jaar

❖ Overlevenden

❖ meestal ernstige handicap

❖ ernstige psychologische en sociale gevolgen

❖ ernstige economische schade : in 2000 geschat

❖ op $9,2 biljard dollar medische kosten en

❖ op $51,2 biljard verlies aan inkomsten

❖ (bron: UpToDate, 2016)

Page 5: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Inleiding❖ Neurotrauma = vaak geassocieerd met andere traumatische pathologie

(“polyneurotrauma”);

❖ Voorbije 20 jaar: ontwikkeling van “guidelines”, met als doel prognose te verbeteren

❖ Ernstig neurotrauma = nood aan neurochirurgische - intensieve zorgen

❖ PREVENTIE van het “primaire letsel”

❖ verplichte autogordel

❖ alcohol-limieten

❖ veiliger wagens

❖ helm

❖ “Secundaire letsel” (ischemie, ICP stijging, …) = therapeutische aangrijpingspunt

Echter: (nog) geen “harde” evidentie, dat dit klopt

Page 6: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

J Neurosurg / Volume 121 / August 2014

The trepanned skull of Chios

329

work (Aidonis A: The trepanation of Chios. The bioar-chaeological background of a surgical intervention from the 2nd century BC. Paper presented at the conference “100 years of archaeological research in Chios”, Chios, Greece, October 20, 2012), anthropological study indicat-ed that the opening was the result of trepanation and the fissure very likely represents a healed linear fracture. The edges of the hole are inclined, the slope is not uniform around its perimeter, and the diameter is greater in the external layer. The lack of cut marks from a trephine or a trepan further supports the assumption that the method used was that of scraping the bone. These morphological features favor trepanation, but there are, of course, patho-logical processes that could be misinterpreted as trepana-tion such as metastatic carcinoma to the skull, some be-nign tumors, congenital defects, tuberculosis, or trauma, but none of these processes fit in this case.31 It is believed that the patient survived several years after the procedure because there is evidence of healing and growth of new bone around the opening, also confirmed by CT. Age es-timation of the skeleton indicated that the man died over the age of 50 years.11

It is not known, of course, who actually performed the trepanation, and the reason he did so. The trepanation took place approximately two centuries after Hippocrates lived, sufficient time for his teaching to have been dis-seminated and established, and the skull defect certainly appears to have been made adjacent to a skull fracture, in accordance with his instructions. It is reasonable to as-sume that the trepanation was performed by a Hippocrat-ic doctor for a head injury. However, the technique was

not unique to the Hippocratic physicians, it had already been used for many centuries and non-Hippocratic phy-sicians also practiced medicine across ancient Greece.22

The discovery of this skull was covered in the na-tional and international press, and since 2003 it has been exhibited in a prominent position in the archaeological museum of the city of Chios.2,27 The following discussion examines the application of Hippocratic teaching on head injuries in association with the trepanned skull of Chios, and compares the rationale behind the ancient practice of trepanation with the principles that govern modern neuro-surgery. It is based on a review of the English translation of the Hippocratic treatise “On injuries of the head” by Francis Adams (1849).16 We have compared the teach-ings contained in this text to the findings on the skele-tal specimen from Chios. We have also tried to assess the therapeutic potential of trepanation in ancient times, based on current scientific knowledge. To the best of our knowledge, this is the first reported case of trepanation performed in accordance with the Hippocratic Corpus.

DiscussionThe word trepanation comes from the Greek word

trypanon (τρυπανον) meaning trepan, or borer. It refers to the surgical procedure of creating an opening in the skull. Trephination is a more recent word and specifically refers to an opening made by a circular saw (trephine), but both terms are used interchangeably in the literature.6

The roots of this technique date back to prehis-tory. Paul Broca and Victor Horsley, both authorities in neuroscience, were among the first to report on ancient trepanned skulls and both proposed theories relating to such primitive cranial surgery.5,13 According to Broca’s theory, people believed that the cranial holes allowed the demons causing convulsions to escape. Horsley, on the other hand, suggested that trepanation originated as a way to treat pain and epilepsy caused by skull fractures.12 Our current knowledge and understanding about this ancient technique derive from saved historical manuscripts of its widespread practice at the time and from bioarchaeologi-cal studies of abundant skeletal specimens that have been discovered in many parts of the world.9,14, 23

Cranial surgery in Greece predates Hippocrates by many centuries. The oldest skeletal evidence of trepana-tion discovered to date was in a Minoan ossuary in Crete (Early Minoan to Middle Minoan period, 2200–1720 BC).3 Trepanned skulls belonging to different periods have also been unearthed in Delphi (Middle Bronze Age period, 1700–1750 BC),21,29 the Peloponnese (Late Hel-ladic period, 1400–1060 BC),25 Crete (8th century BC),19 Abdera (7th century BC),1 and in many other regions, indicating a wide geographic as well as a prolonged chronological distribution. Fabbri et al. presented a case of cranial trepanation that was performed at the begin-ning of the 5th century BC, in a Greek colony in Sicily.10 This procedure was evidently performed in the manner that was described a few decades later in “On injuries of the head.” The lack of relevant skeletal evidence in the geographic area of ancient Greece during and after the

Fig. 1. The trepanned skull of Chios. The arrow points to the healed linear fracture associated with the bur hole. Copyright Hellenic Ministry of Education and Religious Affairs, Cultural Sector, 20th Ephorate of Prehistoric & Classical Antiquities, Archaeological Museum of Chios. Published with permission.

Monro-Kellie❖ Schedel

❖ “gesloten” doos;❖ met een “vast volume”

❖ Normale ICP volwassene < of = 15mmHg (20cm H2O)

❖ In volumes (gemiddeld):❖ 1400mL parenchym❖ 150mL bloed❖ 150mL CSF

80% HERSENPARENCHYM

10% BLOED10% CSF

Page 7: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Y H

Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd ed, Rogers, MC, Williams and Wilkins 1996. p. 646; figure 18.1

Monroe-Kellie principe: ICP is een functie van het volume en de compliance van iedere component van het intracraniële compartiment

Monro-Kellie : aannames

I. Hersenen zijn opgesloten in een gesloten niet-expandeerbare schedel.

II. Het hersenparenchym is quasi niet samendrukbaar.

III. Het intracraniële bloedvolume is quasi constant.

IV. Dus is er een continue uitstroom van veneus bloed nodig om de instroom van arterieel bloed mogelijk te maken.

“Intracraniële Hypertensie”

Page 8: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Autoregulatie curve verschuift bij chronische hypertensie

Rose, neurocrit. care 2004

Cerebral Perfusion Pressure (CPP), Cerebral Blood Flow (CBF) & Autoregulation

CPP = Mean Arterial Pressure - ICP

Normale CPP = of > 50mmHg

Page 9: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Ropper, NEJM, 2012

ICP en Intracranieel volume

❖ Non-lineaire verhouding !

❖ De compliantie neemt AF naarmate het intracraniële volume stijgt.

Page 10: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Ropper, NEJM, 2012

Druk - Volume curves

Page 11: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Y H

Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd ed, Rogers, MC, Williams and Wilkins 1996. p. 646; figure 18.1

Monroe-Kellie principe: ICP is een functie van het volume en de compliance van iedere component van het intracraniële compartiment

Intracraniële Hypertensie

❖ Licht gestegen ICP:

❖ CSF wordt vanuit subarachnoidaal ruimte en ventrikels weggeperst richting spinale axis, doorheen foramen magnum

❖ ook veneus bloed kan via de vv jugulares internae weggestuwd worden

❖ Verder doorstijgen ICP: minder arteriële instroom; ergo daling CPP; ergo ischemie (ICP = MAP : stop van cerebrale circulatie)

❖ hersenoedeem of massa-effect kan herniatie veroorzaken (hersenstam wordt verpletterd)

Page 12: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Intracraniële overdruk : klinisch

❖ Klinisch: Triade van Cushing❖ Arteriële hypertensie❖ Bradycardie❖ Irregulaire ademhaling

❖ Vaak ook pupilafwijkingen (anischorie)

❖ Bewustzijnsstoornissen / Coma

Page 13: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Intracraniële hypertensie: oorzaken❖ Hersenoedeem (cytotoxisch, dus toename intracellulair vocht)

❖ Hyperemie (= normale respons op neurotrauma)

❖ Posttraumatisch massa-effect

❖ epiduraal hematoom

❖ subduraal hematoom

❖ intraparenchymateuze bloeding

❖ vreemd lichaam (bvb kogel)

❖ indeukingsfractuur

❖ Hydrocefalie (hetzij obstructief hetzij communicerend)

❖ Hypoventilatie (hypercapnie, ergo vasodilatatie)

❖ Veneuze sinus trombose (en stuwingsinfarcten)

❖ Status Epilepticus

Page 14: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

“Secundaire” ICP stijging❖ 3 - 10 dagen post neurotrauma

❖ oorzaken:

❖ laattijdige hematoom vorming (epiduraal, subduraal, intraparenchymateus)

❖ cerebraal vasospasme

❖ laattijdig hersenoedeem (meer in pediatrische pten)

❖ hyponatriëmie

Page 15: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1
Page 16: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Behandeling ❖ DOEL

❖ ICP lager dan 20mm Hg (voorkomt “plateau-golven” die de CBF compromitteert , waardoor ischemie en/of hersendood)

❖ CPP hoger dan 50mmHg

❖ CHIRURGISCH

❖ externe ventrikeldrain / ICP sensor (kan geen CSF evacueren)

❖ verwijderen hematoom (epi, sub)

❖ hemicraniëctomie (discussie)

Page 17: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

10-15 % van patiënten met een normale CT-scan na ernstig neurotrauma ontwikkelt hoge intracraniële drukken

Howard, J. Neurosurg 73, 1990 N = 753 N = 45

cave: ICP bij “normale” CT hersenen❖ 10 - 15% van de patiënten met een

normale CT hersenen, zullen overdruk ontwikkelen

❖ Plaatsen ICP sensor en/of EVD❖ GCS 3-8, na reanimatie en met

abnormale CT❖ Normale CT

❖ én ouder dan 40jr ❖ of arteriële hypertensie❖ of uni- of bilaterale

strekbeweging

ALGEMEEN: “suspicion at risk” = wettigt agressieve behandeling

Page 18: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Behandeling : algemeen❖ “algemeen” (routinegewijs)

❖ halfzittende houding

❖ vermijd druk op de nek/hals

❖ vermijd arteriële hypotensie

❖ controleer arteriële hypertensie

❖ vermijd hypoxie

❖ streef naar normocapnie

❖ lichte sedatie (cave: neuro-observatie)

Page 19: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Behandeling : specifiek

❖ “specifiek” (bovenop algemene maatregelen; neuro-intensieve zorgen vereist)❖ diepe sedatie❖ externe ventriculaire

drainage (EVD)❖ hyperventilatie❖ mannitol❖ hypertoon zout

Corticosteroïden hebben GEEN plaats (meer) in behandeling neurotrauma(level I evidentie, oa Lancet 2004, Roberts).

Page 20: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Behandeling : refractaire ICP stijging

❖ Barbituraat coma (cave: cardiovasculaire effecten)

❖ Doorgedreven Hyperventilatie (tot PaCO2 25-30mmHg)

❖ Hemicraniëctomie (of bifrontale decompressie, Kjellberg), al dan niet samen met EVD

❖ Hypothermie (?)❖ Hypertensieve therapie (?)

Page 21: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

The new england journal of medicine

n engl j med 375;12 nejm.org September 22, 2016 1119

established in 1812 September 22, 2016 vol. 375 no. 12

The authors’ full names, academic de-grees, and affiliations are listed in the Appendix. Address reprint requests to Dr. Hutchinson at the Division of Neurosur-gery, Box 167, University of Cambridge, Cambridge Biomedical Campus, Cam-bridge CB2 0QQ, United Kingdom, or at pjah2@ cam . ac . uk.

* A complete list of investigators in the Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure (RESCUEicp) trial is provided in the Supplementary Appendix, available at NEJM.org.

This article was published on September 7, 2016, at NEJM.org.

N Engl J Med 2016;375:1119-30.DOI: 10.1056/NEJMoa1605215Copyright © 2016 Massachusetts Medical Society.

BACKGROUNDThe effect of decompressive craniectomy on clinical outcomes in patients with refractory traumatic intracranial hypertension remains unclear.METHODSFrom 2004 through 2014, we randomly assigned 408 patients, 10 to 65 years of age, with traumatic brain injury and refractory elevated intracranial pressure (>25 mm Hg) to undergo decompressive craniectomy or receive ongoing medical care. The primary outcome was the rating on the Extended Glasgow Outcome Scale (GOS-E) (an 8-point scale, ranging from death to “upper good recovery” [no injury-related problems]) at 6 months. The primary-outcome measure was analyzed with an ordinal method based on the proportional-odds model. If the model was rejected, that would indicate a significant difference in the GOS-E distribution, and results would be reported descriptively.RESULTSThe GOS-E distribution differed between the two groups (P<0.001). The proportional-odds assumption was rejected, and therefore results are reported descriptively. At 6 months, the GOS-E distributions were as follows: death, 26.9% among 201 patients in the surgical group versus 48.9% among 188 patients in the medical group; vegetative state, 8.5% versus 2.1%; lower severe disability (dependent on others for care), 21.9% versus 14.4%; upper severe disability (independent at home), 15.4% versus 8.0%; moderate disability, 23.4% versus 19.7%; and good recovery, 4.0% versus 6.9%. At 12 months, the GOS-E distributions were as follows: death, 30.4% among 194 surgical patients versus 52.0% among 179 medical patients; vegetative state, 6.2% versus 1.7%; lower severe disability, 18.0% versus 14.0%; upper severe disability, 13.4% versus 3.9%; moderate disability, 22.2% versus 20.1%; and good recovery, 9.8% versus 8.4%. Surgical patients had fewer hours than medical pa-tients with intracranial pressure above 25 mm Hg after randomization (median, 5.0 vs. 17.0 hours; P<0.001) but had a higher rate of adverse events (16.3% vs. 9.2%, P = 0.03).CONCLUSIONSAt 6 months, decompressive craniectomy in patients with traumatic brain injury and refractory intracranial hypertension resulted in lower mortality and higher rates of veg-etative state, lower severe disability, and upper severe disability than medical care. The rates of moderate disability and good recovery were similar in the two groups. (Funded by the Medical Research Council and others; RESCUEicp Current Controlled Trials number, ISRCTN66202560.)

a bs tr ac t

Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension

P.J. Hutchinson, A.G. Kolias, I.S. Timofeev, E.A. Corteen, M. Czosnyka, J. Timothy, I. Anderson, D.O. Bulters, A. Belli, C.A. Eynon, J. Wadley, A.D. Mendelow, P.M. Mitchell, M.H. Wilson, G. Critchley, J. Sahuquillo, A. Unterberg, F. Servadei, G.M. Teasdale, J.D. Pickard, D.K. Menon, G.D. Murray, and P.J. Kirkpatrick,

for the RESCUEicp Trial Collaborators*

The New England Journal of Medicine Downloaded from nejm.org on September 25, 2016. For personal use only. No other uses without permission.

Copyright © 2016 Massachusetts Medical Society. All rights reserved.

“RESCUEicp Trial”

Page 22: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

RESCUEicp-Trial

n engl j med 375;12 nejm.org September 22, 20161128

T h e n e w e ngl a nd j o u r na l o f m e dic i n e

ectomy; this situation may have diluted the ob-served treatment effect. Third, 10 patients were excluded from all analyses owing to withdrawal of consent or to a lack of valid consent, and 7 more patients in the medical group were lost to primary follow-up. Fourth, long-term data on cranial reconstruction — a procedure that is usually necessary a few weeks to months after decompressive craniectomy — were not system-atically obtained owing to the pragmatic nature of the trial. This important aspect of treatment needs to be explored in future studies. Finally, the present trial did not examine the effective-ness of primary decompressive craniectomy, which is undertaken more frequently than sec-ondary decompressive craniectomy.19,20

In conclusion, at 6 months, decompressive

craniectomy for severe and refractory intracranial hypertension after TBI resulted in mortality that was 22 percentage points lower than that with medical management. Surgery also was associ-ated with higher rates of vegetative state, lower severe disability, and upper severe disability than medical management. The rates of moderate disability and good recovery with surgery were similar to those with medical management.

Supported by the Medical Research Council (MRC) and man-aged by the National Institute for Health Research (NIHR) on behalf of the MRC–NIHR partnership (grant no. 09/800/16), and by the NIHR Cambridge Biomedical Research Centre, the Acad-emy of Medical Sciences and Health Foundation (Senior Fellow-ship, to Dr. Hutchinson), and the Evelyn Trust. Dr. Hutchinson is supported by a Research Professorship from the NIHR, the NIHR Cambridge Biomedical Research Centre, a European Union Seventh Framework Program grant (CENTER-TBI; grant no. 602150), and the Royal College of Surgeons of England;

Figure 2. Stacked Bar Chart of Extended Glasgow Outcome Scale (GOS-E) Results at 6 Months and 12 Months.

The primary-outcome measure was assessed with the use of the GOS-E, a global outcome scale assessing functional independence, work, social and leisure activities, and personal relationships.12 The eight outcome categories are death, vegetative state (unable to obey commands), lower severe disability (dependent on others for care), upper severe disability (independent at home), lower moderate disability (independent at home and outside the home but with some physical or mental disability), upper moderate disability (independent at home and outside the home but with some physical or mental disability, with less disruption than lower moderate disability), lower good recov-ery (able to resume normal activities with some injury-related problems), and upper good recovery (no problems). See the Supplementary Appendix for additional descriptions of the outcome categories.

0 20 40 60 908010 30 50 70 100

Percent

B GOS-E Results at 12 Mo (secondary end point)

A GOS-E Results at 6 Mo (primary end point)

Dead Vegetativestate

Lowerseveredisability

Lowermoderatedisability

Uppermoderatedisability

Lowergoodrecovery

Uppergoodrecovery

Upperseveredisability

Surgical Group

Medical Group

0 20 40 60 908010 30 50 70 100

Percent

Dead Vegetativestate

Lowerseveredisability

Lowermoderatedisability

Uppermoderatedisability

Lowergoodrecovery

Uppergoodrecovery

Upperseveredisability

Surgical Group

Medical Group

The New England Journal of Medicine Downloaded from nejm.org on September 25, 2016. For personal use only. No other uses without permission.

Copyright © 2016 Massachusetts Medical Society. All rights reserved.

The new england journal of medicine

n engl j med 375;12 nejm.org September 22, 2016 1119

established in 1812 September 22, 2016 vol. 375 no. 12

The authors’ full names, academic de-grees, and affiliations are listed in the Appendix. Address reprint requests to Dr. Hutchinson at the Division of Neurosur-gery, Box 167, University of Cambridge, Cambridge Biomedical Campus, Cam-bridge CB2 0QQ, United Kingdom, or at pjah2@ cam . ac . uk.

* A complete list of investigators in the Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure (RESCUEicp) trial is provided in the Supplementary Appendix, available at NEJM.org.

This article was published on September 7, 2016, at NEJM.org.

N Engl J Med 2016;375:1119-30.DOI: 10.1056/NEJMoa1605215Copyright © 2016 Massachusetts Medical Society.

BACKGROUNDThe effect of decompressive craniectomy on clinical outcomes in patients with refractory traumatic intracranial hypertension remains unclear.METHODSFrom 2004 through 2014, we randomly assigned 408 patients, 10 to 65 years of age, with traumatic brain injury and refractory elevated intracranial pressure (>25 mm Hg) to undergo decompressive craniectomy or receive ongoing medical care. The primary outcome was the rating on the Extended Glasgow Outcome Scale (GOS-E) (an 8-point scale, ranging from death to “upper good recovery” [no injury-related problems]) at 6 months. The primary-outcome measure was analyzed with an ordinal method based on the proportional-odds model. If the model was rejected, that would indicate a significant difference in the GOS-E distribution, and results would be reported descriptively.RESULTSThe GOS-E distribution differed between the two groups (P<0.001). The proportional-odds assumption was rejected, and therefore results are reported descriptively. At 6 months, the GOS-E distributions were as follows: death, 26.9% among 201 patients in the surgical group versus 48.9% among 188 patients in the medical group; vegetative state, 8.5% versus 2.1%; lower severe disability (dependent on others for care), 21.9% versus 14.4%; upper severe disability (independent at home), 15.4% versus 8.0%; moderate disability, 23.4% versus 19.7%; and good recovery, 4.0% versus 6.9%. At 12 months, the GOS-E distributions were as follows: death, 30.4% among 194 surgical patients versus 52.0% among 179 medical patients; vegetative state, 6.2% versus 1.7%; lower severe disability, 18.0% versus 14.0%; upper severe disability, 13.4% versus 3.9%; moderate disability, 22.2% versus 20.1%; and good recovery, 9.8% versus 8.4%. Surgical patients had fewer hours than medical pa-tients with intracranial pressure above 25 mm Hg after randomization (median, 5.0 vs. 17.0 hours; P<0.001) but had a higher rate of adverse events (16.3% vs. 9.2%, P = 0.03).CONCLUSIONSAt 6 months, decompressive craniectomy in patients with traumatic brain injury and refractory intracranial hypertension resulted in lower mortality and higher rates of veg-etative state, lower severe disability, and upper severe disability than medical care. The rates of moderate disability and good recovery were similar in the two groups. (Funded by the Medical Research Council and others; RESCUEicp Current Controlled Trials number, ISRCTN66202560.)

a bs tr ac t

Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension

P.J. Hutchinson, A.G. Kolias, I.S. Timofeev, E.A. Corteen, M. Czosnyka, J. Timothy, I. Anderson, D.O. Bulters, A. Belli, C.A. Eynon, J. Wadley, A.D. Mendelow, P.M. Mitchell, M.H. Wilson, G. Critchley, J. Sahuquillo, A. Unterberg, F. Servadei, G.M. Teasdale, J.D. Pickard, D.K. Menon, G.D. Murray, and P.J. Kirkpatrick,

for the RESCUEicp Trial Collaborators*

The New England Journal of Medicine Downloaded from nejm.org on September 25, 2016. For personal use only. No other uses without permission.

Copyright © 2016 Massachusetts Medical Society. All rights reserved.

Page 23: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

n engl j med 375;12 nejm.org September 22, 20161128

T h e n e w e ngl a nd j o u r na l o f m e dic i n e

ectomy; this situation may have diluted the ob-served treatment effect. Third, 10 patients were excluded from all analyses owing to withdrawal of consent or to a lack of valid consent, and 7 more patients in the medical group were lost to primary follow-up. Fourth, long-term data on cranial reconstruction — a procedure that is usually necessary a few weeks to months after decompressive craniectomy — were not system-atically obtained owing to the pragmatic nature of the trial. This important aspect of treatment needs to be explored in future studies. Finally, the present trial did not examine the effective-ness of primary decompressive craniectomy, which is undertaken more frequently than sec-ondary decompressive craniectomy.19,20

In conclusion, at 6 months, decompressive

craniectomy for severe and refractory intracranial hypertension after TBI resulted in mortality that was 22 percentage points lower than that with medical management. Surgery also was associ-ated with higher rates of vegetative state, lower severe disability, and upper severe disability than medical management. The rates of moderate disability and good recovery with surgery were similar to those with medical management.

Supported by the Medical Research Council (MRC) and man-aged by the National Institute for Health Research (NIHR) on behalf of the MRC–NIHR partnership (grant no. 09/800/16), and by the NIHR Cambridge Biomedical Research Centre, the Acad-emy of Medical Sciences and Health Foundation (Senior Fellow-ship, to Dr. Hutchinson), and the Evelyn Trust. Dr. Hutchinson is supported by a Research Professorship from the NIHR, the NIHR Cambridge Biomedical Research Centre, a European Union Seventh Framework Program grant (CENTER-TBI; grant no. 602150), and the Royal College of Surgeons of England;

Figure 2. Stacked Bar Chart of Extended Glasgow Outcome Scale (GOS-E) Results at 6 Months and 12 Months.

The primary-outcome measure was assessed with the use of the GOS-E, a global outcome scale assessing functional independence, work, social and leisure activities, and personal relationships.12 The eight outcome categories are death, vegetative state (unable to obey commands), lower severe disability (dependent on others for care), upper severe disability (independent at home), lower moderate disability (independent at home and outside the home but with some physical or mental disability), upper moderate disability (independent at home and outside the home but with some physical or mental disability, with less disruption than lower moderate disability), lower good recov-ery (able to resume normal activities with some injury-related problems), and upper good recovery (no problems). See the Supplementary Appendix for additional descriptions of the outcome categories.

0 20 40 60 908010 30 50 70 100

Percent

B GOS-E Results at 12 Mo (secondary end point)

A GOS-E Results at 6 Mo (primary end point)

Dead Vegetativestate

Lowerseveredisability

Lowermoderatedisability

Uppermoderatedisability

Lowergoodrecovery

Uppergoodrecovery

Upperseveredisability

Surgical Group

Medical Group

0 20 40 60 908010 30 50 70 100

Percent

Dead Vegetativestate

Lowerseveredisability

Lowermoderatedisability

Uppermoderatedisability

Lowergoodrecovery

Uppergoodrecovery

Upperseveredisability

Surgical Group

Medical Group

The New England Journal of Medicine Downloaded from nejm.org on September 25, 2016. For personal use only. No other uses without permission.

Copyright © 2016 Massachusetts Medical Society. All rights reserved.

Page 24: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Prognose : parameters (CRASH trial, BMJ, 2008)

Page 25: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Key-messages❖ Neurotrauma kan aanleiding geven tot ICP stijging

❖ bloedingen

❖ hersenoedeem

❖ schedelfracturen

❖ ICP én CPP worden behandeld op neuro-intensieve zorgen

❖ medisch

❖ chirurgisch: EVD, hemicraniëctomie (?)

❖ Indien patiënt overleeft, meestal matige tot ernstige blijvende deficieten (neurocognitief !)

Page 26: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

DANK U !

VRAGEN ? Discussie ?

Page 27: BASIS PATHOFYSIOLOGIE BIJ HERSENTRAUMATAverzekeringsgeneeskundevlaanderen.be/assets/upload/cache/Opleidi… · Neurotrauma (“Traumatic Brain Injury”, TBI) = doodsoorzaak nr 1

Bronnen

❖ Greenberg, “Handbook of Neurosurgery”, 8th Edition, Thieme, 2016

❖ UpToDate, 2016, “Management of Acute Severe Traumatic Brain Injury”

❖ Werner C, Engelhard K, “Pathophysiology of traumatic brain injury”, Br J Anaesth 99 (1): 4-9, 2007