This document provides an overview of the neurological management of severely injured patients. It discusses the pathophysiology of neurotrauma and emphasizes the importance of preventing secondary brain and spinal cord injuries through careful management of factors like hypotension, hypoxia, intracranial pressure, seizures and temperature. The initial assessment and priorities on scene and in the emergency department are outlined. Medical and surgical management strategies for head injuries, spinal injuries and monitoring of intracranial pressure are summarized, along with guidelines for interventions like osmotherapy, blood transfusion thresholds and timing of surgery. Key evidence-based recommendations are highlighted.

1. Neurological Management of
Severely Injured Patient
Presented By:
Dr.Mohammed Alsiraj
MBBS,MRCS1(ED),MRCS2(ED)
Surgery Resident

2. In the management of severe trauma, time is critical starting
from the time of impact

4. Pathophysiology of neurotrauma
Prolonged ischemia compromises,ATP production by disrupting
oxidative phosphorylation.This ATP deficit causes immediate
malfunction of ATP-dependent ion pumps, leading to increased
intracellular sodium and calcium and potassium efflux. Membrane
depolarization then occurs, which in turn causes release of
excitatory amino acids, and oxygen-free radical formation. This
cascade of events leads to cellular necrosis & apoptosis causing the
secondary injury.

5. Cerebral Autoregulation:
is the ability of the brain to maintain a constant critical
level of cerebral blood flow (CBF) {45–50 ml /100 g/min ,
20 ml/100 g/min in white matter to 70ml/100 g/min in
gray matter}over a wide range of mean arterial pressures
(MAP) {60–150 mmHg} in a sigmoidal pattern.

7. The Goal of Management
• To Prevent secondary injuries
to the brain and spinal cord
which are worsened by :
– Hypoxia,
– Hypotension,
– Raised intracranial
pressure
– Seizures,
– Hyperthermia,
– Hypercarbia
• To Improve outcome and
lower mortality & morbidity

8. THE MANAGEMENT STARTS ON THE SCENE

9. Initial Assessment & management
A,B,C ,Including Spine Immobilization (ATLS protocol)
Treat/Prevent hypotension and hypoxemia
GCS

10. The pupils are examined for symmetry and reaction to light;

11. The back is examined using the log roll locking for spinal
tenderness or deformities indicating spinal injuries

12. Priorities for Initial Evaluation and Triage of
Patient with Severe Brain Injuries

13. If SBP <100 despite aggressive
Fluid resuscitation :
• 1st priority is to Establish the cause of
Hypotention
• Neurosurgical evaluation has 2nd
priority
• DPL/FAST exam may be performed in
ED.
• May require urgent OR for
laparotomy,CT scan after laparotomy
• If there is clinical evidence of
Intracranial mass ,diagnostic Burr hole
or craniotomy may be undertaken in OR
while the laparotomy performed.
If SBP >100 after resuscitation +
clinical evidence of intracranial mass :
• 1st priority to obtain CT head sacn.
• A DPL/FAST exam may be performed
in ED,CT area or in OR,but patient
neurologic evaluation or treatment
should not be delayed.

14. Secondary survey
A,B,C ,maintain Spine Immobilization
GCS and Pupils
Focused neurological examination including brainstem reflexes

15. The head is inspected for signs of trauma including Scalp
lacerations, hematomas,areas of skull depression, raccoon eyes,
Battle’s sign,bleeding per nose or ear,hemotympanum, rhinorrhea,
and otorrhea “halo effect” or “double ring sign“

16. • ASIA classification
• ASIA impairment scale
Motor and sensory function is assessed by :

17. Neurogenic shock
• Spinal Lesions above D6
• Minutes – hours (fall of
catecholamines may take 24
hrs)
• Disruption of sympathetic
outflow from D1 - L2
• Unapposed vagal tone
• Peripheral vasodilatation
• Triad of :
– Hypotension,
– Bradycardia ,
– Hypothermia

18. Spinal shock
• Transient physiological reflex
depression of cord function
• Loss anal tone, reflexes,
autonomic control within 24-
72hr
• Flaccid paralysis bladder &
bowel and sustained Priapism
• Lasts even days till reflex
neural arcs below the level
recovers.

19. Head Injury
Closed
MILD
(GCS 14-15)
MODERATE
(GCS 9-13)
SEVERE
(GCS 3-8)
Penetrating
MILD
(GCS 14-15)
MODERATE
(GCS 9-13)
SEVERE
(GCS 3-8)

20. Spinal injury
Spinal column injury
Stable unstable
Spinal cord injury
Complete incomplete

21. NICE guidelines for Computerised Tomography (CT)
in head injury
■ Glasgow Coma Score (GCS) < 13 at any point
■ GCS 13 or 14 at 2 hours
■ Focal neurological deficit
■ Suspected open, depressed or basal skull fracture
■ Seizure
■ Vomiting > one episode
Urgent CT head scan if none of the above but:
■ Age > 65
■ Coagulopathy (e.g. on warfarin)
■ Dangerous mechanism of injury (CT within 8 hours)
■ Antegrade amnesia > 30 min (CT within 8 hours)

22. Depressed skull fracture
Look for under lying EDH,
Patients with depressed skull fractures have an
increased incidence of post-traumatic seizures

23. Epidural hematoma
appears as lenticular hyperdense lesion

24. Subdural hematoma
appears as crescent-shape hyperdensity

25. Subarachnoid hemorrhage
appears as fingerlike projections of hyperdensities as it tracks
along the sulci

26. Intraventricular hemorrhage
May require ventreculostomy

27. Intracerebral hemorrhage

28. Cerebral odema
severe cerebral edema with obliteration of both basal cisterns and lateral
Ventricles indicating raised ICP

29. Cerebral contusion
Initially the contusion is primarily hemorrhagic.
Cerebral contusions, especially frontal or temporal,
are also characterized by a high incidence of posttraumatic
seizures

30. Pneumocephalus

31. Hydrocephalus
If hydrcephalus is present in the upper CT cuts,look for hematoma
(EDH,SDH,SAH) in the posterior fossa compressing & obstructing the 4th
ventricle.

32. Spinal fracture

33. Management

34. Evidence-Based Medicine
• The Brain Trauma Foundation first published the
Guidelines for the Management of Severe Traumatic
Brain Injury in 2000 and it was most recently updated
in 2007.
• These guidelines utilize current evidence-based
methodology to make specific recommendations for
the uniform management of patients with severe TBI.
• Retrospective studies indicate implementation of these
guidelines may decrease mortality, hospital stay, and
improve clinical outcomes.

35. Medical management
Head injury:
• Prevent hypotension
– SBP > 90 mmHg
• Prevent hypoxemia
– paO2 > 8
• Prevent hypercarbia
– paCo2 < 35
• Control of Raise intracranial
pressure
– ICP < 20 mmH2O
• Maintain Cerebral perfusion
pressure
– CPP >65 mmHg
• Sedation :
– Midazolam + sufentanil
– Propofol (propofol infusion sn)
• Analgesia
• GI bleeding prophylaxis
• DVT/PE prophylaxis
• Nutrition
• Skin care

36. THE BRAIN TRAUMA FOUNDATION. THE AMERICAN ASSOCIATION OF NEUROLOGICAL
SURGEONS. THE JOINT SECTION ON NEUROTRAUMA AND CRITICAL CARE. USE OF
MANNITOL. J NEUROTRAUMA 2000;17(6/7): 521–525.
Mannitol is recommended in most neurosurgical guidelines for the
control of ICP following TBI.
MANNITOL

37. BRATTON SL, CHESTNUT RM, GHAJAR J ET AL. GUIDELINES FOR THE MANAGEMENT
OF SEVERE TRAUMATIC BRAIN INJURY. II. HYPEROSMOLAR THERAPY. J NEUROTRAUMA
2007; 24(SUPPL 1): S14–20.
Mannitol with frequent dosing can result in hypovolemia, so
diligence in maintaining euvolemia is important. If utilizing
osmotic diuretic therapy sodium and serum osmolality
should be monitored frequently. Mannitol 20% (0.25–1 g/kg
IV) given over 10–20 minutes can act as a rapid plasma
expander by increasing tonicity of blood and help to reduce
cerebral edema.
MANNITOL

38. FRANCISCA MUNAR, ANA M. FERRER, MIRIAM DE NADAL, MARÍA A. POCA, SALVADOR
PEDRAZA, JUAN SAHUQUILLO, AND ANGEL GARNACHO. JOURNAL OF NEUROTRAUMA.
JANUARY 2000, 17(1): 41-51. DOI:10.1089/NEU.2000.17.41.
The administration of 7.2% HS in patients with traumatic brain injury
significantly reduces ICP without significant changes in relative global CBF
(expressed as 1/AVDO2), increases CI and transiently increases PAOP,
without changing MABP and urine output.
HYPERTONIC SALINE (7.2%)

39. PAUL R. COOPER, M.D., SARAH MOODY, R.N., W. KEMP CLARK, M.D., JOEL KIRKPATRICK,
M.D., KENNETH MARAVILLA, M.D., A. LAWRENCE GOULD, PH.D., AND WANZER DRANE,
PH.D.JOURNAL OF NEUROSURGERY,SEPTEMBER 1979 / VOL. 51 / NO. 3 / PAGES 307-316
Dexamethasone in either high or low dosages has no significant
effect on morbidity and mortality following severe head injury.
DEXAMETHASONE

40. BRATTON SL, CHESTNUT RM, GHAJAR J ET AL. GUIDELINES FOR THE MANAGEMENT OF
SEVERE TRAUMATIC BRAIN INJURY. XIV. HYPERVENTILATION. J NEUROTRAUMA 2007;
24(SUPPL 1): S87–90.
Hyperventilating results in reduced cerebral oxygenation
particularly in injured areas, which can exacerbate cerebral
hypoxia.
HYPERVENTILATION

41. ROBERTS I. BARBITURATES FOR ACUTE TRAUMATIC BRAIN INJURY.
COCHRANE DATABASE SYST REV 2008; ISSUE 1. ART. NO: CD000033.
Outcome was no different with Barbiturates in
severe TBI.
BARBITURATES

42. BRATTON SL, CHESTNUT RM, GHAJAR J, ET AL. ANTISEIZURE
PROPHYLAXIS.J NEUROTRAUMA 2007; 24(S1): S83–S86.
Phenytoin was effective when used as prophylaxis against early post-TBI
seizures given for seven days following TBI.
The same study reviewed current data on the use of AED in late (>7 days)
post-TBI seizures. From their review, they concluded that the data do not
support use of phenytoin for more than seven days because there was no
difference in late post-TBI seizures in the AED treated (10.0%) group
versus placebo (8.4%) group.
ANTI-EPILEPTIC MEDICATIONS

43. GADKARY CS, ALDERSON P, SIGNORINI DF. THERAPEUTIC HYPOTHERMIA
FOR HEAD INJURY (COCHRANE REVIEW). IN: THE COCHRANE LIBRARY, ISSUE 1, 2002.
OXFORD: COCHRANE DATABASE SYST REV 2002;(1): CD 001048.
There is no evidence that hypothermia is beneficial and the
risk of pneumonia is increased. The use of this treatment
modality is not recommended outside of controlled trials.
THERAPEUTIC HYPOTHERMIA

44. ASSOCIATION OF HEMOGLOBIN CONCENTRATION AND MORTALITY IN CRITICALLY ILL
PATIENTS WITH SEVERE TRAUMATIC BRAIN INJURY, SEKHON MS, MCLEAN N, HENDERSON
WR, CHITTOCK DR, GRIESDALE DE, CRITICAL CARE (LONDON, ENGLAND)[2012, 16(4):R128]
A mean 7-day hemoglobin concentration of < 90g/L is associated with
increased hospital mortality in patients with severe traumatic brain injury
ANAEMIA

45. TRANSFUSIONS AND LONG-TERM FUNCTIONAL OUTCOMES IN TRAUMATIC BRAIN INJURY
,MATTHEW A. WARNER, B.S.,1 TERENCE O’KEEFFE, M.B.CH.B., M.S.P.H.,5,PREMAL
BHAVSAR, B.A.,1 RASHMI SHRINGER, B.A.,1 CAROL MOO RE, M.A.,1,CARYN HARPER,
M.S.,1 CHRISTOP HER J. MADDEN, M.D.,2 RAVI SARODE, M.D.,4,LARRY M. GENTILELLO,
M.D.,3 AND RAMO N DIAZ-ARRASTIA, M.D., PH.D.1, J NEUROSURG 113:539–546, 2010
Transfusions may contribute to poor long-term functional outcomes in
anemic patients with TBI. Transfusion strategies should be aimed at patients
with symptomatic anemia or physiological compromise, and transfusion
volume should be minimized
BLOOD TRANSFUSION

46. THERAPEUTIC ANTICOAGULATION CAN BE SAFELY ACCOMPLISHED IN SELECTED
PATIENTS WITH TRAUMATIC INTRACRANIAL HEMORRHAGE. WORLD J EMERG
SURG.2012 JUL 23;7(1):25
RESULTS:
There were 42 patients with a traumatic intracranial hemorrhage that
subsequently developed a thrombotic complication. Thirty-five patients developed a
DVT or PE. Blunt cerebrovascular injury was diagnosed in four patients. 26 patients
received therapeutic anticoagulation, which was initiated an average of 13 days after
injury. 96% of patients had no extension of the hemorrhage after anticoagulation was
started. The degree of hemorrhagic extension in the remaining patient was minimal
and was not felt to affect the clinical course.
CONCLUSION:
Therapeutic anticoagulation can be accomplished in selected patients with
intracranial hemorrhage, although close monitoring with serial CT scans is necessary
to demonstrate stability of the hemorrhagic focus.
ANTI-COAGULATION

47. SHORT D, HARRISON P (2007) SYSTEMIC EFFECTS OF SPINAL CORD INJURY KEY POINTS:
NEUROLOGICAL SYSTEM. IN: MANAGING SPINAL CORD INJURY: THE FI RST 48 HOURS
(2ND EDN) (ED HARRISONP), 64–66. SPINAL INJURIES ASSOCIATION, MILTON KEYNES
Evidence of potential harm from steroids in SCI far outweighs
the evidence of potential improvement and the use can no
longer be justified.
STERIODS

48. Surgical intervention
• Closed, linear, non-depressed skull fractures
heal spontaneously, and surgery is not
necessary
• Treatment of a basilar skull fracture is
conservative unless cranial nerve injury
mandates surgical decompression.
• Open fractures or fractures depressed more
than the thickness of the skull require
surgical elevation and repair.
• The most critical factors in deciding whether
to operate on a traumatic intracranial
hematoma are :
– The patient’s neurological status,
– The imaging findings,
– The presence and severity of extracranial
lesions.

49. ICP monitoring :
• Intraventricular catheter (can
drain CSF)
• Subarachnoid screw or bolt (less
invasive, CSF cannot be drained)
• Epidural catheter or sensor
• Subdural catheter
• Fiberoptic transducer tipped
pressure sensor (most common
device for ICP monitoring)
Craniotomy

50. • Surgical intervention is decided more readily for temporal lobe and
posterior fossa lesions, in which a relatively small lesion may lead to
compression and irreversible brainstem damage within a shorter period of
time.

51. DENT DL, CROCE MA, MENKE PG ET AL. PROGNOSTIC FACTORS AFTER ACUTE
SUBDURAL HEMATOMA. J TRAUMA 1995; 39: 36–42
Time to surgery of less than 4 h was associated with a significantly higher
rate of functional outcome when compared with surgery delayed for
longer than 4 h.
TIME OF SURGERY

52. Spinal Surgical Decompression and/or Fusion
• Indications
– Decompression of the neural
elements (spinal cord/nerves)
– Stabilization of the bony
elements (spine)
• Time :
– Emergent
• Incomplete SCI with
progressive neurologic deficit
– Elective
• Complete SCI(3-7 days post
injury)
• Central cord syndrome (2-3
weeks post injury)

53. TIMING OF SURGICAL DECOMPRESSION FOR ACUTE TRAUMATIC CERVICAL SPINAL CORD
INJURY: A MULTICENTER STUDY QI CHEN, PHD, FENG LI, PHD, ZHONG FANG, PHD,
ZHENGUO ZHANG, PHD, YONG ZHANG, MPHIL, WEI WU, MM, AND GUANGQIN YAO, MM
NEUROSURG Q VOLUME 22, NUMBER 1, FEBRUARY 2012
Urgent surgical decompression improved cervical spinal cord function
more quickly than early surgical decompression. No neurological benefits
were obtained in the delayed surgery group. Urgent and early surgical
decompression decreased the morbidity of DVT and pressure ulcer, and
lowered the increase in the morbidity of autonomic dysreflexia, more
effectively than delayed surgical decompression. However, the timing of
surgical decompression did not affect the morbidity of hypostatic
pneumonia
TIME OF SURGERY

54. U.S. standard U.K. standard
• Complete and irreversible
loss of entire brain and
brainstem activity.
• Complete and irreversible
loss of brainstem function.
BRAIN DEATH

55. PALLIS C, HARLEY DH. ABC OF BRAIN STEM DEATH. BMJ
PUBLISHING GROUP, 1996, P.30
“Published studies of patients meeting the criteria for brain stem death
or whole brain death – the American standard which includes brain stem
death diagnosed by similar means – record that even if ventilation is
continued after diagnosis, the heart stops beating within only a few
hours or days”
BRAIN DEATH

56. • The concept of brain death is specific.
• It does not apply to patients existing in a :
– Persistent vegetative state
– other severe degrees of brain damage from causes
such as metabolic derangements, drug
intoxication etc.

57. Resolution of the Council of Islamic Jurisprudence on
Resuscitation Apparatus
Decision No. (5) D 3/07/86
• The council of Islamic Jurisprudence in its third meeting held in Amman, capital of
Jordan from 8 to 13 Safar 1407 H corresponding to 11 to 16 October 1986 and
after discussing all relevant aspects of resuscitation apparatus and after hearing
the detailed explanation from specialist doctors, decide the following:
A person is pronounced legally dead and consequently, all dispositions of the
Islamic law in case of death apply if one of the two following conditions has been
established:
– There is total cessation of cardiac and respiratory functions, and doctors have ruled that such
cessation is irreversible.
– There is total cessation of all cerebral functions and experienced specialized doctors have
ruled that such cessation is irreversible and that brain has started to undergo autolysins.
• In this case, it is permissible to take the person off resuscitation apparatus, even if
the function of some organs e.g., heart are still artificially maintained.

58. Saudi Center for Organ Transplantation
Who is responsible for the
diagnosis of brain death ?
• It is mandatory that a
– Neurologist,
– Neuro-surgeon,
– Internist,
– ICU physician,
– Anesthesiologist,
– Pediatrician
– consultant physician with experience
in evaluation of brain-dead patients
performs the examinations.
• Neither a nephrologist nor a
transplant surgeon should be
involved in the establishment of
diagnosis of brain death.
Who is responsible for the care
of patients with brain death ?
• The following professionals
are responsible for the care
of the brain-dead patient:
– ICU physician,
– Anesthesiologist,
– Internist,
– Neurosurgeon
– Neurophysician in
cooperation with-a
nephrologist

59. Summary
• Spine Immobilization
• Prevent/treat Hypotention
• Prevent/treat Hypoxemia
• Control Intracranial pressure
• Urgent surgical intervention

60. Thank you