This course is designed for nurses in emergency room in hospital

1. Head and spinal cord injuries
Department of Neurology
LF UPJŠ Košice
6.12.2017

2. Brain/head injury
• Brain and spinal cord injuries
and post-traumatic conditions is a serious medical
and socio-economic problem (permanent
consequences, disability, financial costs, ...)
• Most often in traffic accidents, sports and
occupational accidents
• Craniocerebral injury is damage to the skull, brain,
or both, an injury mechanism
• Splitt into : - open and closed
- focal and diffuse

3. Brain/head injury - mechanism of
action
• Translating - head collision with second body
• Acceleration - linear or rotary
• The patient may also fall as a result of the disease condition:
– Syncope
– Epileptic seizure
– Intoxication
– Stroke

4. Head injuries: classification
• Primary – occur at the time of the accident
- Diffuse: Brain concussion, Brain contusion, Diffuse axonal injury-DAI
- Focal/multifocal: Brain contusion
• Secondary – occur later (the result of an accident)
• A) intracranial - complications of primary injury (epidural bleeding,
subdural bleeding, intracerebral and traumatic subarachnoid
haemorrhage)
• B) extracranial - brain damage eg. hypotension, hypovolemia, etc.
• Interdisciplinary approach: traumatologist, anesthetist, neurologist and
neurosurgeon, physiotherapist, orthopedic ...

5. Introduction: Craniocerebral Injuries
• Effect of an external force on the skull and the
brain tissue with permanent or transient
impairment of brain functions
1. CLOSED
2. OPEN
– Impairment of the dura mater integrity

6. Skull fractures
• Types: open and closed
• Fracture lines - the most common temporal and skull base area
Skull fractures- Location:
• Skull vault fractures:
– Cracks (fissurae) – linear, partial (affect only lamina interna) and complete
– if they do not cross the course of meningeal arteries or venous sinuses, they do not usually
have a more pronounced clinical significance
– sharp/fritter and impressive/sqeeze fractures - by a sharp object with a risk of brain damage
• Skull base fractures: serious prognosis
– Brain base injury, hypothalamus, brain stem and cranial
nerves injury
– Indirectly after an injury to the vault or face bones
– „Eyeglasses-like“ hematoma
– Processus mastoideus ecchymosis – Battle sign
– Risks/complications: neuroinfection (purulent meningitis,
brain abscess), CSF fistula, IC hypotension syndrome
(CFS), n. I and n.II. injury, deafness, n.VII. damage
• CSF - cerebrospinal fluid

7. Skull fractures - diagnosis
- Clinical physical evaluation- palpation - local pain, edema, or decline
- Skull X-ray or brain/skull CT (bone window)
- Liquorrhea nasalis (CSF leakage through broken meninges)
- Otorrhea

8. Skull fractures- therapy
• Linear skull fractures (fissurae calvae)
• Mostly without clinical symptoms and requiring no surgical treatment
• Observation to exclude the development of extracerebral hematoma
• Impressive skull fractures with significant bone dislocation
• surgical repositioning of debris
• under great impression - rupture of the dura and brain contusion on
the brain surface with expansive character
• in the frontal area - even less impression is elevated in a case when
cosmetically significant defect is posed to the patient
• for skull base fractures - ATB coverage is recommended, risk of
pathogens /bacterias entry from oropharynx and airways

9. PRIMARY BRAIN INJURY
• Diffuse - Brain concussion - mTBI
- Diffuse axonal injury - DAI
• Focal

10. 1. BRAIN CONCUSSION
(COMMOTIO CEREBRI, MILD TRAUMATIC BRAIN INJURY- MTBI)
• 2 definitions:
• 1. Reversibile,global brain function failure (transient lost of synaptic function)
- generalised asynapsia, reticular formation dysfunction
- disturbance of consciousness (revised definition from 2008)
• 2. Brain injury caused by external mechanical energy on the head area
associated with a subsequent CNS disorder
• Appearance: 70 – 90 % of all cranio-cerebral injuries
• men are twice as likely to be affected
• the most at risk is the age group 15 – 24 years
• Reasons: traffic accidents and falls
• in which the brains are shuffled back and forth

11. • Sharp acceleration or deceleration of head movement
• Relative displacement of adjacent parts of the brain with inertia
• Mechanism of mTBI: Diffuse Axonal Injury- DAI (or Diffuse Axonal
Damage-DAD) = Functional or structural traumatic damage to the
axons of brain white matter, mainly reticulo-cortical pathways
• Loss of consciousness in mTBI - correlates with axonal damage,
may also have image of qualitative change of consciousness
(disturbance of the outer world perception)

12. DAI
• Functional or structural traumatic axonal damage (brain white matter)
• Differential movement of adjacent brain regions during acceleration and
deceleration
• DAI is major cause of prolonged coma after TBI, probably due to disruption of
ascending reticular connections to cortex, Angular forces > Oblique/ Sagital Forces
• Stretched axons = functional impairment , reversible impairment
• Sheared axons = their ascend. and descendent degeneration, permanent
damage

13. MTBI - MILD TRAUMATIC BRAIN INJURY
• always comes suddenly
• duration of symptoms - different (a few seconds to hours)
• Injury mechanism:
– either by moving the head that is stopped by the motionless object or the
impact of the moving object on the head
– direct attack on the head, face, neck, or any part of the body with inertial
force transfer to the brain region
Unconsciousness and retrograde amnesia without the presence and evident
structural brain lesion, which will take off without consequences

14. MTBI : clinical picture
• Neurological evaluation + score of GCS (Glasgow Coma Scale)
• mTBI: GCS 13 – 15 and duration of unconsciousness (if present)
within 30 minutes
• Clinical picture must meet at least one of the following criteria :
1) confusion and / or disorientation
2) Unconsciousness of up to 30 minutes (may or may not be) - DAI
3) Post-traumatic amnesia up to 24 hours (the lost memory of the event)
4) Other transient neurological symptomatology – focal
neurological deficit, convulsion and detected intracranial lesion,
not required neurosurgical intervention

15. MTBI: clinical picture
• Areflexia, bradycardia and hypotension, nauzea
• Gradually, the patient takes over, is disoriented, can not make simple commands,
confused, behavior changes, slow reactions, incoherent speech, motion
coordination disorder, restlessness, crying (disappear within minutes)
• Post-traumatic stunning (obnubilation) state:
• restlessness, aggression, uncritical status
• more often alcoholics and people with brain damage already before
the accident
• amnesia covers the entire time of the obnubilation
• Post- mTBI convulsions:
• specific non-epileptic phenomenon
• occurs within 2 seconds of the crash
• short-term tonic stiffness and subsequent two-sided, often
asymmetrical myoclonic jerks up to 3 minutes (similar to convulsive syncope)

16. POST-CONCUSSION SYNDROME
• Occurs when trying to start a normal personal and working life after head injury
• Symptoms retreat within a few days or weeks
• Improvement after mTBI – within 3 to 12 months
• 5 % - 1 or more symptoms are persistent even one year after the injury (headache,
dizziness, fatigue, attention deficit, memory and selected executive functions problems)
• Somatic and vegetative: headache, dizziness, nausea, vomiting, smell deficit,
insomnia, rapid tiredness, pathological fatigue, visual problems, hypersensitivity
to light and noise
• Cognitive: disturbance of attention, memory, slowing of thinking, faults in
executive functions, decreased performance
• Emotional : emotional lability, depression, anxiety, nervousness, apathy

17. MTBI - DIAGNOSIS
• History + neurological (without focal symptoms/deficit) + traumatological investigation
• transient (several hours) may be pyramidal irritation symptoms or tendon jerk hyperreflexia
mTBI - 3 categories by risk:
– 1 ) GCS 15, without serious and with maximum 1 less serious risk factor, after head injury without
brain injury, who can be released without head and brain CT scan for home observation unless
another reason for hospitalization is known
– 2 ) GCS 15 with serious or multiple minor risk factors
– 3 ) GCS 13–14, required brain CT
• Brain CT : usually a negative finding
• Brain MRI : changes in tissue signal (hypersignal) in corpus callosum, subcortical white matter, in the
thalamus and brainstem

18. MTBI – DIFFERENTIAL DIAGNOSIS
• Other states of short-term loss of consciousness:
• Epileptic seizure
• Syncope
• Arhytmia
• Intoxication
• Diabetic coma
• Patient with an uncertain history, is approaching
laboratory examination of biochemical parameters in
order to exclude metabolic disorders, cardiac disorders
/ECG/, etc.

19. MTBI – THERAPY
• 1) In the case of negative brain CT, and negative neurological findings and amnesia up to
maximally 60 minutes - patient may be released
• 2) Observation
– Focal neurological deficit
– GCS < 15 points + prolonged posttraumatic amnesia/ agitation
– Headache of high intensity
– Persisting vomitus
– Liquorrhea with suspected skull base fracture
– Polytrauma
– Koagulaopathy
– Alcohol or drug intoxication
– Suspected non- traumatic damage
Mode: repeatedly evaluated neurological status
– GCS < 15..... every 30 minutes
– GCS = 15..... every 30 minutes for the first 2 hours and if there is no deterioration every 1 hour for
the next 4 hours and then once every 2 hours
– Patient observation should be at least 12-24 hours

20. MTBI – THERAPY
• Acute state:
• physical and mental relax until symptoms disappear, followed by gradual
loading
• analgetics (inappropriate non-steroidal anti-inflammatory drugs, ASA-risk of
bleeding higher + opiates - effect on consciousness)
• Prognosis : generally favorable
• spontaneous disappearance of post-mTBI symptoms
• Profylaxy:
• use of helmets (bicycles, motorbikes), education of adults and children about
the brain injury risks and consequences
• adjustment of risk working practices in individual jobs

21. POST-CONCUSSION SYNDROME
(POST-MTBI SYNDROME)
• Definition
• a set of multiple defined persistent post-concussion symptoms
• Occurrence: 50 % of cases of mTBI
• either immediately after the concussion or with latency of a few days after the
accident
• Substrate: unknown
• Headache, attention disturbance, sleep disordres, fatigue, inefficiencies, dizziness,
vegetative dysfunction, 2-12 months, EEG – slight patologic pattern
• 5 – 20 % - lasts up to one year
• Chronic traumatic encephalopathy
• Repeated head injuries ! (boxers, epileptic falls, physically abused persons) can
trigger a neurodegenerative cascade - progressive tau-pathies

22. 2. Contusio cerebri – cerebral contusion
• Definition: focal/multifocal crush of
brain tissue that results from non-
penetrating head trauma
• Structural brain injury/damage with
1. edema/ swelling
2. bleeding / haematoma
3. hypoxic-ischemic changes
• Contusion at the point of crush - par coup
• In the opposite direction to the crush side -
par contre coup – these are more serious
and clinically significant

23. 2. Contusio cerebri – cerebral contusion
• Local or multiplicit (multifocal) cerebral contusions
• On the hemisheral surface:
– In the areas of anterior and posterior temporal lobe pole
– Frontal lobe anterior pole
• In the deep brain structures:
– Periventricular areas
– Basal ganglia
• The degree of brain tissue damage is different: petechial bleeds until extensive lacerations
• Characteristic sign – multiplicit, multifocal lesions
• Contused tissue = necrosis, edema and bleeds = followed by postmalatic necrosis = healing
by cerebromeningeal scar, +/- uncousciousness, focal neurological deficit
• The first 24-48 hours brain edema is worsening

24. 2. Cerebral contusion
• Clinical symptoms and disease course: depends on the extent and
location of lesions
• totally asymptomatic ... up to heavy contusions with unconsciousness
• Clinically manifested brain contusion:
• always present disorder of consciousness (qualitative and quantitative) and
focal neurological deficit (e.g. hemiparesis, aphasia, agnosia, epileptic seizures)
• qualitative consciousness changes – prefrontal syndrome = behavioral
disturbance, affectivity change, restless, loss of orientation in space, lack of
criticism and deliberation
• sleepiness can be alternated with restlessness, agitation and confusion state

25. 2. Cerebral contusion
• In the beginning, unconsciousness may be present - usually longer! as in brain
concussion (mTBI) (hours to days)
• an amnesia for head injury is always present
A) a temporal - lucide interval (short wakefulness) may occur and the
development of the focal symptoms due to perifocal edema continues = again
a disturbance of consciousness arise
B) in many cases the lucide interval is missing = the patient is unconscious from
the beginning
• GCS ≤ 7 = serious state, poor prognosis
• GCS ≥ 9 = better prognosis (the border is GCS = 8 points)
• GCS- Glasgow Coma Scale

26. 2. Cerebral contusion - diagnosis
• History + clinical neurological and traumatological
investigation
• Brain CT: hyperdense places of brain crushing,
dynamic pattern– enlargement a few days after injury
- development of these lesions is unpredictable
• Event relatively favorable course may suddenly be
complicated by expansion of contusion or worsening
of surrounding edema
• Brain CT should be repeated 24 - 48 hours
• Scars (glial scars), posttraumatic necrosis, pseudocysts
• Patient monitoring /ICU: continual observation and
vital function monitoring, neurological state changes,
vital function correction (BP, heart freq., respiration
parameters, pO2 saturation), X-ray cervical spine,
fundoscopy (optic disc n.II. edema = brain edema)

27. 2. Cerebral contusion – therapy and prognosis
• Ensuring vital functions - ventilation and circulatory functions
• positioning of the head and neck - optimal head with an elevation of 30 - 45
degrees
• Therapeutic approach: symptomatic or surgical
• Antiedematous therapy – manitol, anti- convulsants, decubites profylaxy
• Intracranial pressure monitoring – in a case of malign brain edema is
indiated decompressive partial craniectomy
• Fyziotherapy
• Prognosis is different
• depends on the extent of brain damage
• GCS score
• in many cases - sustained focal deficit, cognitive and
psychiatric disorders, posttraumatic epilepsy

28. Gunshot wound and stab brain
injuries
• Penetrating injuries= gunshot injuries
• Perforating injuries = stab injuries
• are an open type of head injury
• there is an injury to the skull and the
brain by penetrating subject – e.g. rod,
knife, cutting and stab object
• The extent of the brain injury depends on
the kinetic energy of the penetrating
object
• Complications - neuroinfection,
meningitis, meningoencephalitis, brain
abscess

29. Gunshot wound brain injury
• The range and severity depend on the velocity, caliber and character of the
projectile and the trajectory of the shot (the higher the kinetic energy of the shot,
the greater the destruction of the tissue)
• Usually extensive brain tissue devastation is present
• Gunshot brain injuries - two types
• Perforating gunshot wound – the projectile penetrates the skull and the brain, creates a fire channel
with fragments of bone and flies out of the head
• Penetrating gunshot wound – the projectile penetrates the skull and the brain, but it is trapped
intracranially
• Complications (may be fatal): brain edema, neuroinfection - meningitis,
meningoencephalitis, cerebral abscess

30. Gunshot wound brain injury
• Diagnosis:
• Inspection of the entry site /shot
• X-ray, CT scan – skull injury, bone fragments in the fire channel and
locating the projectile (at the aperture)
• brain CT- brain tissue damage, brain contusion around the fire
channel and hematoma
• Therapy: surgical + antibiotics (14 days)
• Prognosis:
• always very severe damage
• total mortality - 90 %
• up to 70 % of patients die before hospital treatment

31. Stab brain injuries
• sharp object – a stick, needle, knife, sword, fork ... with low speed
• narrow fracture of the skull + puncture channel with bloody brain tissue in the area of ​​the
puncture canal and its surroundings
• there is no concentration zone of coagulatting necrosis, nor diffuse brain damage around the
puncture channel
• degree of disability and prognosis depend on the location and depth of penetration
• Prefrontal area – personality changes, relatively good prognosis
• Temporal lobe – risk of injury of important structures- thalamus, brainstem, Willis circle
vessels, cranial nerves - high mortality!
• The penetrating object under the first aid principles is not removed from the wound - the
wedged object creates a tamponade of important vessels

32. Stab brain injuries
• Diagnosis
– Brain CT - clarifies the depth and magnitude of brain damage
– CT brain- bone window - useful for indicating skull plastic surgery or
removal of bone fragments, foreign body from brain tissue
– AG brain vessels – suspected vascular posttraumatic complications
• Therapy- perforating brain injuries - surgical
– craniotomy and with the revision of the punch or fire channel
– drainage of bloody brain tissue
– removing available foreign bodies and bone fragments
– surgical treatment does not interfere with deep structures! (brainstem,
thalamus)
– maximal carefully review and treatment of the speech and visual cortex!
– antibiotics - an infection profylaxy

33. Stab brain injuries
• 35 % - complications : neuroinfections, inflammatory-
type complications, especially if the puncture canal
passes through the paranasal sinuses
– meningoencephalitis
– abscess
– ventriculitis
• 30 % - complications with brain vessels damage
– pseudoaneurysm – up to 50 % of them bleed
during the first week and lead to death in 30-50 %
of cases
– vazospasms
– vessel occlusion
– arterio-venous fistula
• Because of these complications and their high
mortality, it is recommended to perform an AG
-angiographic examination as soon as possible

34. Secondary brain injuries
• Primary head injury can cause secondary brain
injury
1. Epidural bleeding
2. Subdural bleeding
3. Intracerebral traumatic bleeding
4. Traumatic subarachnoidal bleeding

35. Epidural haematoma
• Arterial bleeding between skull bone and dura mater after head injury
• Source: most common a. meningea media at the fracture site (with
patietal and temporal bone fractures)
• arterial bleeding (high pressure) does not have tendency to stop
spontaneously
• up to 75% - a skull fissure is present
• after the 60th is rare (firm adhesion of the thorn to the bone of the skull)
• supratentorial localisation, rarely infratentorialy (venous sinus)

36. Epidural haematoma
• Small hematoma - may be asymptomatic
Larger hematomas - progressive character:
• Typical disease course: initial coma (DAI) – lucid interval
(few hours) - development of rapid progression
uncousciousness + focal brain symptoms/deficit – sy ICH +
brain herniation (temporal conus) and craniocudial
deterioration (occipital conus) – death
• In case of severe injuries and extensive haematomas, the
disturbance of consciousness from the beginning and no
stroke interval
• Posterior fossa hematoma- occipital conus, respiratory
failure
• Syndrome ICH- intracranial hypertension
• Epileptic seizure

37. Epidural haematoma: diagnosis and
treatment
• History + neurological evaluation
• Skull X ray – fissura, fracture crossing
a.meningea media
• Brain CT: typical convex shape lens-like
hyperdense lesion- hematoma
• Treatment:
• surgery, urgent blood aspiration-
evacuation + revision of affected artery
and dural space
• In most cases life-saving procedure
• progressive expansion of hematoma with
compression of the brain, the risk of brain
cones - does not delay!
• Without therapy- fatal brainstem
compression /brain herniation- temporal
and occipital conus/

38. Subdural haematoma
• Traumatic venous bleeding between dura mater and arachnoidea
• Source: rupture of brain bridging veins (surface veins of the brain in the section
prior to sinus entry) or of the pial vessels
• Most often - frontal and parietal, in 15-20% of cases it is on both sides
• Venous bleeding – low pressure, slow, may stop spontaneously
• size varied - from small cloaks to large
• Occurrence: the most at risk: old people with atrophy of the brain
Classification – disease course:
» acute
» subacute
» chronic

39. Acute subdural haematoma
• Focal neurological deficit- similar to epidural hematoma
• the most common type of traumatic intracranial bleeding
• manifests itself within 24-48 hours after injury
• development of focal symptoms from direct hematoma to brain
pressure or brain herniation (coma), may also be associated
with cerebral contusion
• may coincide with the image of epidural hematoma with lucid
interval and focal symptoms, but the dynamics of consciousness
disorder is not so dramatic
• Diagnosis: brain CT - semilunar shape of haematoma
• Therapy:
• Large hematomas- urgent surgery, blood evacuation
• Small hematomas- observation

40. Subacute subdural hematoma
• manifests itself within 3 weeks of injury
• more frequent in older age
• dominated progressive consciousness
disorder, headache, dizziness and light palsy/
hemiparesis

41. Chronic subdural haematoma
• Slow progressive or persistent symptoms
• Less severe disease course and symptoms
• The onset of several weeks to months after the head injury
• Own bleeding does not clinically occur in the acute phase
• Chronic headache, ICH syndrome, hemiparesis, psychic changes, apathy, balance
disorders, speech disorder (aphasia), epileptic seizures
• Occurrence: chronic alcoholics, people with blood clotting disorder, infants
• In the elderly - even after the banal head injury
• Can be undiagnosed or silent
• Unrecognized - an image of progressive dementia, incontinence, walking disorders, and can be
mistakenly evaluated as Alzheimer's disease, brain tumor in the frontal region, dementia of alcoholics
• Often slight head injury
• Haematoma- blood/Hb metabolic changes are osmotic active – water, lesion enlargement
= hygroma
• Complications: ICH syndrome, brain herniation

42. Chronic subdural haematoma: diagnosis
and therapy
• Diagnosis: History + neurol. evaluation
• Brain CT - typical moon shape hematoma /hyperdensity
• Chronic stage- hypodensity (hygroma)
• Therapy:
• relatively rigid capsula even after evacuation of the hygroma it can be repeatedly filled
with fluid - require open operation with removing of the hematoma sleeve
• Small subdural haematoma – conservative approach- observation
• Surgery indications:
• hematoma thickness 10-12 mm, taking into account the degree of cerebral atrophy and
the manifestations of hematoma expansion to surrounding structures
• Urgent surgery: posterioir fossa (infratentorial) hematoma- risk of brainstem compression
• Prognosis- depends on hematoma volume and brain compression
• Generally good prognosis

43. Intracerebral traumatic bleeding
• Intracerebral traumatic hematoma
• Focal symptoms
• occurs at the time of injury or delay -6 hours apart
• usually with heavy head injuries
• Cause: rupture or vessel wall distention
• Localized on the head injury side, contralateral, or both sides
• Mainly frontal lobe, temporal lobe
• may be combined with bone fracture, subdural hematoma, brain
contusion and diffuse axonal injury
• Clinical picture: focal neurological symptoms
small hematomas - asymptomatic
large hematomas - ICH syndrome, conus of the brain
• Diagnosis: brain CT

44. Traumatic subarachnoidal
haemorrhage (SAH)
• Associated with cranial injuries
• Often accompanied by brain
contusion
Clinical picture: meningeal
syndrome, ICH sy, hydrocephalus
•
Diagnosis:
CT brain
AG
• CSF - finding a blood in a CSF

45. Postraumatic syndromes
1. Brain edema and ICH syndrome
Brain congestion, neuroinfection (meningitis, brain
abscess), likvorhea
2. Epileptic seizures and posttraumatic epilepsy
3. Hydrocephalus
4. Posttraumatic syndrome, irritability, instability,
diziness, sleep problems, emotions, mood, ...
5. Dementia pugilistica
6. Posttraumatic parkinsonism

46. Posttraumatic complications and
syndromes
• The critical period for the development of secondary brain damage is the
period immediately after the injury
• Clinical status progression and secondary brain damage can also be caused by
many extracerebral causes:
• hypovolaemia
• hypotension
• hypoxia or hypercapnia
• respiratory distress
• pulmonary embolism, adult respiratory distress syndrome (ARDS)
• infection
• disseminated coagulopathy, organ failure
• arhytmia

47. ICH syndrome
• Brain edema: Generalized, local or around focal lesion
• Hemispheric edema - is caused by the progression of focal edema
Edema is vasogenic, less cytotoxic
ICH sy = syndrome of intracranial hypertension:
• worsening of cerebral perfusion
• promotes further worsening of edema
• overpressure of central structures to contralateral side ide by more than 10-12 mm - it
is necessary to consider decompressive partial craniectomy
• Early detection of critical IC pressure increase – by IC pressure monitoring
• Diagnosis of brain edema: brain CT
Treatment: conservative-anti-edematous (mannitol)
malignant edema - decompressive partial craniectomy (temporary
local removal of calves beyond the largest edema)

48. Posttraumatic complications
• Brain congestion (vascular swelling, brain hyperaemia)
increased cerebral blood volume, followed by increased brain volume
• stasis in the vein brain system, post-vasoprevention and vasodilation
• Neuroinfections - complications of open penetrating skull injuries:
• meningitis, meningoencephalitis, abscess of the brain
• Liquorrhea - CSF (5 to 10% of patients with skull base fracture)
• pathological communication (fistula) between the subarachnoid and extra-
cranial space: the nasal leakage=rhinorhea, or the ear=otorhea
• the risk of posttraumatic cranial hypotension and bacterial meningitis
DG: isotopic examination by radionuclide
Treatment: head lift, antibiotics, if it lasts for more than 2 weeks, while fistula
persists, recommended plastic surgery of the dura mater

49. ICH syndrome
Brain herniation
• Head elevation up to 30o
• Slight hypothermia
• Arterfic. hyperventilation
• Antiedematous th – Manitol,
Kortikoids ?
• Dekompressive surgery
• Hematoma evacuation
• Decompressive craniectomy

50. Posttraumatic complications
Hydrocephalus
• slowed CSF reabsorption after brain injury
• communicating normotensive hydrocephalus - cognitive impairment (dementia),
walking disorder and incontinence, DG: Brain CT
Treatment: surgery = temporary or permanent shunt - ventriculoperitoneal drainage
with removal CSF from the ventricle into the peritoneal abdominal cavity
Epileptic seizures
• 5-10% of patients with craniocerebral trauma
• Early post-traumatic epileptic seizures (within 1-2 weeks of injury) – symptomatic
• Late - the development of epilepsy
• brain injury have a 29-fold higher risk of developing epilepsy than a normal population
• Cause: hematomas, contusive lesions, fragments of bone with impression
The greatest risk of late seizures - 0.5-2 years from head injury and <10 GCS
Treatment: anti-convulsants (2 weeks after head / brain injury)

51. Spine and spinal cord injuries

52. Spine and spinal cord injury

53. Spinal injury
• Spinal injury: damage to one or more vertebrae,
luxation, fracture of the body or arc, or
combination of luxation and fracture, ligament
damage and fixation muscle corset
• Occurrence: relatively common, rarely associated
with injury to nerve structures (spinal cord and spinal
cord)
• Injury of bone and soft backbone structures (mainly
dislocation of vertebral fractures) may cause spinal
cord compression and spinal cord disruption
• Injury mechanism: fracture, penetrating bony
fractures, contusion, gunshot
• either alone or together with a spinal cord injury
• In spinal cord injuries - always very serious
consequences for the life of the affected person, his
physical and mental health
• Often, young adults in productive age are affected

54. Spinal injury
• World incidence of traumatic spinal cord injuries:15 to 30 cases per million
inhabitants per year
USA: 28-50 cases/million inhabitants per year
Slovakia: 20 cases/million inhabitants per year, of which about ¼ is a complete lesion
of the spinal cord
• Up to 80% is between 18-35 years of age
• Men are 2,5 to 3 times more than women
• 55 % of spinal cord injuries are reported in road accidensts
• 30 % in industry and 15% in sport
• The most common causes of spinal cord trauma are road accidents, sports injuries,
height drops, violent and gunshooting injuries

55. Commotio medullae spinalis
• Reversible spinal cord injury, no organic changes
• Reversible loss of spinal functions followed by full improvement within 24 - 72 hours
(usually several minutes to hours)
• Causes: fall from a height or crush
Most common levels: C 5-7, Th 10 - L1 and Th5
KO: spinal shock, acute transversal spinal lesion with quadriplegia or paraplegia and
urinary retention
– Cause: spinal cord edema, temporary ischemia or depolarization of cell membranes. There is no complete
transversal spinal cord lesion, as some functions remain preserved; typical is the volatile and transient
finding of a neurological deficit
• Therapy:
• Lihgt form: do not required treatment, sponatneous complete improvement
• Severe forms: steroids (methylprednisolone i.v. )
• Analgetics, sedatives, thrombosis profylaxy (low molec. Heparins)
• Prognosis: generally good, most cases improve ad integrum

56. Spinal cord injury
• most commonly associated with spinal cord injury
• as a result of luxation or vertebral fractures, spinal cord or spinal cord
compression occurs
• rarely spinal cord injury is present without simultaneous spinal vertebres (in
children and adolescents)
• Mechanism of action- spinal cord injury:
• direct spinal cord destruction by injury
• spinal cord compression by hematoma, bone fragments, prolapsed
intervertebral disc
• spinal cord ischemia due to spinal artery injury or compression

57. Spinal cord injury
• Depending on the extent of injury we divide the traumatic lesions of the spinal cord:
• A – partial, incomplete spinal cord lesion – 55 % spinal cord injuries
– Some modality of sensitivity or motor function remains preserved (e.g. central spinal
cord lesion syndrome)
– Right after the injury, some incomplete spinal lesions may be manifested by a picture of
complete plegia as a result of spinal shock
• B – total, complete transverzal spinal cord lesion – 45 % spinal cord injuries
– The spinal cord is affected by necrosis due to ischemia or tissue dilaceration
– There are no motor and sensory functions preserved distally to the wound site
– Interruption of sympathetic nerves leads to hypotension and below the level of injury is loss of
blood vessels tonus, stagnation of venous blood flow (risk of venous thrombosis)
– Bradycardia - the result of predominance of parasympathetic tonus
– This condition is part of the „neurogenic shock“ - characterized by haemodynamic triad of
hypotension, bradycardia and peripheral vasodilation from discontinuation of sympathetic
innervation in acute spinal cord injury, especially above the level of Th6 segment

58. Primary spinal cord injury
• In spinal cord injury: primary and secondary spinal cord injury occurs
• Primary injury: mechanical spinal cord injury by concussion, tearing, squirting,
compression, or indirectly by extradural processes - hematoma, tumor,
metastasis
• It occurs at the time of injury and is most often caused by bone structures -
fractures, or sequestration of the intervertebral disc
• The result is bleeding and necrosis of the tissue from the oppression and shear force
• Tachycardia, later bradycardia and blood pressure fluctuation, hypotension and hypoxia
• Local auroregulation changing mechanisms leads to bleeding occurs mainly in the spinal
cord gray matter, leads to vasospasms and thrombosis

59. Secondary spinal cord injury
• consequence of auto-destruction, disturbances in blood supply to the tissue, disturbed
vascular supply by arterial injury, thrombosis, or hypoperfusion and spinal shock
hypoxia
• massive release of cytokines, neurotoxins, arachidonic acid, free radicals and
prostaglandins, which further aggravate the state of already damaged tissue
• These factors leads to worsening of blood flow in the spinal cord and aggravate edema,
which extends several segments up and down from the site of damage
• Capillary damage, haemorrhage - traumatic hematomyelia and
• secondary ischaemia of mainly spinal cord gray matter - myelomalatia and necrosis
occur
• Protection of the spinal cord from immediate damage resulting from primary injury is
not possible
• therapy may only be aimed at avoiding secondary changes in the tissue
• Secondary changes begin already in the first hours after the injury and have a
significant impact on the outcome

60. Spinal cord injury
• The clinical picture depends on the location and extent of spinal cord injury
• Neurological symptoms + respiratory distress, restlessness, anxiety, agitation,
paleness, cyanosis - breathing disorder and lost sympathetic innervation
• Segment C1 – C2: vit.respiratotry capacity 5 – 10 % of normal value, coughing is
impossible, death
• Below C5: quadruparesis/plegia, diaphragmal breathing only
• Th2 – Th4: vit.respiratotry capacity 30 – 50 %, coughing is weak, LL paraplegia

61. • Below Th11: minimal rspir. insufficiency, LL paraplegia
• Brown-Séquard syndrome
• Syndrome anterior spinal cord lesion- ventral spinal compression, syndrome
a.spinalis anterior, syndrome of syringomyelic dissociation
• Syndrome central spinal cord injury
• Syndrome posterior spinal columns
• Syndrome epiconus medullaris: segment L4 – S2
•
• Syndrome conus medullaris: segmentov S3 – Co3
• Syndrome cauda equina: roots L3 – S5

62. Spinal cord injury- spinal shock
• Transient depression of all sensitive and motor functions connected to
autonomous innervation lost right after spinal injury
• the loss of all spinal functions and reflexes distal to the site of the injury
• at the beginning, we find the image of the flaccid plegia (2 weeks to several
months)
• then develops spastic paresis / plegia (usually spastic paraplegia of the lower
limbs with a disorder of urinary and stool control)
• An unfavorable prognostic symptom:
- presence of a complete transverse lesion more than 24 hours
- priapism (pathological painful penile erection)
- prolonged plantar leg flexion

63. Spinal cord injury
• Spinal cord contusion
• Focal /segmental persistent disorder of motor, sensitivity
and sphincter functions
• In lesions at the level above the C4 segment - disturbed
diaphragma innervation and the patient requires artificial
ventilation
• Whiplash injury
• traumatic neck injury is typical for traffic accidents
• sudden movement of the fuselage and cervical spine,
severe hyperflexia and subsequent hyperextension give rise
to a movement similar to whiplash
• a muscular and connective tissue injury of the neck portion
sometimes associated with the dislocation or fracture of
the vertebrae
• symptoms develop only after hours - pain and stiffness,
headache, shoulders and chest spine between the
shoulders
• Rare spinal cord injuries may also occur

64. Spinal cord injury
• Diagnosis
• Neurological, traumatological, neurosurgical evaluation
• motor, all sensitivity modalities and sfincter difficulties
• Spinal CT and MRI (fractures, fissure, hematoma, necrosis,
edema, ischemia, contusion, disc lesion)
• It is important to determine the lesion boundary, which is
the most caudal segment that has a preserved motoric and
sensitive function
• The last picture of spinal damage is composed of primary
mechanical damage and subsequent self-destructive
processes in the first 4 hours after injury
• For the objective range of spinal trauma is used Frankel ´s 5 degreescale:

65. Spinal cord injury
• Therapy
• Dynamic process
• the full range of injury can only occur after some time
• Incomplete lesion may go to complete, the extent of the injury is aggravated by one to two
segments above the initial level in hours and days
• Respiratory complication of spinal trauma
• First Aid and Patient Transport Principles:
• stabilization and fixation of the injured spine during patient's transport
• minimize manipulation, maintain normal spinal axis position
• transport on a hard pad or in a vacuum mattress
• fix the neck with a hard - Philadelphia collar
• it is necessary to predict spinal cord injury and to take precautions to prevent deterioration of the
spine, correction of respiratory distress (supportive breathing, intubation and artificial ventilation),
cardiac activity and possible hypotension

66. Spinal cord injury
• Early administration of corticosteroids
Methylprednisolone high dose 30 mg/kg i.v. for 45 minutes and after 15 minutes
- 5.4 mg / kg for 23 hours (the procedure is valid if the 1st dose is administered within 3 hours after
the injury
- If corticosteroids can be administered from 3 to 8 hours after the injury, it is continued
continuously for 48 hours
- The aim of corticotherapy is to reduce secondary changes in the spinal cord
• Surgery
• to prevent further deterioration of the neurological condition
• to create optimal conditions for restoration of functions and to ensure
decompression of the spinal cord, reposition and stabilization of bone structures

67. Spinal cord injury
• Symptomatic therapy
• Analgetics, prevention of decubitus and infections, treatment of spasticity, disorders of
autonomic regulation, psychotherapy
• Sexual dysfunction therapy
• Transuretral catheterization – sfincter problems
• Suprapubic epicystostomy
• neurogenic reflex bladder: spinal cord lesion above segment S2 - S4, the patient does not feel the bladder filling,
the bladder is emptied spontaneously, reflexively, automatically
• atonic bladder: spinal cord injury at or below the Budge Center, the bladder must be emptied passively.
• Rehabilitation:
• the focus of concurrent treatment of spinal cord injuries
• restoring the affected functions and making the best use of preserved functions and
muscle potential
• preventing the development of muscular atrophy

68. Spinal cord injury- prognosis
• Prognosis is individual, depends on severity and location
• neurological deficit may increase even further over the hours and days after
the injury
• extending neurological deficits cranially is a sign of deterioration
• complete spinal lesions have an adverse prognosis, with permanent loss of
motor activity, sensitivity, sphincter control, and impotence
• upper cervical segments lesion – may progress to ascendent necrosis of
medulla oblongata
• Complications: decubites, aspiration, hypothermia and respiratory problems
• At complete spinal cord lesion - only about 5 % of the recovery is available
• The dynamics of the change in the first hours and days is important:
– if complete paralysis persists for more than 72 hours – improvement is not possible
– if at least minimal sensitive innervation is maintained – 50 % chance of restoring the ability
to walk