Head Injury + Coma Flashcards

1
Q

What is the difference between: coma, stupor, confused and delirium?

A
  • coma → unresponsive, unrousable state
  • stupor → unresponsive, rousable state
  • confused → alert, but disorientated
  • delirium → like confusion, but also agitated + restless
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2
Q

What are clinical features of a coma?

A
  • unconscious (lasting 6+hrs)
  • unrousable
  • fails to respond normally to pain, light + sound
  • lacks a normal sleep-wake cycle
  • does not initiate voluntary movement
  • GCS 3-8
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3
Q

How do you calculate the Glasow Coma Scale?

A
  • E4 V5 M6
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4
Q

What are the differentials for coma?

A
  • epilepsy
  • trauma → concussion, haematoma
  • vascular → stroke
  • infective → meningitis, encephalitis, cerebral abscess
  • circulatory → MI, septic shock, hypovolaemia
  • metabolic → Na, glucose, calcium, uraemia, hepatic failure, DM
  • endo → adrenal crisis
  • toxins → alcohol, sedatives, TCAs, CO
  • psych → catatonia, psychogenic
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5
Q

On what 3 structures in the brain does consciousness depend on?

A
  • pontomesencephalic reticular formation
  • thalamus + hypothalamus
  • diffuse cortical projections
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6
Q

Predictors of prognosis of coma include causes of coma, depth + duration as well as clinical signs present. After head injury, prognosis is directly proportional to initial GCS.

What causes are associated with a good and bad prognosis?

A
  • GOOD:
    • drug overdose → high proportion of good recovery if adequately treated
    • metabolic → 25% good recovery
  • BAD:
    • cerebrovascular disease → 75% die, 3% fully recover
    • hypoxic-ischaemia → 60% die, 8% recover
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7
Q

What are some complications of coma and how can we prevent them?

A
  • bedsore → good nursing care eg turning pt every 2-3hrs
  • infection → pneumonia due to aspiration, lack of gag reflex or from feeding tube - ensure careful feeding + monitoring, can tilt patient up, UTIs 2o to long-term catheters
  • atelectasis → chest physio, alteration of ventilator settings
  • malnutrition → NG feeding + fluid resuscitation
  • contractures → physio
  • persistent vegetative state → coma becomes permanent
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8
Q

Initial assessment + management includes ABCDE resuscitation.

What are some examples of treatment for reversible causes of unconsciousness/coma?

A
  • glucose infusion for hypoglycaemia → 50ml of 50% glucose IV
  • IV thiamine → alcoholism or unclear diagnosis
  • drug overdose antidotes:
    • naloxone → for opiates, 0.4-2mg IV
    • flumazenil → benzodiazepines, if airway compromise
  • if signs of infection:
    • meningitis → cefotaxime
    • encephalitis → aciclovir
  • anticonvulsants if pt is in status epilepticus → lorazepam
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9
Q

What is meant by ‘vegetative state’?

A
  • complete loss of awareness
  • with preserved wakefulness + wake-sleep cycles
  • thalamocortical function severely disrupted
  • commonly due to:
    • severe cerebral cortical damage → anoxia-ischaemia or hypoglycaemia
    • damage to white matter of cerebrum → diffuse axonal injury from TBI
    • thalamic damage → anoxia-ischaemia or structural lesions
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10
Q

What is meant by ‘brain death’?

A
  • irreversible total destruction of all brainstem functions
  • including capacity for alertness, cranial nerve functions + apnoea
  • must never be diagnosed without an aetiology
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11
Q

Guidelines have been drawn up to diagnose brainstem death. What certain preconditions need to exist before testing can take place?

A
  • patient requires ventilatory support in the absence of drugs
  • there is a known cause for coma, capable of resulting in brainstem death
  • patients core temperature + any metabolic abnormality or effects of drugs must be normalised
  • effects of any sedation must have worn off
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12
Q

Brain death testing should be undertaken by two appropriately experienced doctors on two separate occasions.

Both should be experienced in performing brain stem death testing and have at least 5 years post graduate experience. One of them must be a consultant. Neither can be a member of the transplant team (if organ donation contemplated).

What brainstem reflexes are used in diagnosis of brain death?

A
  • absent pupillary responses to light → pupil fixed + unresponsive
  • absent oculocephalic reflexes → eyes move passively in direction of horizontal or vertical head movements, rather than maintaining their position of gaze while head is being moved by examiner
  • absent corneal reflexes → no blink w/ corneal stimulation
  • firm supraorbital pressure → no grimace in response to facial pain
  • absent vestibulo-ocular response → intact reflex consists of transient tonic deviation of eye towards stimulated side when 20-50ml of ice-cold water is instilled into the ear
  • absent gag reflex
  • no cough in response to pharyngeal or tracheal stimulation + suction
  • absence of any resp effort, even after fully oxygenating pt and then allowing PCO2 to rise to 50-60mmHg
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13
Q

Head injury is defined as any trauma to the head, with or without injury to the brain. Traumatic brain injury (TBI) is a non-specific term describing blunt, penetrating, or blast injuries to the brain.

How do you classify brain injury by broad aetiology?

A
  • blunt → occurs when external mechanical force leads to rapid acceleration or deceleration w/ brain impact, typically found in setting of motor vehicle-related injury, falls, crush injuries or physical altercations
  • penetrating → occurs when object pierces skull + breaches dura matter, seen commonly in gunshot + stab wounds
  • blast → after bombings or warfare, due to combo of conact + inertial forces, overpressure + acoustic waves
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14
Q

The GCS has been used extensively to classify TBI into levels of severity and prognosis. After traumatic brain injury, there is an inverse relationship between the GCS score and the incidence of positive findings on CT; in fact, the rate of intracranial injury (ICI) and need for neurosurgical intervention doubles when the GCS drops from 15 to 14.

What is the classification by clinical severity (GCS)?

A
  • minor/mild TBI → GCS 13-15; mortality 0.1%
  • moderate TBI → GCS 9-12; mortality 10%
  • severe TBI → GCS <9; mortality 40%

There is a grey area around a GCS of 13 as some argue it should be classed as moderate due to the increased morbidity

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15
Q

TBI can be primarily classified by area involved, as in diffuse or focal, although the two types frequently coexist.

What do these terms mean?

A
  • diffuse → includes diffuse axonal injury, hypoxic brain injury, diffuse cerebral oedema or diffuse vascular injury
  • focal → lesions such as contusions, haematomas, infarctions, axonal tears, cranial nerve evulsions + skull fractures

The above refer to causes of primary brain damage, secondary brain damage occurs after impact - it is preventable + treatable.

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16
Q

For brain injury, immediate management includes ABCDE following ATLS guidelines. CT head must be performed immediately + analysed within 1 hour.

Who should be admitted into hospital?

A
  • anyone w/ GCS <15
  • any signs of raised ICP - headache + vomiting
  • causes for concern - distracting injuries, meningism, NAI, CSF leak
  • CT abnormalities
17
Q

For adults who have sustained a head injury, perform a CT head scan within 1hr of the risk factor being identified.

What are the criteria for performing a CT head?

A
  • GCS <13 on initial assessment
  • GCS <15 2hrs after injury on assessment
  • suspected open or depressed skull fracture
  • any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, CSF leakage)
  • post-traumatic seizure
  • focal neurological deficit
  • >1 episode of vomiting
  • pre-event amnesia >30mins before event

If anyone failing to recover in 24hrs or deteriorating –> repeat CT

18
Q

C-spine should be immobilised until damage is excluded. What patients would require immediate ventilation, upon assessment?

A
  • GCS 8 or less
  • PaO2 <9kPa (air) or <13kPa (O2), or PaCO2 >6kPa
  • spontaneous hyperventlation (PaCO2 <3kpa)
  • respiration irregular
19
Q

After initial resuscitation and management of ABCDs, a focused history should be performed on every patient with a TBI or unknown cause of altered mental status

What questions would you be asking?

A
  • witness / collateral history useful
  • mechanism of injury + detailed description
  • LoC, amnesia, lucid periods?
  • seizures, confusion, mental status progress?
  • vomiting or headache?
  • drugs/alcohol → currently intoxicated? chronic problems?
  • PMHx → CNS surgery, past trauma, haemophilia, seizures
  • current meds incl anticoagulants
  • age → TBI in older age has poorest outcome
20
Q

A thorough physical examination must be performed after the initial ABCDs have been addressed. In addition to vigilance for occult injuries, the physician should perform the physical examination with careful attention to what?

A
  • GCS + pupillary examinations every 15 mins until pt stable
  • inspect cranial nerves, periorbital + postauricular ecchymoses, CSF rhinorrhoea or otorrhoea, haemotmpanum
  • fundoscopy → retinal haemorrhage + papilloedema
  • palpation of scalp → haematoma, crepitance, laceration + bony deformity
  • auscultate → carotid bruits
  • spinal cord injury → cervical spine tenderness, paraesthesias, incontinence, extremity weakness, pripaism
  • obv foreign bodies not to be removed until dura opened in OR
  • continuous cardiac + serial BP monitoring - watch out for hypotension
  • continuous puls ox + end-tidal CO2 capnography in intubated pts - watch out for hypoxia
  • upper and lower limb motor + sensory examination
21
Q

For head injury, what should the pupils be examined for?

A
  • size, symmetry, direct/consensual light reflexes, duration of dilatation/fixation
  • abnormal reflexes → herniation, brainstem injury, orbital trauma, drugs or direct CN III trauma
  • normal diameter of pupil = 2-5mm, both should be equal but 1mm diff is normal
  • abnormal symmetry may result from compression of CN III
  • opthalmological meds may slow down light reflexes
  • increased ICP may account for sluggish pupillary responses
22
Q

For brain injury, what should baseline laboratory investigations include?

A
  • FBC including platelets
  • U+Es
  • serum glucose
  • coagulation status: PT, INR, activated PTT
  • blood alcohol level + toxicology screening if indicated
  • urine analysis
23
Q

Patients should not be discharged until they have a GCS of 15. Minor head injury (GCS 14-15 initially) can often be discharged as long as there are no criteria for CT imaging or admission. Verbal and written information should be given at discharge.

What advice should be given to patients w/ a minor head injury?

A

The patient should be told to return to A+E if they develop:

  • loss of or reduced consciousness
  • new onset: deafness, ataxia, weakness
  • vomiting
  • bleeding from ear or clear fluid from eyes and nose
  • seizures
  • difficulties understanding speech
  • severe headaches not relieved by paracetamol

It is important to make sure patient has someone with them at home. Aspirin and sedatives should be avoided, as well as avoiding contact sport for 3 weeks, returning to work when ready and to avoid driving unti feeling better.

Some symptoms are normal for up to 2 weeks after - headaches, dizziness, nausea, sleep difficulties, mood/concentration disturbance, difficulties problem solving, fatigue + depression.

24
Q

There are 2 common forms of herniation syndrome that present following trauma.

How does uncal herniation present?

A
  • ipsilateral pupillary dilation (early sign)
  • complete ipsilateral 3rd nerve palsy
  • loss of consciousness
  • contralateral hemiplegia (2o to mass)
  • ipsilateral hemiplegia (compression of contralateral cerebral peduncle against edge of tentorium)
  • flaccid paralysis
25
Q

Tonsillar hernation is when displacement of the cerebellar tonsils through the foramen magnum compresses the cervico-medullary junction. Can be precipitated by LP in presence of a posterior fossa mass.

What are signs of tonsillar herniation?

A
  • AKA ‘coning’
  • head tilt or neck pain
  • ataxia
  • up going plantar reflexes
  • respiratory arrest
  • loss of consciousness
  • flaccid paralysis

Treat with mannitol

26
Q

How do you manage skull fracture?

A
  • depressed → consider surgery if:
    • significant mass effect
    • underlying haematoma
    • compound depressed/comminuted → surgery = wound debridement + closure, if there is dural laceration + further surgery is required
27
Q

How do you manage extradural haematoma?

A
  • presents w/ a lucid interval
  • CT shows clear dural edge to haematoma
  • manage with craniotomy + evacuation of clot
28
Q

How do you manage acute subdural haematoma?

A
  • results from more severe impact than EDH
  • more likely to present w/ coma than EDH
  • two causes:
    • clot forms around parenchymal laceration
    • tearing of the bridging veins
  • CT shows less defined edge, effacement of ipsilateral ventricle + midline shift
  • treatment → craniotomy + evacuation of clot
29
Q

How do you manage traumatic intracerebral haemorrhage?

A
  • often burst out of parenchyma into subarachnoid + subdural spaces
  • extensive peri-haemorrhagic oedema → raised ICP
  • treatment = surgery
    • surgery reduces risk of deleterious consequences of raised ICP
    • but unlikely to improve neurologic deficit
30
Q

CSF leak occurs in ~2% of severe head injuries and can appear years later.

How do you manage cerebrospinal fluid leak?

A
  • rhinorrohoea → confirm w/ dipstick for glucose, B2-transferrin is another identifier
    • most are self-limiting within 1 month
    • risk of meningitis, however!!
  • otorrhoea
    • smaller/negligible risk of meningitis
    • does not require repair, normally self-limiting

If unresolving, can do LP or lumbar drain or operative intervention (craniotomy)

31
Q

Head injury can lead to a variety of long-term neurological sequalae depending on the severity of the injury and early complications.

What are these long-term complications?

A
  • cognitive deficit
  • hemiparesis
  • cranial nerve palsies
  • carotico-cavernous fistulae
  • BPPV
  • post-traumatic amnesia
  • post-concussion syndrome
  • epilepsy
  • critical illness myopathy