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ACC > Pt w/ Headache / Head Injury > Flashcards

Pt w/ Headache / Head Injury Flashcards

1
Q

What signs and symptoms might there be if someone has a head injury?

A

In the absence of OBVIOUS TRAUMA and/or a HISTORY people might present in the following way:

  • Nausea and Vomiting
  • Impaired consciousness
  • Memory problems
  • Vision changes (including pupils)
  • Headache
  • Weakness
  • Otorrhoea
  • Rhinorrhoea
  • Cushing’s response
  • ABG changes
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2
Q

Why is it important to get an ABG in someone who has had a head injury?

A

Close monitoring of their PaCO2 is really important. Even small increase will lead to vasodilation and marked vasodilation increasing the ICP

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3
Q

What is the cerebral perfusion pressure equation?

What is the CPP at which we would start to become concerned?

A

CPP = MAP - ICP

CPP: 70mmHg or below is concerning

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4
Q

Was does the Monroe-Kellie doctrine state and what does this mean in the context of head injuries?

A
  • Cerebral/skull volume is fixed meaning that if ICP increases for any reason (due to a bleed or a SOL) this will have the affect of decreasing the CPP.
  • Even small increases in ICP will lead to clinical signs and larger increases may even lead to brain herniation
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5
Q

What are the early symptoms of raised ICP?

A

Altered consciousness
Confusion
Drowsiness

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6
Q

When ICP increase considerably where does the herniation occur and what affect does this have?

A
  • Into the tentorial hiatus which leads to compression of the parasympathetic portion of the oculomotor nerve (which runs in this tract)
  • Clinically this leads to FIXED DILATED PUPILS
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7
Q

What if the ICP continues to rise despite tentorial hiatus herniation?

How will this present?

A
  • Brain continues to herniate out of the skull
  • Initially this will cause CONTRALATERAL HEMIPARESIS and then as the brainstem becomes compressed it can lead to CARDIOPULMONARY ARREST
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8
Q

What affect can increasing ICP have on haemodynamics? (name of response?)

A

CUSHING’S RESPONSE (triad)

  1. Hypertension
  2. Bradycardia
  3. Irregular breathing
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9
Q

What are some more specific symptoms of a basal skull fracture? (6)

What medication do you give for skull fracture?

A

BASAL SKULL FRACTURE

  • Haemo-tympanum (blood in ear)
  • Otorrhoea (CSF leak in ears)
  • Rhinorrhoea (CSF leak in rose )
  • Battle’s sign (bruising over mastoids)
  • Panda eyes (bilateral orbital bruising)
  • Subconjunctival haemorrhage (red sclera)

Give IV cefurOxime for skull fracture (O looks like panda eyes)

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10
Q

What are the two types of head injury?

A

PRIMARY (occurs at the time of accident) - axonal shearing or haemorrhage

SECONDARY (preventable and reversible factors)
-Hypoxia, hypovolaemia, infection, hyperglycaemia
↓Cerebral perfusion, ↑ICP, intracranial haematoma

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11
Q

How do you examine/assess brain injury?

A
  • A-E assessment
  • GCS(if GCS<8 call anaesthetist)
  • C-SPINE assessment - immobilise until happy no fracture (Canadian C-Spine rules)

Bedside

  • Monitor obs closely (HR + BP + RR)
  • Smell of alcohol on the patient
  • Pupils - size, movements, reflexes
  • Full PNS and CNS
  • PR exam
  • ECG

Bloods
-Bloods (FBC, UsEs, glucose, clotting)

Imaging

  • Head and neck CT (make sure radiology is available to interpret)
  • IV abx for compound skull fracture (IV cefuroxime)

Make ICU, anaesthetics and neurosurgery aware

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12
Q

What factors are really important to ask about in the history of someone who’s had a head injury?

A

When it happened

  • Mechanism of injury (MoI)
  • Did they lose consciousness? Before or after hitting their head? Did they have a seizure?
  • Do they remember the event or do they have AMNESIA?
  • Ask about symptoms above (rhinorrhoea, pyorrhoea etc.)
  • PMH (cardiac arrhythmias, diabetes, epilepsy, prev HI)
  • DH: alcohol, other drugs, regular meds
  • SH: is their home situation suitable for discharge?
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13
Q

How do you manage/treat brain injury?

A

REDUCE RISK OF SECONDARY BRAIN INJURY
• Avoid hypotension - maintain MAP above 90 with medications
• Encourage venous drainage - sit patients up by elevating head to 30-40 degrees
• Restrict fluids to less than 1.5L per day
• Osmotic agents such as mannitol
• Control seizure with lorazepam or buccal midazolam
• Avoid hypoxia - maintain PaO2 above 11
• Avoid hypercapnia - hyperventilate if ventilated and keep PaCO2 between 4-4.5kPa
(Hypercapnia>vasodilation> ICP)
•Infection: In skull fracture give 1.5g of cefuroxime

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14
Q

What are the criteria for CT scan in the ED in adults with head injury? (within 1 hour and within 8 hours)

A

Criteria for CT head

WITHIN 1 HOUR if:
• GCS < 13 at initial assessment
• GCS < 15 at 2 hrs post-injury
• Post-traumatic seizure 
• Focal neurological deficit
• more than 1 episode of vomiting
• Any signs of basal skull fracture 
• Suspected open or depressed fracture

WITHIN 8 HOURS if:
•LOC or amnesia with ONE of the following:
•If on anticoagulants (warfarin/DOACS)
•If 65years+
•If clotting or bleeding disorders
•If dangerous mechanism of injury (hit by car,5 stairs, ejection from car, fall 1m)
•If >30mins retrograde amnesia of events before injury

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15
Q

What are some presenting clinical features of meningitis?

A

Symptoms of meningitis

  • Headache
  • Fever
  • Photophobia
  • Neck stiffness/myalgia
  • Reduced consciousness level
  • Irritability
  • Vomiting/anorexia
  • Children may get URTI symptoms (especially viral)
  • Signs of raised ICP

NON-BLANCHING SKIN RASH - meningococcal septicaemia (can present with or without meningitis)

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16
Q

What are some common bacterial organisms that cause meningitis? (and specifically for neonates)

A 
Causes of meningitis 
NEONATES 
• Group B strep(g+ve)
• Listeria monocytogenes(and elderly)(g+ve) 
• E coli(g-ve)

INFANTS/ADULTS
• H influenzae(g-ve)-invaccinated
• N meningitides(g-ve)
• S pneumoniae(g+ve)

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17
Q

What are some non infective causes of meningitis?

A 
Non infective causes of meningitis 
• Malignant cells
• Drugs - NSAIDs, trimethoprim
• Lyme disease Borrelia burgdorferi 
• Sarcoidosis
• SLE
• Behcet's disease (painful moth and genital sores)
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18
Q

What investigations should be done in a patient with suspected meningitis?

Initial, bloods, imaging, special

A

ABCDE assessment (ECG, ABG)

  1. First do blood cultures
  2. Then do LP if not contraindicated (only do before AB if stable)

Other bloods
•FBC(↑Neut – bacterial), Us+Es, ↑↑CRP, Glucose (for LP comparison), clotting screen, viral PCR

Imaging
•CT scan if suspicion of raised ICP

Special
•Rapid antigen screen – blood or urine (quick and easy)
•Nasal + Throat swab culture – obtains bacterial + viral

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19
Q

How should suspected cases of meningitis be managed initially in hospital?

A

Initial treatment of meningitis

  1. RESUSSATIVE TREATMENT where needed (O2, fluids)
  2. ANTIBIOTICS IMMEDIATELY (don’t wait for results)
    Wide spectrum cephalosporin penetrate CSF
    • CEFOTAXIME or CEFTRIAXONE
      + Amoxicillin for those at risk of listeria infection (<3 months or >55 years or immunocompromised)
  3. IV DEXAMETHASONE with starting dose of AB to reduce meningism (must be >3 months)

then CONSULT MICROBIOLOGY AND REFER TO TRUST GUIDELINES

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20
Q

How does a SAH classically present and what are some other ket symptoms?

A
  • SUDDEN SEVERE HEADACHE (THUNDERCLAP/’KICKED IN THE HEAD’)
  • Worst at onset
  • Meningism (neck pain, photophobia, N+V)
  • LOC might occur - may make diagnosis more difficult
  • Drowsiness and confusion
  • Unilateral eye pain
  • Warning headaches can occur
  • Fits

-In 25% exertional activities precede the event

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21
Q

What is the aetiology of an SAH?

What is most common?

A

Either trauma (most common overall) or Aneurysm (berry Aneurysm in the circle of Willis most common site)

-Ask about family history because aneurysms have a considerably familial link

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22
Q

What investigations should be done for a patient with suspected SAH? (bedside, bloods, imaging, special)

A

Investigations SAH
Bedside
-Regular observations (Cushing’s response to raised ICP: hypertension, bradycardia and irregular breathing)
-Look for focal/global neurology-CNS and PNS exam
(oculomotor never palsy indicates berry aneurysm in the posterior communication circulation)
-ECG (high risk for arrhythmias)

Bloods
-Bloods (FBC/UsEs/Glucose/clotting)

Imaging

  • Chest Xray- Neurogenic pulmonary oedema
  • CT head ASAP (within 6 hours)

Special
-Admit for LP 12 hours after onset even if CT normal (xanthochromia)

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23
Q

How should a patient with a suspected SAH be managed initially?

A

Managment SAH

  • AE assessment
  • Analgesic (codeine) and laxative (consipation-to reduce strain)
  • Anti emetic
  • Bed rest (reduce strain)
  • NIMODIPINE (to prevent vasospasm)
  • Mannitol IV if evidence of raised ICP
  • Carefully maintain BP
  • HDU/ICU
  • Involve neurosurgery (if aneurysm-clip/coil)
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24
Q

What are sequelae of SAH? (7)

A

Sequelae of SAH

  • DEATH (50%)
  • seizure +/- epilepsy
  • ischeamia (can lead to TIA/stroke)
  • hydrocephalus
  • SIADH (hypopituitry axis is affected)
  • re bleed
  • aneurysm re-occurance
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25
Q

What clinical features would make you begin to consider SOL?

A 
SYMPTOMS OF SOL 
-Long lasting headache (dull, achey, made worse by lying down or straining)-due to increase in ICP) 
-Focal neurology pathology:
 •Cranial nerve palsys (abducens most common) 
 •Vision changes 
 •Motor/sensory changes (speech, walk) 
 •Personality changes 
 •ICP (vomiting/seizures/papilloedema)
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26
Q

What sorts of things classify as a SOL?

A
  • Big brain aneurysms
  • Abscesses
  • Subdural haematoma
  • Granuloma
  • Cyst
  • Tumour
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27
Q

What investigations should be done in a patient who has a suspect SOL?

A

Space occupying lesions

  • CT head
  • FBC, Us+Es, Glucose
  • ECG
28
Q

How should a patient with SOL be managed in ED?

A

NOT MANAGED IN ACUTE SETTING - refer to neurology

  • Do ABCDEG assessment and symptom control (analgesic for headache)
  • Dexamethasone can be useful in treating cerebral oedema
29
Q

What is temporal arteritis?

What are some common causes / associations with temporal arteritis?

A

-Temporal arteritis is autoimmune vasculitis affecting the medium and large vessels (including posterior ciliary arteries)

Common associations

  • AGE (unheard of in under 55)
  • F>M
  • 50% associated with polymyalgia rheumatica

CONSIDER IN ALL PATIENTS OVER 50 WITH RECENT SUDDEN ONSET HEADACHE

  • if younger <55 and FEMALE = Takayasu’s
30
Q

How does a patient with temporal arteritis present?
History
Examination (including retina)

A

Temporal arteritis
• Headache (normally unilateral, temporal)
• Scalp tenderness e.g. when combing hair
• Tongue/jaw claudication - pain on chewing
• Reduction/loss in vision (Amaurosis fugax curtain descending-must act soon, can become irreversible)

Extra-cranial symptoms include:
• Malaise(tiredness)
• Dyspnoea(breathing problems due to pulm haemorrhage)
• Weight loss
• Low grade fever
• Night sweats
• Unequal or weak pulses
• Splinter haemorrhages
• Signs of PRM (proximal weakness + stiffness in shoulder/hips)

O/E
Retina:
• Pale papilledema
• Pale, waxy, elevated disc - ischaemia

o/e: Area over temporal artery might be red, tender and pulseless

31
Q

What investigations should be done in someone with temporal arteritis?
(bedside, bloods, fundoscopy)

A

Investigations for temporal arteritis
ESR first line, Biopsy definitive

Bedside
-FUNDOSCOPY - really important

Bloods

  • FBC (↑Platelets, ↓Hb (low grade), ↑WCC,)
  • LFT (1/3 ALP will be high)
  • CRP, ESR (ESR will be really high > 40mm/h - although if normal does NOT exclude Temporal arteritis)

Special tests
TEMPORAL BIOPSY IS DEFINITIVE with characteristic skip lesions-conduct within 7 d of starting steroids

32
Q

Temporal arteritis

  • Who should you refer to and when?
  • What is a complication if not treated?
  • Treatment?
  • Long term treatment?
A

Management of temporal arteritis
MEDICAL EMERGENCY
-Ideally same day referral to rheumatology (3 days latest)
-If any visual loss (tangent or permanent)>SAME DAY URGENT OPHTHALMOLOGY REFERRAL
(irreversible bilateral visual loss can occur suddenly if not treated)
-Start ORAL PREDNISOLONE 40-60mg immediately (higher dose for those with visual problems) and reassess within 48 hours (should’ve improved)
-Consider PPI protection and bone protection (bisphosphonates)

Long term: typically 2 year course, wean when ↓symptoms + ↓ESR

33
Q

What is a venous sinus thrombosis?

Where does it most commonly occur?

A

Venous sinus thrombosis

  • Acute thrombosis (blood clot) in the dural venous sinuses which normally drain blood from the brain
  • Causes cerebral infarction

Commonly the:

  1. Sagittal sinus
  2. Transverse sinus
34
Q

What are some important causes/risk factors of venous sinus thrombosis?

A 
Causes of venous sinus thrombus 
(anything that causes hypercoag state) 
-Pregnancy/post partum  
-Malignancy 
-Combined OCP
-Dehydration 
-Head injury 
-Recent LP 
-Brain tumours (pressure)
-Infections
35
Q

What investigations is it important to do in people who have a suspected venous sinus thrombosis?

A

Investigations for venous sinus thrombosis
-Important to rule out SAH and meningitis

  • Bloods: thrombophilia screen, cultures to r/o meningitis
  • LP (if not contra indicated)
  • CT head/MRI (may show absence of sinus, delta sign?)
  • Check for meningitic symptoms
  • MRI T2 weighted might be useful for visualising thrombus and seeing infarction (venous infarction will cross boundaries between arterial territories)
36
Q

How will a dural venous sinus thrombosis present?

A

Venous sinus thrombosis presentation
-gradual onset (days/weeks)
-signs of raised ICP
>headache, visual losses, papilloedema, vomiting, seizures

Cortical vein thrombosis

  • extends to cortical veins (infarction in venous territory)
  • focal, stroke like symptoms that develop over days -headache may come on suddenly (thunderclap headache)
37
Q

How should venous sinus thrombi be managed initially?

A
  • Rule out other things (meningitis, SAH) then NEURO referral
  • Heparin/LMWH to anticoagulate
  • Start warfarin to reach INR 2-3 (even if secondary heamorrage)
  • If unresolved, give thrombolysis or mechanical thrombectomy (futile in large infarcts and impending herniation)
38
Q

How might we treat a raised ICP?

A

MANNITOL - increases the osmotic pressure of the blood drawing fluid out of the tissues. (risk of rebound increase in ICP if used over prolonged period of time)
HYPERTONIC SALINE can be used for the same reasons - increasing osmotic pressure of blood
POSITIONING - elevate the head by 15-30 degrees

39
Q

What are some symptoms of concussion?

A

These symptoms are very common but can cause anxiety in patients and relatives. Common symptoms that are not specifically concerning include:

  • Headache - occurs in most patients and can persist for up to 2 months (intermittent and worse on exertion)
  • Dizziness - non specific
  • Lethargy
  • Inability to concentrate
40
Q

When can we make a diagnosis of concussion?

A

When other symptoms e.g. rhinorrhoea, otorrhoea, bruising, neck pain, photophobia, vomiting have been RULED OUT

Always make sure to safety net about symptoms getting worse or coming back unusually.

41
Q

What drug can be used to reduce ICP?

A

MANNITOL (200mL 10%)

42
Q

What are some signs of cerebellar damage?

A 
DANISH 
Dysdiadochokinesia 
Ataxia 
Nystagmus 
Intention tremor 
Slurred/Staccato speech
Hypotonia
43
Q

What are some sequelae of meningitis? (acute-4 and delayed-2)

A

Sequelae of meningitis

  • raised ICP (look out for Bradycardia, hypertension, irregular respiration)
  • DIC (disseminated intravascular coagulation)
  • Cerebral absess (swining pyrexia and ↑ICP)
  • pericardial effusion

Delayed complications

  • hearing loss (most common-do hearing test post infection)
  • encephalopathy
44
Q

How will a bacterial meningitis LP look and what will it contain?

A

Bacterial meningitis will look cloudy.

  • Neutrophils ++++polymorphs
  • Low glucose <0.4 (may be normal) <1/2 of plasmaglucose
  • High protein (>1g) (may be normal)
45
Q

How will a viral meningitis LP look and what will it contain?

A

Viral meningitis will have clear appearance.
Lymphocytes ++++(mononuclear cells)
-Normal protein (<1g), normal glucose (>1/2 plasma glucose)

46
Q

How will a TB meningitis LP look and what will it contain?

A

TB meningitis LP will look cobwebby/fibriny

  • Very high protein +++ >1-5g/L
  • Low glucose <1/2 of plasmaglucose
  • Lymphocytes ++++ (mononuclear)
47
Q

Specific signs of cavernous sinus thrombosis?

A

Cavernous sinus thrombosis

  • Chemosis(conjunctiva swelling)
  • Swollen eyelids
  • Proptosis
  • Painful ophthalmoplegia
  • Fever
48
Q

What is the difference in onset between sub-dural and extradural haematoma?

How do the pattern of consciousness differ?

A

-Sub-dural haematoma is SLOWER (Subdural Slow)
you tend to get fluctuation in conciseness over several DAYS

  • Extra-dural is faster (hours) (Extradural Emergency)
  • ‘Talk and die’ lucidity sequelae. LOC>full recovery>rapid neuro degeneration and LOC
49
Q

What is the difference in pathophysiology in subdural and epic/extradural heamatoma?

What vessel does extradural normally involve and why?

A

SUBDURAL-rupture in bridging vein between brain and dura, can happen with little force

EXTRADURAL/EPIDURAL -arterial rupture (often middle meningeal) from skull trauma (often temporal bone fracture), a lot of force is required!

50
Q

Who is more at risk of subdural heamatoma?

A

Alcoholics/elderly more at risk of SUBDURAL(dehydrated veins)

51
Q

Viral causes of meningitis?

Managment of viral meningitis?

A

Viral meningitis (more common, less severe)

  • Enterovirus e.g. coxsackie (most common)
  • HSV1 & 2 (both can be quite sev)
  • EBV
  • Adenovirus

Acyclovir (if not sure yet then cover for both)

52
Q

Managment of bacterial meningitis

A
  1. ANTIBIOTICS
    Wide spectrum cephalosporin penetrate CSF
    -50mg CEFOTAXIME
    -OR
    -80mg CEFTRIAXONE
    + Amoxicillin in children under 3 months (or>55 years) for listeria cover
  2. STEROIDS (ASAP before/at same time as AB)
    (reduce risk of neurological complications, particularly deafness and death. Within 12 hours if cant give immediately)
    -although not if <3 months
    -DEXAMETHASONE
  3. FLUIDS if in shock
    - 0.9% NaCl fluid bolus (monitor response and monitor Ca and K)
  4. PHE should be notified (contact prophylaxis might be required) and TREAT contacts prophylactically
  5. SAFTEY NET AND FOLLOW UP
    - follow up with pads and hearing test
    - safety net: come back if any hearing or developmental problems (memory)
53
Q

Treatment for close contact of MENINGOCOCCAL meningitis?

A

Prophylactic Ciprofloxacin one off dose for all close contacts in past 7 days (regardless of vaccination status)

  • Rifampicin is second line (also if caused by HiB)
  • Partner
  • Sharing kitchen
  • Exposed to respiratory droplets

***PHE alert

54
Q

Explain the canadian C spine rules for head injury

A
  1. Any high risk factors? (65, drive, deprived)
    -sixty five
    -fast drive (dangerous mechanism)
    -sensory deprived (paraethesia in extremities)
    IF YES>CT (image if alive) IF NO> go to question 2
  2. ANY low risk factors?
    -slow wreck (simple mechanism)
    -slow neck (delayed neck pain)
    -sitting down
    -walking round (ambulatory at any time)
    -C spine fine (absence of midline C spine tenderness)
    IF YES>range the spine IF NO>CT
  3. Able to rotate neck 45 degrees left and right?
    IF YES> DONT CT IF NO>CT
55
Q

Complications of temporal arteritis?

A

Complications of temporal arteritis

  • Stroke and TIA- if involving carotid or vertebral artery
  • Visual loss- if involving temporal.a →ischemic optic neuropathy
56
Q

How do you differentiate between subdural and extra dural haematoma on CT head?

A

Both have positive mass effect-push brain away

Subdural haematoma

  • crescent shape of bleeding
  • sliver - venous bleed between dura and arachnoid
  • CANNOT CROSS MIDLINE (because under dura)
  • CAN cross sutures of skull (long areas)

Extradural haematoma

  • lens shape of bleeding (eggstradural)
  • Usually arterial (needs pressure to tear dural away from skull)
  • CAN CROSS MIDLINE (not confined by dura)
  • CANNOT cross sutures of skull (located to one area)

subarachnoid-loss of sulk and gyrus

57
Q

What is the managment of subdural heamatoma?

A

SUBDURAL HEAMATOMA

  • stop anticoagulants
  • reverse clotting abnormalities urgently if possible
  • Surgical managment depends on the size of the bleed the timeline and size
  • generally, >10mm or with >5mm midline shift have surgery (BURR HOLE drainage)
  • adress the cause (falls/trauma)

either conservative (monitor with serial CT) or surgical (drainage with burr holes).

58
Q

What is the managment of extradural heamatoma?

A

EXTRA DURAL HEAMATOMA

  • stop anticoagulants
  • reverse anticoagulants if possible
  • potentially mannitol to decrease BP
  • evacuation via a CRANIOTOMY
59
Q

What is 1st line investigation for SAH?

What should you do if this investigation is normal?

A

SAH
1st line: CT head ASAP (within 6 hours)

If normal: admit for LP 12 hours after onset even if CT normal (xanthochromia)

60
Q

What is really important to check with head injury?

A

Head injury

  • eye movements (proptosis/visual acuity
  • pre bulbar heamatoma>optic nerve compression>blindless
61
Q

What is Kernigs sign

A

Kernig’s sign (sign of meninginism)

  • leg is flexed at 90 degrees
  • pain and resistance when attempt to extend leg

‘legs in K-Kannot extend’

62
Q

What is Brudinskis sign

A

Brudinskis sign (sign of meninginism)

  • move their neck
  • their legs flex
63
Q

What treatment must be given ASAP by GP if suspected meningococcal septicaemia (with RASH)

A

MENINGOCOCCAL SEPTICEAMIA
-IM benzylpenicillin given ASAP and then urgent hospital transfer (can also give to simple bacterial meningitis- if remote and unable to urgently get to hospital)

64
Q

Presentation of meningococcal septicaemia

A

MENINGOCOCCAL SEPTICEAMIA

  • Signs of sepsis (↑Temp, ↑HR, ↓BP, ↓Sats)
  • Dehydration (mottled skin, ↑CRT, dry m. membranes, shock)
  • Non-blanching purpuric rash!
  • Seizures
  • Bloods – ↑PT ↑APTT ↓Platelets = DIC!! Give FFP ASAP!!

DONT DO AN LP until stabilised

65
Q

Contraindications to LP?

A 
LUMBAR PUCTURE CONTRAINDICATIONS
MENINGOCOCCAL SEPTACEMIA! DO NOT DO LP 
-Raised ICP 
• Papilodema 
• Cushings reflex  (bradycardia, ↑BP, irregular breathing)
- Focal neurology 
-Infection at site 
-Coagulopathy (deranged LFTs)
-Thrombocytopenia 
-Cardio/resp instability
66
Q

What ECG finding might you mind in SAH?

A

inverted T waves

67
Q

Acute management of cluster headache?

Prophylactic managment fo cluster headache?

A

Acute: 100% oxygen and subcutaneous triptan

Prophylaxis: verapamil is the drug of choice. There is also some evidence to support a tapering dose of prednisolone

ACC (23 decks)

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