Neurosurgery Flashcards
219 You are the ED intern on duty. You are asked to see a 20 year old who was struck on the left side of his head by a cricket ball. Initially he was drowsy and a bit confused, then he appeared to recover completely. He is now mildly confused, he has a severe headache and has vomited 4 times. His pulse is 60 bpm and regular, and his BP is 170/110mmHg. During the examination his GCS drops rapidly to 8/15. What is your differential diagnosis and what investigations would you like?
Working diagnosis: extra-dural haemorrhage
- Clearly defined head trauma + transient LOC
- Subsequent lucid interval
- Symptoms of raised ICP: ongoing severe headache, confusion, vomiting
Cushing’s triad (reflexive response to raised ICP):
1) Increased BP - early sympathetic activation → peripheral vasoconstriction
2) Bradycardia - parasympathetic compensation to increased BP by aortic bodies → reduced HR
3) Irregular breathing - herniation → compression of pontine respiratory centre
DDx: sub-dural haemorrhage, sub-arachnoid haemorrhage, vertebral/carotid dissection
What has happened:
1) Blunt-force trauma to the head has fractured the skull, most likely at the pterion region (where the frontal, parietal, sphenoid, and temporal bones all join)
- Skull is very thin at this point
2) Tear to (middle) meningeal artery → bleeding into potential space between cranium and parietal dura
- Pterion overlies the anterior division of middle meningeal artery
3) Haematoma expansion causes stripping of dura from cranium → severe headache
4) Further expansion raises ICP and creates a mass-effect, causing:
- Headache
- Vomiting
- Drowsiness/confusion
- Aphasia
- Seizures
- Hemiparesis
5) Further raised ICP and mass-effect → eventual brain herniation and death
Investigations: #1 CT head = localise cause of bleed and assess for skull fracture - EDH = biconvex, evidence of mass-effect, containment by cranial sutures
Other useful investigations:
- Continuous neuro obs to monitor for LOC
- Fundoscopy (changes due to raised ICP)
- Bloods: FBC, UEC, LFTs, coags, ABG, BGL
- ECG
- MRI brain (if strong suspicion but no evidence on CT)
220 You are the ED intern on duty. You are asked to see a 20 year old who was struck on the left side of his head by a cricket ball. Initially he was drowsy and a bit confused, then he appeared to recover completely. He is now mildly confused, he has a severe headache and has vomited 4 times. His pulse is 60 bpm and regular, and his BP is 170/110mmHg. During the examination his GCS drops rapidly to 8/15. What is your differential diagnosis and what has happened to cause this problem?
Working diagnosis: extra-dural haemorrhage
- Clearly defined head trauma + transient LOC
- Subsequent lucid interval
- Symptoms of raised ICP: ongoing severe headache, confusion, vomiting
Cushing’s triad (reflexive response to raised ICP):
1) Increased BP - early sympathetic activation → peripheral vasoconstriction
2) Bradycardia - parasympathetic compensation to increased BP by aortic bodies → reduced HR
3) Irregular breathing - herniation → compression of pontine respiratory centre
DDx: sub-dural haemorrhage, sub-arachnoid haemorrhage, vertebral/carotid dissection
What has happened:
1) Blunt-force trauma to the head has fractured the skull, most likely at the pterion region (where the frontal, parietal, sphenoid, and temporal bones all join)
- Skull is very thin at this point
2) Tear to (middle) meningeal artery → bleeding into potential space between cranium and parietal dura
- Pterion overlies the anterior division of middle meningeal artery
3) Haematoma expansion causes stripping of dura from cranium → severe headache
4) Further expansion raises ICP and creates a mass-effect, causing:
- Headache
- Vomiting
- Drowsiness/confusion
- Aphasia
- Seizures
- Hemiparesis
5) Further raised ICP and mass-effect → eventual brain herniation and death
Investigations: #1 CT head = localise cause of bleed and assess for skull fracture - EDH = biconvex, evidence of mass-effect, containment by cranial sutures
Other useful investigations:
- Continuous neuro obs to monitor for LOC
- Fundoscopy (changes due to raised ICP)
- Bloods: FBC, UEC, LFTs, coags, ABG, BGL
- ECG
- MRI brain (if strong suspicion but no evidence on CT)
221 A 56 year old woman is brought to the ED by her partner. She had complained of a sudden onset, severe headache immediately before collapsing, unconscious on the floor. She has regained consciousness after a few minutes, and now complains of neck stiffness. PMH is completely unremarkable, other than being a long term smoker. What is the likely diagnosis and what are the causes?
Likely diagnosis: sub-arachnoid haemorrhage (bleeding into sub-arachnoid space between arachnoid and pia mater, containing veins and arteries)
Symptoms: “thunderclap” headache, vomiting, collapse, drowsiness/seizure/coma
Signs: neck stiffness, Kernig’s sign (takes 6hrs), retinal bleed, focal neuro deficit
Aetiology:
- Ruptured berry aneurysm (85%)
- AV malformation (15%)
- Arterial dissections
- Anticoagulant use
- Trauma (associated with cerebral contusion)
Risk factors playing a causative role:
- Hypertension
- Smoking
- Fx (3-5x)
- Females > males (~3:2)
- Connective tissue disease
- Bleeding disorders
- Mycotic aneurysm
222 A 56 year old woman is brought to the ED by her partner. She had complained of a sudden onset, severe headache immediately before collapsing, unconscious on the floor. She has regained consciousness after a few minutes, and now complains of neck stiffness. PMH is completely unremarkable, other than being a long term smoker. What is the likely diagnosis, and how would the patient’s neurological condition best be monitored clinically during initial assessment?
Likely diagnosis: sub-arachnoid haemorrhage (bleeding into sub-arachnoid space between arachnoid and pia mater, containing veins and arteries)
Symptoms: “thunderclap” headache, vomiting, collapse, drowsiness/seizure/coma
Signs: neck stiffness, Kernig’s sign (takes 6hrs), retinal bleed, focal neuro deficit
Clinical monitoring:
1) Full initial neurological examination
2) Glasgow Coma Scale (4 eyes, 5 voice, 6 motor)
Eyes:
1 = no eye opening
2 = eyes open to pain
3 = eyes open to verbal command
4 = eyes open spontaneously
Voice:
1 = no verbal response
2 = incomprehensible sounds
3 = inappropriate words
4 = confusion
5 = oriented
Motor:
1 = no motor response
2 = decerebrate/extensor posturing (implies midbrain damage BELOW level of red nucleus)
3 = decorticate/flexor posturing (implies midbrain damage ABOVE level of red nucleus)
4 = withdrawal response to pain
5 = localising response to pain
6 = follows verbal commands
3) Neuro obs prescribed for half-hourly until GCS 15 is achieved/if GCS has deteriorated, then half-hourly for 2hrs → hourly for 4hrs → 2-hourly thereafter
4) Early referral to ICU or specialised neurological/neurosurgical unit
223 A 56 year old woman is brought to the ED by her partner. She had complained of a sudden onset, severe headache immediately before collapsing, unconscious on the floor. She has regained consciousness after a few minutes, and now complains of neck stiffness. PMH is completely unremarkable, other than being a long term smoker. What is the likely diagnosis and how would the diagnosis be confirmed?
Likely diagnosis: sub-arachnoid haemorrhage (bleeding into sub-arachnoid space between arachnoid and pia mater, containing veins and arteries)
Symptoms: “thunderclap” headache, vomiting, collapse, drowsiness/seizure/coma
Signs: neck stiffness, Kernig’s sign (takes 6hrs), retinal bleed, focal neuro deficit
Confirming diagnosis:
1) Non-contrast CT
2) Lumbar puncture
3) CT/MR angiograph (determining the site of aneurysm or other vascular malformation)
Other: FBC, UEC, coagulation, ECG, troponin
224 A 56 year old woman is brought to the ED by her partner. She had complained of a sudden onset, severe headache immediately before collapsing, unconscious on the floor. She has regained consciousness after a few minutes, and now complains of neck stiffness. PMH is completely unremarkable, other than being a long term smoker. What is the likely diagnosis, and what is the usual treatment if this diagnosis is confirmed?
Likely diagnosis: sub-arachnoid haemorrhage (bleeding into sub-arachnoid space between arachnoid and pia mater, containing veins and arteries)
Symptoms: “thunderclap” headache, vomiting, collapse, drowsiness/seizure/coma
Signs: neck stiffness, Kernig’s sign (takes 6hrs), retinal bleed, focal neuro deficit
Treatment:
1) Admission to ICU or specialist neurosurgical unit for constant haemodynamic and neurologic monitoring
- IV fluids targeting euvolemia and normal electrolyte balance
- Anticoagulation reversal
- ICP monitoring
- BP control ~<160
- Stool softners
2) Definitive aneurysm treatment
a) Coiling - intraluminal insertion of platinum coil to induce thrombus to plug aneurysm
b) Clipping - external microsurgical clip placement via craniotomy
3) Prevention of vasospasm and delayed cerebral ischaemia
- On-going monitoring and neuro obs
- Nimodipine (Ca2+-channel blocker) = improves outcomes but no convincing evidence of vasospasm control
- “Triple-H therapy” = induced haemodilution + hypertension + hypervolemia (lack of strong evidence but may help
4) Management of complications
- Symptomatic vasospasm = balloon angioplasty, intra-arterial vasodilators
- Hydrocephalus = ventricular drain
- Hyponatremia = NaCl tabs, 3% NaCl infusion, monitor Na+ every 6hrs
- Seizures = AEDs (levetiracetam, carbamazepine
225 You are the ED intern on duty. You are asked to see a 75 yoa man who has been brought into the hospital from home where he has been becoming increasingly confused and clumsy. He was previously well and independent. He had a fall about 3 weeks ago, when he cut his forehead. He has little medical history of note, he used to smoke and still drinks about 30 standard units of alcohol per week. On direct questioning he is confused in time and place. Physical and neurological examination are normal. What is your differential diagnosis? What investigations would you like?
Provisional diagnosis = chronic subdural haematoma
DDx: delirium, alcohol withdrawal, stroke
Investigations:
1) Bloods: FBC, UEC, BGL, LFTs, coags, tox screen
2) CT brain non-contrast = localise cause of bleed, skull #
3) Plain skull x-ray = skull # (but CT better and warranted in this case)
4) MRI brain = determine degree of brain injury, areas of ischaemia/hypoperfusion/infarction
5) On-going regular neuro obs (incl. GCS)
226 You are the ED intern on duty. You are asked to see a 75 yoa man who has been brought into the hospital from home where he has been becoming increasingly confused and clumsy. He was previously well and independent. He had a fall about 3 weeks ago, when he cut his forehead. He has little medical history of note, he used to smoke and still drinks about 30 standard units of alcohol per week. On direct questioning he is confused in time and place. Physical and neurological examination are normal. A CT head shows a subdural haematoma. What has happened inside this man’s head? What treatment is required?
Diagnosis: chronic subdural haematoma (symptoms have developed after 21 days)
Rupture in the bridging veins which connect the superficial cerebral veins to the dural venous sinuses
Blood has collected beneath the dura in the subarachnoid space
Treatment
General
- Reverse anticoagulation, serial observations, close monitoring for deterioration/neurological function
Conservative
If no signs of herniation, stable neurological status, midline shift < 5mm and haematoma < 10mm
Monitor with serial CT scans
Surgical decompression - trephination (burr holes) or craniotomy and evacuation
227 What is the importance of the primary and secondary brain injuries when managing an acute head injury?
Once a primary brain injury has been identified, the main objective of management is to prevent secondary brain injuries
Primary injury = occurs at the time of the initial traumatic event
Secondary injury = potentially preventable and reversible injury occurring as a consequence of primary injury due to pathophysiological evolution
Common primary injuries:
- Brain contusion (direct trauma, acceleration-deceleration)
- Skull fracture (direct trauma)
- Haemorrhage or haematoma (EDH = meningeal artery tear by #, SDH = tearing of bridging veins during rapid acceleration-deceleration injury, SAH = bleeding from pial vessels due to fall or MVA, ICH = tear of parenchymal vessels)
Diffuse axonal injury (stretching/tearing of axons due to rapid rotational or deceleration force)
Common secondary injury manifestations include:
- Cerebral oedema
- Raised intracranial pressure
- Haemorrhage
- Ischaemia
- Seizures
- Infection
228 What are the methods most commonly used for clinical assessment of a head injury?
1) History and physical examination
- Mechanism of injury
- Risk factors
- Clinical signs correlating with particular pathologies
2) GCS
- Can give indication of global neurological impact of intracranial pathology
3) CT Brain - Marshall CT classification of traumatic brain injury, primarily concerned with:
- Degree of swelling as determined by midline shift and/or compression of basal cisterns
- Presence and size of contusions/haemorrhages
4) Post-Traumatic Amnesia Scale
- Westmead PTAS most commonly used in Australia and New Zealand
- Provides assessment for formation of new memory by allowing the patient to learn information that will form part of additional memory questions on subsequent testing
