Intracranial Haemorrhage Flashcards
Pituitary Apoplexy
Sudden enlargement of pituitary tumour secondary to haemorrhage or infarction
Features
sudden onset headache similar to that seen in subarachnoid haemorrhage
vomiting
neck stiffness
visual field defects: classically bitemporal superior quadrantic defect
extraocular nerve palsies
features of pituitary insufficiency e.g. Hypotension secondary to hypoadrenalism
Pituitary Apoplexy - Diagnosis: Example Question
A 28-year-old female presents to the emergency department with a severe headache and lethargy. The headache came on fairly quickly whilst she was watching television. She is otherwise fit and well, has no medical problems and takes no regular medications. She lives at home with her husband and two-year-old daughter. Whilst in the emergency department she is given two co-codamol for her persisting headache but then vomits. On examination, there is no focal neurology but she is slightly drowsy and her GCS is 14/15.
Hb 126 g/l Platelets 274 * 109/l WBC 10.9 * 109/l Na+ 124 mmol/l K+ 5.0 mmol/l Urea 4.1 mmol/l Creatinine 124 µmol/l
What is the most likely diagnosis?
Tension headache Addison's disease > Pituitary apoplexy Sub-arachnoid haemorrhage Cranial diabetes insipidus
A sudden onset headache with altered consciousness and vomiting is very suspicious for an intra-cranial event such as a subarachnoid bleed. The hyponatraemia, in this case, would not be explained by a sub-arachnoid haemorrhage alone however. Bleeding into, or from, a pituitary adenoma can cause features similar to an aneurysmal subarachnoid bleed. It might, as in this case, cause secondary hypoadrenalism which would explain the hyponatraemia. One would expect hypernatraemia with diabetes insipidus.
Subarachnoid Haemorrhage - Causes
Causes 85% are due to rupture of berry aneurysms (conditions associated with berry aneurysms include adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta) AV malformations trauma tumours
Investigations
CT: negative in 5%
lumbar puncture: done after 12 hrs (allowing time for xanthochromia to develop)
Complications
rebleeding (in 30%)
obstructive hydrocephalus (due to blood in ventricles)
vasospasm leading to cerebral ischaemia
Management
neurosurgical opinion: no clear evidence over early surgical intervention against delayed intervention
post-operative nimodipine (e.g. 60mg / 4 hrly, if BP allows) has been shown to reduce the severity of neurological deficits but doesn’t reduce rebleeding*
*the way nimodipine works in subarachnoid haemorrhage is not fully understood. It has been previously postulated that it reduces cerebral vasospasm (hence maintaining cerebral perfusion) but this has not been demonstrated in studies
SAH - Typical CT Findings
SEE PASSMED SAH
‘The CT shows diffuse subarachnoid haemorrhage in all basal cisterns, bilateral sylvian fissures and the inter-hemispheric fissure. This case demonstrates the typical distribution that takes the blood into the subarachnoid space in a subarachnoid haemorrhage.’
Subdural Haemorrhage - Basics
Basics
most commonly secondary to trauma e.g. old person/alcohol falling over
initial injury may be minor and is often forgotten
caused by bleeding from damaged bridging veins between cortex and venous sinuses
Features
headache
classically fluctuating conscious level
raised ICP
Mx:
Needs Neurosurgical Review ?Burr hole
Subdural Haemorrhage - Diagnosis: Example Question
An 85 year old woman was referred by her General Practitioner to the stroke team on an urgent outpatient basis after her rest home staff reported a unusual episode the previous week. The patient normally suffered from mild dementia but was independent with activities of daily life with minimal assistance from care staff. One week previously, she had been found unusually drowsy in an armchair at her home. Staff recalled that she had been inconsistent with following commands and in particular was unable to raise her left arm in the air and was unable to stand. The drowsiness and arm weakness had resolved within 30 minutes, however the patient had subsequently been more confused than normal with reduced mobility. On direct questioning, rest home staff than a few days prior to the above episode the patient had lost her balance and had sat down heavily on the ground. The care worker with her at the time was certain that the patient had not hit her head during this incident.
Past medical history included mild dementia, myocardial infarction and atrial fibrillation. Regular medications included aspirin 75 mg daily, ramipril 2.5 mg daily, bisoprolol 2.5 mg daily, simvastatin 20 mg daily and warfarin (target INR 2-3). Review of recent blood test monitoring showed that the patients INR had been well controlled over recent months with no results outside of the therapeutic range. The patient did not drink and was a long-term ex-smoker. As mentioned above, the patient normally needed minimal assistance with self-care and was fully continent.
Examination in clinic demonstrated a significant cognitive impairment (abbreviated mental test score 4/10) but without evidence of dysphasia. Pupils were equal and reactive to light with no papilloedema on fundoscopy. There was a full range of conjugate eye movements. No facial weakness or sensory loss was demonstrated. Tongue and palate function was unremarkable with no weakness of trapezius muscle. Examination of the peripheral nerves was unremarkable except for possible slight pronator drift in the left arm and an up going left plantar response. Cardiovascular examination was unremarkable except for an irregular pulse. Respiratory and abdominal examination was unremarkable.
Results of investigations performed at the time of clinic assessment are given below.
Electrocardiogram: atrial fibrillation at rate 80 bpm, normal axis, inferior T wave inversion
Chest x-ray: clear lung fields
Carotid doppler: no significant stenosis in right internal carotid artery; 50 % stenosis in left internal carotid
Transthoracic echocardiogram: mild left ventricular systolic impairment, normal valvular function, no mural thrombus
What is most likely finding on CT brain scan performed after clinic review?
Sub-arachnoid haemorrhage Cerebral infarction Intracerebral haemorrhage Normal pressure hydrocephalus > Sub-dural haematoma
The diagnosis of sub-dural haematoma can be challenging, especially in those individuals with underlying dementia. In particular, a high index of suspicion is required in elderly patients treated with anti-coagulant drugs. Sub-dural haemorrhage commonly occurs after minor injury, with up to 50 % of cases preceded by a fall without head injury. Transient focal neurological deficit can occur in up to 20 % of cases, leading to potential for diagnostic confusion with transient ischaemic attack.
In this case the patients history of a fall, anticoagulation and worsening confusion all point towards sub-dural haematoma as the most likely underlying pathology. The lack of risk factors for cerebral infarction other than appropriately treated atrial fibrillation make this less likely. The history is less likely to be consistent with the other possible answers.
Superficial Siderosis
Superficial siderosis
Superficial siderosis describes the chronic deposition of iron in neurons of the central nervous system. The most common cause is chronic bleeding secondary to either a subarachnoid haemorrhage or subdural haemorrhage.
Features sensorineural hearing loss ataxia dementia anosmia anisocoria
Presentation with anosmia, bilateral symmetrical ataxia, cognitive impairment and sensorineural hearing loss = classical symptoms of superficial siderosis, which would be demonstrated on MRI head, with siderosis typically prominent in the posterior fossa.
The underlying cause for iron deposition is thought to be due to chronic or previous intracerebral haemorrhages.eg berry aneurysms in ADPKD, previous neurosurgery or head trauma. There is no current treatment for superifical siderosis but case reports have demonstrated possible improvements with lipid soluble iron chelators.
Superficial Siderosis - Example Question
A 57 year old male presents with a 3 months history of increasing clumsiness in his hands and arms. He has a complicated past medical history: 22 years ago, he underwent a renal transplant after progressive deterioration in his renal function following diagnosis with autosomal dominant polycystic kidney disease aged 25. His transplant has functioned well since but the patient has since undergone two resections of squamous cell carcinomas and one serious lengthy hospital admission for a systemic fungal infection. He stopped working a year ago as a wine merchant, after complaining that he was no longer able to differentiate ‘the smells of his wines as he got older’.
On examination, he is alert and orientated. Questioning was challenging due to his hearing impairment, despite bilateral hearing aids. He scored 17/30 on a mini-mental examination. Pupils were reactive with a full range of eye movements. Facial power and sensation were normal, with symmetrical palatal elevation and no tongue deviation. He was profoundly deaf bilaterally. Tone, power and sensation were normal, reflexes were present with downgoing plantars. However, you note significant bilateral finger-nose dysmetria and heel-shin malco-ordination.
Which investigation is likely to produce the unifying diagnosis?
Lumbar puncture for cerebrospinal fluid including 14-3-3, S100 EEG > MRI head Neurogenetic testing Nerve conduction studies and EMG
The patient has presented with anosmia, bilateral symmetrical ataxia, cognitive impairment and sensorineural hearing loss, classical symptoms of superficial siderosis, which would be demonstrated on MRI head, with siderosis typically prominent in the posterior fossa. The underlying cause for iron deposition is thought to be due to chronic or previous intracerebral haemorrhages. In the case of this patient, the association of polycystic kidney disease with brain aneurysms are likely to be significant. In other patients, previous neurosurgery or head trauma can similarly result in siderosis. There is no current treatment for superifical siderosis but case reports have demonstrated possible improvements with lipid soluble iron chelators.
How to reduce Cx post-SAH?
Patients presenting following SAH may suffer from cerebral vasospasm - occurs in 30% patients
This may result in further ischaemia due to a reduction in distal blood flow
In these patients we do not want to decrease the blood pressure acutely because a higher BP may be required to drive the same cerebral perfusion pressure
All patients are therefore prescribed a CCB to prophylactically prevent vasospasm from occurring
e.g. NIMODIPINE (dihydropyridine CCB) post-op 60mg/4hrly if BP allows
This has been shown to reduce the severity of neurological deficits but does not reduce rebleeding
Subdural Haematoma - Challenging Diagnosis
The diagnosis of sub-dural haematoma can be challenging, especially in those individuals with underlying dementia. In particular, a high index of suspicion is required in elderly patients treated with anti-coagulant drugs. Sub-dural haemorrhage commonly occurs after minor injury, with up to 50 % of cases preceded by a fall without head injury. Transient focal neurological deficit can occur in up to 20 % of cases, leading to potential for diagnostic confusion with transient ischaemic attack.
