Stroke Flashcards
What is a neurovascular unit?
It is a functional unit of the CNS.
Composed of neurons, glial cells and endothelium (including BBB).
How does a stroke occur?
There is a hypoperfusion of the endothelial lumen which causes a reduction in available glucose and O2. This leads to reduction in ATP synthesis and so any processes requiring ATP will be affected.
Membrane transport is the ATP dependent process mostly affected, where this is the process underlying the generation of AP.
An AP is an ‘all or nothing’ pattern of firing. Therefore if there is a low ATP in the NVU the AP won’t set off and so move from the ability of achieving neuronal transmission to total cessation. I.e. the symptoms of stroke will present suddenly, without any progression in symptoms.
What are the typical symptoms of stroke?
Sudden onset- this is due to the loss of AP firing, so any gradual onset symptoms would imply an alternative diagnosis.
Focal- Since only a branch of the cerebrovasculature is affected, only the NVU in this area are impacted.
Loss of function- Since have a cessation of AP.
Collection of symptoms can relate back to the vascular territory of hypoperfusion.
Symptoms do not typically migrate in a stroke syndrome since the loss of AP is a sudden change, commonly visual and sensory symptoms will migrate in common stroke mimics.
Episodes do not typically stereotype- i.e. the symptoms do not repeat in an identical fashion, in relation to a stroke this would mean embolization to the same vessel, which is highly unlikely.
What is capsular warning syndrome?
Intermittent hypoperfusion of the lenticulostriate arteries/the equivalent in the PCA and ACA leads to the appearance of intermittent/fluctuating impairments. These recurrent events recur over minutes to hours and so is different from non vascular stereotyping occurring over days/weeks/years.
What are the different groups of stroke mimics?
Group 1- Readily identifiable on imaging i.e. cerebral abscess, brain tumour, MS, subdural haematomas, where MRI may be more useful than CT.
Group 2- Distinguishable from stroke on clinical grounds i.e. BPPV, vestibular neuronitis, Bell’s palsy, syncope syndrome etc.
Group 3- Exclusion from stroke syndrome requires specialist stroke assessment using brain imaging i.e. migraine with aura, focal seizures, functional syndrome etc.
What are some types of stroke mimics?
1) BPPV- Vertigo is a common presentation of stroke syndrome and common stroke mimics. Vertigo on changing positions, associated vomiting, examine and confirm with Dix-Hallpike test and Epley maneuver.
2) Vestibular neuronitis- Sudden onset vertigo, since isolated presentation of vertigo it is less likely to be stroke. Head thrust test will confirm the diagnosis.
3) Transient Global Amnesia- Dysfunction of ‘episodic’ memory, whilst procedural memory stays in tact. Px memory affected at the stages of registration, storage and retrieval, where Px will repeatedly ask the same Qs and once the TGA resolves, they have no recollection of the event, having a ‘gap’ in their memory.
4) Migraine with aura- There is a migration of symptoms due to cortical spreading depression.
5) Functional syndrome
6) Apparent neurological deficits- Areas of gliosis (scarring of the brain) exist, where during ‘optimal conditions’ the Px functions normally. In suboptimal conditions i.e. hypoglycaemia, hypoxia, sepsis, dehydration, poor sleep there is underperformance and so symptoms become apparent.
7) Focal seizures
What are some possible chameleons of stroke?
Venous infarct Small cortical strokes Limb shaking TIA Occipital stroke Stroke amnestic syndromes Stroke mimicking vestibular dysfunction
What is the cause of the stroke?
What are the complications of stroke?
Complications arise as a result of Px being in a state of having had a stroke. Sensory/functional loss from the stroke do not constitute the complciations.
Recurrent stroke
Immobility- Pressure sores, DVT, constipation
Raised ICP- hydrocephalus, malignant oedema.
Infections
Mood/cognitive issues
Post stroke fatigue
Post stroke pain
Spasticity, contractures, secondary epilepsy
How are complications of stroke prevented?
Anticipate them!
Surveillance- daily review of obs, mood, chest, bowel etc
Timely bloods- CRP looking for infection, Hb
How would you manage and prevent the complications of stroke?
Complications of a stroke:
-Care bundle; admit to stroke unit, revascularisation*, surveillance, nutritional support, secondary prevention, rehabilitation.
*Revascularisation:
IV alteplase in 4.5hr therapy window
Thrombectomy in Px with large vessel occlusion, in 6hr therapy window.
NIHSS- examination of stroke Px giving clues about aetiology, prognosis, therapy, recovery and/or deterioration.
Secondary prevention of a stroke:
- Aeitology
- Antithrombotic therapy
- BP control
- Lipid control
- Glycaemic control
- Carotid endarterectomy
- Lifestyle changes i.e. smoking cessation, weight loss, optimising sleep, exercise etc.
How is an intracerebral hemorrhage managed?
The haematoma will result in an increased ICP therefore need to anticipate this and manage with BP control, correcting clotting derangements, managing glycaemic control.
Can also consider neurosurgery for managing increased ICP, although this requires a balance between surgical accessibility and neurological stability.
What are the prognostic groups of stroke Px?
Unstable- Requiring multiple assessments to evaluate the usefulness of interventions.
Stable but high risk of stroke complocations- Need close surveillance
Stable- Standard attention and review.
What is the current pathway for stroke presentation?
Call 999
Paramedic do FAST test
If +ve then refer to LRI ED, where stroke team are alerted.
If -ve then discuss other possible routes.
What are the 5 priorities following a stroke presentation to ED?
Confirm diagnosis, weigh Px, find out if for thrombolysis, bloods, CT, obs Identify any contraindications Gain consent/assent Imaging Bolus and infusion
What are the indications of alteplase?
- Alteplase can be administered within 4.5 hrs
- Disabling impairments (NIH >4, dysphasia, inability to self care or mobilise independently, visual field defect, dysphagia).
- No contraindications
What are the contraindications of alteplase?
Blood pressure > 185/110 mmHg after 2 attempts to reduce levels
Seizure at onset of stroke
Symptoms suggestive of a subarachnoid haemorrhage
Stroke/head injury within the last 3 months
Active internal bleeding
Severe haematology abnormalities
INR>1.7 or APTT>40
On dabigatran with abnormal APTT or thrombin time >100 seconds
On rivaroxaban / apixaban / edoxaban
On high-dose LMWH
Platelet count <50 x 109/L
etc
What are the relative contraindications of alteplase?
What are the optimal areas to image for a stroke presentation?
Pipes- Blood vessels using CT angiography (may use MR). Confirms large vessel occlusion so would be the starting point for thrombectomy. Can also show evidence of good collateral circulation.
Parenchyma- Explore the tissue, using non contrast CT or MRI
Perfusion- Identify tissue at risk- hypo perfused to give symptoms but no cell death.
Penumbra- Identify tissue at risk- hypo perfused to give symptoms but no cell death. Use perfusion scans which will represent areas of hypoperfusion on one image and areas of infarction on another image of the same area- the area of penumbra = hypo perfused area - the infarct volume.
What are the important points of consenting a Px for thrombolysis?
The earlier the treatment is given the better the odds of recovery.
Giving alteplase:
- 1/3 benefit compared to not having alteplase.
- 1/10 have a chance of full recovery.
- 1/50 chance of allergic reaction.
Practical details of giving the infusion, details of monitoring.
Explain the risk of bleeding.
What is thrombolytic therapy?
The use of alteplase in an ischaemic (80% of all strokes) stroke.
Steps of stroke management:
1) FAST +ve
2) ED notified
3) Px imaged and haemorrhagic stroke ruled out, contraindications assessed, consent obtained.
4) Alteplase adminstered
Alteplase:
Given if Px presents within 4.5hrs of stroke onset.
Dose calculated based of weight.
10% given as an initial bolus over 1-2 minutes.
Remaining 90% given as an infusion over 1hr.
How is a Px on thrombolytic therapy monitored?
Potential of many complications.
Monitored neurologically and haemodynamically every 15 mins during the infusion, checking pulse, BP, GCS, pupil reaction, asking about headaches, vision changes etc.
If any suspected anaphylaxis or bleeding then infusion paused and Px is imaged.
After 24hrs the Px will undergo a CT head to pick up any potential causes of raised ICP, which were not apparent on regular monitoring.
What are the complications of thrombolysis?
Adverse effect of thrombolysis and alteplase
Evolution of stroke causing rising ICP-
- Oedema
- Hydrocephalus
Seizure
Infection
Metabolic disturbance
Bleeding is the main and feared risk of alteplase infusion. If this is the case, pause the alteplase treatment, image, give reversal drugs, blood transfusion, may require surgery also. Extracerebral haemorrhage- -Thin thready pulse, drop in BP - Maleena - Distended abdomen
Intracerebral haemorrhage-
- Neurological decline
- New headache
- Rising BP
- N+V
Why is alteplase not effective with large vessel occlusion?
Alteplase is a fibrinolytic agent, so therefore requires a communication with fibrin. In larger vessels, the thrombus is such that most of the firbin is hidden and so can’t communicate with the alteplase, rendering it ineffective.
What is thrombectomy?
The management of choice in large vessel occlusion stroke, pre stroke MRS score of 0/1, NIHSS>/= 5/
Within 6hrs of stroke symptoms onset.
At the time of the CT, patient should also have a CT angiography, where the quality of collateral circulation should also be assessed.
What is the process of a thrombectomy?
- Catheter inserted through the femoral artery then through the carotid.
- A microcatheter is pushed out (from the point at the carotid artery) and pushed along through the offending clot.
- A Merci Retriever is pushed through the catheter and the catheter withdrawn.
- The stent will open up, where the blood flow will push the stent up against the clot, adhering the clot to the stent.
- A balloon at the level of the carotid catheter is inflated to stop any blood flow, and create blood flow illusion towards the carotid artery balloon*.
- The stent is withdrawn along with the adhered clot, through the carotid balloon.
*This creates a ‘vacuum’ so that if any pieces of the clot were to break off, they are removed from the body as opposed to being allowed to distally circulate.
What is a haemorrhagic transformation?
Complication of an ischaemic stroke, usually post cardioembolic strokes. This is because this is a sudden event, where the collateral arteries do not have time to be recruited and so there is a lack of protection of the BBB, as opposed to carotid disease which is a more gradual course.
BBB dysfunction leads to peripheral blood extravasation into the brain.
Developing 2-14 days post stroke
Can still give anti-platelets as treatment, if indicated.
What is the importance of AF in stroke?
A common cause of stroke, where the outcomes are more severe due to lack of collateral circulation mobilisation.
AF is becoming more prominent due to the aging population.
Can identify AF through clinical examination, ECG and prolonged cardiac monitoring.
As a primary prevention technique CHA2DS2VASc score is used to identify the risk of stroke.
HASBLED is used to identify the bleeding risk of a Px.
Mainstay secondary prevention is anticoagulation, where DOACS (rivaroxaban, apixaban, edoxaban and dabigatran) are preferred to Warfarin.
If anticoagulation is contraindicated then left atrial appendage closure is recommended as the alternative method of secondary prevention.
What is the importance of temporal arteritis and stroke?
Increases the risk of ischaemic stroke.
Need to start high dose steroid therapy, even without the confirmation of a diagnosis.
What is the importance of metabolic syndrome in stroke?
Metabolic syndrome is a combination of obesity, dyslipidaemia, insulin resistance and HTN.
This is a risk to developing a stroke and so stroke prevention would include measures such as; -Weight loss -Good BP control -Lipid control -Glycaemic control -Smoking cessation -Alcohol reduction -Optimisation of sleep etc.
What are the complications of metabolic syndrome?
- Vasculopathy- stroke, IHD, PVD
- Obstructive sleep apnoea- Even with good BP control, there can be nocturnal spikes in BP which can lead to a ‘hypertensive’ ICH.
- Non-alcoholic steatohepatitis can lead to liver cirrhosis.
- Malignancy
- Osteoarthritis
- Chronic venous insufficiency leading to ulcers, complex regional pain syndrome.
- Difficulties with conception.
- Cognitive dysfunction- Can include cerebrovascular disease or a normal sleep deprived brain.
What is the importance of carotid disease and stroke?
Disease progression at the carotid artery due to;
1) Disturbance of laminar flow at the carotid bifurcation, therefore usual location of carotid stenosis.
2) Endothelial damage- This can be due to turbulent flow, HTN, toxins (from smoking) etc.
Arethomatous plaques are the equivalent of ‘scar tissue’, growing over the damaged endothelium. The plaque progression depends on the cells involved, i.e. a diabetic Px or one with controlled dyslipidaemia will have a macrophage dense plaque with foam cells.
A stable plaque has a nice layer of endothelium over the plaque, so regardless of the reduced lumen size, is unlikely to embolise.
An unstable plaque has a raw top layer engaging in inflammation/clotting so will easily embolise.
What are the secondary preventative management plans for stroke induced by carotid disease?
Either through plaque stabilisation or plaque removal.
1) BMT (Best medical therapy)- Induces endothelial repair and reduce repeated injury, which in turn would reduce the promotion of plaques. I.e. Smoking cessation, aggressive BP control, dual antiplatelet therapy, high dose statin therapy, maintenance of good glycaemic control in diabetics.
2) Carotid endarterectomy- Additional benefit beyond that of BMT, good recovery where the disease is ipsilateral. Threshold is 50% lumen reduction, need to assess the risk of surgery and the time in which the stroke occurred (unstable plaque provides a benefit, stable plaque either no benefit or even harm). Risk of stroke recurrence reduces over time and so CEA becomes unbeneficial after some time.
3) Carotid stenting- Although an option, is not as beneficial as CEA, and post surgery there is a risk of death and stroke.
What is the difference between ischaemia and infarction?
Ischaemia is a reduced blood flow, where the metabolic demands of a tissue are not met. This leads to cerebral hypoxia and poor oxygen supply. This may be reversible.
Ischaemia may lead onto infarction i.e. tissue death, which is irreversible.
Post infarction, damage to the BBB can lead to a leakage of peripheral blood into the infarct, resulting in a haemorrhagic transformation.
What is a TIA?
Brief episode of neurological dysfunction, due to focal brain/spinal cord/retinal ischaemia.
Clinical symptoms will last <1hr and there is no evidence of an acute infarct. Resolves completely within 24hrs.
How is a TIA managed?
A Px with suspected TIA should be started on Aspirin 300mg, unless contra indicated.
If already on regular low dose aspirin, this should be continued w/o the addition of 300mg Aspirin.
Px referred for specialist investigation and assessment, within 24hrs of symptom onset.
If symptoms >24hrs then consider diagnosis as a stroke.
If Px has a bleeding disorder, need an urgent CT to rule out any ICH.
What are the 4 ages of an infarct?
1) Hyperacute (within first 6hrs)
2) Acute (within 7 days)
3) Subacute (upto 4 months)
4) Chronic (after 4 months)
What is the management of a hyperacute infarct?
Do urgent unenhanced CT to rule out haemorrhagic cause or any stroke mimics or show potential targets/thrombosed vessels or may identify infarcts too big or too old for thrombolysis.
Obtain consent
Alteplase infusion within the first 4.5hrs of the stroke.
How do cerebral infarct present on an unenhanced CT?
Hypoattenuating (Whiter) areas
Cortical-subcortical
Within a vascular territory
Sensitivity to infarction increases with time.
Sensitivity is also relevant to size, location, ‘background brain’ and radiological technique.
When is an MRI useful in detecting infarcts?
It is +ve for an infarct from 2hrs to 3 weeks.
Useful if:
There is previous CVD making the CT difficult to interpret
The location of the infarct is difficult for the CT to capture i.e. posterior fossa.
The case is ambiguous i.e. potential tumour.
In a TIA clinic, where a more sensitive imaging is required
Can also do an MRA
What is a perfusion CT?
A CT with contrast, where rather than taking images at different levels, repeated images are taken of the same level.
As the contrast passes through the vessel- this gives a transient hyperattenuation.
Software can then be used to work out the mean transit time (MTT) and cerebral blood volume (CBV). These values will give the cerebral blood flow.
Reduced CBV= Irreversible infarction.
Reduced CBF BUT maintained CBV= Ischaemic penumbra i.e. still salvageable. Therefore thrombolysis only works on ischaemic penumbra, so Px w/o ischaemic penumbra will not benefit from thrombolysis. Therefore sometimes time may not be relevant in the decision to thrombolyse. A Px may present after 6hrs of symptoms BUT with massive areas of potentially salvageable ischaemic penumbra. If the Px not thrombolysed this potentially salvageable tissue is lost.
What are important considerations of a brainstem infarct?
Slower to appear
Slower to evolve
Likely longer therapeutic window
What is an intracranial haemorrhage?
When would you suspect ICH?
This is a cause of ~15% of strokes.
Occurring usually in the cerebellum, thalamus, putamen and pons.
Suspect with: Underlying condition Hx of headache Seizures Reduced consciousness on admission
What are the causes of ICH?
Primary-
Usually small vessel
-HTN
-Cerebral amyloid angiopathy (CAA)
Secondary-
- Haemorrhagic transformation of an infarct
- Tumour
- Vascular i.e. aneurysm
- Coagulopathy
- Alcohol, cocaine
What are the effects of ICH?
Neurological deficit
ADD
What is the prognosis of an ICH?
Mortality-
Early: Surgical complications
Late: Medical complications
Poor outcome is dependent on the size of the ICH, location (where thalamus and BS have poorer prognosis) and the intraventricular component.
Also mortality is increased with age >80yrs and GCS<9.
What are the types of ICH?
Extradural Subdural Subarachnoid Intraparenchymal Intraventricular
How are ICH diagnosed?
Need rapid non-contrast CT to image the acute bleed and the immediate complications of the bleed. Highly sensitive and specific and key to an early diagnosis. Reveals size, location and intraventricular extension, mass effect, hydrocephalus and early signs of herniation.
How is an ICH managed?
1) Supportive management and CT.
2) Labetalol 10mg +/or hydralazine 10mg.
Nicardipine infusion
Mannitol
Coaggulopathy
3) Is the Px for surgery?
What are the management options for ICH?
Neurosurgery i.e. decompression craniotomy is the choice of management for a cerebellar haemorrhage.
Neurosurgery i.e. Intraventricular shunting is a required management plan of hydrocephalus.
Medically- Need supportive treatment- stabilise airway, breathing and circulation to prevent secondary hypoxaemia. O2 Control of seizures, mass effect, BP. Secondary prevention
How do the different stages of ICH appear on a CT?
Hyperacute- Initial stage of blood leaking so the density is parenchymal.
Acute- As the clot forms and the serum is extruded, the density increases. Start to get perilesional oedema, with a lower density than the brain.
Subacute- At this point the globin particle is being broken down and digested by macrophages. This results in a decreased density.
Chronic- There is a residual haematoma cavity, indistinguishable from a previous infarct.
What is hypertensive ICH?
HTN as a primary cause of ICH.
Common cause, especially with Asians due to poor primary care of BP and/or poor compliance.
Can prevent through anti hypertensives.
What is CAA induced ICH?
Cerebral amyloid angiopathy as a primary cause of ICH.
This is where there is amyloid plaque deposition in the small cerebral vessels. These can rupture and cause ICH, usually lobar.
Genetic predisposition to ICH and Alzheimer’s.
80% have Alzheimer’s.
What is an intratumoural haemorrhage?
A secondary cause of ICH.
Clues include a stuttering onset, oedema, irregular nature of the clot.
Contrast MRI needed immediately.
Malignancy can be primary or metastasis.
What are the complications of ICH?
Mass effect
Raised ICP
What is ICH mass effect?
Loss of ventricular space either partial or complete
Displaced ventricles
Midline shift
Twisted ventricles- continue to dilate with CSF secretion
Hydrocephalus
Cerebral herniation i.e. subfalcine, uncal, tenting (transtentorial), coning.
Raised ICP
What is intracranial pressure monitoring?
Raised ICP refers to increase by >20mmHg.
A complication of ICH includes increased ICP.
Cerebral perfusion pressure refers to the difference between MAP and ICP.
In mass effect the ICP reduces and so the CPP is increased.
NB CCP <70mmHg leads to reduced tissue perfusion and so ischaemic injury.
Therefore need to ensure a BP <130 to reduce further bleeds and >90 to maintain CCP.
What is an extradural haematoma?
Skull fracture leading to the collection of blood between the outer dura mater and the bone.
More common in young.
Common following head injury.
Acute presentation.
May ‘pass out’ then seem normal.
Bleed is usually due to arterial vessel, commonly the middle branch of the MMA, so very high pressure.
Appears lens shape on CT.
What is a subdural haemorrhage?
Collection of blood between the arachnoid and dura mater.
Usually in elderly.
Torn bridging veins, brain atrophy and so these vessels are more prone to tear. Low pressure since veins.
Can be due to an acceleration-deceleration injury.
Convex on CT.
What is a subarachnoid haemorrhage?
Thunderclap headache.
Sudden onset.
Ruptured aneurysm in the Circle of Willis.
What are the uses of MRI in ICH?
MRI is more useful for imaging the later stages of the bleed i.e. subacute and chronic etc, but are also useful in the differentiation of the stages. Also MRI can be used to image potential causes i.e. haemorrhagic transformation of an infarct, tumour, aneurysm, venous sinus thrombosis.
What are the 5 principles of rehabilitation?
Realisation of potential
Re-ablement; maximising the functional independence
Resettlement; providing safe transfer of care
Role fulfilment; to establish personal autonomy
Readjustment; to adapt a new lifestyle
What is early supported discharge?
40% of stroke Px are eligible
Hospital level therapy at home, therefore reducing hospital stay.
Px either transferred independently or with a carer.
Px rehabilitation goals are identified.
Suitable home environment
Can be referred from rehab, TIA clinic or acute stroke unit.
What are the criteria needed for rehabilitation transfer, post stroke?
Usually transfer at roughly day 7. Medically stable NG tube w/o the risk of refeeding Stroke consultant review twice a week Needing less than 24% O2
What are the characteristics of stroke rehabilitation?
Stroke rehab has been found to be more beneficial to stroke Px compared to a general rehab.
Brain plasticity means peak neurological recovery is within 1-3 months.
Initial phase- Reperfusion of hypoxi brain and reduction of brain oedema.
Late phase- Brain remodelling
Use of ischaemic penumbra is the key to good improvement post stroke.
What are good prognostic factors for stroke rehabilitation?
Absence of coma
Early motor recovery
Continence
What are the poor prognostic factors of stroke rehabilitation?
Severe communication deficit Old age Incontinence Neglect No leg movement at week 2 Severe upper limb weaknss at 4 weeks.
Who are the members of the MDT associated with stroke rehabilitation?
Specialist- Nurses SALT OT PT Dietician Neuropsychologist
What are common problems during stroke rehab?
Dysarthria and aphasia Dysphagia Sensation loss Spasticity and contractures Fatigue Hydration and nutrition Leg movement Shoulder pain Neuropathic pain Anxiety and depression Cognitive impairment Mouth care Continence Balance and walking
How is aphasia and dysarthria managed in rehab?
Aphasia- Difficulty producing speech- 1/3 Px
Dysarthria- Unclear articulation of speech
Assessed by SALT during rehab
How is dysphagia managed in rehab?
Difficulty swallowing
40-80% of Px
After acute stroke if Px has dysphagia then;
-Consider for fluids
-Specialist assessment of swallowing SALT
-Consider NG tube within 24hrs
-Referred to dietician
If Px unable to tolerate NG tube or can’t adequately swallow food/fluid by 4 wks then consider gastrostomy feeding.
How is nutrition and hydration managed in rehab?
Within first few weeks 1/4 Px are malnourished
Px need referral to dietician, SALT, advice, assessment and monitoring.
NG tube within 24hrs of admission
How is balance and walking managed in rehab?
80% Px become weaker Assessment Provided and trained on mobility aids Balance training Functional task specific training Lower limb strengthening exercises
How is fatigue managed in rehab?
Common after stroke
Px offered assessment of mental and physical potential contributing factors.
How is continence managed in rehab?
Urine incontinence increases risk of skin damage and ulceration
Faecal incontinence associated with more severe stroke
Manage with; Timed toileting Review caffeine intake Medication review Bladder retraining Pelvic floor exercises Minimise constipating drugs Oral laxatives
How is spasticity and contractures managed in rehab?
Spasticity affects 1/4 Px
Spasticity can be reduced with positioning, passive movements, pain relief. If focal then botulinum injection. If generalised then skeletal muscle relaxants i.e. baclofen
How is sensation loss managed in rehab?
80% Px affected
Trained on how to avoid injury in areas of reduced sensation
How is mouth care managed in rehab?
Important aspect of care. Poor oral hygiene results in;
Ulcers
Soreness
Cracked lips
Increased bacteria in mouth and saliva so if Px has dysphagia then can lead to sepsis/aspiration pneumonia
Mouthcare should be TDS
How is cognitive impairment managed in rehab?
Associated with poor outcomes
Interventions aimed at developing compensatory behaviours and learning adaptive skills
Receive specialist assessment and treatment from neuropsychologist
How is anxiety and depression managed in rehab?
Depression affects 1/3 Px Anxiety affects 1/4 Px Improve through; Social interaction Increased exercise Psychosocial education groups
How is neuropathic pain managed in rehab?
Affects 20% Px
Control since it affects spasticity, mood and engagement in rehab
Need neuropathic pain relief
How is shoulder pain managed in rehab?
Affects 20% Px In weak arm manage through; -Careful positioning -Simple analgesia -Local joint injection, if above are no effective`
What is the amber care bundle?
Advance care plan
Discussed with family
Documented in discharge letter to GP
For Px who are unwell and don’t qualify for rehab
