- Post stroke complications
- Recognise complications
- Preventing stroke complications
- Managing post-stroke complications
Complications after stroke can greatly affect outcome. They can be divided into those that occur from onset of the stroke are early complications as seen below and those more likely to occur during the first few weeks and later. They can affect the opportunities and stamina needed for therapy and rehabilitation. They can affect swallowing and nutritional status and add to the psychological post stroke burden. They can be life-threatening and affect short and long-term outlook. It is important to not only predict or at least react to diagnose issues but to have protocols in place to address particular problems. Most medical complications are seen within the first month. In the early days swallowing, fever, coma, cerebral oedema and sepsis are all major factors and patients are most vulnerable. Later as mobility is gained issue such as falling, ongoing continence issues and venous thromboembolism are more concerning. All the members of the multidisciplinary team play a role in minimising and pre-empting complications. Stroke renders patients weak with sensory loss, visual and cognitive and psychological and other issues. The main complication is simply the results of profound immobility and others which are listed below. It is important to have a plan to prevent and manage complications. Stroke renders patients weak with sensory loss, visual and cognitive and psychological and other issues. The main complication is simply the results of profound immobility and others which are listed below. It is important to have a plan to prevent as well as to detect and manage complications.
Epilepsy after stroke
Epilepsy after stroke is dealt with here
Post Ischaemic stroke disorder of cell function leads to the development of cytotoxic oedema usually accompanies infarction and is seen in lesions after about 24 hrs and tends to peak at the 48-72 hr period. Oedema is usually cytotoxic and is due to a failure of cellular pumps due to ischaemia. Later oedema can be vasogenic due to break down in normal vascular blood brain barrier and it is this that causes raised ICP. It is cytotoxic oedema that we see on DWI causing restricted diffusion. Oedema is often a transient phenomenon but becomes more malign when a stroke involves a large volume of the brain causing a significant rise in intracranial pressure usually due to a large vessel occlusion - MCA or Internal carotid. There is no role for steroids. Vasogenic oedema is seen with tumours and does respond to steroids. As ICP rises patients may require decompressive surgery such as hemicraniectomy for large lobar strokes and to reduce pressure and prevent coning or with suboccipital decompression for malignant cerebellar infarcts. Patients with oedema are given isotonic fluids, e.g. N-Saline rather than Dextrose to try to reduce excess free water and oedema. Fluid restriction may even be considered in this period however there are concerns that this may be prothrombotic or reduce cerebral perfusion in those with stenotic lesions. Cerebral oedema can also be managed medically often as a bridge to surgery using either IV Mannitol or Hypertonic saline or Barbiturates or elevated head position at 30-45 degrees.
Haemorrhagic Infarction (HI)/Transformation
Following an Ischaemic stroke there can be a form of secondary haemorrhage into the infarcted tissue and this is often termed haemorrhagic infarction or transformation. It is more common in embolic strokes, larger stroke and following spontaneous or therapeutically driven recanalisation with thrombolysis (especially intraarterial) and/or thrombectomy. Thrombectomy seems to have an increase of asymptomatic HI but symptomatic HI is unaffected. The rate seems to be higher with delayed recanalisation e.g. Alteplase after 3 hours. Poorly controlled hypertension is a risk and is one of the reasons to control blood pressure after thrombolysis. Severe hyperglycaemia may also be a risk. It tends to happen early within the first few days, but it can be as late as 2 weeks. It is often clinically silent especially as at this time there is rarely any need to do brain imaging. Blood is more clearly seen on MRI GRE and T2 star. Often the response is to omit antiplatelets for several days. If the patient presents late it can be difficult to distinguish haemorrhagic transformation from a primary intracerebral haemorrhage. HT is possibly due to the reopening of occluded blood vessels with flow into tissues with a damaged capillary bed due to local ischaemic necrosis. It is always a worry in re-establishing flow that haemorrhage will occur. However, there is a distinct difference between mild to moderate haemorrhage into already damaged brain and de novo haemorrhage into undamaged brain adding to the overall stroke burden. There is a radiological classification and an excellent review article here.
|Haemorrhagic Infarction Type 1||Small hyperdense petechiae||No change|
|Haemorrhagic Infarction Type 2||Confluent hyperdensity in infarct zone no mass effect||No change|
|Parenchymal haematoma type 1 (PH1)||Confluent hyperdensity in infarct zone taking up < 30% infarct area with some mass effect||No change|
|Parenchymal haematoma type 2 (PH4)||Confluent hyperdensity in infarct zone taking up > 30% infarct area and beyond with oedema and mass effect||Increased|
An obstructive hydrocephalus can be seen after both ischaemic and haemorrhagic strokes and may need urgent neurosurgical intervention both for the stroke itself and the insertion of an external drain into the lateral ventricle to allow the external drainage of CSF so that intracranial pressure falls. It is dealt with in more detail. It usually presents with a general worsening and a fall in GCS which should initiate a new clinical reassessment and CT scan. This subject is dealt with in more detail here
Fever may be seen post stroke and can be multifactorial. Fever is associated with worsened outcomes. Pyrexia correlates with infarct size and severity. Infective causes should be explored and treated. General examination and bloods such as WCC, Urinalysis, CRP and blood cultures can be helpful. Anecdotally pontine lesions appear to cause pyrexia. Treatment should be with antipyretics such as IV/PO paracetamol and ensure euvolaemia. Caution with overhydration and worsening cerebral oedema.
This is seen in 20-40% of patients post stroke. Hyperglycaemia may often be seen in diabetic patients whose management may be difficult due to loss of oral intake, acute physiological stress pushing up glucose and possible sepsis. In complicated settings, a variable rate insulin infusion (VRII) may be appropriate. Once all has settled patients may be restarted on oral agents or on their Insulin balanced with some oral/NG intake. The concern about using hypoglycaemia agents is rendering a comatose patient hypoglycaemic which may not be detected due to coma and causing further brain injury. In that case many prefer sugars not to be too tightly controlled. A level of 5-15 mmol/l is recommended by the RCP guidance. Animal and laboratory studies suggested that poor glycaemic control can worsen stroke-related brain injury. Clinical studies suggest that hyperglycaemia is associated with worse clinical outcomes.
Many patients are elderly and frail and may have co-existing ischaemic or valvular heart disease, hypertension or diabetes and be at high risk for heart failure. Both systolic and diastolic heart failure are common, and it is important to keep a close watch on input and output especially as this can change after stroke and decide on whether to continue routine diuretics or other heart failure medications. If there is diagnostic uncertainty the CXR may show cardiomegaly, upper lobe diversion and pleural effusion, the ECG will often be abnormal with LVH, old MI and dynamic changes and screening tests such as BNP will be abnormal too. An echocardiogram can often give a good assessment of LV contractile function as well as valve issues. Acute symptomatic management involves IV or oral loop diuretics and long-term prognosis is improved with use of ACE inhibitors and beta blockers. Ischaemic and valvular heart disease and Hypertension should be managed. Saline is the fluid of choice immediately post stroke, but care must be taken to avoid overload and pulmonary oedema particularly seen in the frail older patients with cardiac and renal disease. Weekly weights if possible can give a good idea of short term changes in fluid balance.
AF is seen in 10% of those over 80 and is a common cause of stroke. They may also have tachyarrhythmias such as Fast AF and maybe compromised. Usually the AF predates the stroke but any form of sepsis or other problem can potentially precipitate AF. More information here. These patients will need CHADS-VASC and HASBLED score and consideration for anticoagulation.
Post Stroke seizures
Seizures after stroke are uncommon and seen in about 5%. They may be early or late. Early may occur within the first 1-2 days after a stroke. Usually, the stroke is large and cortical. There may be anything from a single seizure to status epilepticus. Early seizures can be one-off events in the acute stroke period and do not always herald a diagnosis of epilepsy and can quickly settle and may not need long-term anticonvulsants. Late onset seizures several months or even years post-stroke are treated as epilepsy. The underlying aetiology for seizures is complex but one suggestion is an excess of the excitatory neurotransmitter glutamate. Locally our first line therapy is often levetiracetam (Keppra) but Valproate is often used. Phenytoin is restricted for status epilepticus.
VTE covers the incidences of Deep vein thrombosis and pulmonary embolism. DVT is common in those who are mobile in the hospital and is often asymptomatic. The more immobile the greater the risk. There are various strategies to try to prevent VTE and these are discussed below. If one performs venography at Day 10 in stroke patients a great deal of small and distal clots can be found of uncertain risk. The main preventative strategy is early mobilisation, hydration and intermittent pneumatic compression (IPC).
Chest Infections/Aspiration Pneumonia
Chest infections can be seen in as many as 20% post stroke. Pneumonia is a major cause of morbidity and mortality after stroke. Pneumonia after stroke is associated with older age, dysarthria/aphasia, severity of post-stroke disability, cognitive impairment, and an abnormal water swallow test. Severe stroke and increasing age were shown to be the main early predictors for infections after stroke. There is no clear definition of post-stroke pneumonia. Some divide them into acute and chronic forms, with 1-month post-stroke being the cut off-threshold. Chest infections may happen for various reasons. Chest infection can result from simply being bed bound with basal atelectasis and immobility. It is commoner in those with severe neurological impairment, the elderly and diabetes and those needing mechanical ventilation. Chest infection carries an almost 3-fold increase in risk of death. The diagnosis of stroke-associated pneumonia requires often symptoms of breathlessness and malaise, auscultatory findings though most older patients may have lung crackles, percussion findings, fever, secretions, raised CRP, microbiological (e.g. sputum cultures) and radiological signs
Aspiration can result from impaired swallowing and so an initial swallowing assessment is key, and this helps to prevent inappropriate oral intake. A bedside swallow should be performed on all new stroke patients within the first few hours. If this fails, then patients should remain NBM and have IV fluids or consideration for an NG tube. The neurology of swallowing involves centres in the frontal lobe and brainstem. Swallowing is a complex neurological function that depends on multiple muscle groups acting together to direct food from the oral cavity into the upper oesophagus allowing and avoiding and aspiration. It is not surprising that in many patients with stroke that it often parallels initial drowsiness. Swallowing is often the dominant disability in those with a Lateral medullary syndrome. An excellent paper is available here. Risk Factors Reported in the Literature for Development of Post Stroke Pneumonia.
Prophylactic antibiotics have been shown to be useful in animal models this has not translated fully into the human experience with a small reduction in infections and no affect on mortality.
The treatment can involve physiotherapy to aid expectoration, adequate hydration and regular sitting out to help ensure respiratory function. Pure aspiration is partially a chemical pneumonitis if low pH material is aspirated. One of the common issues is about NG feeding of patients with poor upper airway protection and the real risks of gastro-oesophageal reflux and aspiration of feeds. There are always the concerns of the never event where a patient is fed via NG, but the tip of the line is within a main bronchus. This should be preventable with pH testing and CXR if needed ensuring the NG tube remains in the midline in its passage though the chest. Avoid the "whoosh test" which is unreliable.
- Wartenberg, KE, Stoll A,Funk A, AndreasMeyer, Schmidt MJ, Berrouschot J. Infection after Acute Ischemic Stroke: Risk Factors, Biomarkers, and Outcome. Stroke Research and Treatment Volume 2011. doi:10.4061/2011/830614
- Sellars C, Bowie L, Bagg J, Sweeney, Miller H, Tilston J, Langhorne P, Stott DJ. Risk Factors for Chest Infection in Acute Stroke. Stroke. 2007;38:2284-2291
Urinary tract infection (UTI)
Urinary tract infection is often related to the need to catheterise patients who are in retention after stroke. UTI may be seen in 11-23% of patients with stroke within 7-10 days. Almost a quarter of hospitalised patients have an indwelling catheter at some point. Catheter-associated UTI is very common and can lead to a systemic sepsis. Catheters are not the full story and there may be associated causes such as stroke-related immunosuppression or bladder dysfunction. An added note is that physicians often neglect the fact that patients have a catheter as time goes by. It is something that should be discussed as part of the weekly MDT. Catheters are a two-edged sword with many benefits but some significant risks and needs some discussion. The most important message is that Indwelling catheters should not be used as a substitute for nursing care in those with incontinence. Instead they need a continence plan that is personalised for them. Those who experience UTI will have a longer stay in hospital and will be at greater risk of bacteraemia. A UTI can cause delirium and sickness and can leave a patient unable to get on with rehabilitation. There will be fever. Exposure to antibiotics can lead to further consequences such as diarrhoea.
|Reasons Catheters used post stroke|
|Alternatives to indwelling urethral catheters:|
Bladder dysfunction is common after stroke. Continence issues are common in those with language and cognitive dysfunction associated with severe functional impairment. Continence issues greater with larger and cortical infarcts and there is no real lateralisation.
|Algorithm to reduce need for catheterisation|
|A||Every 2 hours, patient should be assessed and asked if he/she needs to void.|
|1.||If able to ambulate (per orders and safety assessment), they should be assisted to the bathroom.|
|2.||If unable to ambulate (per orders and safety assessment), consider assisting patient to a bedside commode if appropriate.|
|3.||If unable to ambulate to bathroom or use bedside commode, consider use of a urinal for male patients or bedpan for female patients.|
|4.||If unable to use the urinal or bedpan, consider using a diaper/brief.|
|B.||For urinary retention (no void for 4 hours or complaints of bladder fullness or inability to void)|
|1.||Perform a bladder scan.|
|2.||If bladder scan shows >250 mls of urine in bladder, perform an intermittent straight catheterization (ISC).|
|3.||After one episode of urinary retention, begin bladder scans every 4 hours, or after patient voids (postvoid residual). Continue ISC every 4 hours for bladder scan showing >250 mls of urine in bladder.|
|1.||Perform a post-void residual bladder scan once every shift. If scan shows >250cc of urine, follow instructions under B.|
|2.||Place a brief/diaper on patient.|
|3.||Assess patient frequently, asking if they need to void and following instructions in A.|
|4.||Perform skin checks for skin breakdown with every brief/diaper change and clean-up. If skin breakdown is present, notify clinical nurse specialist for further care.|
|D.||If concerned that patient needs catheter, call house officer on call for the patient.|
The only way to completely prevent falls in a patient recuperating following stroke is to not allow patients to walk but this creates a whole set of other problems. The aim of rehabilitation when possible is to enable a patient to walk safely. This may require the use of various walking aids. Falls without syncope may be due to many factors, weakness, poor vision, ataxia, apraxia, anxiety. Falls associated with low BP should be managed medically and the cause addressed as much as is possible prior to ongoing therapy.
The patient will enter a catabolic state if deprived of calories post stroke. The challenge is always how to give calories as safely as possible. In many frail older patients there may already be some weight loss. Patients may have chronic illnesses associated with weight loss such as COPD or even known or occult malignancies. With dementia type processes the interest and desire to eat may be reduced. Patients may simply forget to eat and need support and prompting. Other issues in older patients include poor dentition, odynophagia, candidiasis and oral issues. Some may have an undetected oesophageal malignancy, so an accurate history must be taken and an OGD may be needed in some. In some patients with lateral medullary syndromes where the issue is predominately a defective swallow then rapid NG to PEG will quickly resolve nutritional issues and the PEG can be removed when swallow is safe enough to allow normal intake. It is important that patients are evaluated for nutrition as part of the weekly MDT. Tools such as MUST below can help to identify at-risk patients.
|Issues weight loss and feeding|
|MUST Tool: add up the scores|
|Calculate BMI||Calculate Weight loss in 3-6 months||Acutely ill and no food for 5 days|
|0||BMI > 20||0||< 5%||0||No|
|1||BMI > 18.5-20||1||5-10%||2||yes|
|2||BMI > <18.5||2||>10%|
|Total Score||Actions Recommended are|
|1||Review and watch nutrition and ensure help is given and any issues addressed|
Strokes are often life-changing events and carry with them psychological trauma for the patient and those close to them. There is often a loss, physical, function and a loss of confidence and independence which can be devastating. It takes time for patients to readjust to new circumstances and many patients with time recover psychologically. Psychological treatment can include counselling or therapy for feelings that result from clinical depression. Types of treatment may include antidepressant medication, psychotherapy or both. You may also be referred to a local stroke support group. I will often discuss mood on more than one occasion with patients and discuss if they wish to consider antidepressants which is usually a six-month course and they can then withdraw gradually under supervision of their primary care physician.
There is available NICE guidance:psychological care after stroke. They pinpoint various times when psychological issues should be assessed.
- One month after stroke or just before discharge, or at six week follow-up
- Three months after stroke, usually post-discharge to judge persistence of early-onset problems and emergence of new problems
- Six months after stroke when much physical and social recovery has stabilised and likely longer-term problems can be assessed
- Assessment at six month and annual reviews will allow identification of those with long-term problem
|Level||The Nice guidance groups patients into several tiers with different levels of need|
|LEVEL 3||Severe and persistent disorders of mood and/or cognition that are diagnosable and require specialised intervention, pharmacological treatment and suicide risk assessment and have proved resistant to treatment at levels 1 and 2. These would require the intervention of clinical psychology (with specialist expertise in stroke) or neuropsychology and/or psychiatry.|
|LEVEL 2||Mild/Moderate symptoms of impaired mood and or cognition that interfere with rehabilitation. These may be addressed by non psychology stroke specialist staff, supervised by clinical psychologists (with special expertise in stroke) or neuropsychologists.|
|LEVEL 1||Sub-threshold problems at a level common to many or most people with stroke. General difficulties coping and perceived consequences for the person lifestyle and identity. Mild and transitory symptoms of mood and/or cognitive disorders such as a fatalistic attitude to the outcome of stroke, and which have little impact on engagement in rehabilitation. Support could be provided by peers, and stroke specialist staff|
Which cognitive assessment tools to use?
Assessment measures should only be carried out by staff trained to administer these tests. Some assessments require specific training from the company who provide the assessment, such as the AMPS. Assessment tools vary in purpose and should be selected according to need. Some assessment tools aim to give a broad picture of cognitive ability such as the MOCA, ACE-R or RBANS. Other assessments are targeted at specific cognitive skills for example:
- Attention: TEA
- Memory; Rivermead Behavioural Memory Test,
- Perceptual skills; BIT, RVPB
- Executive Functions;BADS
Links to Tests
- Addenbrookes cognitive Examination-III English Version A (2012)
- The Rivermead Behavioural Memory Test 3. Used to screen for memory problems and can measure changes over time. Used in those following Brain Injury, head Injury, stroke, neurological dysfunction. Takes 30 mins.
Skin Integrity issues
Poor skin care can lead to skin breaks and even pressure ulcers in vulnerable areas e.g. heals, buttocks. The problem is worse after stroke as there may be paralysis such that the patient cannot move the affected limb and so pressure points are not changed and breakdown occurs. Also patients may have sensory loss and so will not have any awareness or pain. Spasticity and contractures can distort normal anatomy and so cause skin pressure issues. Much of this is preventable from good nursing care. Most patients who are immobile are turned every 2 hours.
The integrity of the shoulder joint depends on the muscles surrounding it in terms of holding the joint together, the so-called rotator cuff group of muscles. Shoulder pain - stems from lack of support of an arm due to weakness or paralysis. This usually is caused when the affected arm hangs resulting in pulling of the arm on the shoulder.
- Medical complications after stroke Sandeep Kumar, Magdy H Selim, Louis R Caplan.Lancet Neurol 2010; 9: 105-18
- Spasticity after stroke: Physiology, assessment and treatment. Brain Inj, Early Online