Stroke Complications

From Stroke Education
Jump to: navigation, search

Learning objectives

  • Post stroke complications
  • Recognise complications
  • Preventing stroke complications
  • Managing post stroke complications

Introduction

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 after late complications. 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 preempting 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 and manage complications.

Cerebral oedema

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. 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 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.

Fever

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.

Hyperglycaemia

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 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. 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.

Post Stroke seizures

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 lifelong anticonvulsants. Later onset seizures several months or even years post-stroke are treated as epilepsy.

Venous Thromboembolism

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).

Poor Swallow and Aspiration Pneumonia

The 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 also in the 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.

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 maybe 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

  • Acute urinary retention or obstruction
  • Measurements of urinary output in critically ill patients
  • Hygiene for open sacral or perineal wounds in incontinent patients
  • Prolonged immobilization (e.g. uncleared thoracic or lumbar spine)
  • To improve comfort for end of life care if needed


Alternatives to indwelling urethral catheter

  • Condom catheter drainage (when appropriate)
  • Intermittent catheterisation
  • Bladder ultrasound can measure volume and can help reduce need for catheter insertions.

Continence

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

Every 2 hours, patient should be assessed and asked if he/she needs to void.

  • If able to ambulate (per orders and safety assessment), they should be assisted to the bathroom.
  • If unable to ambulate (per orders and safety assessment), consider assisting patient to a bedside commode if appropriate.
  • If unable to ambulate to bathroom or use bedside commode, consider use of a urinal for male patients or bedpan for female patients.
  • If unable to use the urinal or bedpan, consider using a diaper/brief.

For urinary retention (no void for 4 hours or complaints of bladder fullness or inability to void

  • Perform a bladder scan.
  • If bladder scan shows >250 mls of urine in bladder, perform an intermittent straight catheterization (ISC).
  • 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.

For incontinence

  • Perform a post-void residual bladder scan once every shift. If scan shows >250cc of urine, follow instructions under B.
  • Place a brief/diaper on patient.
  • Assess patient frequently, asking if they need to void and following instructions in A.
  • 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.
  • If concerned that patient needs catheter, call house officer on call for the patient.

Falls

The only way to completely prevent falls in a patient recuperating following stroke is to not allow patients to walk abut 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.

Nutrition

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
  • New and older Cognitive defects
  • Malabsorption - coeliac, pancreatic
  • Difficulty eating - pain, weakness, apraxia
  • Issues of care - needing help to feed, language
  • Lack of access to appropriate food
  • Chronic and acute illness
  • Fatigue, Poor vision, Breathlessness
  • Low mood and depression



MUST Tool
Calculate BMI
0 BMI > 20
1 BMI > 18.5-20
2 BMI > <18.5
Calculate Weight loss in 3-6 months
0 < 5%
1 5-10%
2 >10%
Acutely ill and no food for 5 days
0 No
2 yes
TotalActions
0 Weekly review
1Review and watch nutrition and ensure help is given and any issues addressed
2+
  • Identify contributory causes and address them
  • Weekly discussion at MDT and monitoring
  • Dietician referral and high energy drinks and supplements
  • Full fat milk and multivitamins
  • NG tube/PEG may be considered if appropriate
  • TPN in selected cases when there are issues with enteral feeding.


Mood/Cognition

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.

<A href="https://www.nice.org.uk/media/default/sharedlearning/531_strokepsychologicalsupportfinal.pdf">NICE guidance:psychological care after stroke</a>

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

LevelThe 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 1Sub-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

Spasticity post stroke

Increased tone or spasticity as it is better known. Tone is usually reduced initially and then can increase and if excessive is termed spasticity. Spasticity is seen in 30% of post stroke patients. It has been defined as a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.There is however no universal definition. Spasticity is a dynamic phenomenon which can be seen early or late post stroke and may be transient. It can vary with posture, position, activity, pain, infection and mood. Spasticity can induce pain, poor positioning, skin pressure issues, tendon retraction and muscle weakness. It can reduce the potential success of rehabilitation. Scales have been used and the most common is the Modified Ashworth Scale (MAS) which measures the level of resistance to passive movement but does not assess other factors but is easy and quick to use and has been the basis of much related research.

Modified Ashworth Scale
0No increase in muscle tone
1Slight increase in muscle tone, manifested by a catch or by minimal resistance at the end of the range of motion (ROM) when the affected part(s) is (are) moved in flexion or extension
1+Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM
2More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved
3Considerable increase in muscle tone, passive movement difficult
4Affected part(s) rigid in flexion or extension


Summary of the most common patterns observed in the upper motor neuron syndrome, the muscles involved and the most observed side-effects. Adapted from [6].
Pattern Muscles involvedSide-effects
Adducted/internally rotated shoulder Pectoralis major, Teres major, Latissimus dorsi, Anterior deltoid, Subscapularis
  • Muscle contractures and pain
  • Shoulder stiffness and painful passive range of motion
  • Skin maceration, breakdown and malodour in the axilla
  • Difficulties for dressing
  • Limitation of the reaching-forward behaviour
Flexed elbow Teres major, Latissimus dorsi, Long head of triceps, Posterior deltoid
  • Muscle contractures and pain
  • Persistent elbow flexion during sitting, standing and walking
  • Difficulties for transfer (no fulcrum), dressing and reaching objects
  • Skin maceration, breakdown and malodor in the antecubital fossa
  • Disfiguring appearance
  • Stretch injury to the ulnar nerve (at the bend of the elbow). The nerve is vulnerable to

repeated trauma and can be compressed in the cubital tunnel leading to intrinsic muscle atrophy in the hand and weakness of ulnar wrist and finger flexion

Pronated forearm Pronator teres, Pronator quadratus
  • Muscle contractures and pain
  • Difficulties to reach underhand to a target
  • Limitations to turn the patients hand palm side up for fingernail trimming

(important for patients with fingers that are flexed into the palm secondary to a clenched fist deformity)

  • Difficulties to feed (e.g., hold a spoon)
Flexed wrist Flexor carpi radialis, Flexor carpi ulnaris, Palmaris longus, Extensor carpi ulnaris
  • Muscle contractures and pain
  • Compression of the median nerve at wrist with carpal tunnel syndrome and hand pain
  • Disfiguring appearance
  • Awkward hand placement during reaching and impairs positioning of objects held
  • Weakened grip strength
Clenched fist Flexor digitorum sublimis and profundus
  • Patients cannot perform the reach phase to grasp an object
  • Fingernails digging into palmar skin with pain
  • Nail bed infections
  • Pain when somebody attempts to pry fingers open to gain palmar access
  • Disfiguring appearance
  • Skin maceration, breakdown and malodour in the palm
  • Difficulties to wear gloves or hand splints
  • Limitation for grasping, manipulation and release of objects
  • Development of muscle, skin and joint contractures
Thumb-in-palm Flexor pollicis longus and brevis deformity, Adductor pollicis, First dorsal interosseaous
  • Difficulties to wear gloves or hand splints
  • Limitation of thumb extension and abduction that open up the web space before grasp
  • Difficulties to execute grasp patterns (three-jaw chuck, lateral grasp and tip pinch)
Flexed hip

Iliopsoas, Rectus femoris, Pectineus Adductors longus and brevis

  • Interfered with positioning on a chair, sexuality and gait
  • Walking with a crouched gait pattern and compensatory knee flexion to maintain

balance (leading to fatigability)

Adducted thigh Adductor longus and brevis, Adductor magnus, Gracilis, Iliopsoas, Pectineus
  • Scissoring thighs interfere with perineal care, sexual intimacy, sitting, transfers,standing and walking
  • Difficulties with limb clearance and advancement during swing phase of gait
Stiff kneeRectus femoris, Vastus intermedius, medialis and lateralis, Gluteus maximus
  • Gait deviation with the knee remaining extended through the gait cycle
  • Functional lengthening of the leg during the gait with dragging of the toe and risk to trip and fall
  • Need of leg elevation support when seated
  • Problems for standing, climbing stairs and transfers
Flexed knee Medial and lateral hamstrings
  • Compensation of ipsilateral hip flexion during stance phase with flexed knee and

contralateral hip and knee flexion (crouch gait pattern)

  • Muscle contraction and pain
  • Difficulties with transfers and wheelchair positioning
  • Limitation of limb advancement due to the lack of knees extension during the

terminal swing (short step lengths)

  • When acting to the hip joint, hamstring cause the extension of the trunk leading to the
deformity slide forward in the wheelchair
Equinovarus foot Medial and lateral gastrocnemius, Soleus, Tibialis anterior and posterior, Long toe flexor, Extensor halluces longus
  • Compression of the lateral border of the foot against the mattress, bed rail, footrest or floor
  • Skin breakdown on the fifth metatarsal head
  • Pain upon weight bearing over the lateral border of the foot
  • Difficulties to put on and wear shoes
  • Limitation of dorsiflexion during early and mid stance
  • Short contralateral steps
  • Deviant knee flexion during pre-swing
  • Occurrence of an early swing phase foot drag

Skin Integrity issues

Poor care can lead to skin breaks and even pressure ulcers in vulnerable areas e.g. heals, buttocks. This is preventable from good nursing care. Most patients who are immobile are turned every 2 hours.

Shoulder syndromes

  • 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.

References