ISCHEMIC STROKE / COMPLICATIONS
Acute stroke complications
Created 20/02/2023, last revision 23/08/2023
- usually, the neurological deficit is maximal at the onset of the stroke and may improve in the following period (spontaneously or thanks to recanalization therapy)
- however, stroke patients are at risk for a wide range of complications that can cause death or clinical deterioration, manifested by:
- deficit progression or appearance of new symptoms (new occlusion, progression of existing thrombosis, edema, hemorrhage)
- quantitative or qualitative impairment of consciousness
- delirium
- epileptic seizures
- intracranial hypertension
- mood disorders
- worsening of existing comorbidities (cardiac, respiratory, etc.)
- onset of new systemic disorders (infection, VTE, infarction, etc.)
- complications can be divided into intracranial and extracranial; a brief overview follows
Diagnostic evaluation
- general and neurological physical examination
- check medication (sedatives, delirium-inducing drugs)
- follow-up CT/MR of the brain (large edema? hemorrhage? new infarct lesion? hydrocephalus?)
- follow-up vascular imaging (neurosonography/MRA/CTA)
- occlusion in another segment? reocclusion of recanalized artery?
- hemodynamically significant stenosis?
- collateral circulation failure?
- EEG exam (or EEG monitoring)
- ECG monitoring
- other imaging studies
- chest X-ray
- abdominal ultrasound
- CT scan of the chest, abdomen, or pelvis
- laboratory tests:
- the basic metabolic panel, CBC + coagulation tests
- ASTRUP method for determination of arterial pH, pCO2, and “base excess”
- CRP, procalcitonin
- cardiac enzymes
- Mg, Ca, ammonia
- the basic metabolic panel, CBC + coagulation tests
- detection of infection
- sputum and urine analysis, culture swabs
- blood cultures
Intracerebral complications
- approximately 30% of acute stroke patients experience progression of neurological deficits, including quantitative or qualitative disturbances of consciousness
- deterioration may occur gradually (typically due to edema or thrombus progression) or suddenly (new embolism, abrupt failure of collateral circulation, intracranial bleeding, etc.)
Hemorrhagic transformation of ischemia
- hemorrhagic component is easily detected on CT and even better on MR GRE
[Arnauld, 2003] - hemorrhagic transformations occur most frequently in the initial 48 hours; increased risk is associated with a large ischemia, late recanalization, and early anticoagulation
- hemorrhagic transformation is often asymptomatic
- antiplatelet therapy/LMWH should be discontinued if major bleeding occurs
Brain edema, intracranial hypertension
- edema usually develops on days 2-5
- initially intracellular (cytotoxic)
- a vasogenic component can be seen from day 5
- more severe edema can be expected in large supratentorial ischemias and cerebellar infarcts
- clinical presentation:
- worsening of the neurological deficit (including LOC) within 24-36h
- gradual progression over several days
- initial deterioration is followed by a plateau and gradual improvement over a week (except malignant edema)
- efficacy of pharmacotherapy is unclear (AHA/ASA 2013 IIb/C)
- ventricular drainage and/or craniectomy is recommended if acute hydrocephalus develops as a result of the posterior fossa stroke (AHA/ASA 2013 I/C)
- decisions regarding decompressive craniectomy should be made early in cases of malignant ischemia
→ intracranial hypertension syndrome
Ischemia progression / early stroke recurrence
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Acute symptomatic epileptic seizures (ASS)
- according to various sources, stroke is the responsible for up to 60% of all acute symptomatic seizures (ASS)
- seizures are mainly focal with possible secondary generalization
- 50-70% of ASS occur in the first 48 hours after stroke onset
- the increased risk of ASS is associated with large cortical ischemia
- prophylactic use of anti-seizure medication (ASM) is not recommended (AHA/ASA 2013 III/C)
Delirium
- delirium (historically known as acute confusional state) presents with disturbances of attention, awareness, and higher-order cognition
- usually caused by:
- brain lesion
- extracerebral causes: medication, metabolic disorders, alcohol withdrawal syndrome, infection, etc.
- Alcohol Withdrawal Syndrome (AWS) is a set of symptoms that can occur following a reduction in alcohol consumption after a period of excessive and/or prolonged use
- combination of both
| Delirium-inducing drugs |
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anticholinergic drugs
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Addictive substances and alcohol (acute toxicity/ withdrawal)
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H2-blockers (cimetidine, ranitidine)
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opioid analgesics
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antimalarial drugs (mefloquine)
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antiviral drugs (acyclovir)
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others (lithium, barbiturates, benzodiazepines flunitrazepam, NSAIDs indomethacin, digoxin, corticosteroids, centrally acting myorelaxants, antihypertensives
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Failure of collateral circulation
- the risk of collateral circulation failure is increased in the presence of concurrent extra-intracranial stenoses and/or hypotension
- typical watershed infarcts can be seen in such a setting
- maintain MAP >110 mmHg in normotensive patients, >130 mmHg in patients with known hypertension for the first 24 hours
- administer plasma expanders/vasopressors if needed
Extracerebral complications
Infectious complications
- fever is most commonly caused by respiratory infection
- prevention of aspiration bronchopneumonia: early detection of dysphagia, early indication for NG tube
- urinary tract infections (catheter)
- catheter-related bloodstream infections (sepsis)
Metabolic disorders
- hydration disorders (usually dehydration)
- ionic imbalances (most commonly hyponatremia, hypokalemia, hypophosphatemia, etc.)
- renal or prerenal uremia
Cardiovascular complications
- several heart conditions (valvular heart disease, atrial fibrillation, myocardial infarction) are significant risk factors for stroke
- acute stroke can also induce cardiac dysfunction (e.g., arrhythmias) or other cardiac complications
- worsening of premorbid cardiomyopathy (CMP) or congestive heart failure
- a risk factor for increased stroke morbidity and mortality
- acute decompensation due to MI, tachyarrhythmias, transfusion, antiedema therapy
- acute stress cardiomyopathy (Tako-Tsubo)
- bulging of the apical part of the ventricle, ST-segment elevation with negative T waves in V3 and V4
- cardiac enzymes are normal
- females are more commonly affected
- myocardial infarction with hypokinesia may be a source of cardiac embolism, but MI may also be a consequence of stroke (autonomic dysregulation, stress)
- elevation of cardiac enzymes due to neurogenic myocardial damage (myocytolysis) is a frequent finding; it is always necessary to exclude MI
- more common in polymorbid patients with previously diagnosed CAD and vascular risk factors (diabetes, hyperlipidemia, peripheral artery disease)
- decompensated hypertension or hypertensive crisis (emergency) occurs in up to 80% of stroke patients
- etiology is complex (a compensatory mechanism that improves perfusion, stress response, etc.)
- hypotension (low blood pressure) is generally defined as SBP < 90 mm Hg or DBP < 60 mm Hg
- the clinical threshold (leading to hypoperfusion symptoms including border zone infarction) is individual (higher in hypertensive patients)
- most common causes of hypotension in acute stroke patients are:
- heart failure
- hypovolemia/shock
- anemia
- sepsis
- arrhythmias (dysrhythmias) are irregularities in the heartbeat and are a common complication of acute stroke
- the most common are supraventricular arrhythmias
- sinus tachycardia
- atrial fibrillation/flutter
- arrhythmias may cause:
- hemodynamic instability with hypotension (↑risk of hypoperfusion injury)
- congestive heart failure with pulmonary edema, etc.
- atrial fibrillation/flutter increases the risk of cardioembolism
Respiratory complications
- hypoxia leads to a progression of brain damage with a transition from penumbra to necrosis and possible worsening of neurological deficit
- most common causes of respiratory failure are:
- impaired airway toilet
- congestion, difficulty coughing (bulbar syndrome, somnolence) ⇒ hypoxemia, hypercapnia
- airway obstruction
- aspiration pneumonia
- often a combination of aspiration and congestion/difficulty coughing
- increased risk in drowsy patients and those with a bulbar syndrome
- early screening for dysphagia may prevent pneumonia → see below
- central respiratory disorders (primary and secondary brainstem lesions)
- pulmonary edema, atelectasis
- pulmonary embolism
- decompensation of asthma bronchiale (cave beta-blockers)
- impaired airway toilet
Gastrointestinal complications
- dysphagia is present in 42% – 67% of patients with acute stroke in the first three days
- the most severe dysphagia is seen in patients with brainstem lesions
- dysphagia is associated with an increased risk of aspiration
- the incidence of aspiration in the first five days ranges from 20% to 42%
- aspiration/silent aspiration is a common cause of bronchopneumonia
- systematic screening for dysphagia reduces the risk of aspiration bronchopneumonia
- recommendations:
- initial screening for dysphagia before initiating per os intake (including medication) is effective in identifying patients at increased risk of aspiration (AHA/ASA 2019 I/C-LD)
- optimally, it should be performed by a speech and language therapist or other specially trained professional
- standardised protocol is recommended
- implementation of oral hygiene protocols
- early NG tube placement is indicated with evidence of dysphagia, followed by training of swallowing
- dietary modification in milder cases
- if dysphagia does not improve after 2-3 weeks, percutaneous endoscopic gastrostomy (PEG) should be indicated (AHA/ASA 2019 IIa/C-EO)
- initial screening for dysphagia before initiating per os intake (including medication) is effective in identifying patients at increased risk of aspiration (AHA/ASA 2019 I/C-LD)
- screening tests
- GUSS test
- water swallow test (original and modified)
- objective instrumental examinations:
- FEES (fiberoptic examination of swallowing function)
- videofluoroscopy (VF) – X-ray during swallowing of barium contrast agent
- FEES (fiberoptic examination of swallowing function)
- procedure
- the patient is seated in a chair and is given a cup containing 30 mL of water
- the patient is then asked to drink the cup
- monitor and assess:
- time to empty a cup
- drinking profile
- drinking episodes
- the patient is seated in a chair and is given a cup containing 30 mL of water
- drinking profiles
- 1. patient can drink all the water in 1 gulp without choking
- 2. patient can drink all the water in ≥ 2 gulps without choking
- 3. patient can drink all the water in 1 gulp, but with some choking
- 4. patient can drink all the water in ≥ 2 gulps, but with some choking
- 5. patient often chokes and has difficulty drinking all the water
- drinking episodes
- sipping, holding water in the mouth while drinking, water coming out of the mouth, a tendency to try to force himself/herself to continue drinking despite choking, drinking water cautiously, etc.
- diagnosis
- normal : profile 1 completed within 5s
- suspected : profile 1 completed in > 5s, or profile 2
- abnormal : profiles 3-5
- procedure
- the patient is given 3 mL of cold water in the oral vestibule and then instructed to swallow the water
- if possible, give more water and ask to swallow 2 more times; the worst swallowing activity is to be assessed
- if the patient meets criteria 1-4, a maximum of 2 additional attempts (a total of 3 attempts) should be made, and the worst assessment is recorded as the final result
- assessment criteria
- 1. failed to swallow with choking and/or respiratory changes
- 2. swallowed successfully without choking but with changes in breathing or wet hoarseness
- 3. swallowed successfully with choking and/or wet hoarseness
- 4. swallowed successfully with no choking/wet hoarseness
- 5. criteria 4 + 2 successful swallowing within 30 s
- 1. failed to swallow with choking and/or respiratory changes
- GUSS is divided into 2 parts
- preliminary assessment – indirect swallowing test
- direct swallowing test – 4 items with 3 subtests (semisolid, liquid, and solid) to be performed sequentially
- before starting the GUSS procedure, the patient should be seated in bed in the upright position (of at least a 60°)
- because neglect and apraxia can alter the test, the investigator should ensure that the patient can see the examiner’s face, the spoon, and the textures in front of him/her
- patients must be fully awake before bolus testing
- evaluation:
- in the indirect swallowing test, additional evaluation is performed for vigilance, voluntary coughing, deglutition of saliva, drooling, and voice change
- the evaluation criteria used in the direct swallowing test are: deglutition, involuntary cough, drooling, and voice change
- deglutition – effectual larynx elevation
- voice change – particularly wet and gurgling voice qualities after swallowing or permanent, were found to be reliable parameters for detecting aspiration
- drooling – easy to assess
- a weak or absent voluntary cough and/or throat clearing, as well as spontaneous coughing before, during, or after swallowing, are considered predictive of aspiration risk
- Indirect Swallowing Test – a simple saliva swallow is performed. Patients who cannot produce enough saliva because of dry mouth are given saliva spray as a substitute. Vigilance, voluntary cough, throat clearing, and saliva swallowing are assessed
- Semisolid Swallowing Trial – water is thickened with an instant food thickener to the pudding consistency. One-third to one-half teaspoon is offered as an initial bolus, followed by 5 more half-teaspoons. The investigator should observe the patient closely after each spoonful. Abort the investigation if 1 of 4 aspiration signs (deglutition, cough, drooling, and voice change) is positive.
- Liquid Swallowing Trial – starting with 3 mL of aqua in a cup, the patient should be observed closely while swallowing the first amount. If swallowed successfully, the test continues with increasing amounts of 5, 10, and 20 mL Finally, the patient should drink the 50 mL as quickly as possible
- Solid Swallowing Trial – a small piece of dry bread is the first bolus at the beginning of this subtest. The test is repeated 5 times. Ten seconds have been established as the time limit for a small solid bolus (including the oral preparation phase)
- the most common cause of GI bleeding is either a preexisting lesion or newly developed “stress ulcer”
- disruption of the integrity of the upper GI mucosa due to extreme physiological stress, typically in critically ill patients
- often develops within a few hours after the initial insult
- can result in bleeding or perforation ⇒ ↑ mortality and intensive care stay
- incidence approx. 3% when on prophylactic medication
- risk factors for GI bleeding
- coagulopathies, including iatrogenic
- history of GI bleeding/peptic ulcer
- mechanical ventilation > 48h
- traumatic brain/spinal cord injury
- sepsis
- corticosteroids use
- renal and hepatic impairment
- malignancy
- sever stroke
- prophylaxis should be administered only to patients at increased risk and discontinued in a timely manner (due to the increased risk of nosocomial pneumonia, Clostridium difficile infection, drug interactions, or hepatotoxicity); routine use of PPIs does not reduce mortality
- proton pump inhibitors (PPIs) – OMEPRAZOLE, PANTOPRAZOLE
- 20-40 mg once daily PO or IV
- PPIs are more expensive and significantly more effective than H2-blockers [Buendgens, 2016]
- use H2 blockers if PPIs are contraindicated
- FAMOTIDINE 40 mg once daily, or 20 mg twice daily PO
- FAMOTIDINE 40 mg once daily, or 20 mg twice daily PO
- SUCRALFATE
- 1g PO or via nasogastric tube every 6-8 hours
- used in peptic ulcer prevention and treatment or to reduce hyperphosphatemia
- antacids
- proton pump inhibitors (PPIs) – OMEPRAZOLE, PANTOPRAZOLE
- initiate enteral nutrition as soon as possible!
- induced by a clonic contraction of the diaphragm with simultaneous closure of the glottis
- benign causes predominate in short-term hiccups
- distention of the esophagus and stomach, intake of carbonated fluids, irritation of the digestive tract with spices)
- emotions, excitement
- sudden change in temperature): drinks (hot/cold), shower, air, etc.
- more serious causes:
- pulmonary and mediastinal diseases (pneumonia, lung tumors, mediastinitis, and mediastinal tumors)
- abdominal cavity diseases (direct irritation of the diaphragm – ileus, peritonitis, stomach and liver tumors and metastases, liver abscess, pancreatitis, and pancreatic tumors, etc.)
- heart diseases (pericarditis, MI)
- esophageal diseases (oesophageal obstruction by solid food or tumor, or esophagitis)
- metabolic causes (uremia, diabetes decompensation), acid-base disorders, mineral imbalances (hyponatremia)
- central (direct or indirect brainstem lesions) – tumors, stroke, trauma
- alcohol and drugs (dexamethasone, methyldopa, sulfonamides, antiepileptic drugs)
- severe forms are often resistant to symptomatic treatment
- treat potential causes
- pharmacotherapy (see table), including combination therapy (e.g., omeprazole + baclofen + gabapentin)
- psychotherapy
- acupuncture
| BACLOFEN the both peripheral and central effect |
PO 5-20 mg every 8-12 hours (max dose 60 mg/d) |
| Anticonvulsive drugs |
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| gabapentin (NEURONTIN) | PO 300 mg every 8 hours |
| valproate (ORFIRIL, DEPAKINE) |
PO up to 15 mg/kg/24h divided into 3-4 doses |
| Neuroleptics (central effect) | |
| HALOPERIDOL | PO 1-4 mg 1-3x daily
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| chlorpromazine (PLEGOMAZIN) |
PO 25-50 mg every 6-8 h (if PO form available) after 3 days, increase the dose to 25-50mg every 3-4h |
| Prokinetic drugs |
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| metoclopramide |
PO 10 mg every 6-8 hours |
| PPI (if GER is suspected) | |
| omeprazole pantoprazole |
PO 20-40 mg once daily |
Urogenital complications
- urinary incontinence
- urinary tract infections (up to 15%)
- may lead to the worsening of clinical condition
- prevention:
- avoid unnecessary catheterization
- use prophylactic urinary antiseptics
- use antimicrobial (antibiotic-coated) catheters
Deep vein thrombosis/pulmonary embolism
Other complications
- Post-Stroke Depression (PSD) is quite common (up to 33% of patients)
- depressed patients are less compliant with physical therapy and medical treatment and have worse outcomes compared to non-depressed patients
- early drug treatment (tricyclics, SSRIs, SNRIs) is important
- anxiety
- Vascular Cognitive Impairment (VCI)
- pressure sores usually occur on the back of the head, shoulders, elbows, sacrum and buttocks, hips, and heels
- prevention of pressure sores:
- regular repositioning of the patient (every 2h), physiotherapy, massages
- prevention devices:
- antidecubitus mattress
- anti decubitus fleece
- antidecubitus mattress
- minimize the pharmacologic sedation in agitated patients
- ensure adequate hydration and nutrition (monitor protein and albumin levels)
- rule out fracture or luxation (often caused by a fall caused by sudden onset of paresis)
