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 |
anticholinergic drugs
|
|
Addictive substances and alcohol (acute toxicity/ withdrawal)
|
H2-blockers (cimetidine, ranitidine)
|
opioid analgesics
|
antimalarial drugs (mefloquine)
|
antiviral drugs (acyclovir)
|
others (lithium, barbiturates, benzodiazepines flunitrazepam, NSAIDs indomethacin, digoxin, corticosteroids, centrally acting myorelaxants, antihypertensives
|
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)
- 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 |
|
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
|
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 |
|
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:
- rule out fracture or luxation (often caused by a fall caused by sudden onset of paresis)