• typically, the neurological deficit is maximal at the onset of the ischemic stroke and may subsequently improve (either spontaneously or due to recanalization therapy)
  • however, stroke patients are at risk of a variety of complications that may lead to death or clinical deterioration, manifested by:
    • progression of existing deficits or appearance of new symptoms (due to new occlusion, progression of existing thrombosis, edema, or hemorrhage)
    • quantitative or qualitative impairment of consciousness
      • delirium
      • epileptic seizures
      • intracranial hypertension
    • mood disorders
    • worsening of preexisting comorbidities (cardiac, respiratory, etc.)
    • onset of new systemic disorders (infection, venous thromboembolism, infarction, etc.)
  • complications can be divided into intracranial and extracranial; a brief overview follows

Diagnostic evaluation

  • general and neurological examination
    • global x focal deficits?
    • delirium syndrome (ICU-CAM)?
    • NIHSS, GCS
    • vital signs (O2 saturation, blood pressure + heart rate)
    • look for discrete signs of focal seizure (e.g., facial twitching, etc.)
  • review 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)
    • new occlusion in another segment? reocclusion of recanalized artery?
    • hemodynamically significant stenosis?
    • collateral circulation failure?
  • EEG examination (or EEG monitoring)
  • ECG monitoring
  • other imaging studies
    • chest X-ray
    • abdominal ultrasound
    • CT scan of the chest, abdomen, or pelvis
  • laboratory tests:
    • basic metabolic panel, CBC + coagulation tests
    • arterial blood gas (ABG) analysis (arterial pH, PaO2, PaCO2, and “base excess”
      • test provides valuable information about the patient’s acid-base balance, oxygenation, and ventilation status, which are crucial in the management of stroke and other critical conditions
      • normal arterial pH: 7.35-7.45
    • CRP, procalcitonin
    • cardiac enzymes to assess the myocardial injury
      • troponin T (TnT) and troponin I (TnI)
      • creatine kinase-MB (CK-MB)
    • Mg, Ca, ammonia
  • 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 be gradual (typically due to edema or thrombus progression) or sudden (new embolism, abrupt failure of collateral circulation, or intracranial bleeding, etc)

Hemorrhagic transformation of ischemia

  • the hemorrhagic component is easily detected on CT and even better on MR GRE   Asymptomatic hemorrhagic transformation of ischemia detected by MR GRE   [Arnauld, 2003]
  • hemorrhagic transformation most commonly occurs within the first 48 hours; increased risk is associated with extensive ischemia, late recanalization, and early anticoagulation
  • hemorrhagic transformation is often asymptomatic
  • antiplatelet therapy/LMWH should be discontinued if major bleeding occurs
Bleeding classification after Stroke and Reperfusion Therapy (ECASS II)

Brain edema, intracranial hypertension

  • edema usually develops between days 2-5
    • initially intracellular (cytotoxic)
    • a vasogenic component can be seen from day 5
  • symptomatic edema can be expected in large supratentorial ischemias and cerebellar infarcts
  • clinical presentation:
    • worsening of the neurological deficit (including loss of consciousness) within 24-36 hours
    • gradual progression over several days
    • initial deterioration is followed by a plateau and gradual improvement over a week (except for malignant edema cases)
  • 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 a posterior fossa stroke (AHA/ASA 2013 I/C)
  • decisions regarding decompressive craniectomy should be made early in cases of malignant ischemia  Malignant infarction in MCA and ACA territory Cerebellar ischemia with hydrocephalus managed by with decompressive craniectomy

Ischemia progression / early stroke recurrence

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Acute symptomatic epileptic seizures (ASS)

  • according to various sources, stroke is responsible for up to 60% of all acute symptomatic seizures (ASS)
  • seizures are typically focal, with possible secondary generalization
  • most seizures occur in the first 48 hours after stroke onset; increased risk of ASS is associated with large cortical ischemia and intracerebral bleeding


  • delirium (historically known as acute confusional state) presents with disturbances in attention, awareness, and higher-order cognition
  • commonly attributable to:
    • brain lesion
    • extracerebral causes: medication, metabolic disorders, alcohol withdrawal syndrome (AWS), 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 (besides delirium,  tremor, anxiety, nausea, hallucinations, or seizures can be seen)
    • combination of both intracerebral and extracerebral factors
Delirium-inducing drugs
anticholinergic drugs
  • tricyclic antidepressants (amitriptyline, imipramine)
  • prothiaden, fluoxetine, trazodone, lithium
  • conventional neuroleptics (chlorpromazine, thioridazine)
  • anticholinergic antiparkinsonian drugs (triphenidyl, biperiden, diethazine, benztropine), levodopa, pramipexole
  • atropine
  • spasmolytics (buscopan, oxybutynin)
  • 1st generation antihistamines (diphenhydramine)
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 settings  Border zone infarcts (BZI)
  • maintain a mean arterial pressure (MAP) >110 mmHg in normotensive patients and >130 mmHg in patients with known hypertension for the first 24 hours
  • administer plasma expanders or vasopressors if needed

Extracerebral complications

Infectious complications

  • fever is most commonly caused by respiratory infections
    • preventive measures for aspiration bronchopneumonia include early detection of dysphagia and early indication for NG tube placement
  • urinary tract infections are associated with catheter use
  • 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 (such as valvular heart disease, atrial fibrillation, and myocardial infarction) are significant risk factors for stroke
  • acute stroke can also induce cardiac dysfunction (e.g., arrhythmias) or lead to other cardiac complications
  • worsening of preexisting cardiomyopathy (CMP) or congestive heart failure (CHF)
    • a risk factor for increased morbidity and mortality
    • acute decompensation may occur due to myocardial infarction (MI), tachyarrhythmias, transfusion, or antiedema therapy
  • acute stress cardiomyopathy (Tako-Tsubo)
    • characterized by bulging of the apical part of the ventricle, ST-segment elevation with negative T waves in leads V3 and V4
    • cardiac enzymes are typically 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; exclusion of MI is imperative
  • more common in polymorbid patients with previously established coronary artery disease (CAD) and vascular risk factors (such as diabetes, hyperlipidemia, etc.)
  • decompensated hypertension or hypertensive crisis (emergency) occurs in up to 80% of stroke patients
  • etiology is complex, involving compensatory mechanisms aimed at improving perfusion and stress response

→ blood pressure management in the acute stroke

  • hypotension 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 heart rhythm 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, potentially leading to pulmonary edema, etc.
    • atrial fibrillation/flutter increases the risk of cardioembolism

Respiratory complications

  • hypoxia leads to a progression of brain damage, transitioning from penumbra to necrosis and potential worsening of neurological deficit
  • the most common causes of respiratory failure are:
    • impaired airway clearance
      • congestion, difficulty coughing (due to bulbar syndrome or somnolence) ⇒ hypoxemia, hypercapnia
    • airway obstruction
    • aspiration pneumonia
      • often a combination of aspiration and congestion/difficulty in coughing
      • increased risk in drowsy patients and those with bulbar syndrome
      • early screening for dysphagia may prevent pneumonia
    • central respiratory disorders (due to primary and secondary brainstem lesions)
    • pulmonary edema, atelectasis
    • pulmonary embolism  Pulmonary embolism on CTA
    • decompensation of asthma bronchiale (caution when using beta-blockers)

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 frequent cause of bronchopneumonia
    • systematic screening for dysphagia reduces the risk of aspiration-related bronchopneumonia
  • recommendations:
    • screening for dysphagia before initiating per os intake (including medications) – effective in identifying patients at increased risk of aspiration (AHA/ASA 2019 I/C-LD)
      • optimally, screening should be performed by a speech and language therapist or other specially trained professional
      • a standardized protocol is recommended
    • implementation of oral hygiene protocols
    • early nasogastric  (NG) tube placement if dysphagia is evident, followed by swallowing training
    • dietary modifications for milder cases
    • if dysphagia persists beyond 2-3 weeks, percutaneous endoscopic gastrostomy (PEG) should be indicated  (AHA/ASA 2019 IIa/C-EO)
  • screening tests
    • GUSS test
    • water swallow test (original and modified)
  • objective instrumental examinations:
    • FEES (fiberoptic examination of swallowing function)  FEES
    • videofluoroscopy (VF) – X-ray during swallowing of barium contrast agent  Videofluoroskopie
Water swallow test (original)
  • 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 required to empty the cup
      • drinking profile 
        • 1. the patient can drink all the water in 1 gulp without choking
        • 2. the patient can drink all the water in ≥ 2 gulps without choking
        • 3. the patient can drink all the water in 1 gulp, but with some choking
        • 4. the patient can drink all the water in ≥ 2 gulps, but with some choking
        • 5. the patient often chokes and struggles to consume all the water
      • drinking episodes

        • sipping, holding water in the mouth while drinking, water leaking from the mouth, a tendency to try to force oneself to continue drinking despite choking, cautious water consumption, etc.
  • diagnosis
    • normal: profile 1 completed within 5 seconds
    • suspected: profile 1 completed in > 5 seconds, or profile 2
    • abnormal: profiles 3-5
Water swallow test (modified)
  • procedure
    • the patient is given 3 mL of cold water in the oral vestibule and is instructed to swallow the water
    • if possible, additional water is given, and the patient is asked to swallow 2 more times; the worst swallowing activity is 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 score 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 alterations in breathing or wet hoarseness
    • 3. swallowed successfully with choking and/or wet hoarseness
    • 4. swallowed successfully without choking/wet hoarseness
    • 5. criteria 4 + 2 successful swallows within 30 s
GUSS test
  • GUSS is divided into 2 parts
    • preliminary assessment – indirect swallowing test
    • direct swallowing test – comprises 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 an upright position (at an angle of at least 60°)
    • because neglect and apraxia can alter the test, the examiner should ensure that the patient can see the examiner’s face and the spoon
    • patients must be fully awake before bolus testing
  • evaluation:
    • the indirect swallowing test includes additional scoring 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 laryngeal elevation
      • voice change – notably wet and gurgling voice qualities after swallowing or permanent, are reliable indicators of 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 increased aspiration risk
  • Indirect Swallowing Test – a simple saliva swallow is performed. Patients unable to produce enough saliva because of dry mouth are provided with a saliva spray substitute. Vigilance, voluntary coughing, throat clearing, and saliva swallowing are assessed
  • Semisolid Swallowing Trial – water is thickened to pudding consistency using an instant food thickener. One-third to one-half teaspoon is offered as an initial bolus, followed by 5 additional half-teaspoons. The investigator should observe the patient closely after each spoonful. Abort the testing if 1 of 4 aspiration signs (deglutition, cough, drooling, and voice change) occurs
  • Liquid Swallowing Trial – starting with 3 mL of aqua in a cup, the patient should be closely observed. 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 used as the initial bolus; the test is repeated five times. A time limit of ten seconds has been established for a small solid bolus
GUgging Swallowing Sreen (GUSS) test
  • the most common cause of GI bleeding is either a preexisting lesion or a 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
    • severe stroke
  • initiate enteral nutrition as soon as possible!
  • 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)


  • PPIs are more expensive and significantly more effective than H2-blockers [Buendgens, 2016]
  •  use H2 blockers if PPIs are contraindicated


  • 40 mg once daily, or 20 mg twice daily PO
    • 1g PO or via nasogastric tube every 6-8 hours
    • used in peptic ulcer prevention and treatment or to reduce hyperphosphatemia
  • caused by a clonic contraction of the diaphragm with simultaneous closure of the glottis
  • short-term hiccups are mostly benign and can be attributed to factors such as:
    • 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 underlying 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, myocardial infarction)
    • esophageal diseases (oesophageal obstruction by solid food or tumor, or esophagitis)
    • metabolic causes (uremia, diabetes decompensation), acid-base disorders, mineral imbalances (hyponatremia)
    • central causes (direct or indirect brainstem lesions) – tumors, stroke, trauma
    • alcohol and drugs (dexamethasone, methyldopa, sulfonamides, antiseizure medications)
  • severe forms of hiccups are frequently resistant to symptomatic treatment
  • treat potential causes
  • pharmacotherapy (see table) – combination therapy may be effective (e.g., omeprazole + baclofen +  gabapentin)
  • psychotherapy (cognitive-behavioral therapy or other psychological interventions may be beneficial for stress-induced hiccups)
  • acupuncture (may provide symptomatic relief, particularly for hiccups resistant to pharmacotherapy)

→ overview of treatment options see here

(has a peripheral and central effect)
  • initial dose: 5-10 mg PO every 8 hours
  • maintenance dose: 10-20 mg PO every 8 hours
  • max dose 60-80 mg per day
  • abrupt discontinuation should be avoided to prevent withdrawal symptoms
Anticonvulsive drugs
gabapentin (NEURONTIN)
  • initial dose: 300 mg PO every 8 hours
  • the dose may be titrated up based on patient response and tolerance. Commonly used regimens include 300 mg every 8 hours or 600 mg twice a day
  • initial dose: 250 mg PO every 12 hours
  • maintenance dose: 500-1000 mg divided into 2 or 3 doses
Neuroleptics (central effect)
  • initial dose: 0.5-2 mg PO every 8 hours
    • titrate gradually (sometimes 1-2 mg per night is enough); fewer AEs occur at this dose
  • maintenance dose:  1-4 mg every 8 hours
chlorpromazine (PLEGOMAZIN)
  • initial dose:  25-50 mg PO or IM every 8 hours
  • after 3 days, the dose may be increased to 25-50mg every 4h
  • chlorpromazine may cause extrapyramidal symptoms, QT prolongation, or other serious side effects and may interact with other medications. Monitoring for adverse effects is recommended.
Prokinetic drugs
PO 10 mg every 6-8 hours (max 40 mg/d)
PPI (use if GER is suspected)
PO 20-40 mg once daily

Urogenital complications

  • urinary incontinence
  • urinary tract infections (up to 15%)
    • may lead to worsening of the clinical condition
    • prevention:
      • avoid unnecessary catheterization and regularly review the necessity of an indwelling catheter and remove it as soon as clinically feasible
      • employ sterile technique during catheter insertion and maintenance
      • use antibiotic-coated or silver-alloy catheters to reduce the risk of bacterial colonization
      • perform routine urine tests to detect early signs of infection
      • ensure adequate fluid intake to promote urinary flow and dilute bacteria
      • encourage early mobilization

Deep vein thrombosis/pulmonary embolism

Other complications

  • Poststroke Depression (PSD) is quite common (in up to 33% of patients)
    • depressed patients are less compliant with physical therapy and medical treatment and have worse outcome compared to non-depressed patients
    • early drug treatment (tricyclics, SSRIs, SNRIs) is important
  • anxiety
  • 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 2 hours), physical therapy, massages
    • prevention devices:
      • antidecubitus mattress  Antidekubitální pomůcky
      • antidecubitus fleece  Antidekubitální pomůcky   Antidekubitální pomůcky
    • minimize pharmacologic sedation in agitated patients
    • ensure adequate hydration and nutrition (monitor protein and albumin levels)
Pressure sore
  • rule out fracture or luxation (often caused by a fall due to sudden onset of paresis)

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Acute stroke complications
link: https://www.stroke-manual.com/acute-stroke-complications/