• the management of patients with acute stroke includes
    • diagnosis and specific stroke treatment (recanalization, surgery, etc.)
    • management and prevention of general medical problems
      • cardiac and pulmonary care, fluid and ion balance restoration, metabolic maintenance, blood pressure control
      • prevention and treatment of complications (infection, VTE, intracranial hypertension, bed sores, etc.)
    • evaluation of stroke etiology and initiation of individualized secondary prevention
    • early initiation of rehabilitation (incl. speech therapy, ergotherapy, etc.)
  • the proper management of general conditions and complications is equally important as specific therapy (although the latter may sometimes attract more attention)

Stroke unit care

  • it is recommended to admit the patient to a stroke unit (AHA/ASA 2019 I/A)
    • for a minimum of 24 hours, preferably for 48-72 hours
  • care is provided by a specialized multidisciplinary team
  • treatment in a stroke unit results in a relative reduction in mortality and dependency compared to treatment in a regular ward  [Langhorne, 1997] 
    • treating 100 patients using this approach can result in a reduction of 5 patients who would die or remain dependent (NNT 20)
    • the benefit is universal and applicable to all types of stroke and patients of varying degrees of severity

Basic monitoring

  • oximetry (maintain sat O2 > 94%)
    • use a finger or earlobe sensor
    • oxygen should be provided to maintain oxygen saturation >94%  (AHA/ASA 2019, I/C)
    • do not administer oxygen in nonhypoxic patients (AHA/ASA 2019 III/B-R)
  • blood pressure
    • check BP every 30 minutes in stabilized patient
    • otherwise, proceed per specific protocols (→ Blood pressure management in acute stroke, hypertensive urgency protocols, etc.)
    • hypotension and hypovolemia should be corrected to maintain necessary systemic perfusion levels
    • the usefulness of drug-induced hypertension in patients with AIS is not well established  (AHA/ASA 2019, IIb/B)
  • ECG
    • record 12-lead ECG on admission, then monitor with 3-lead ECG
    • especially infarctions in the right insula can lead to autonomic system failure and cardiac complications (ST depression, T wave inversion, troponin elevation in the laboratory)
    • look for arrhythmias (particularly atrial fibrillation)
  • monitoring the state of consciousness and neurostatus (GCS, NIHSS)
    • adjust the frequency of evaluations based on the patient’s condition and underlying diagnosis (more frequent in extensive SAH, ICH, malignant edema)
    • in unconscious patients, repeatedly assess cranial nerves and brainstem reflexes
  • search for additional symptoms such as headache, nausea, vertigo, singultus

Extended neuromonitoring

  • recommended in patients with severe stroke (~ 24-48h); a 10-20 or 2-4 channel EEG system with adhesive electrodes is used
  • monitoring of SE treatment (always) and depth of anesthesia
  • NCSE diagnosis
    • sensitivity and specificity of standard EEG is low
    • clinical manifestations are none or only subtle and often escape attention (facial twitching, short eyeball deviation, autonomic signs)
  • DDx of non-epileptic seizures
  • monitoring of metabolic coma
  • SSEP (prognostic value in coma vigile)
  • BAEP (brain death diagnosis in patients with decompressive craniectomy)
  • ERP (event-related potential)
    • detection of P300 wave in a coma is associated with a good prognosis
  • indications for ischemic stroke patients are ambiguous
  • probably advantageous in patients with GCS ≤ 8 with extensive hematoma, SAH, or hydrocephalus
  • intraparenchymal or intraventricular sensors are available
  • doppler signs
    • decrease in velocities, increase in resistance and pulsatility index (RI and PI), then disappearance of diastolic flows, and finally systolic spikes or biphasic flow curve → TCCD in the diagnosis of brain death
    • ICP=(10.927* PI)-1.284
    • ↓ vasomotor reactivity
  • B-mode signs
    • optic nerve sheath enlargement or head prominence (transorbital approach)
    • midline shift (transtemporal approach)

→ neurosonology in intensive care

  • a special catheter is inserted into the bulb of the internal jugular vein to monitor venous blood O2 saturation
  • global information is provided, and therefore may not reflect localized issues; take into account body temperature and the effect of medication)
  • normal values: 55-80%
    • SjO2 < 50% with normal arterial O2 saturation indicates either ↓ CBF (e.g., when cerebrovascular resistance is increased) or increased consumption (↑CMRO2)
    • SjO2 > 85% indicates either hyperemia with ↑CBF or ↓CMRO2
  • 2 sensors are placed on the forehead; emitted beams penetrate to about 4 cm
  • from the reflected light, the oxygenation of the brain tissue is derived
  • direct measurement of parenchymal oxygenation near the sensor
  • standard 20-45 mm Hg
  • ischemic threshold (depending on the type of sensor < 15-20 mm Hg)
  • measurement of extracellular metabolite levels in the CNS ( glucose, lactate, pyruvate, lactate/pyruvate ratio, glutamate, glycerol)

Intravascular access

Peripheral venous system
  • ensure intravascular access via a venous cannula in every acute stroke patient (bilaterally if thrombolysis is planned)
    • uncomplicated insertion and management, prefer disinfection with 0.5% chlorhexidine in alcohol during insertion
    • some drugs and concentrated solutions cannot be administered (limit < 600 mosm/l)
    • insertion time: 72-96h
    • remove if not used > 24h or no further use is probable
    • replace in case of local  (e.g., pain, swelling, skin discoloration, skin temperature change, hardening, resistance to flushing) or systemic (fever) complications
  • for longer use, prefer the midline catheter (approx. 14 days – 3 months)
    • can be used for blood sampling
    • drugs with osmolarity < 600 mOsm/l and  nutrition < 800 mOsm/l can be administered
  • when peripheral IV access is required for > 3 months, prefer PICC catheter
    • it is placed under ultrasound guidance in the cavoatrial junction (when maximum P wave is seen in ECG)
    • may be retained for several months
Central venous system
  • central venous catheters (lines) are commonly placed in the internal jugular, subclavian, or femoral veins (usually using a 2 or 3-way cannula)
    •  order chest X-ray to exclude pneumothorax 3 hours after subclavian vein cannulation
  • central catheter enables:
    • administration of all types of drugs and concentrated solutions
    • measuring central venous pressure (CVP)
      • normally 5-12 cm H2O, subtract PEEP in ventilated patients
  • adhere to aseptic treatment incl. sterile cover, and daily checks
  • complications:
    • during insertion: pneumothorax, artery puncture  RTG - pneumothorax po kanylaci v.scl. vpravo
    • late complications: venous thrombosis, catheter sepsis
  • insertion time: 1-3 weeks
  • use PICC or tunneled catheters when prolonged central venous access is required

Major indications for the use of central venous catheters

  • difficult peripheral venous access
  • delivery of certain medications or fluids
    • medications such as vasopressors, chemotherapeutic agents, or hypertonic solutions that damage the peripheral veins
    • additionally, catheters with multiple lumens enable the delivery of several parenteral medications simultaneously
  • prolonged intravenous therapies
  • specialized treatment
    • hemodialysis, plasmapheresis, transvenous cardiac pacing, and invasive hemodynamic monitoring

Classification of intravascular access according to the expected time of insertion

Classification of intravascular access according to the expected time of insertion
► Short-term

  • peripheral cannula – 3-4 days
  • central venous catheter – 1-3 weeks
► Mid-term   (→ care)
  • midline catheter – 1-3 months
  • PICC (Peripherally Inserted Central Catheter) – 3 -12 months
► Long-term
  • tunneled catheters with cuff – years
  • ports – years

Ventilation and respiration

  • ensure adequate oxygenation (O2 saturation > 94%)
    • SO2S  trial showed no benefit from routine O2 administration ⇒ O2 administration is not recommended in nonhypoxic patients
  • test breathing reflexes and regularly assess the risk of aspiration (many patients have bulbar or pseudobulbar syndrome) → see water swallow test below
    • a common cause of acute respiratory insufficiency is aspiration and/or accumulation of mucus and saliva in the airways due to inadequate expectoration
  • in cases of respiratory infection,  administer antibiotics empirically after collecting sputum and swabs. Adjust the therapy according to cultures and sensitivity results
  • in case of respiratory failure, initiate early intubation and mechanical ventilation
    • before intubation, consider the patient´s prior wishes, general condition, and prognosis
  • Hyperbaric Oxygen Therapy (HBOT) is not recommended, except for stroke caused by air embolization   (Murphy, 2019)   (AHA/ASA 2019 III/B)
    • the limited data show no benefit
    • HBO thus should be offered only in the context of a clinical trial or for individuals with cerebral air embolism
Signs of respiratory failure
  • dyspnoea, involvement of auxiliary respiratory muscles
  • tachycardia
  • respiratory rate > 35/min
  • hypoxemia < 60 mm Hg (7.59 kPa) (at FiO2 0.4 by mask)
  • hypercapnia > 55 mm Hg (7.3 kPa) (except in patients with chronic hypercapnia)

ECG monitoring, arrhythmias

  • acute stroke is associated with an increased risk of cardiac arrhythmias, affecting up to 25% of hospitalized stroke patients
    • the incidence is greatest within the first 24 hours
    • tachycardia is more common than bradycardia
    • arrhythmias are more prevalent in patients with hemispheric lesions
  • while some arrhythmias are benign (such as ventricular/atrial extrasystoles), persistent tachyarrhythmias may lead to hypotension or cardiac failure, potentially contributing to stroke progression
  • atrial fibrillation should be excluded as a potential cause of the stroke
  • ECG monitoring is recommended for ≥ 24 hours (AHA/ASA 2019 I/B-NR)
  • ECG changes are common in acute stroke
    • the ST segment is most commonly affected; these changes may mimic myocardial infarction (ST elevation can be present, but not depression) ⇒ exclude myocardial infarction in such cases
  • the situation is further complicated by frequent elevation in troponin levels, which is usually attributable to cerebral infarction rather than myocardial infarction

Fluids and minerals, glycemia

  • monitor fluid balance every 6-24h and aim to maintain normovolemia or mild hypervolemia
    • measure central venous pressure (CVP) if needed
    • avoid fluid restriction as it increases the risk of ischemic deficit (especially in SAH)
    • hypervolemic hemodilution and vasodilator therapy are not recommended
  • monitor biochemical parameters (ion levels, urea, creatinine, C-reactive protein, hepatic enzymes, and osmolality) as well as complete blood count (CBC) +coagulation profile
    • adjust thefrequency of sampling based on the patient’s condition and any detected abnormalities
  • acid–base balance checks
    • acutely to detect conditions such as hypoxemia, hypercapnia, acidosis/alkalosis
    • stable patients on UPV should be checked  twice daily

Glycemia

  • glucose serves as the primary energy source for the brain; >90% of the brain’s energy derives from the oxidation of glucose. Even during hypoglycemia, glucose remains the most important substrate for brain metabolism
  • the brain/serum glucose ratio (typically 0.6-0.7) drops to 0.2-0.4 in cases of brain injury (esulting in increased sensitivity to hypoglycemia)
  • hyperglycemia (stress hyperglycemia, stress diabetes) is present in up to 2/3 of stroke patients, worsening the outcome of all types of stroke and traumatic brain injuries (TBI)
    • a meta-analysis focus on in-hospital mortality in critically with hyperglycemia showed that even mild hyperglycemia (6.1-8.0 mmol/l) in non-diabetics is associated with a 3.9-fold higher risk of death compared to completely normoglycemic individuals   [Capes, 2000]
  • according to the NICE-SUGAR study, the optimal target glycemia in intensive care is < 10 mmol/L;  hypercorrection to levels < 6 mmol/L increases mortality
    • maintain glycemia around 7.8-10 mmol/L  (140-180 mg/dL) (AHA/ASA 2019 IIa/C-LD)
    • closely monitor and treat hypoglycemia when levels drop below 3.3 mmol (60mg/dL)  (AHA/ASA 2019 I/C-LD)
      • intensive glycemic control can lead to hypoglycemia
      • microdialysis studies indicate that intensive insulin therapy may lead to brain glucose deprivation and and elevated levels of lactate and glutamate  [Vespa, 2006]
  • check glycemia every 6h (glycemic profile); monitor more frequently during continuous insulin administration
  • use repeated boluses of subcutaneous insulin or continuous IV infusion → per insulin protocol

Fever

  • maintain normothermia
  • identify and treat sources of hyperthermia (body temperature >38°C)
  • administer antipyretic medication to hyperthermic patients   (AHA/ASA 219 I/C)
  • the benefit of induced hypothermia is uncertain

Nausea and vomiting

  • most commonly occurs in ICH, SAH, and brainstem ischemia

Prevention and management of GI complications

  • gastrointestinal (GI) complications are common and significantly worsen morbidity and mortality
  • most common complications:
    • stress ulcer
    • gastroesophageal reflux (GER)
    • gastroparesis
    • intestinal paralysis (paralytic ileus)
      • ⇒ X-ray, abdominal SONO or CT
      • endoscopic desufflation
    • constipation/diarrhea
    • singultus
  • 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
    • SUCRALFATE
      • 1g PO or via nasogastric tube every 6-8 hours
      • used in peptic ulcer prevention and treatment or to reduce hyperphosphatemia
    • antacids
  • 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

→ overview of treatment options see here

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

  • titrate gradually (sometimes 1-2 mg per night is enough); fewer AEs occur at this dose
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

Pain management

  • pain is typically present in SAH, less commonly in ICH and ischemic stroke
  • untreated pain may contribute to elevated blood pressure, tachycardia, or patient agitation
  • rule out fractures or dislocations, which are often caused by falls due to sudden paresis

Dysphagia screening, oral hygiene

Nutrition

  • catabolic state is common in the acute phase of stroke
  • the total energy demand depends on the basic metabolic rate (BMR) and other factors
  • early initiation of nutrition (within 24 hours) reduces the risk of various complications (malnutrition increases the risk of infection, muscle loss, etc.)
  • enteral nutrition is preferred; if parenteral nutrition is necessary, use it for the shortest possible duration
  • in patients with significant dysphagia, insert a nasogastric tube (NGS) for the prevention of aspiration bronchopneumonia
  • follow oral hygiene protocols  (AHA/ASA 2018 IIb/B-NR)
  • Harris-Benedict formula basal metabolic rate (BMR) [kcal/day]
    • men = 66,47 + 13,75 x weight [kg] + 5 x height [cm] – 6,67 x age [years]
    • women = 65,10 + 9,56 x weight [kg] + 1,85 x height[cm] – 4,68 x age [years]
    • total energy demand = BMR x A factor x T factor (kcal/day)
    • kJ = 4.18 * kcal
  • for obese people (with a BMI > 30) prefer the Mifflin−St. Jeor (MSJ) equation  → calculator
    • men(kcal/day) = 5 + 10× weight (kg) + 6.25× height (cm) − 5× age (years)
    • women(kcal/day) = −161 + 10× weight (kg) + 6.25× height (cm) − 5× age (years)
A factor
(activity)
immobile patient   1.2
mobile patient   1.3
T factor
(trauma)
surgery
minor-moderate 1.0-1.1
major 1.1-1.2
infection
light 1.0-1.2
moderate 1.2-1.4
severe 1.4-1.8
trauma
1.2-1.35
polytrauma
1.6
burn injury
< 20%     1.0-1.5
20-40%   1.,5-1.85
> 40%     1.85-1.95

Prevention of infection

  • adhere to barrier measures when in contact with the patient, secure careful hand washing by staff
  • follow protocols for the prevention of aspiration and early detection of impaired airway hygiene
  • regularly evaluate the necessity of each invasive access, and replace them regularly
    • risk of complications increases significantly:
      • from day 3 for cannula
      • from day 5 for urinary catheter
      • from day 7 for central venous catheter (CVC)
  • microbiological screening
    • repeated sputum (throat and nasal swab) and urine cultures twice a week in the ICU
    • take cultures after transfer from another department
    • isolate the patient if necessary (especially after  transfers from ICU, neurosurgery)
  • prophylactic administration of antibiotics is not indicated (AHA/ASA 2018 III/B-R)

Early rehabilitation and speech therapy

  • start rehabilitation and ergotherapy ASAP, including early verticalization
    • however, overly aggressive therapy in the first 24h is not beneficial (AVERT study)  (AHA/ASA 2019 III/B-R)
  • mechanical aids have a positive effect  
    • ReStore exosuit was approved by FDA in 6/2019 Exosuit ReStore
  • effect of fluoxetine on improving motor function is not proven
  • timing and intensity of rehabilitation in SAH and ICH must be individualized

Delirium, anxiety, depression

  • search for signs of delirium, depression, or anxiety and treat them properly
  • in patients without depression, fluoxetine therapy is not effective in enhancing poststroke functional status

→ Delirium

Preventing pressure ulcers

  • paralysis and weakness lead to extended periods of bedrest, increasing the chance of pressure sore development
  • pressure sores typically located on the back of the head, shoulders, elbows, sacrum and buttocks, hips, and heels
  • measures for preventing pressure sores are crucial:
    • regular repositioning of the patient (every 2h), physiotherapy, massages
    • skincare
    • adequate hydration and nutrition (monitor protein and albumin levels)
    • early mobilization
    • prevention devices:
      • anti-decubitus mattress  Antidekubitální pomůcky
      • anti-decubitus fleece  Antidekubitální pomůcky   Antidekubitální pomůcky
    • minimize pharmacological sedation for agitated patients

Brain edema, intracranial hypertension

→ Intracranial hypertension
 → Malignant cerebral infarction

Prevention of venous thromboembolism (VTE)

  • deep vein thrombosis is detected in the first 2 weeks in up to 50% of immobile patients  [Brandstater, 1992]

Prophylaxis and management of acute symptomatic seizures

→ see Acute symptomatic seizures

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General management of acute stroke patients
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