PREVENTING AND MANAGING COMPLICATIONS POST 24 HOURS

After the patient’s stroke has stabilized for 12–24 hours, collaborative care shifts from preserving life to preventing complications, reducing disability, and attaining optimal functioning. This most often requires intensive care in a unit staffed by ICU nurses who are trained to recognize and manage intracranial complications.

Postprocedural Care

For patients who have had surgery, complications may develop within 24–48 hours of catheter sheath removal. The site should be monitored for:

  • Arterial spasm
  • Pain
  • Swelling
  • Bruising
  • Erythema
  • Groin hematoma/excessive bleeding
  • Pulsatile mass
  • Drainage from the puncture site
  • Retroperitoneal bleed
  • Pseudo-aneurysm or arteriovenous fistula
  • Arterial occlusion
  • Distal pulse assessment every 15 minutes for 1 hour, every 30 minutes for 1 hour, every 1 hour for 4 hours
    (Rodgers et al., 2021)

Deterioration of Neurologic Functioning

Early neurologic deterioration following an acute stroke is associated with poor outcomes. The key to managing complications in the stroke ICU is recognizing them quickly. The deterioration in a patient’s neurologic status is always a signal to search quickly for a complication.

Therefore, a core responsibility for stroke nurses is the monitoring and management of neurologic status. This is often very frequent in hyperacute stroke care, where observations may be required every 15 minutes for the first 2 hours, every 30 minutes for the next 2 hours, and every 60 minutes until 24 hours have passed. Assessment includes:

  • Level of consciousness (e.g., Glasgow coma score)
  • NIHSS
  • Pupil responses
  • Motor function
  • Vital signs

Neurologic deterioration is defined as an increase in the NIHSS score by ≥4 points and a decrease of ≥2 points on the Glasgow coma score. Patients are also assessed every 15 minutes for the first 2 hours for signs of change, which include nausea, vomiting, headache, and seizure (Clukie & Rudd, 2020).

ISCHEMIC BRAIN SWELLING

Injured brain tissue swells from edema, and sufficient swelling will push the brain against the skull or nondispensable edges of the dura. In these situations, the brainstem is often squeezed, and the patient will show signs of cerebral herniation. Cerebral herniation should be suspected when new neurologic signs include:

  • Abnormal breathing pattern
  • Unintended muscle contractions
  • Cranial nerve problems, especially asymmetry, loss or reduction of pupillary responses
  • Peripheral motor deficits
  • Headache
  • Irregular respirations
  • Neck pain or stiffness
  • Nausea and vomiting
  • Increasing sleepiness
  • Loss of consciousness

Brain herniation is a life-threatening emergency, and ventriculostomy or decompression craniectomy may be a necessary treatment option for many patients (Ishida, 2022; Nehring et al., 2022).

INCREASED INTRACRANIAL PRESSURE

Both ischemic and hemorrhagic strokes sometimes increase intracranial pressure indirectly as a result of brain edema. Hemorrhagic strokes can also increase intracranial pressure directly by adding extravascular blood to the restricted intracranial space.

Clinically, elevated ICP presents with:

  • Headache
  • Vomiting
  • Decreased level of consciousness
  • Papilledema (optic disc swelling)
  • Periorbital bruising
  • Cushing triad (bradycardia, irregular respiration, hypertension)

(Cushing triad is controversial, but many believe it is related to brainstem compression and is an especially ominous sign requiring urgent intervention.)

Patients with signs of increased ICP or herniation should be intubated and hyperventilated. But excessive hyperventilation is to be avoided, as it may potentiate vasospasm and ischemia. Other interventions for increased ICP include:

  • Osmotic agents (e.g., mannitol), which can decrease ICP dramatically (by 50% 30 minutes post administration)
  • Although controversial, intravenous steroids (e.g., dexamethasone)
  • Diuretics (carbonic anhydrase inhibitors) such as acetazolamide

Patients must remain on strict bedrest, with head of the bed elevated at 30 degrees to ensure optimal venous drainage. Barbiturates can be considered in cases where sedation and usual methods of treatment are not successful in reducing the ICP (Pinto et al., 2022).

INTRACRANIAL REBLEEDING

Another cause of deteriorating neurologic functioning in the stroke ICU is additional intracranial bleeding. This problem can be recognized using brain imaging, usually CT scan.

  • Ischemic strokes. Symptomatic intracerebral hemorrhage can be a catastrophic complication of acute ischemic stroke, with poorer clinical outcomes at 3 months. Hemorrhage transformation represents the conversion of an ischemic infarction into an area of hemorrhage. Hemorrhagic transformation of an ischemic infarct usually occurs within 7–14 days post ictus. Ischemic tissues have a natural tendency to bleed, as acute cerebral ischemia leads to the death of capillary cells, which causes vascular permeability and extravasation of blood in the brain parenchyma. Vasospasm can also lead to hemorrhagic transformation, and intravenous thrombolysis has been shown to increase the risk of mild to severe intracranial hemorrhage (Charbonnier et al., 2021).
  • Intracerebral hemorrhages. Enlargement of blood clot occurs in the first 24 hours after onset in about one third of patients and is a major concern. One major factor in the rebleed is the use of anticoagulant medication. Fifty percent of patients admitted with brain hemorrhage while on anticoagulation deteriorate in the first 24–48 hours due to additional bleeding, with a high mortality rate of 64% by 6 months. For rebleed prevention, blood pressure management for a target BP of 130/80 mmHg is recommended when the patient is medically and neurologically stable (MCN, 2022; Kim et al., 2022).
  • Subarachnoid hemorrhages. The most dreaded early complication of SAH is rebleeding, the greatest risk being within the first 72 hours after ictus, and it is associated with a 60% case-fatality rate. Measures to prevent rebleeding include bed rest in a quiet, darkened room; analgesia; and sedation. Stool softeners are given to prevent the Valsalva maneuver, with resultant peaks in SBP and ICP. The only effective treatment is prevention by obliterating the ruptured aneurysm via clipping surgically or occluding endovascularly with a coil (Calviere et al., 2022).

Pulmonary Complications

PNEUMONIA

Pneumonia develops in 4%–10% of patients with acute stroke and is associated with a higher mortality and poorer long-term outcomes.

Aspiration is the cause of about 60% of poststroke pneumonia. Aspiration pneumonia following stroke is usually due to stroke-related dysphagia or to a decreased level of consciousness that results in compromised cough reflex and glottic closure.

Measures to prevent aspiration include keeping the patient NPO initially and subsequently modifying the diet for those who have a persistent dysphagia.

The patient is screened on admission for swallowing problems using a formal screening protocol by a trained healthcare professional. Patients who fail the swallowing screening are referred to a speech pathologist for a comprehensive assessment. Additional preventive measures include patient mobilization when neurologically stable and good pulmonary care (Ishida, 2022).

COMPLICATIONS RELATED TO INTUBATION AND MECHANICAL VENTILATION

For intubated patients, risk reduction measures include daily assessment for potential extubation, minimizing sedation, suctioning of secretions, elevating the head of the bed when possible, and maintaining ventilator circuits. Avoid prophylactic antibiotics and agents that suppress gastric secretions. Additional preventive measures include patient mobilization when neurologically stable and good pulmonary care (Ishida, 2022).

ABNORMAL BREATHING PATTERNS

Stroke may disrupt breathing either by causing a disturbance of central rhythm generation, interrupting the descending respiratory pathways leading to a reduced respiratory drive, or causing bulbar weakness leading to aspiration.

Abnormal breathing patterns are a common consequence of stroke. Among the recognized abnormal respiratory patterns are Cheyne-Stokes breathing, periodic breathing, apneustic breathing, central sleep apnea, ataxic breathing, and failure of automatic breathing:

  • Cheyne-Stokes breathing involves a period of rapid and shallow breathing followed by slow, heavier breathing along with periods of apnea.
  • Apneustic breathing is characterized by regular deep inspirations with an inspiratory pause followed by inadequate expiration. This respiratory pattern carriers a poor prognosis.
  • Ataxic breathing is a pattern characterized by complete irregularity of breathing, with irregular pauses and increasing periods of apnea.

Close observation of the stroke patient for these potential disturbances and implementation of prophylactic measures can prevent significant morbidity and mortality (Schmutzhard, 2019).

OXYGEN DESATURATION

Stroke patients may exhibit a decline of more than 50% in respiratory function. Mild hypoxia is common and may lead to supplementary brain damage as a result of reduced blood supply. The underlying condition causing hypoxia must be treated to manage and improve patient outcome.

Body position may have a significant impact on oxygenation. A semi-sitting position is better at improving ventilation-perfusion matching. This position affects oxygenation and arterial blood gas parameters by rising SpO2, PaO2, and decreasing PaCO2.

The semi-Fowler position maximizes lung volumes, flow rate, and capacities; decreases abdominal contents’ pressure on the diaphragm; and increases respiratory system compliance, resulting in increased oxygenation and decreased PaCO2.

Patients with very low oxygen levels must be treated with oxygen, and so it is important to monitor oxygen levels to maintain oxygen saturation >95%. However, there is clear and unambiguous evidence that stroke patients do not need routine oxygen and that it does not improve recovery from stroke (Ali et al., 2021).

NEUROGENIC PULMONARY EDEMA (NPE)

Neurogenic pulmonary edema is rare and most often develops abruptly and progresses quickly after a neurologic insult. NPE is an increase in interstitial and alveolar fluid that can occur following stroke, particularly subarachnoid hemorrhage, and can be fatal. The patient presents with dyspnea, tachycardia, tachypnea, cyanosis, pink frothy sputum, crackles, and rales on auscultation. Blood tests reveal hypoxemia. Aspiration pneumonia, ventilator-associated pneumonia, and ventilation-induced lung injury have similar symptoms and must be ruled out.

General supportive care for NPE includes supplemental oxygen to correct hypoxemia and mechanical ventilation if necessary. With the use of low inflation volumes, positive end-expiratory pressure (PEEP) is added to prevent compression atelectasis (Zhao et al., 2020; Naik, 2020).

Cardiovascular Complications

CARDIAC PROBLEMS

Cardiac complications include arrhythmias, myocardial infarction, congestive heart failure, and neurogenic cardiac injury. MI occurs in approximately 1%–2% of patients with acute stroke during initial hospitalization and is associated with poor outcomes.

Elevation of troponin and other cardiac enzymes after acute stroke may be related to stroke-induced elevation of circulating epinephrine and activation of the sympathoadrenal system contributing to myocardial damage.

Neurogenic cardiac damage may be due to underlying coronary disease, but this may not be the only mechanism, as it can occur in patients with subarachnoid hemorrhage, who are often young and do not have underlying heart disease.

Cardiac arrhythmias in the first 72 hours following an admission for acute stroke occur in approximately 25% of patients, atrial fibrillation being the most common. Cardiac events and cardiac death after acute stroke may be caused by acute myocardial infarction, heart failure, ventricular arrhythmias such as ventricular tachycardia or fibrillation, and cardiac arrest.

Other causes include focal atrial tachycardia, undetermined supraventricular tachycardia, ventricular ectopy, nonsustained ventricular tachycardia, and atrial flutter. Bradyarrhythmias have been found to be caused by atrial fibrillation.

Cardiac myofibrillar degeneration (myocytolysis) in the area of cardiac nerves has been found on autopsy in patients who died from acute stroke. The lesion differs from necrosis due to coronary disease because it is visible within minutes and the cells die in a hypercontracted state.

Initial ECG monitoring is undertaken for all patients with stroke. The duration and mode of monitoring is generally recommended for at least the first 24 hours, but for patients with embolic stroke of uncertain source, longer-term ECG monitoring (external or implantable) is used (Ishida, 2022; Carrarini et al., 2022).

HYPERTENSION

Elevated BP during the acute phase of intracranial hemorrhage (ICH) has been found to be associated with hematoma expansion, perihematomal edema, rebleeding, neurologic deterioration, and death. The first step in managing ICH is to reduce blood pressure as quickly as possible. IV antihypertensive drugs are standard treatment in this instance, while medications may also be prescribed to counteract any blood thinners the patient may be taking.

The consensus is that for ICH patients with systolic BP of 150–220 mmHg and without contraindications, acute lowering of systolic BP to 140 mmHg is considered safe and may improve functional outcomes.

The majority of patients with ischemic stroke have hypertension, and lowering BP may be critical in preventing recurrent stroke. However, if BP is lowered rapidly in the acute phase, adverse renal events may occur. Studies of antihypertensive treatment have shown evidence that in the acute ischemic stroke setting, antihypertensive treatment does not change cerebral perfusion. It is recommended that moderate hypertension in most patients who are not candidates for fibrinolytic therapy be permitted, and most patients will experience spontaneous reduction in BP over the first 24 hours without treatment. Guidelines state that there is no one ideal blood pressure reading for patients with ischemic stroke. Guidelines also recommend carefully lowering blood pressure in patients who are otherwise eligible for treatment with fibrinolysis.

In some instances, part of the treatment goals for ischemic stroke is to enhance blood flow through a blocked vessel that may partially reopen, allowing some blood to flow through. One strategy to accomplish this is to increase blood pressure to push the blood through those narrower vessels. If a patient is on antihypertensives, they are stopped and blood pressure is allowed to rise. This is referred to as permissive hypertension (Moawad, 2021; Pressman, 2021; Kim et al., 2022).

VENOUS THROMBOEMBOLISM (VTE)

Venous thromboembolism includes deep vein thrombosis (DVT) and pulmonary embolism (PE). DVT may develop as early as 24–48 hours after stroke onset and has a peak incidence between 2–7 days. Pulmonary embolism, often unassociated with clinically recognized DVT, accounts for up to 25% of early deaths after stroke and is the most common cause of death at its peak occurrence about 2–4 weeks after stroke onset. Patients with hemiparesis are predisposed to DVT development. Additional risk factors include advanced age, high stroke severity, and immobility.

VTE prophylaxis is indicated for all patients with acute stroke and restricted mobility using thigh-length intermittent pneumatic compression (IPC), starting on admission, for patients within 72 hours of acute stroke. IPC is contraindicated in those with evidence of leg ischemia due to peripheral vascular disease, leg ulcerations, dermatitis, severe leg edema, or confirmed DVT.

Additionally, pharmacologic VTE prophylaxis is recommended for select patients within 48 hours of acute ischemic stroke onset who have restricted mobility. This may include subcutaneous low molecular weight (LMW) heparin once daily or subcutaneous low dose unfractionated heparin two to three times daily. This recommendation applies only to patients for whom the benefit of anticoagulation is assessed to outweigh the risk of bleeding.

IPC is the mainstay for prevention of venous thromboembolism in patients with acute intracerebral hemorrhage (ICH) and should be started on admission. Once bleeding has stopped, low-dose LMW or unfractionated heparin after 1–4 days of onset for patients with lack of mobility should be started. Risk of hematoma expansion may weigh against the use of anticoagulation.

For patients with subarachnoid hemorrhage and decreased mobility, IPC is started on admission and prior to aneurysm treatment. Heparin (LMW or unfractionated) can be added once the aneurysm is secured for those who continue to have restricted mobility.

Once patients become fully ambulatory, mechanical and pharmacologic interventions are generally discontinued (Ishida, 2022).

Other Common Complications

Other complications that occur frequently in ICU stroke patients include hyperthermia, hyperglycemia, dysphagia, and infections.

HYPERTHERMIA

Fever is independently associated with poor outcomes. All stroke patients should have their temperature monitored at least four times a day for 72 hours. Sources of hyperthermia (temperature >100.4 °F) are identified and treated with antipyretic medications such as acetaminophen. Elevated temperature in the first 24 hours of being admitted to ICU has been associated with an increased risk of in-hospital death.

The benefit of hypothermia is not well established and should only be offered in the context of ongoing clinical trials. Studies suggest that induction of hypothermia is associated with an increased risk of infection, including pneumonia (Powers et al., 2019).

HYPERGLYCEMIA AND HYPOGLYCEMIA

Hyperglycemia is believed to decrease reperfusion. Persistent hyperglycemia during the first 24 hours after onset of AIS is associated with worse outcomes and an increase in 30-day mortality rate, and it is an independent risk factor for greater infarct growth and hemorrhage stroke conversion. Considering available evidence, it is reasonable to maintain blood glucose between 140–180 mg/dL during hospitalization with subcutaneous or IV insulin when needed, being aware that IV insulin increases risk of hypoglycemia. Studies have found that aggressive methods for reducing high blood sugar are not more effective than standard lower-risk treatment.

Hypoglycemic patients with glucose <60 mg/dL should be treated to achieve normoglycemia with IV dextrose 50% to reach a level ≥80 mg/dL. The brain requires glucose for metabolism, and the metabolic requirement of the brain is high; therefore, episodes of hypoglycemia can decrease repair of the brain (Hui et al., 2022; Anadeani et al., 2022).

DYSPHAGIA

Poststroke dysphagia is a very common complication and is the major risk factor for aspiration pneumonia. Independent predictors of dysphagia include male gender, age older than 70, disabling stroke, impaired pharyngeal response, incomplete oral clearance, and palatal weakness or asymmetry. Dysphagia will usually improve spontaneously with return of safe swallowing function by two weeks in about 90% of patients.

Patients with acute stroke should have their swallowing screened within four hours of arrival at the hospital and before being given any oral food, fluid, or medication. Personnel specifically trained in swallowing screening using a validated tool should perform the screening to observe how well swallowing muscles move and to help determine which nerves, muscles, and reflexes are impaired.

The water swallowing test (WST) is a bedside screening tool used to assess for aspiration in clinical practice, but it is limited in its accuracy. Different food texture and viscosity might be used according to the levels of dysphagia, which cannot be demonstrated by WST. A more ideal bedside screening tool is the volume-viscosity swallow test (V-VST), which uses boluses of different volumes and viscosities of food. It has an advantage by indicating the appropriate diet for stroke patients in order to minimize the risk of complications.

Patients who fail the swallowing screening are referred to a speech pathologist for a comprehensive assessment, which may include instrumental examination. Video-fluoroscopy (VFS) with modified barium swallow may also be performed once the patient is stable in order to assess severity of dysfunction and risk of aspiration. Intravenous hydration with normal saline is administered to maintain volume status.

Patients with acute stroke who cannot take food and fluids orally due to persistent dysphagia, altered mental status, and/or mechanical ventilation should receive nutrition and hydration via nasogastric nasoduodenal, or percutaneous endoscopic gastrostomy tube feedings while undergoing efforts to restore swallowing (Ishida, 2022).

URINARY TRACT INFECTION

Urinary tract infection is a common problem following stroke and occurs in approximately 11%–15% of patients who are followed for up to three months. It is a serious complication that impairs stroke recovery, is associated with poorer neurologic outcomes and longer hospital stays, and can be life-threatening in about 1% of cases. UTI is also a common complication in patients who have been followed for up for 30 months.

The main risk factors for UTI are:

  • Female sex
  • Older age
  • High modified Rankin Scale score (a measure of poststroke disability)
  • Postvoid residual volume greater than 100 ml

It is a common practice to place an indwelling catheter in patients with stroke due to incontinence, immobility, or convenience. This is an important risk factor for infection, and the duration of catheterization is directly related to the risk. Therefore, an indwelling catheter should be avoided whenever possible. The use of external catheter systems or intermittent catheterization are alternatives associated with a lower risk of urinary tract infections (Ishida, 2022).

GASTROINTESTINAL COMPLICATIONS

Gastrointestinal (GI) hemorrhage is one of the more common complications and has both serious and nonserious manifestations in about 1.5%–3% of stroke patients. These patients have worse outcomes, including a higher rate of dependency and mortality. Overt GI bleeding may be severe or even life-threatening. Occult bleeding is generally less serious.

Risk factors for GI hemorrhage include:

  • Older age
  • Severe stroke
  • Posterior circulation stroke
  • Prestroke dependence
  • History of peptic ulcer disease or cancer predating stroke

Stress ulcer prophylaxis with proton pump inhibitors or H2 antagonist is effective for reducing overt GI bleeding but may increase the risk of nosocomial pneumonia. Therefore, prophylaxis is not routinely used for patients with acute stroke but is reserved for select patients who require intensive care management or are otherwise at high risk.

Evidence suggests that enteral nutrition alone may reduce the risk of overt GI bleeding due to ulceration and that stress ulcer prophylaxis may be ineffective or harmful among patients who are receiving enteral nutrition (Ishida, 2022).

DELIRIUM

Delirium is a common poststroke complication associated with poor outcomes and increased mortality. Up to 25% of stroke patients experience delirium in the acute phase of stroke, and up to two thirds of these patients experience delirium within 24 hours of admission. Stroke patients with delirium have been found to have more severe stroke-related disabilities on admission and do not show improvement during their stay in a stroke unit. This may likely be due to disturbances in cerebral neurotransmitters and cerebral networking, with more severe strokes leading to a high risk of delirium.

Prevention of delirium and minimizing its negative consequences should be a priority in stroke care. However, there is little evidence about the efficacy of delirium prevention intervention in stroke patients, and not all interventions can easily be applied to this patient population. Surveys have shown that less than half of clinicians have standardized delirium management and less than one third are using a valid assessment frequently. A standardized delirium management includes both pharmacologic and nonpharmacologic measures. Delirium management can include:

  • Delirium screening three times within 24 hours using one of the following:
    • Nursing Delirium Screening Scale (Nu-DESC) with DSM-V criteria for validation
    • 4 Assessment Test for Delirium (4AT)
    • Confusion Assessment Method ICU (CAM-ICU)
  • Interprofessional evaluation of possible underlying causes and treatment using checklists
  • Nonpharmacologic interventions such as reorientation, education, and mobilization
  • In case of persisting symptoms, specific pharmacologic intervention as an option
    (Thomsen, 2020; Nydahl et al., 2022)