NEUROLOGY
In this section, you will learn about the following topics:
ICU Delirium/Sedation & Analgesia
Drug Overdoses
Encephalopathy
Approach to the Acute Stroke Patient
Seizures and Status Epilepticus
ICU Delirium/Sedation & Analgesia
In the fast-paced world of modern medicine, our intensive care units play a crucial role in saving lives and providing essential care to critically ill patients. However, the complex interplay between sedation, analgesia, and the development of ICU delirium presents a unique challenge to healthcare professionals.
ICU Delirium
ICU delirium is a common and serious neurological challenge that occurs in critically ill patients. It is characterized by an acute change in mental status, with fluctuating levels of consciousness, attention, and cognition. Delirium is often underdiagnosed and undertreated in the intensive care unit (ICU), leading to increased morbidity, mortality, and long-term cognitive impairment in survivors.
Causes and Risk Factors
ICU delirium can have multiple causes, including underlying medical conditions, medications, and environmental factors. The most common risk factors for developing delirium in the ICU include advanced age, pre-existing cognitive impairment, severity of illness, use of sedatives and analgesics, mechanical ventilation, and prolonged ICU stay.
Pathophysiology: The exact pathophysiology of ICU delirium is not fully understood, but it is believed to involve a complex interplay of neurotransmitter imbalances, inflammation, oxidative stress, and neuronal dysfunction. The disruption of normal brain function in delirium is thought to result from a combination of direct effects of critical illness, systemic inflammation, and the use of sedative and analgesic medications.
Clinical Presentation: ICU delirium can present with a wide range of symptoms, varying from hypoactive to hyperactive delirium. Hypoactive delirium is characterized by lethargy, decreased responsiveness, and withdrawal, while hyperactive delirium is characterized by agitation, restlessness, and hallucinations. Mixed delirium, which combines features of both hypoactive and hyperactive delirium, is also common.
Diagnosis: The diagnosis of ICU delirium is primarily clinical and relies on the recognition of characteristic symptoms. Validated screening tools, such as the Confusion Assessment Method for the ICU (CAM-ICU) or the Intensive Care Delirium Screening Checklist (ICDSC), can aid in the diagnosis and monitoring of delirium in the ICU. These tools assess the patient's level of consciousness, attention, and cognitive function.
Impact on Patient Outcomes: ICU delirium is associated with numerous adverse outcomes, including increased mortality, prolonged ICU and hospital stays, higher healthcare costs, and long-term cognitive impairment. Delirium in the ICU has been shown to be an independent predictor of mortality, even after adjusting for other factors. Additionally, delirium is associated with an increased risk of complications, such as ventilator-associated pneumonia, deep vein thrombosis, and pressure ulcers.
Management and Treatment: The management of ICU delirium involves a multifaceted approach that includes prevention, early recognition, and treatment of underlying causes. Non-pharmacological interventions, such as early mobilization, sleep promotion, orientation protocols, and minimizing the use of sedatives and analgesics, are key components of delirium prevention. Pharmacological interventions, such as antipsychotic medications, may be considered in cases of severe agitation or distress.
Prognosis and Long-term Outcomes: The long-term outcomes of ICU delirium can be significant, with many survivors experiencing persistent cognitive impairment and functional decline. Delirium in the ICU has been associated with an increased risk of developing dementia and accelerated cognitive decline in the months and years following critical illness. Rehabilitation and cognitive rehabilitation programs may be beneficial in improving long-term outcomes for patients who have experienced ICU delirium.
Sedation Management
Sedation is a crucial aspect of critical care management in the intensive care unit (ICU). It plays a vital role in ensuring patient comfort, facilitating mechanical ventilation, and reducing anxiety and agitation. However, the management of sedation in the ICU requires a delicate balance between achieving the desired level of sedation and minimizing potential adverse effects.
The primary goals of sedation in the ICU are to alleviate patient discomfort, promote cooperation with medical interventions, and prevent complications such as self-extubation or accidental removal of invasive lines. Additionally, sedation aims to reduce the physiological stress response, optimize patient-ventilator synchrony, and facilitate diagnostic procedures.
To effectively manage sedation in the ICU, healthcare providers utilize sedation scales to assess the level of sedation and titrate medications accordingly. Commonly used sedation scales include the Richmond Agitation-Sedation Scale (RASS) and the Sedation-Agitation Scale (SAS). These scales provide a standardized approach to evaluate sedation levels, ranging from deep sedation to agitation. At Piedmont, we mainly use RASS. This is a scale that ranges from -5 to +5.
Regular assessment of sedation is essential to ensure that patients are neither over-sedated nor inadequately sedated. Continuous monitoring of vital signs, including heart rate, blood pressure, and oxygen saturation, is crucial in assessing the patient's response to sedation and adjusting medication doses accordingly.
Several pharmacological agents are commonly used in our ICU.. The choice of medication depends on various factors, including the patient's clinical condition, underlying comorbidities, and desired level of sedation. Some commonly used sedatives include:
Benzodiazepines: Drugs such as midazolam (Versed) are frequently used for sedation in the ICU. They provide anxiolysis, sedation, and amnesia. However, benzodiazepines are associated with a risk of respiratory depression, delirium, and prolonged sedation.
Propofol: This intravenous sedative-hypnotic agent has a rapid onset and short duration of action, making it suitable for short-term sedation. Propofol provides excellent sedation and amnesia but can cause hypotension and respiratory depression.
Dexmedetomidine (Precedex): This selective alpha-2 adrenergic agonist has gained popularity in recent years due to its unique properties. Dexmedetomidine provides sedation, anxiolysis, and analgesia while preserving respiratory drive and allowing for easy arousal. It is particularly useful in patients requiring light to moderate sedation.
Opioids: Medications such as fentanyl and morphine are commonly used for analgesia in the ICU. While opioids provide effective pain relief, they can also cause respiratory depression and sedation. Careful titration is necessary to balance pain control with the risk of oversedation.
DO NOT oversedate. To ensure consistent and safe sedation practices, many ICUs have implemented sedation protocols or guidelines. These protocols provide a framework for the initiation, titration, and weaning of sedative medications. They aim to minimize the use of excessive sedation, promote early mobilization, and reduce the duration of mechanical ventilation. However, it is important to recognize that each patient's sedation requirements may vary. Individualized care is crucial to tailor sedation strategies to the specific needs of each patient. Factors such as age, underlying medical conditions, and the presence of delirium or agitation should be considered when determining the appropriate sedation regimen.
In addition to pharmacological agents, non-pharmacological approaches can also be employed to enhance patient comfort and reduce the need for sedative medications. These approaches include:
Environmental modifications: Creating a calm and quiet environment can help reduce patient agitation and promote restful sleep. Measures such as minimizing noise, adjusting lighting, and maintaining a regular day-night cycle can contribute to a more conducive ICU environment.
Communication and reassurance: Effective communication with patients and their families is essential in reducing anxiety and promoting cooperation. Providing clear explanations, reassurance, and involving patients in decision-making can help alleviate distress and minimize the need for sedation.
Multimodal analgesia: Adequate pain control is crucial in minimizing the need for sedation. Utilizing a multimodal approach to analgesia, which combines different classes of analgesic medications and non-pharmacological techniques, can help optimize pain management and reduce sedative requirements.
Resources to complete:
FCCS Ch. 8
Marino 3rd ed: Ch. 49 and 50
Pulmcast: ICU Liberation: The Alphabet Soup of A-F Bundle
Drug Overdoses
Drug overdoses are a significant concern in critical care settings, as they can lead to severe neurological complications and require immediate intervention. The ICU often sees patients who have overdosed on various substances, including prescription medications, illicit drugs, and alcohol. Understanding the common drug overdoses encountered in the ICU is crucial for providing appropriate management and optimizing patient outcomes.
Opioid Overdose
Opioid overdose is a prevalent and potentially life-threatening condition seen in the ICU. Opioids, such as morphine, fentanyl, and oxycodone, are commonly prescribed for pain management but can be misused or accidentally overdosed. These drugs act on the central nervous system, binding to opioid receptors and causing respiratory depression, sedation, and analgesia. In overdose situations, opioids can lead to severe respiratory depression, hypoxia, and even cardiac arrest.
The management of opioid overdose in the ICU involves immediate resuscitation and stabilization of the patient's airway, breathing, and circulation. Administration of naloxone, an opioid receptor antagonist, is the mainstay of treatment. Naloxone rapidly reverses the effects of opioids, restoring normal respiration and consciousness. Close monitoring of the patient's vital signs and respiratory status is essential during the recovery phase.
Benzodiazepine Overdose
Benzodiazepines, such as diazepam, lorazepam, and midazolam, are commonly prescribed for anxiety, insomnia, and sedation in the ICU. However, these medications can be misused or accidentally overdosed, leading to significant neurological effects. Benzodiazepines enhance the inhibitory effects of gamma-aminobutyric acid (GABA) in the brain, resulting in sedation, muscle relaxation, and anticonvulsant properties. In overdose situations, benzodiazepines can cause excessive sedation, respiratory depression, and even coma.
The management of benzodiazepine overdose in the ICU involves supportive care and close monitoring of the patient's vital signs, including respiratory rate and oxygen saturation. Flumazenil, a benzodiazepine receptor antagonist, can be administered to reverse the sedative effects of benzodiazepines. However, caution should be exercised as flumazenil can precipitate seizures in patients who are dependent on benzodiazepines.
Antidepressant Overdose
Antidepressant medications, such as selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs), are commonly prescribed for the treatment of depression and other psychiatric disorders. In overdose situations, these medications can lead to significant neurological complications. The specific effects depend on the class of antidepressant involved.
SSRIs are generally well-tolerated in overdose and rarely cause life-threatening effects. However, in rare cases of severe overdose, serotonin syndrome can occur, characterized by agitation, confusion, hyperthermia, and autonomic instability. Supportive care and close monitoring of vital signs are the mainstays of management.
TCAs are known for their cardiotoxic and neurotoxic effects in overdose situations. They can cause significant anticholinergic effects, leading to delirium, seizures, and cardiac arrhythmias. The management of TCA overdose in the ICU involves aggressive supportive care, including airway management, administration of sodium bicarbonate to counteract the cardiotoxic effects, and close monitoring of cardiac rhythm.
MAOI overdose is relatively rare but can lead to hypertensive crisis, serotonin syndrome, and delirium. Supportive care, including blood pressure control and close monitoring of vital signs, is essential in managing MAOI overdose.
Sedative-Hypnotic Overdose
Sedative-hypnotic medications, such as barbiturates and non-benzodiazepine sedatives, are commonly used for sedation in the ICU. Overdose situations can occur due to misuse or accidental ingestion. These medications enhance the inhibitory effects of GABA in the brain, leading to sedation, anxiolysis, and anticonvulsant properties. In overdose situations, sedative-hypnotics can cause excessive sedation, respiratory depression, and even coma.
The management of sedative-hypnotic overdose in the ICU involves supportive care, including airway management, respiratory support, and close monitoring of vital signs. Flumazenil can be administered to reverse the sedative effects of non-benzodiazepine sedatives, but caution should be exercised as it can precipitate seizures in patients who are dependent on these medications.
Stimulant Overdose
Stimulant drugs, such as cocaine, amphetamines, and methamphetamines, are commonly abused substances that can lead to significant neurological effects when overdosed. These drugs increase the release and inhibit the reuptake of neurotransmitters, such as dopamine and norepinephrine, resulting in increased alertness, euphoria, and sympathetic stimulation. In overdose situations, stimulants can cause agitation, delirium, seizures, and cardiovascular complications, including hypertension, tachycardia, and arrhythmias.
The management of stimulant overdose in the ICU involves supportive care, including close monitoring of vital signs, management of agitation and delirium, and treatment of cardiovascular complications. Benzodiazepines can be administered to control agitation and seizures. In severe cases, vasopressors may be required to manage cardiovascular instability.
Resources to complete:
Marino 3rd ed: Ch. 53; 4th ed Ch 54-55
ESICM Trauma and Emergency Medicine Module: Major Intoxication section
Must have special access, but this page is a good summary: Click here
FOAMCast 48: Urine Drug Screen, Cocaine, and PCP
EM Cases: Best Case Ever 50: Delirium Tremens
Encephalopathy
Few conditions are as enigmatic and multifaceted as encephalopathy. The ICU serves as a refuge for critically ill patients battling a multitude of ailments, and encephalopathy stands as a formidable adversary often lurking in the shadows of their primary diagnoses. It is a condition that challenges healthcare providers to unravel the intricate web of cognitive dysfunction, delirium, and altered mental states that can confound even the most seasoned clinicians.
The word “Encephalopathy” is a broad term used to describe a dysfunction or disease of the brain that affects its structure or function. It is a common neurological challenge encountered in critical care settings, including the ICU. Encephalopathy can have various causes and can present with a wide range of symptoms, making it a complex condition to diagnose and manage.
Types of Encephalopathy
There are several types of encephalopathy that can occur in the ICU. Understanding the different types is crucial for appropriate diagnosis and treatment. Some common types of encephalopathy encountered in critical care include:
Metabolic Encephalopathy: Metabolic encephalopathy is a condition characterized by brain dysfunction due to metabolic disturbances. It can occur as a result of electrolyte imbalances, liver or kidney dysfunction, hypoxia, or endocrine disorders. Metabolic encephalopathy often presents with confusion, altered consciousness, and cognitive impairment.
Hepatic Encephalopathy: Hepatic encephalopathy is a type of metabolic encephalopathy that specifically occurs in patients with liver dysfunction or cirrhosis. It is caused by the accumulation of toxins, such as ammonia, in the bloodstream, which affects brain function. Hepatic encephalopathy can lead to cognitive impairment, personality changes, and even coma.
Hypoxic-Ischemic Encephalopathy: Hypoxic-ischemic encephalopathy (HIE) occurs when the brain is deprived of oxygen and blood flow. It can result from conditions such as cardiac arrest, respiratory failure, or severe hypotension. HIE can cause significant brain damage and may lead to long-term neurological deficits.
Anoxic Encephalopathy: Post-anoxic encephalopathy refers to brain dysfunction that occurs after a period of inadequate oxygen supply to the brain. It can result from cardiac arrest, near-drowning incidents, or severe respiratory failure. Post-anoxic encephalopathy can cause a range of neurological symptoms, including cognitive impairment, movement disorders, and seizures.
Toxic-Metabolic Encephalopathy: Toxic-metabolic encephalopathy is a type of encephalopathy caused by exposure to toxins or drugs. It can occur due to drug overdoses, substance abuse, or exposure to environmental toxins. Toxic-metabolic encephalopathy can manifest with various neurological symptoms, including confusion, hallucinations, and seizures.
The treatment and management of encephalopathy in the ICU are aimed at addressing the underlying cause, minimizing further brain injury, and providing supportive care to promote recovery.
Resources to complete:
FCCS Ch. 8
Marino 3rd ed: Ch. 50; 4th ed: Ch 44, 51
ESICM Neurocritical care Module: Coma and altered consciousness section (parts 1-4)
Establishing brain death: part 4 Coma ESICM above
Pulmcast - Establishing Clinical Brain Death
Approach To Acute Stroke Patient
When a patient arrives at the intensive care unit (ICU) in the throes of a stroke, every passing moment becomes a vital factor in their prognosis and ultimate recovery. It is in this high-stakes arena that healthcare providers face the formidable challenge of unraveling the mysteries of acute stroke while working tirelessly to save brain function.
The clinical presentation of acute stroke can vary depending on the location and extent of the brain injury. The most common symptoms include sudden onset of focal neurological deficits such as weakness or paralysis of the face, arm, or leg, difficulty speaking or understanding speech, and visual disturbances. Other symptoms may include severe headache, dizziness, loss of balance or coordination, and altered level of consciousness.
It is important to note that not all patients with acute stroke present with classic symptoms. In some cases, especially in patients with posterior circulation strokes, the symptoms may be more subtle and nonspecific, making the diagnosis challenging. Therefore, a high index of suspicion is crucial in the critical care setting.
Assessment Tools
Several assessment tools can aid in the recognition and assessment of acute stroke. The most widely used tool is the National Institutes of Health Stroke Scale (NIHSS), which is a standardized neurological examination that quantifies the severity of stroke-related deficits. The NIHSS assesses various domains including level of consciousness, language function, motor function, sensory function, and visual fields. It provides a numerical score that correlates with the severity of the stroke and helps guide treatment decisions.
In addition to the NIHSS, other assessment tools such as the Cincinnati Prehospital Stroke Scale (CPSS) and the Los Angeles Motor Scale (LAMS) can be used to quickly screen for stroke in the prehospital setting or in the emergency department. These tools focus on identifying specific stroke symptoms such as facial droop, arm weakness, and speech abnormalities.
Imaging and Diagnostic Tests
Imaging plays a crucial role in the assessment of acute stroke. Non-contrast computed tomography (CT) scan of the brain is typically the initial imaging modality used to evaluate patients with suspected acute stroke. CT scan can help identify hemorrhagic strokes, which require different management strategies than ischemic strokes. It can also provide information about the extent of the ischemic injury and help guide treatment decisions, such as the use of thrombolytic therapy.
In some cases, additional imaging studies may be necessary to further evaluate the stroke and its underlying cause. Magnetic resonance imaging (MRI) of the brain can provide more detailed information about the location and extent of the stroke, as well as identify other potential causes of the patient's symptoms. Magnetic resonance angiography (MRA) and computed tomography angiography (CTA) can be used to evaluate the blood vessels in the brain and identify any occlusions or stenosis that may have caused the stroke.
Diagnostic tests such as electrocardiogram (ECG), echocardiogram, and carotid ultrasound may also be performed to assess the patient's cardiac and vascular health and identify any potential sources of emboli that may have caused the stroke.
Time is Brain
In the management of acute stroke, time is of the essence. The concept of "time is brain" emphasizes the importance of early recognition and treatment to minimize the extent of brain damage and improve patient outcomes. The goal is to initiate treatment within the first few hours of symptom onset, as the efficacy of certain interventions, such as thrombolytic therapy, decreases with time.
Therefore, it is crucial for healthcare providers in the critical care setting to have a high level of suspicion for acute stroke and to rapidly initiate the appropriate diagnostic workup and treatment. This requires a multidisciplinary approach involving emergency physicians, neurologists, radiologists, and critical care specialists working together to provide timely and effective care.
Resources to complete:
FCCS Ch. 8
AHA Guidelines for the Management of Spontaneous ICH
Marino 3rd ed: Ch. 52; 4th ed: Ch. 46
EmCrit Podcast 11: Ischemic Stroke 2013
EmCrit Podcast 8: Subarachnoid Hemorrhage
EmCrit Podcast 78: Increased ICP and Herniation
Seizures/Status Epilepticus:
Seizures are often the heralds of underlying neurological challenges that can tip the balance between life and death. Throughout this learning, you will shine a light on the multifaceted causes of seizures in the ICU, including metabolic disturbances, traumatic brain injury, infections, and pharmacological triggers. We will explore the vital role of neuroimaging and electroencephalography (EEG) in deciphering the underlying pathology.
The clinical presentation of seizures can vary widely depending on the location and extent of the abnormal electrical activity in the brain. Seizures can manifest as motor movements, altered consciousness, sensory disturbances, or a combination of these symptoms. It is important to obtain a detailed history from the patient, family members, or witnesses to accurately describe the seizure event. The information should include the duration, frequency, and characteristics of the seizures, as well as any precipitating factors or associated symptoms
Several diagnostic tests can aid in the diagnosis and evaluation of seizures in the ICU. These tests help identify the underlying cause of the seizures and guide appropriate management. The following tests are commonly used:
Electroencephalography (EEG): EEG is a valuable tool for diagnosing and characterizing seizures. It records the electrical activity of the brain using electrodes placed on the scalp. Continuous EEG monitoring is particularly useful in the ICU setting, as it can detect subclinical seizures and provide real-time information about the patient's brain activity. EEG findings can help differentiate between different types of seizures and guide treatment decisions.
Neuroimaging: Neuroimaging studies, such as computed tomography (CT) and magnetic resonance imaging (MRI), are essential in evaluating patients with seizures. These tests can identify structural abnormalities, such as tumors, strokes, or brain lesions, that may be causing the seizures. Additionally, neuroimaging can help rule out other potential causes of seizures, such as intracranial hemorrhage or brain infections. CT heads can be ordered with stroke protocol acutely, while MRIs often take a long time due to the nature of the imaging type.
Laboratory Tests: Laboratory tests are important in the evaluation of seizures, as they can help identify metabolic or toxic causes. Blood tests, including CBC, electrolyte panel, liver function tests, and toxicology screens, should be performed to assess for any underlying abnormalities or drug-related causes of seizures. Specific tests, such as cerebrospinal fluid analysis or autoimmune panels, may be indicated in certain clinical scenarios.
The following monitoring techniques are commonly used to monitor for seizures:
Bedside Clinical Observation: Documentation of seizure events, including their duration and characteristics, is important for accurate diagnosis and treatment.
Routine EEG: You can order a one time routine EEG that is done by a tech in the ICU. They come to bedside and measure only a moment of time.
Continuous Video EEG Monitoring: Video EEG monitoring combines continuous EEG recording with simultaneous video surveillance. This technique allows for the correlation of clinical events with EEG findings, providing valuable information about the type and localization of seizures. Video EEG monitoring is particularly useful in patients with unexplained spells or suspected non-convulsive seizures.
Resources to complete:
FCCS Ch. 8
Marino 3rd ed: Ch. 51; 4th ed: Ch 45