Emergency Management in Neurocritical Care

Edward Manno

• Publisher: Wiley-Blackwell
• Year: 2012
• ISBN:
  9781118297155
• Edition: 1
• Topic: Medicina
• Subtopic: Medicina de emergencia y cuidado crítico

Rapid response, assessment and management are crucial for neurocritical situations

Acute neurological illness is traumatic for patients and their families. Physicians caring for these patients are often under great distress and need to rapidly assess the situation to allow appropriate stabilization and management.

Emergency Management in Neurocritical Care gives you the tools you need to perform under pressure in the neurocritical or emergency care unit. The no-nonsense approach corresponds to the attitude needed in both acute emergencies and in the neurocritical care unit. Packed with handy tips to improve your care of patients, and written by internationally renowned experts, the book covers:

• Acute Management of Neurological Emergencies
• Cerebrovascular Critical Care
• Infections of the Nervous System
• Neuromuscular Complications Encountered in the Intensive Care Unit
• Neurological Complications and Consultations in General Intensive Care Units
• Acute Neuroimaging and Neuromonitoring in Neurocritical Care

Clinical in approach, practical in execution, Emergency Management in Neurocritical Care will help you perform better in pressure situations.

Part I

Acute Management of Neurological Emergencies

Chapter 1

Hypertensive Emergency

Laurie McWilliams

Neurocritical Care Unit, Cerebrovascular Center, Department of Neurology and Neurosurgery, Cleveland Clinic, Cleveland, OH, USA

Introduction

Hypertension and neurologic disease coexist frequently, either as a cause or consequence of the underlying neurologic disease. In addition, the management of elevated blood pressures in this setting has significant impact on outcomes. Hypertension is defined as systolic blood pressure greater than 140 mmHg or diastolic blood pressure greater than 90 mmHg. The National Health and Nutrition Survey (NHANES) is conducted by the Centers for Disease Control and Prevention obtaining data from US household individuals regarding health and nutrition for the purpose of improving the US health through policy. The NHANES 2005 to 2006 data reported that 29% of the United States population 18 years and older are diagnosed with hypertension. Of the population with treated hypertension, greater than 64% has controlled hypertension. Men have a higher rate of hypertension until the age of 45 when the incidence of hypertension equalizes between men and women.

In 2006 the mortality from hypertension was reported in 56,561 individuals. Both the prevalence from hypertension and mortality has increased from the late 1990s to the 2000s. The estimated direct and indirect cost of hypertension for the year 2010 was 76.6 billion US dollars.

The sequelae of hypertension include strokes, myocardial ischemia, aortic dissection, and renal insufficiency. The remaining text of the chapter will focus on the management of blood pressure in the specified acute neurologic diseases.

Hypertensive crisis is defined as an abrupt elevation of blood pressure, to a point that the blood vessels are unable to maintain constant blood flow in the setting of increasing perfusion pressures to specific organs, also known as disruption of autoregulation. The end result leads to end-organ damage from ischemia or hemorrhage. The end result leads to end-organ damage from ischemia or hemorrhage.

Patients with blood pressure elevations greater than 180/110 mmHg are categorized into the following diagnoses:

1. Severe hypertension: no to mild symptoms and no acute end-organ damage

2. Hypertensive urgency: significant symptoms and mild acute end-organ damage. Mild end-organ damage is defined as dyspnea and headaches.

3. Hypertensive emergency: severe symptoms with life-threatening end-organ damage.

Life-threatening end-organ damage is defined as acute ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, acute aortic dissection, myocardial infarction, acute heart failure, eclampsia, renal insufficiency, and acute pulmonary edema, to name a few. The first instinct when dealt with this situation as a practitioner is to acutely correct the problem. However, there are some considerations prior to acutely correcting the blood pressure in a hypertensive crisis. The remainder of the chapter will discuss these considerations in relation to neurologic emergencies.

Hypertensive urgencies include 25% of ED medical visits, while hypertensive emergencies are one-third of the cases. CNS complications are the most frequent of the hypertensive emergencies. The hypertensive emergent patient with neurologic sequelae needs urgent attention, with hourly blood pressure monitoring and neurologic examination in an intensive care unit. Prior to discussing blood pressure management, a discussion of cerebral autoregulation and the parental antihypertensive agents will be reviewed.

Cerebral Autogregulation

Cerebral blood flow (CBF) is tightly controlled under the normal conditions, with cerebral perfusion pressures (CPP) ranging from 50 to 150 mgHg. Cerebral perfusion pressures can be calculated from mean arterial pressure (MAP) minus jugular vein pressure (JVP). Intracracranial pressure (ICP) is substituted for JVP under conditions where the ICP is greater than the JVP. Cerebral autogregulation involves arteriole caliber changes in response to changes in the blood pressure; however, there are upper and lower limits that lead to a disruption of this system with resultant ischemia or cerebral edema (Figure 1.1).

Figure 1.1. Autoregulation maintains cerebral blood flow relatively constant between 50 and 150 mmHg mean arterial pressure. The range is right shifted in chronically hypertensive patients. (Reproduced from Ruland and Aiyagari. Hypertension 2007; 49: 978, with permission from Wolters Kluwer Health.)

The underlying mechanisms of autoregulation that allow for vessel caliber changes are myogenic and metabolic. When the MAP decreases, the arterioles constrict to increase the CBF; however, if hypotension persists beyond the lower limit threshold, resultant cerebral ischemia exists. If the blood pressure continues to increase above the higher limit threshold, the result is hyperemia and cerebral edema. However, in brain dysfunction, the blood–brain barrier and cerebral endothelium is disrupted, leading to leaky blood vessels with subsequent fibrinoid deposition into the cerebral vasculature. This results in vascular narrowing, with compensatory vasodilation. In these circumstances the autoregulation curve follows a more linear pattern with the CBF being dependent on perfusion pressures.

Normal CBF is 50 mL/100 g brain tissue per minute. Reversible injury, occurs at 15–20 mL/100 g/min, and irreversible injury is less than 15 mL/100 g/min. The occurrence of cell death is based on the product of the degree and length of time of ischemia. The ischemic penumbra is vulnerable tissue with impaired autoregulation and low blood flow despite high oxygen extraction. Therefore the tissue is salvageable but has a high risk of becoming ischemic if the blood flow is not recovered in a short period of time.

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Scientific Evidence

An EEG is a useful tool for monitoring seizures, but also for detecting cerebral blood flow. In the operation room, older studies have shown that EEG can detect real-time ischemia. When cerebral blood flow reaches 25–30 mL/100 g/min, an EEG demonstrates a change in morphology, amplitude, and frequency. When the CBF decreases to less than 15 mL/1006/min, the EEG becomes isoelectric. The neurons that produce the excitatory post-synaptic potential (EPSP) and inhibitory post-synaptic potential (IPSP) for the electrodes are the same neurons (pyramidal neurons) that are sensitive to hypoxia.

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Antihypertensive Agents

Hypertensive emergency can be fatal, and needs prompt treatment. The initial treatment is blood pressure control, in a reliable and controlled fashion, therefore oftentimes, requiring parental agents and arterial blood pressure monitoring. There are multiple classes of antihypertensives one has to choose from; however, there are also many factors to consider prior to administration. The most important factor to consider in neurologic damage is increased intracranial pressure. A few class of antihypertensive agents work via vasodilatory mechanisms, which can lead to further increases in intracranial pressure and potentially further worsening of neurologic injury. Another factor is the onset and duration of action. Rapid fluctuations of hypotension and hypertension can lead to worsening cerebral injury. An agent that can be turned off and out of the system quickly is more desirable in case of an acute hypotensive episode.

Preferred Agents for Hypertensive Emergencies with Brain Dysfunction

Beta Blockers

Labetalol is a selective alpha-1 and nonselective beta antagonist. The onset of action is 2–5 minutes with a peak effect seen in 5–15 minutes. The hypertensive effect can last for 2–4 hours. Beta action does cause a decrease in heart rate but maintains the cardiac output. Similarly, cerebral perfusion is maintained with the use of beta blockers.

Start with a loading dose of 20 mg, increasing subsequent doses from 20 to 80 mg every 10 minutes to the desired effect. In the author's institution, if repeat labetalol boluses do not result in the desired effect, an infusion is initiated starting at 1–2 mg/min.

Esmolol is a short-acting beta antagonist, with no direct affect on the peripheral vasculature. Decreased blood pressure is secondary by decreasing cardiac output. The onset of action is 60 seconds, with a duration of action of 10–20 minutes. esmolol has a unique metabolic profile, being metabolized by red blood cell (RBC) esterases. In the setting of anemia, Esmolol can have a prolonged effect. Due to its pure beta action, caution should be used in patients with COPD. Similarly it should be avoided in patients in decompensated heart failure, due to compromising myocardial function.

Start with a loading dose of 500–1000 μg/kg, with a continuous infusion at 50 μg/kg/min to a maximum of 300 μg/kg/min.

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Tips & Tricks

Beta blocker toxicity can present with bradycardia, hypotension, bronchospasm, and hypoglycemia. An ECG can be helpful with detecting PR prolongation. QT prolongation can sometimes be detected. It should be treated with atropine for bradycardia, intravenous fluids and vasopressors for hypotension. Glucagon is a well-known antedote for the treatment of beta blocker toxicity.

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Calcium Channel Blockers

Three types of calcium channel blocker exist: dihydropyridines, phenylalkylamines, and benzothiapines. The two types of calcium channels that exist in the vasculature are L-type and T-type.

The action of calcium channel blockers on L-type channels decrease calcium influx, resulting in elevated GMP levels. The elevated GMP levels lead to vascular smooth muscle relaxation, vasodilation and decrease systolic...

Table of contents

• Cover
• Title Page
• Copyright
• List of Contributors
• Series Foreword
• Preface
• Part I: Acute Management of Neurological Emergencies
• Part II: Cerebrovascular Critical Care
• Part III: Infections of the Nervous System
• Part IV: Neuromuscular Complications Encountered in the Intensive Care Unit
• Part V: Neurological Complications and Consultations in General Intensive Care Units
• Color Plates
• Index