916 Pages

Practice Guidelines for Acute Care Nurse Practitioners - E-Book


Gain access to the library to view online
Learn more


PRACTICE GUIDELINES FOR ACUTE CARE NURSE PRACTITIONERS, 2nd Edition is the only comprehensive clinical reference tailored to the needs of advance practice nurses. With discussions of more than 230 of the most common conditions experienced by adult patients in acute care, this reference includes everything you need on a day-to-day basis. Plus, quick reference is easy with a spiral binding and content organized by body system. Each condition lists a concise outline of defining terms, incidence/predisposing factors, subject and physical examination findings, diagnostic tests, and management strategies so you can find everything you need to know quickly. Includes discussion of body systems, nutritional considerations, fluid/electrolyte imbalances, shock, trauma, gerontological concerns, professional issues, and trends in advanced practice.
  • Nursing guidelines for more than 230 of the most common conditions experienced by adult patients in acute care serve as an invaluable resource in the field.
  • Conditions are organized by body system for quick reference when treating patients.
  • Each condition lists defining terms, incidence/predisposing factors, subjective and physical examination findings, diagnostic tests, and management strategies to provide help every step of the way.
  • Coverage also includes discussion of body systems, nutritional considerations, fluid/electrolyte imbalances, shock, and trauma for a complete look at patient care and diagnosis.
  • An entire chapter dedicated to congestive heart failure gives you a deeper look at the disease.
  • Specific content, as well as online references, for diseases such as SARS and West Nile Virus give you the most current information available on these evolving diseases.
  • New chapters on admission, pre-op and post-op orders prepare you for every step of the patient treatment process.
  • Addition of ICD-9 codes within the chapters makes classifying diseases with ICD codes easy.
  • New content on Parkinson's disease, gout, testicular cancer, multiple sclerosis, bite management (including spider, snake, animal, and human) better prepare you for these situations.
  • Updated and expanded content reflects changes in current guidelines and evidence-based practice, an important part of working in the field.
  • Updated and expanded content on coronary artery disease and inclusion of the new JNC 7 national hypertension guidelines features more information on these common diseases.
  • Expanded and updated coverage of postmenopausal women and hormone replacement therapy.



Published by
Published 26 December 2007
Reads 0
EAN13 9781416069218
Language English
Document size 1 MB

Legal information: rental price per page 0.0222€. This information is given for information only in accordance with current legislation.

Table of Contents
Cover Image
CHAPTER 1. Cerebrovascular Accidents: Brain Attack
CHAPTER 2. Structural Abnormalities
CHAPTER 3. Peripheral Neuropathies
CHAPTER 4. Neurologic Trauma
CHAPTER 5. Central Nervous System Disorders
CHAPTER 6. Seizure Disorders
CHAPTER 7. Dementia
CHAPTER 8. Cardiovascular Assessment
CHAPTER 9. Hypertension
CHAPTER 10. Coronary Artery Disease and Hyperlipidemia
CHAPTER 11. Angina and Myocardial Infarction
CHAPTER 12. Adjunct Equipment/Devices
CHAPTER 13. Peripheral Vascular Disease
CHAPTER 14. Inflammatory Cardiac Diseases
CHAPTER 15. Heart Failure
CHAPTER 16. Valvular Disease
CHAPTER 17. Cardiomyopathy
CHAPTER 18. Ectopy and Arrhythmia Emergencies
CHAPTER 19. Diagnostic Concepts of Oxygenation and Ventilation
CHAPTER 20. Measures of Oxygenation and Ventilation
CHAPTER 21. The Chest X-ray
CHAPTER 22. Differential Diagnosis of Pulmonary Disorders
CHAPTER 23. Pulmonary Function Testing
CHAPTER 24. Obstructive (Ventilatory) Lung Diseases
CHAPTER 25. Restrictive (Inflammatory) Lung Diseases and Congestive Heart
Failure/Pulmonary Edema
CHAPTER 26. Pathophysiologically Derived Therapy for Respiratory Dysfunction
CHAPTER 27. Pulmonary Hypertension and Pulmonary Vascular Disorders
CHAPTER 28. Chest Wall and Secondary Pleural Disorders
CHAPTER 29. Respiratory Failure
CHAPTER 30. Pneumothorax
CHAPTER 31. Lower Respiratory Tract Pathogens
CHAPTER 32. Obstructive Sleep Apnea
CHAPTER 33. Oxygen Supplementation
CHAPTER 34. Mechanical Ventilatory Support
CHAPTER 35. Peptic Ulcer Disease
CHAPTER 36. Liver Disease
CHAPTER 37. Biliary DysfunctionCHAPTER 38. Inflammatory Gastrointestinal Disorders
CHAPTER 39. Anatomic Intestinal Disorders
CHAPTER 40. Gastrointestinal Bleeding
CHAPTER 41. Urinary Tract Infections
CHAPTER 42. Renal Insufficiency and Failure
CHAPTER 43. Benign Prostatic Hyperplasia
CHAPTER 44. Renal Artery Stenosis
CHAPTER 45. Nephrolithiasis
CHAPTER 46. Diabetes Mellitus
CHAPTER 47. Diabetic Emergencies
CHAPTER 48. Thyroid Disease
CHAPTER 49. Cushing's Syndrome
CHAPTER 50. Primary Adrenocortical Insufficiency (Addison's Disease) and Adrenal Crisis
CHAPTER 51. Pheochromocytoma
CHAPTER 52. Syndrome of Inappropriate Antidiuretic Hormone
CHAPTER 53. Diabetes Insipidus
CHAPTER 54. Arthritis
CHAPTER 55. Subluxations and Dislocations
CHAPTER 56. Soft Tissue Injury
CHAPTER 57. Fractures
CHAPTER 58. Compartment Syndrome
CHAPTER 59. Back Pain Syndromes
CHAPTER 60. Anemias
CHAPTER 61. Sickle Cell Disease/Crisis
CHAPTER 62. Coagulopathies
CHAPTER 63. Leukemias
CHAPTER 64. Lymphoma
CHAPTER 65. Other Common Cancers
CHAPTER 66. HIV/AIDS and Opportunistic Infections
CHAPTER 67. Autoimmune Diseases
CHAPTER 68. Integumentary Disorders
CHAPTER 69. Ectopic Pregnancy and Sexually Transmitted Infections
CHAPTER 70. Eye, Ear, Nose, and Throat Disorders
CHAPTER 71. Headache
CHAPTER 72. Fever
CHAPTER 73. Pain
CHAPTER 74. Psychosocial Problems in Acute Care
CHAPTER 75. Management of the Patient in Shock
CHAPTER 76. Nutritional Considerations
CHAPTER 77. Fluid, Electrolyte, and Acid-Base Imbalances
CHAPTER 78. Poisoning and Drug Toxicities
CHAPTER 79. Wound Management
CHAPTER 80. Infections
CHAPTER 81. Chest, Abdominal, and Eye Trauma
CHAPTER 82. Solid Organ TransplantationCHAPTER 83. Burns
CHAPTER 84. Hospital Admission Considerations
CHAPTER 85. Managing the Surgical Patient
CHAPTER 86. Guidelines for Health Promotion and Screening
CHAPTER 87. Major Causes of Mortality in the United States
CHAPTER 88. Immunization Recommendations
APPENDIX. 2007 Asthma Guidelines, National Heart, Lung, and Blood Institute
AbbreviationsC o n t r i b u t o r s
Hector Alvarez, MSN, APRN, BC, ACNP
Acute Care Nurse Practitioner, Orthopaedic Surgery Specialists, Burbank, California
46. Diabetes Mellitus, 47. Diabetic Emergencies
Judith Azok, MSN, APRN, BC, GNP
Clinical Assistant Professor, University of South Alabama, College of Nursing, Mobile, Alabama
19. Diagnostic Concepts of Oxygenation and Ventilation, 30. Pneumothorax
Thomas W. Barkley Jr., DSN, APRN, BC, ACNP
Associate Professor and Coordinator, Acute Care Nurse Practitioner Program, California State
University, Los Angeles, School of Nursing
President, Barkley & Associates, Los Angeles, California
8. Cardiovascular Assessment; 9. Hypertension; 10. Coronary Artery Disease and
Hyperlipidemia; 11. Angina and Myocardial Infarction; 12. Adjunct Equipment/Devices; 13.
Peripheral Vascular Disease; 14. Inflammatory Cardiac Diseases; 15. Heart Failure; 16.
Valvular Disease; 17. Cardiomyopathy; 18. Ectopy and Dysrhythmia Emergencies; 22.
Differential Diagnosis of Pulmonary Disorders; 23. Pulmonary Function Testing; 24. Obstructive
(Ventilatory) Lung Diseases; 25. Restrictive (Inflammatory) Lung Diseases and Congestive Heart
Failure/Pulmonary Edema; 26. Pathophysiologically Derived Therapy for Respiratory
Dysfunction; 27. Pulmonary Hypertension and Pulmonary Vascular Disorders; 28. Chest Wall
and Secondary Pleural Disorders; 29. Respiratory Failure; 31. Lower Respiratory Tract
Pathogens; 32. Obstructive Sleep Apnea; 46. Diabetes Mellitus; 47. Diabetic Emergencies; 48.
Thyroid Disease; 49. Cushing's Syndrome; 50. Primary Adrenocortical Insufficiency (Addison's
Disease) and Adrenal Crisis; 51. Pheochromocytoma; 52. Syndrome of Inappropriate Antidiuretic
Hormone; 53. Diabetes Insipidus; 66. HIV/AIDS and Opportunistic Infections; 81. Chest,
Abdominal, and Eye Trauma; 83. Burns; 84. Hospital Admission Considerations
Catherine Blache, MSN, RN, CCRC
Director of Research, University of South Alabama, College of Medicine, Mobile, Alabama
79. Wound Management
Otto “Joey” Bonin Jr., MSN, APRN, BC, ACNP, ANP-C
Adult/Acute Care Nurse Practitioner, Cardiovascular Institute of the South, Zachary, Louisiana
72. Fever
Lorris J. Bouzigard, MSN, APRN, BC, ACNP, ANP-C
Cardiovascular Nurse Practitioner, Slidell Memorial Hospital, Slidell, Louisiana
72. Fever
Barbara Ann Shelton Broome, PhD, RN
Associate Dean and Chair, Community/Mental Health, University of South Alabama, College of
Nursing, Mobile, Alabama
87. Major Causes of Mortality in the United StatesKimberly Riley Bryan, MSN, APRN, BC, CCRN
Adjunct Clinical Professor, University of South Alabama, College of Nursing, Mobile, Alabama
82. Solid Organ Transplantation
R. Michael Culpepper, MD
Professor of Medicine, Associate Professor of Physiology, University of South Alabama, Mobile,
Alabama;, Attending Physician, Director of Dialysis, University of South Alabama Medical
Center, Mobile, Alabama
77. Fluid, Electrolyte, and Acid-Base Imbalances
Gladys D. Field, MSN, APRN, BC, ACNP
Lecturer, California State University, Los Angeles, Los Angeles, California
24. Obstructive (Ventilatory) Lung Diseases
Denise R. Fortenberry, MSN, APRN, BC, ACNP
Acute Care Nurse Practitioner, Hoag Hospital, Newport Beach, California
24. Obstructive (Ventilatory) Lung Diseases
Jennifer Ramos Javier, MSN, APRN, BC, ACNP
Acute Care Nurse Practitioner, Los Angeles, California
9. Hypertension, 10. Coronary Artery Disease and Hyperlipidemia
Jesse A. Lopez, MSN, APRN, BC, ACNP, CCRN
RN Educator, Kaiser Permanente, Los Angeles, California
66. HIV/AIDS and Opportunistic Infections
Sylvia Russell Love, MEd, MSN, APRN, BC, ACNP, ANP
Clinical Assistant Professor, University of South Alabama, College of Nursing, Mobile, Alabama
60. Anemias, 61. Sickle Cell Disease/Crisis, 62. Coagulopathies, 63. Leukemias, 64. Lymphoma,
68. Integumentary Disorders, 71. Headache
Sara Clarkson Majors, PhD, MSN, MPH, CRNA, CPNP
Clinical Assistant Professor, Program Coordinator, Advanced Child Health, University of South
Alabama, College of Nursing, Mobile, Alabama
73. Pain
Robert Demetric Martin, MSN, RN, NP
Clinical Assistant Professor of Emergency Medicine Associate Director, USC Center for Life
Support Training, Keck School of Medicine, University of Southern California, Los Angeles,
18. Ectopy and Dysrhythmia EmergenciesTom Meyer, MSN, APRN, BC, CCRN, CNS
Clinical Assistant Professor, Adult Health, University of South Alabama, College of Nursing,
Mobile, Alabama
20. Measures of Oxygenation and Ventilation, 21. The Chest X-Ray, 33. Oxygen Supplementation,
34. Mechanical Ventilatory Support
Diantha D. Miller, MSN, APRN, BC, ACNP, PNP
Adjunct Faculty, University of South Alabama, Mobile, Alabama
Nurse Practitioner, Laser and Skin Care Center of Mobile, Mobile, Alabama
70. Eye, Ear, Nose, and Throat Disorders
Sally K. Miller, PhD, APRN, BC, ACNP, ANP, GNP, FAANP
Chair, Department of Physiologic Nursing, University of Las Vegas School of Nursing, Las
Vegas, Nevada
67. Autoimmune Diseases, 85. Managing the Surgical Patient
Charlene M. Myers, MSN, APRN, BC, ACNP, CCRN
Clinical Assistant Professor, Program Coordinator, Adult Acute Care Nurse Practitioner
Program, University of South Alabama, College of Nursing, Mobile, Alabama
1. Cerebrovascular Accidents: Brain Attack, 2. Structural Abnormalities, 3. Peripheral
Neuropathies, 4. Neurologic Trauma, 5. Central Nervous System Disorders, 6. Seizure Disorders,
7. Dementia, 23. Pulmonary Function Testing, 28. Chest Wall and Secondary Pleural Disorders,
35. Peptic Ulcer Disease, 36. Liver Disease, 37. Biliary Dysfunction, 38. Inflammatory
Gastrointestinal Disorders, 39. Anatomic Intestinal Disorders, 40. Gastrointestinal Bleeding, 41.
Urinary Tract Infections, 42. Renal Insufficiency and Failure, 43. Benign Prostatic Hyperplasia,
44. Renal Artery Stenosis, 45. Nephrolithiasis, 75. Management of the Patient in Shock
Sandra J. Ogawa, MSN, APRN, BC, ACNP
Acute Care Nurse Practitioner, Thoracic Surgery, Assistant Coordinator, Esophageal Disease
Center, Heart Institute at St. Joseph's Medical Center, Phoenix, Arizona
84. Hospital Admission Considerations
Marian Elizabeth Peters, MSN, RN, WHNP, CNS
Clinical Assistant Professor, University of South Alabama, Mobile, Alabama
69. Ectopic Pregnancy and Sexually Transmitted Infections
Luisa Maria Schulman, MSN, RN, ANP-C, CCRN
Adult Nurse Practitioner, Private Practice, Pasadena, California
Lecturer, California State University, Los Angeles, School of Nursing, Los Angeles, California
66. HIV/AIDS and Opportunistic Infections
Martha N. Surline, MS
Director of Student Services, University of South Alabama, College of Nursing, Mobile, Alabama76. Nutritional Considerations
Paula K. Vuckovich, PhD, APRN, BC
Assistant Professor, School of Nursing, California State University, Los Angeles, California
Relief Supervisor, Aurora Las Encinas Hospital, Pasadena, California
74. Psychosocial Problems in Acute Care
Elizabeth A. Vande Waa, PhD
Associate Professor, Department of Adult Health, University of South Alabama, College of
Nursing, Mobile, Alabama
78. Poisoning and Drug Toxicities
John A. Vande Waa, DO, PhD
Associate Professor of Medicine, Consultant in Infectious Diseases, Immunodeficiencies,
Traveler's Health, University of South Alabama, Mobile, Alabama
80. Infections
Colleen R. Walsh, RN, MSN, APRN, BC, ACNP, ONC, CS
Faculty, Graduate Nursing, University of Southern Indiana, College of Nursing and Health
Professions, Evansville, Indiana
Acute Care Nurse Practitioner, Jenkins Community Hospital, Jenkins, Kentucky
54. Arthritis, 55. Subluxations and Dislocations, 56. Soft Tissue Injury, 57. Fractures, 58.
Compartment Syndrome, 59. Back Pain Syndromes, 65. Other Common Cancers
Gail Washington, DNS, RN
Assistant Professor, California State University, Los Angeles, School of Nursing, Los Angeles,
69. Ectopic Pregnancy and Sexually Transmitted Infections
Carolyn Mathis White, JD, MSN, APRN, BC, FNP, PNP, CCRN
Clinical Assistant Professor, University of South Alabama, Mobile, Alabama
Nurse Practitioner, Victory Health Partners, Mobile, Alabama
70. Eye, Ear, Nose, and Throat Disorders; 86. Guidelines for Health Promotion and Screening
Kimberly A. Williams, DNSc, APRN, BC, ANP, PMHNP
Assistant Professor, University of South Alabama, College of Nursing, Mobile, Alabama
Adult Health Nurse Practitioner, Gulf Coast Medical Center, Biloxi, Mississippi, Garden Park
Medical Center, Gulfport, Mississippi, Hancock Medical Center, Bay St. Louis, Mississippi,
Memorial Hospital, Gulfport, Mississippi, Ocean Springs Hospital, Ocean Springs, Mississippi,
Select Specialty Hospital, Gulfport, Mississippi
88. Immunization RecommendationsP r e f a c e
Practice Guidelines for Acute Care Nursing Practitioners is a succinct and comprehensive pocket
text for advanced practice nurses. The text is organized in a systematic fashion, addressing over 250
of the most common conditions experienced by adult patients in acute care. Using an easy-to-read
outline format, coverage of each condition includes defining terms, incidence/predisposing factors,
subjective and physical examination findings, diagnostic tests, and management strategies.
The text has been written to provide the practitioner with a quick overview of evidence-based
practice guidelines. In this light, the text builds on previous knowledge of anatomy, physiology, and
pathophysiology concepts that have not been separately emphasized. Although many practitioners
may be highly specialized, this text was designed as a useful tool for the entire scope of acute care
nursing practice, including settings such as clinics, emergency departments, medical/surgical
departments in hospitals, as well as critical care units. Although this text was developed based on
research and expertise, we also feel strongly that collaborative practice with other experts and
clinicians is essential to successfully meeting patient goals.
Thomas W. Barkley Jr. and Charlene M. MyersA c k n o w l e d g m e n t s
We gratefully acknowledge the outstanding contributors and reviewers for this text. Without the
expertise of these scholars, this work would not have been possible.
We also thank the following people at Elsevier:
Thomas Eoyand, former Editor, for believing in our potential as editors for the first edition
Barbara Nelson Cullen, former Executive Publisher
Sandra Brown, Senior Acquisitions Editor
Sophia Oh Gray, Developmental Consultant
Cheryl Abbott, Senior Project Manager
whose combined efforts have produced what we believe is a state-of-the art, evidence-based,
excellent resource for the profession.
Thomas W. Barkley Jr. and Charlene M. MyersR e v i e w e r s
Nancy J. Bekken, RN, MSN, CCRN
Spectrum Health, Grand Rapids, Michigan
Susan Duhon-Johnston, MSN, FNP-BC
Hospital-based Internal Medicine, Ochsner Health System, New Orleans, Louisiana
Lynn S. Eckhardt, BSN, MSN, NP
Director of Dementia Clinic, Neurology Department, Ochsner Health System, New Orleans,
Pamela L. Isbell, MSN, CEN
Staff Nurse, Relief Charge Nurse, Orlando Regional Medical Center, Orlando, Florida
Suzanne Lazare-Ellis, RN, MSN, CCRN, CNS
Intensive Care Unit Staff Nurse, San Francisco VA Medical Center, San Francisco, California
Allyson E. Mobley, MSN, CRNP
Neurology, Alabama Neurological Institute, Birmingham, Alabama
Ted Rigney, MS, RNP, CCRN, ACNP
Assistant Director Nurse Practitioner Program, University of Arizona College of Nursing, Tucson,
Nancy Evans Stoner, RN, MSN
Hospital of the University of Pennsylvania, Clinical Nutrition Support Service, Philadelphia,
Scott Carter Thigpen, RN, MSN, CCRN, CEN
Assistant Professor of Nursing, South Georgia College, Douglas, Georgia
Joseph E. Williams, RN, MSN, ACNP-C, ANP-C
Lead Nurse Practitioner, Hospitals Division, Department of Internal Medicine, Ochsner Health
System, New Orleans, LouisianaCHAPTER 1. Cerebrovascular Accidents: Brain Attack
Hemorrhagic stroke, 431
Ischemic stroke, 434.91
Stroke/brain attack, 434.91
Transient ischemic attack, 436
I. Definition
A. Classic definition: sudden or rapid onset of neurologic deficit caused by focal ischemia that
lasts for a few minutes and resolves completely within 24 hours
B. Recently proposed revision of classic definition: brief episode of neurologic dysfunction
caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than 1
hour and no evidence of acute infarction
II. Etiology/incidence/prevalence
A. Incidence is 160/100,000; prevalence is 135/100,000.
B. Carotid or vertebral artery disease
C. Cardiac emboli as seen in arrhythmia (atrial fibrillation), myocardial infarction, congestive
cardiomyopathy, and valvular disease
D. Hematologic causes
1. Red blood cell (RBC) disorders
a. Increased sludging
b. Decreased cerebral oxygenation such as in severe anemia
c. Polycythemia, sickle cell anemia
2. Platelet disorders
a. Thrombocytosis
b. Thrombocytopenia
3 . Myeloproliferative disorders, leukemia with white blood cell (WBC) count greater than
4. Increased viscosity/hypercoagulable conditions
a. Antiphospholipid antibody syndrome (e.g., lupus anticoagulant, anticardiolipin antibody)
b. Oral contraceptive use
c. Antithrombin III deficiency
d. Protein S and C deficiency
e. Tissue-type plasminogen activator (t-PA) and plasminogen deficiencies
f. Patients particularly at risk for a hypercoagulable state
i. Older than age 45
ii. History of thrombolytic event
iii. History of spontaneous abortion
iv. Related autoimmune conditions (e.g., lupus)
v. Stroke of unknown cause
vi. Family history of thrombotic eventsE. Intracranial causes
1. Brain tumor
2. Focal seizure
3. Hemorrhage
a. Subdural hematoma (SDH)
b. Subarachnoid hemorrhage (SAH)
c. Intra cerebral hemorrhage (ICH), which may cause cerebrovascular dysfunction due to
leakage of blood outside the normal vessels
F. Subclavian steal syndrome
1. Localized stenosis or occlusion of a subclavian artery proximal to the source of the
vertebral artery, so that blood is stolen from that artery
2. Blood pressure is significantly lower in the affected arm than in the opposite arm.
G. Others
1. Transient hypotension
2. Osteophytes that cause compression of neck vessels
3. Kinking of neck vessels during rotation of the head
4. Cocaine abuse
5. Hypoglycemia
III. Risk factors
A. TIA: Individuals are at risk for stroke in the months, as well as the years, immediately after
the initial TIA; therefore, proper treatment of attacks is important. Approximately one third of
stroke patients have a history of TIA.
B. Hypertension
C. Cardiac disease, such as the following:
1. Mitral valve disease
2. Anterior wall myocardial infarction
3. Congestive myopathy
4. Arrhythmia (e.g., atrial fibrillation)
D. Smoking
E. Obesity
F. Hyperlipidemia
G. Elevated homocysteine levels in the elderly
H. Advanced age
I. Diabetes
J. Alcohol and recreational drug abuse
IV. Clinical manifestations
A. Carotid artery syndrome
1. Ipsilateral monocular blindness (amaurosis fugax) described as similar to a shade coming
down over one eye
2. Paresthesia/weakness of contralateral arm, leg, and face (may be episodic)
3. Dysarthria, transient aphasia4. Ipsilateral, vascular-type headache
5. Carotid bruit may be present.
6. Microemboli, hemorrhage, and exudate may be visualized in the ipsilateral retina.
B. Vertebrobasilar artery syndrome
1. Visual disturbance bilaterally (blurred vision, diplopia, complete blindness)
2. Vertigo, ataxia, tinnitus
3. Nausea and/or vomiting
4. Sudden loss of postural tone in all extremities while consciousness remains intact (drop
5. Dysarthria
6. Perioral or facial paresthesia
7. Acute confusional state
V. Diagnostics/laboratory findings
A. Laboratory evaluation should include the following:
1. Complete blood count (CBC), platelet count, prothrombin time (PT), partial
thromboplastin time (PTT), and international normalized ratio (INR) to detect these
a. Anemia
b. Polycythemia
c. Leukemia
d. Thrombocytopenia
e. Hypercoagulopathy
2. Anticardiolipin antibodies (immuno globulin [Ig]G, IgM, IgA) and assay for lupus
anticoagulant for suspected antiphospholipid antibody syndromes
3. Assays for antithrombin III, proteins S and C, plasminogen, and t-PA
4. Electrolytes, glucose to detect the following:
a. Hyponatremia
b. Hypokalemia
c. Hypoglycemia
d. Hyperglycemia
5. Sedimentation rate, to detect these conditions:
a. Vasculitis
b. Infective endocarditis
c. Hyperviscosity
d. Giant cell arteritis
6. Lipid profile
a. Detects hyperlipidemia
7. In selected patients, antinuclear antibody (ANA), Venereal Disease Research Laboratory
test (VDRL), and toxicology screen
8. Homocysteine level
a. An amino acid
b. Elevated plasma level associated with increased risk of vascular eventsB. Computed tomography (CT) scan of the head
1. May reveal “silent” ischemia or ischemic images, as well as hemorrhage or infarct and
2. 10% to 20% of patients with TIAs have an infarct in the territory relevant to their
C. Magnetic resonance imaging (MRI), particularly diffusion-weighted imaging (DWI) and
perfusion-weighted imaging (PWI)
1. More sensitive than CT scan to early pathologic changes of ischemic infarction because of
its excellent detection of brain edema
2. MRI is also preferred for the detection of lacunar or vertebrobasilar TIAs, or when
vascular territory is not well defined.
D. Single photon emission computed tomography (SPECT)
1. Injection with 99mTc-labeled agent
2. Multiple views of emission projection data
3. Essentially, a VQ (ventilation/quantification) scan of the brain
E. Duplex ultrasonography
1. 85% sensitivity and 90% specificity
2. Useful in identifying hemodynamically significant carotid stenosis
F. Magnetic resonance angiography (MRA)
1. Alternative to ultrasound studies
2. No contrast medium is needed.
3. Can be obtained at the same time as an MRI scan
4. Good means for assessment of extracranial and intracranial vessels
G. Carotid Doppler ultrasound has limited usefulness.
H. Echocardiography and a 24-hour Holter monitor are used to evaluate for a cardiac source of
I. Trans esophageal echocardiography (TEE) to detect vascular tree abnormalities and stenosis
J. Cerebral angiography for patients whose symptoms suggest involvement of the carotid
circulation and who are candidates for carotid endarterectomy (CEA)
K. Chest x-ray for enlarged heart
L. Blood cultures to monitor for infective endocarditis
M. Temporal artery biopsy to detect giant cell arteritis
N. Cardiac enzymes to detect an acute myocardial infarction
O. Electroencephalography (EEG) indicated in patients suspected of having a seizure disorder
associated with stroke, as well as an underlying toxic-metabolic disorder that may cause seizure
VI. Management
A. Address the following underlying risk factors:
1. Hyper tension (HTN)
2. Diabetes mellitus (DM)
3. Obesity
4. Hyperlipidemia5. Smoking
B. Carotid TIAs
1. Greater than 70% obstruction: CEA is indicated for those who are a good surgical risk.
2. Less than 30% obstruction: Surgery is not indicated.
3. Recently, carotid angioplasty and stenting (CAS) has emerged as an alternative in high-risk
surgical patients, or when CEA is contraindicated for technical or medical reasons.
C. Anticoagulation if caused by a cardioembolic event
1. May prevent recurrent cardioembolic events
2. Begin with heparin (loading dose of 5000-10,000 units for those not at risk for
hemorrhagic transformation and maintenance infusion of 1000-2000 units/hour).
3. Target PTT should be 1.5 times control.
4. Follow with warfarin (Coumadin), 5-15 mg PO (per os; by mouth), which is indicated for
the following:
a. TIA caused by embolism arising from a mural thrombus after a myocardial infarction
b. TIA caused by embolus in patients with mitral stenosis or prosthetic heart valves
c. Recurrent TIAs despite platelet antiaggregant agents
d. INR of 2 to 3 is considered therapeutic.
D. Antiplatelet therapy is useful for patients who are not candidates for surgery or warfarin
therapy (those with gastrointestinal [GI] bleeding, bleeding tendencies, or severe hypertension,
elderly patients who fall frequently, or uncooperative patients).
1 . Aspirin (ASA [acetylsalicylic acid]) decreases incidence of subsequent stroke by 15% to
30% in male patients with TIAs; dose of 81-325 mg/day is as effective as higher doses and
causes fewer adverse effects.
2. Clopidogrel (Plavix)
a. Antiplatelet agent that is a chemical relative of ticlopidine (Ticlid)
b. Causes far fewer adverse hematologic effects
c. May cause thrombotic thrombocytopenia purpura (TTP) during the first 2 weeks of
d. Indicated for secondary prevention of ischemic stroke, MI, and other vascular events in
patients who cannot tolerate ASA, or in patients who were taking ASA at the time of the
e. Dosage is 75 mg/day PO.
3. Combined dipyridamole (Persantine) (200 mg extended release) and ASA (25 mg
immediate release)
a. Available as fixed-dose formulation under the trade name Aggrenox
b. Both drugs suppress platelet aggregation but do so through different mechanisms.
c. Combination treatment is more effective than either drug alone.
d. Recommended dose is 2 capsules daily—1 in the morning and 1 at night.
e. Significantly more expensive than ASA therapy: approximately $90/month versus
$3/month for ASA therapy alone
I. Definition
A. Rapid onset of a neurologic deficit involving a certain vascular territory and lasting longer
than 24 hoursB. A stroke-in-evolution is an enlarging infarction manifested by neurologic defects that
increase over 24 to 48 hours.
C. Stroke is the leading cause of disability and the third leading cause of death in the U.S.
D. Stroke can be classified as ischemic and hemorrhagic.
E. 80% of strokes are caused by blood clots that produce ischemic areas in the brain; remaining
strokes are caused by intracerebral hemorrhage.
II. Etiology and risk factors
A. Same as for TIA
B. Cocaine-related stroke is increasingly common.
C. Women who use oral contraceptives and who smoke are at high risk.
D. Hyperlipidemia raises the risk of ischemic stroke.
E. Low cholesterol increases the risk of hemorrhagic stroke.
I. Etiology
A. Caused by a thrombus (30%)
1. Progression of symptoms over hours to days
2. Patients often have a history of TIA.
3. This often occurs during the night while the patient is sleeping; the patient may completely
infarct and may be unarousable in the morning.
4. Patient may awaken with a slight neurologic deficit that gradually progresses.
5. Predisposing factors
a. Atherosclerosis
b. HTN
c. DM
d. Arteritis
e. Vasculitis
f. Hypotension
g. Trauma to the head and neck
B. Caused by embolism (25%)
1. Very rapid onset
2. History of TIA uncommon
3. Patient is usually involved in an activity when symptoms occur.
4. Predisposing factors
a. Atrial fibrillation
b. Mitral stenosis and regurgitation
c. Endocarditis
d. Mitral valve prolapse
II. Clinical manifestations (depend on the cerebral vessel involved)
A. Middle cerebral artery
1. Hemiplegia (involves upper extremity and face more often than lower extremity)
2. Hemianesthesia3. Hemianopia (blindness of half the field of vision)
4. Eyes may deviate to the side of the lesion.
5. Aphasia if dominant hemisphere is involved
6. Occlusions of various branches of the middle cerebral artery may cause different findings
(involvement of the anterior division may cause expressive aphasia, and involvement of the
posterior branch may produce receptive aphasia).
B. Anterior cerebral artery
1. Hemiplegia (lower extremity more often than upper extremity)
2. Primitive reflexes (such as thumb sucking)
3. Urinary incontinence
4. Bilateral anterior infarction may cause behavioral changes and disturbance in memory.
C. Vertebral and basilar arteries
1. Ipsilateral cranial nerve findings
2. Contralateral (or bilateral) sensory and motor deficits
D. Deep penetrating branches of major cerebral arteries (lacunar infarction)
1. Most common: less than 5 mm in diameter
2. Associated with poorly controlled HTN or diabetes
3. Contralateral pure motor or sensory deficit
4. Ipsilateral ataxia with crural (pertaining to the leg or thigh) paresis
5. Dysarthria with clumsiness of the hand
6. Prognosis for recovery is high, with partial or complete resolution occurring over 4 to 6
III. Diagnostics/laboratory findings
A. CT scan of the head without contrast should be done initially.
1. Preferable to MRI in the acute stage to rule out cerebral hemorrhage when MRI may not
easily detect hemorrhage in the first 48 hours (especially when anticoagulation is considered),
when signs and symptoms cannot be explained by one lesion, when patient presents with
stroke on anticoagulation therapy, and to rule out abscess, tumor, and SDH
2. Appears as an area of decreased density
3. Lacunar infarcts appear as small, punched-out, hypodense areas.
4. Initial CT scan may be negative, and the infarct may not be visible for 2 to 3 days after its
B. Chest radiography
1. May reveal cardiomegaly or valvular calcification
2. Neoplasm may suggest metastasis rather than stroke as the cause of neurologic deficits.
C. CBC, sedimentation rate, blood glucose, VDRL, lipid profile, INR, PTT prior to
anticoagulation, blood urea nitrogen (BUN)/serum creatinine (Cr) to evaluate renal function
before contrast media may be given, homocysteine level, drug screen, and blood alcohol level
D. Electrocardiogram (ECG) (if unrevealing, may place patient on cardiac monitor/Holter
E. Blood cultures if endocarditis is suspected
F. Echocardiography
G. TEE to detect dysfunction of left atrium (thrombus)H. Carotid duplex ultrasonography
I. MRI/MRA: Diffusion-weighted MRI is more sensitive than conventional MRI in detecting
cerebral ischemia.
J. CT angiography
1. Can provide information regarding vascular anatomy with three-dimensional (3D)
reconstruction (requires the use of contact dye)
2. May allow for rapid evaluation and diagnosis in hospitals without MRI capability
K. Cerebral angiography continues to be gold standard for complete evaluation of intracranial
and extracranial vessels.
1. Injection with 99mTc-labeled agent
2. Multiple views of emission projection data
3. Essentially, a VQ scan of the brain
M. Lumbar puncture (LP)
1. Not always necessary but may be helpful if cause of stroke is uncertain
2. Obtain a CT scan first to rule out cerebral hemorrhage or any expanding mass that could
lead to herniation if LP is performed.
IV. Management
A. Blood pressure (BP) control
1. Acute lowering of systemic BP is not recommended because it may lead to further damage
in the ischemic penumbra, in which autoregulation may be defective, and may clinically
worsen the stroke.
2. Most patients with acute cerebral infarction have an elevated BP, which usually returns to
baseline within 48 hours without any special treatment.
3. BP control may be warranted, however, in the following conditions:
a. Systolic BP (SBP) exceeds 220 mmHg, and diastolic BP (DBP) exceeds 120 mmHg
(malignant hypertension).
b. Hypertensive encephalopathy is present.
c. Vital organs are compromised.
d. Aortic dissection
e. Symptomatic cardiac disease
f. Patient is receiving t-PA therapy. (Some experts recommend decreasing BP in those who
are receiving intravenous heparin therapy as well, although this is not universally
4. When indicated, BP should be lowered gradually to 170 to 180 mmHg systolic and 95 to
100 mmHg diastolic.
5. Sublingual nifedipine (Procardia) is inappropriate because of its precipitous lowering of
BP and possible worsening of a stroke.
6. Sodium nitroprusside (Nipride), nitroglycerin, and calcium channel blockers should be
avoided as well, particularly with large infarcts that may cause the brain to swell and herniate,
because these agents increase intracranial pressure.
7. Esmolol (Brevibloc), 5 g/500 ml intravenous fluid (IVF) titrated to desired BP;
maintenance dose should not exceed 200 mcg/kg/minute
8. Labetalol (Trandate), 20 mg intravenous (IV) push initially; additional doses of 40-80 mg
may be given every 10 minutes as needed, not to exceed 300 mg total dose, or 200 mg/250ml of solution begun at 2 mg/minute and titrated to desired response
9. Enalapril (enalaprilat) IV
B. Anticoagulation
1. Heparin does not reduce the severity of a stroke that has occurred but may prevent
recurrent cardioembolic strokes.
2. It may also be used in patients with stroke-in-evolution and in hypercoagulable states.
3. Heparin may increase the risk of transformation from ischemic stroke to hemorrhagic
stroke and therefore is not recommended for massive stroke.
4. The loading dose of heparin is 5000-10,000 units IV followed by a maintenance infusion
of 1000-2000 units/hour. PTT should be 1.5 times control.
5. Heparin followed by warfarin (5-15 mg/day PO) is indicated in suspected cerebral
embolism resulting from the following:
a. Mural thrombus
b. Mitral stenosis
c. Atrial fibrillation
6. CT scan may be necessary after 48 hours to determine whether any hemorrhaging has
7. Anticoagulation is absolutely contraindicated if CT scan or LP suggests cerebral
hemorrhage, tumor, abscess, SDH, or epidural hematoma.
8. Use cautiously in patients with a history of GI bleeding, bleeding tendencies, severe HTN,
or a large cerebral infarct.
9. May use after a completed stroke if embolization is determined to be the cause
C. Platelet therapy may be used with nonhemorrhagic stroke victims who are not candidates for
surgery or warfarin therapy.
1. ASA, 75-325 mg/day PO
a. ASA continues to be the least expensive and most widely used antiplatelet medication.
b. Recent evidence suggests that low-dose ASA resistance may occur, and that ASA may
not offer desired antiplatelet effect.
2. Ticlopidine (Ticlid), 250 mg twice daily
a. Has reported adverse effects such as agranulocytosis, TTP, and GI intolerance
b. Cost tends to be higher than that of other platelet therapies.
c. Necessitates blood monitoring every 2 weeks for the first 3 months of therapy
3. Clopidogrel (Plavix), 75 mg/day PO
a. Does not produce as many adverse effects as ticlodipine
b. Is prescribed in place of ticlodipine by many practitioners
4. Aggrenox (ASA, 25 mg immediate release, and dipyridamole, 200 mg extended release), 1
tablet twice daily (1 in the morning and 1 at night)
a. Recently approved for stroke prevention
b. Study has shown that this combination may reduce stroke by 22% compared with ASA
therapy alone.
D. Mannitol and/or furosemide (Lasix) can be used for cerebral edema that may occur on the
second or third day.
E . Corticosteroids have been used in an attempt to reduce vasogenic cerebral edema, but the
benefits are unclear.F. Tissue plasminogen activator (TPA) 0.9 mg/kg up to a maximum of 90 mg is now being
used, if appropriate conditions are met, as thrombolytic therapy for acute stroke when the
patient is brought in within 3 hours after the stroke. Such conditions include the following:
1. Availability of a physician with appropriate expertise to diagnose the stroke
2. 24-hour availability of CT scanning to assess for hemorrhage
3. Capability of facility to manage intracranial hemorrhage and other complications of
thrombolytic therapy
4. Patients must seek help early and have a well-defined onset of symptoms.
5. Patient's condition must be carefully examined for contraindications, such as these:
a. Previous and/or current hemorrhage
b. Previous stroke or head trauma within 3 months
c. Major surgery within 14 days
d. Urinary or gastrointestinal hemorrhage within 24 days
e. Seizure at stroke onset
f. Arterial puncture at noncompressible site within 7 days
g. Elevated PTT, PT (longer than 15 seconds)
h. Oral anticoagulants or heparin with elevated PTT within 48 hours
i. Serum glucose level less than 50 or greater than 400 mg/dl
j. SBP greater than 185 mmHg or DBP greater than 110 mmHg
G. Use of calcium channel blockers such as nimodipine (30 mg PO every 6 hours for 4 weeks)
is under study; may reduce deficit caused by cerebral ischemia and morbidity and mortality rates
of stroke.
H. Surgery, CEA may be indicated for those with high-grade extracranial carotid artery disease
(70%-99% stenosis) if not at high risk.
I. Rehabilitation should take a multidisciplinary approach.
J. Correct treatment depends on a correct diagnosis of stroke type; therefore, it is imperative that
diagnostic tests be completed quickly. A report from the National Institute of Neurological
Disorders and Stroke advocates the following goals, which are based on time of arrival:
1. Perform an initial emergency department evaluation within 10 minutes.
2. Notify the stroke team or neurologist within 15 minutes.
3. Start a CT scan within 25 minutes.
4. Obtain a CT scan interpretation within 45 minutes.
5. Administer thrombolytics, if appropriate, within 60 minutes.
6. Transfer the patient to an inpatient bed within 3 hours.
K. Emerging strategies
1. Intra-arterial (IA) t-PA
2. Combined IA and IV thrombolysis
a. According to 1999 Emergency Management of Stroke (EMS) Bridging Trial,
recanalization was better with the use of IV and IA t-PA versus placebo and IA t-PA.
3. Mechanical reperfusion
a. Clot dissolution with saline jets (Angiojet)
b. Clot dissolution with endovascular photoacoustic reperfusion (EPAR); a laser is used to
create a stress wave and then suction.
c. Ultrasound-assisted thrombolysisd. Thrombectomy
4. Neuroprotectants
a. Medications that protect the brain from secondary injury caused by stroke
b. Although only a few are approved for use by the FDA at this time, many are in clinical
c. Several different classes show promise for the future, including the following:
i. Calcium antagonists
ii. Glutamate antagonists
iii. Opiate antagonists
iv. Antioxidants
v. Apoptosis inhibitors, among many others
5. Modulation of the renin-angiotensin-aldosterone system (RAAS) has proved effective in
reducing recurrent cardiac events; experimental evidence has linked the RAAS to the
development and progression of cerebrovascular disease and suggests that it is a promising
target for the secondary prevention of stroke.
6. Another area of research involves experiments with vasodilators. Researchers hope that
vasodilators may aid in the rehabilitation of stroke victims by increasing blood flow to the
7. Gene therapy is also being investigated, but research is in the early stages.
I. Definition
A. Condition resulting from bleeding into the subarachnoid space or brain parenchyma
B. Accounts for approximately 14% of all cerebral infarctions
II. Etiology
1. Ruptured saccular aneurysm (85%)
2. Arteriovenous malformation (AVM) (8%)
3. Cryptogenic
1. Usually associated with HTN
2. May occur during activity
3. Much more likely to result in death or major disability than cerebral infarction or SAH
4. Predisposing factors
a. HTN
b. Use of anticoagulants or thrombolytics
c. Use of illicit street drugs (e.g., cocaine)
d. Heavy use of alcohol
e. Hematologic disorders
III. Clinical manifestations
1. Sudden headache of intense severity that radiates into the posterior neck region and is
worsened by neck and head movements
a. Grade I: Asymptomatic or slight headacheb. Grade II: Moderate to severe headache, stiff neck, no focal signs other than cranial nerve
c. Grade III: Drowsy, mild focal deficit
d. Grade IV: Stupor, hemiparesis
e. Grade V: Deep coma, decerebration
1. Elevation in BP, often to very high levels (90% of patients)
2. Headache (40%)
3. Vomiting is an important diagnostic sign, particularly if the bleed lies in the cerebral
hemisphere (49%).
4. Sudden onset of neurologic deficits that can rapidly progress to coma or death, depending
on area involved (50%)
5. Putamen hemorrhage
a. Eyes deviate conjugately to the side of the lesion.
b. PERRL (pupils equal, round, reactive to light)
c. Contralateral hemiplegia
d. Hemisensory disturbance
6. Thalamic hemorrhage
a. Downward deviation of the eyes, looking at the nose
b. Pupils pinpoint with a positive reaction
c. Coma is common.
d. Flaccid quadriplegia
7. Cerebellar hemorrhage
a. Ipsilateral lateral conjugate gaze paresis
c. Inability to stand or walk
d. Facial weakness
e. Ataxia of gait, limbs, or trunk
f. Vertigo and dysarthria
IV. Diagnostics/laboratory findings
1. CT scan of the head will assist in differentiating between an ischemic and a hemorrhagic
stroke in 75% of patients.
a. Scan may be normal if obtained 48 hours after SAH, or if the bleed is small.
b. Aneurysm itself may be seen in 50% of cases when contrast material is given, depending
on site and size and CT scan quality and whether fine cuts were obtained.
2. LP if CT scan is unavailable or negative and suspicion is high
a. Contraindicated in any expanding mass because it may cause herniation
b. A funduscopic examination must be performed prior to the procedure to rule out
c. Cerebrospinal fluid (CSF) will be uniformly grossly bloody, although this may not occur
3 6 3if the bleed is small. In a true SAH, LP reveals 10 to 10 RBCs/mm .
d. Opening pressure is elevated.e. Xanthochromia is present.
i. Yellowish discoloration of CSF produced by blood breakdown products
ii. Xanthochromia appears no earlier than 2 to 4 hours after bleeding occurs.
iii. Cerebral angiography
(1) Used to determine source of bleed, presence of an aneurysm, and best source of
treatment (medical or surgical)
(2) May demonstrate vasospasm
(3) Should be performed after the patient has been stabilized
3. CT angiography is beneficial in patients who are too unstable to undergo cerebral
angiography or in an emergent setting prior to surgical evacuation of clot.
1. CT scan without contrast
a. To confirm a bleed and determine the size and site
b. May reveal structural abnormalities such as aneurysms, AVMs, or brain tumors that may
have caused the bleed, as well as complications such as herniation, intraventricular
hemorrhage, or hydrocephalus
2. Cerebral angiography may be performed.
a. To determine whether the source is an aneurysm or an AVM
b. Should be considered for all patients without a clear cause of hemorrhage who are
surgical candidates, particularly young, normotensive patients who are clinically stable
c. Timing depends on the patient's clinical state and the neurosurgeon's judgment about the
urgency of surgery, if needed.
3 . MRI and MRA may be useful for detecting structural abnormalities (i.e., AVMs and
aneurysms). Gradient recalled echo MRI (GRE MRI) may be useful in detecting hemorrhage.
4. CT angiography may be used to allow noninvasive imaging of large and medium-sized
5. CBC, platelet count
6. Electrolytes
7. ECG
8. Chest x-ray
9. Bleeding time
10. PT/PTT
11. Liver enzymes
12. Renal studies
13. LP is contraindicated: may cause herniation in the presence of a large hematoma
V. Management
1. Strict bed rest in a quiet, stress-free environment
2. Cardiac monitoring
3. Treat symptomatically for headache or anxiety (acetaminophen [Tylenol] and codeine).
4. Have the patient avoid all forms of straining and exertion.
5. Order stool softeners and laxatives (docusate [Colace], 1-2 tablets PO 4 times a day).
6. Phenobarbital (Luminal), 30-60 mg PO 3 times daily7. Maintain SBP at 140 to 160 mmHg.
8. In severe hypertension, lower BP gradually rather than in an extreme manner, but DBP
should not be lower than 100 mmHg. Modest hypotension in these patients can produce
global cerebral ischemia.
9. Cerebral edema can be reduced with mannitol and/or furosemide (Lasix).
10. Cerebral vasospasms
a. Vasospasms occur in approximately 30% of patients.
b. Symptoms, which include headache, ischemia, and increased intracranial pressure (ICP),
may or may not be present.
c. Vasospasm commonly occurs 4 to 14 days after bleeding and is associated with the
presence of a thick clot in the subarachnoid space.
d. Calcium channel blockers (nimodipine) may be used to treat cerebral blood vessel spasm
after SAH from ruptured aneurysms (60 mg every 4 hours for 3 weeks).
e. If symptomatic vasospasm occurs, the patient is usually treated with IV fluid loading
(hypervolemic hemodilution) and induced hypertension.
i. Aim for a hematocrit of about 30%.
i i . Monitor cardiac output, pulmonary wedge pressure, central venous pressure,
pulmonary arterial pressure, and systemic blood pressure.
iii. The goal is to optimize the low shear rate viscosity of the whole blood and to ensure
cerebral perfusion pressure that is adequate to restore regional cerebral blood flow in
perfusion areas beyond the vasospastic vessels.
f. Treatment is less risky if the aneurysm has been clipped.
g. Angioplasty or papaverine may be used for vasospasms resistant to the preceding
h. A new treatment currently under study for refractory cerebral spasm is intrathecally
delivered sodium nitroprusside.
i. 1-4 mg/ml, admixed with the patient's CSF (draw off 5-10 ml from the catheter before
administration, and mix medication with a portion).
ii. Dosing in patients with established vasospasm varies and is intermittent in accordance
with the patient's clinical response. End points of the intervention may include
angiographic reversal of vasoconstriction, failure of treatment to alleviate
vasoconstriction within 30 minutes, and adverse effects (e.g., systemic hypotension,
intracranial hypertension).
iii. Recommended dosing for patients who are treated prophylactically is 4 mg/ml, 1-2
ml given in two divided doses via ventriculostomy.
i. Rebleeding
i. Rebleeding is unpredictable but often occurs between days 2 and 19 after initial
rupture and is thought to originate from fibrinolysis of the clot at the site of the ruptured
ii. 40% of patients rebleed, and approximately half of these rebleeds are fatal; therefore,
efforts to seal off an aneurysm should be made as soon as possible.
iii. Neurologic deterioration is generally abrupt.
iv. A repeat CT scan, and occasionally a repeat LP, is needed to confirm rebleeding.
v. Research is under way on the use of antifibrinolytic therapy in combination with
antiischemic medications (calcium channel blockers), to determine whether this treatment
reduces the rate of rebleeds and results in decreased morbidity and mortality.
j. Surgery may be indicated for aneurysm, depending on the size of the aneurysm, thepatient's age and clinical condition, and the neurosurgeon's opinion.
i. Because the brain is acutely swollen and ischemic, early surgery may trigger more
severe vasospasm than may occur without surgery.
ii. One approach is to take grade I and II patients immediately to angiography and surgery
to evacuate the clot and clip the aneurysm as soon as possible.
iii. In the case of patients with grade III or IV aneurysm, whose prognosis is worse, the
surgeon should wait until they reach grade I or II, if they are to be operated on at all.
k. Coil embolization for ruptured aneurysm: performed by trained radiologist. Nonsurgical
procedure involving the threading of tiny coils through a microcatheter into the aneurysm.
May be used when bleeding is in a difficult to reach area of the brain.
1. Initial management should be directed toward the basic airway, breathing, and circulation
and toward focal neurologic deficits.
2. Intubation is indicated for insufficient ventilation, for hypoxia (partial pressure of oxygen
[PO ] less than 60 mmHg, or partial pressure of carbon dioxide [PCO ] greater than 502 2
mmHg), and for obvious risk of aspiration.
3. Oxygen should be administered to all patients with possible ICH.
4. Control severe HTN.
a. Should not exceed 20% reduction
b. Should be achieved through short-acting agents (sodium nitroprusside 50 mg/250 ml,
dextrose 5% in water [D W] titrated to maintain BP)5
c. Goal is to decrease the risk of ongoing bleeding from ruptured small arteries and
d. Overaggressive treatment of HTN may decrease cerebral perfusion pressure (CPP) and
therefore worsen brain injury, particularly in the setting of increased intracranial pressure.
e. Maintaining a mean arterial blood pressure (MAP) of 130 mmHg is recommended.
5. CPP (MAP − ICP) should be kept above 70 mmHg.
6. Some suggested medications for elevated BP include the following:
a. Labetalol (Trandate), 5-100 mg/hour IV by intermittent bolus dose every 10 minutes of
10-40 mg or continuous drip (2-8 mg/minute), not to exceed 300 mg total for intermittent
and continuous doses. Avoid in patients with asthma.
b. Esmolol (Brevibloc), 500 mcg/kg as a load (IV); maintenance, 50-200 mcg/kg/minute
c. Sodium nitroprusside, 0.5-10 mcg/kg/minute IV
d. Hydralazine (Apresoline), 10-20 mg every 4 to 6 hours IV
e. Enalapril, 0.625-1.2 mg every 6 hours as needed
7. Guidelines for antihypertensive therapy in patients with acute stroke may be used within
the first few hours of ICH.
a. If SBP is above 230 mmHg or DBP is above 140 mmHg on two readings taken 5
minutes apart, institute nitroprusside.
b. If SBP is 180 to 230 mmHg, DBP is 105 to 140 mmHg, or MAP exceeds 130 mmHg
on two readings 20 minutes apart, institute IV labetalol, esmolol, or enalapril, or other
small doses of easily titratable IV medications such as diltiazem, lisinopril, or verapamil.
c. If SBP is less than 180 mmHg and DBP is less than 105 mmHg, defer antihypertensive
d. During the immediate postoperative period, an MAP greater than 110 mmHg should be
avoided.e. If BP falls to less than 90 mmHg, pressors should be given (dopamine, 2-20
mcg/kg/minute; phenylephrine [epinephrine], 2-10 mcg/kg/minute; or norepinephrine
[Levophed], 0.05-0.2 mcg/kg/minute).
8. Maintain ICP at less than 20 mmHg and CPP at greater than 70 mmHg.
a. Mannitol for cerebral edema (0.25-0.5 g/kg of a 20% solution) given IV every 4 hours.
Because of its rebound phenomenon, mannitol is recommended for 5 days or less. To
maintain the osmotic gradient, furosemide (Lasix) (10 mg every 2-8 hours) may be
administered with mannitol. Serum osmolality should be measured twice daily for those
receiving osmotherapy and should be kept at no greater than 310 mOsm/L.
b. Ventricular drain for secondary hydrocephalus
i. Use should not exceed 7 days because of possible infectious complications.
ii. IV antibiotic prophylaxis is recommended.
c. If hyperventilation is used, PCO should be maintained at 30 to 35 mmHg.2
d. Steroids are not recommended.
9. Supportive measures
a. IVFs
i. Excessive administration can worsen cerebral edema.
ii. Goal is euvolemia.
iii. Fluid balance is calculated by measuring daily urine production and adding 500 ml
for insensible losses plus 300 ml per degree in febrile patients.
b. Phenytoin (Dilantin) if seizure activity is noted
c. Nutritional support
d. Maintain body temperature with acetaminophen (Tylenol) 650 mg for temperature
greater than 101.3° F (38.5° C).
e. Physical therapy
f. Skin care/turning
10. Surgery
a. Indicated for patients with cerebellar hemorrhage
b. Indicated for those with surgically accessible cerebral hematoma that shows signs of
temporal herniation
GW Albers, LR Caplan, JD Easton, et al., Transient ischemic attack—proposal for a new definition,
N Engl J Med 347 (2002) 1713–1716.
MJ Alberts, Diagnosis and treatment of ischemic stroke, Am J Med 106 (1999) 211–221.
A Algra, LL De Schryver, J van Gijn, et al., Oral anticoagulants versus antiplatelet therapy for
preventing further vascular events after transient ischemic attack or minor stroke of presumed
arterial origin, Stroke 34 (2003) 234–235.
D Bergman, M Soeding, R Bernstein, et al., Research shows aspirin therapy didn't work in almost
half of stroke patients studied,
Accessed July 21, 2004..
JP Broderick, M William, Feinberg lecture: stroke therapy in the year 2025: burden, breakthrough,
and barriers to progress, Stroke 35 (2004) 205–211.
JP Broderick, HP Adams Jr, W Barsan, et al., Guidelines for the management of spontaneous
intracranial hemorrhage: a statement for healthcare professionals from a special writing group
of the Stroke Council, American Heart Association, Stroke 30 (1999) 905–915.BM Demaerschalk, Diagnosis and management of stroke (brain attack), Semin Neurol 23 (2003)
HM Fernandes, B Gregson, S Siddique, et al., Surgery in intracerebral hemorrhage, Stroke 31 (2000)
FF Ferri, Practical guide to the care of the medical patient. ed 6 (2004) Mosby, St. Louis .
M Fisher, J Bogousslavsky, Further evolution toward effective therapy for acute ischemic stroke,
JAMA 279 (1998) 1298–1303.
JR Fulgham, Management of acute ischemic stroke, Mayo Clin Proc 79 (2004) 1459–1469.
J Gijn, GJE Rinkel, Subarachnoid hemorrhage: diagnosis, causes and management, Brain 124
(2001) 249–278.
S Gilman, Medical progress: imaging the brain: first of two parts, N Engl J Med 338 (1998)
D Harris, Recent developments in hemorrhagic stroke, Geriatr Med 35 (2005) 43–44; 46-48.
J Hinkle, An update on transient ischemic attacks, J Neurosci Nurs 37 (2005) 243–248.
SH Horowitz, Thrombolytic therapy in acute stroke: neurologists, get off your hands!, Arch Neurol
55 (1998) 155–157.
SE Kasner, More than one way to lyse a clot, Stroke 35 (2004) 911–912.
T Kosty, Cerebral vasospasm after subarachnoid hemorrhage: an update, Crit Care Nurs Q 28
(2005) 122–134.
A Luisi, AL Hume, Thrombolysis in acute ischemic stroke, J Am Board Fam Pract 11 (1998)
EM Manno, Emerging medical and surgical management strategies in the evaluation and treatment of
intracerebral hemorrhage, Mayo Clin Proc 80 (2005) 420–433.
H McNaughton, Management problems of spontaneous ICH, Hosp Med 66 (2005) 229–234.
In: (Editors: SJ McPhee, MA Papadakis, LM Tierney) Current medical diagnosis and treatment ed
46 (2007) McGraw Hill/Appleton & Lange, New York.
Merck & Co., Inc, Hemorrhagic stroke, http://merck.com/mmhe/sec06/ch086/ch086d.html; Accessed
July 23, 2007..
National Institute of Neurological Disorders and Stroke (NINDS), Stroke hope through research,
www.ninds.nih.gov/disorders/stroke/detailstroke.html; Accessed July 23, 2007..
N Pouratian, NF Kassell, AS Dumont, Update on management of intracerebral hemorrhage,
Neurosurg Focus 15 (2003); article 3.
RE Rakel, Saunders manual of medical practice. ed 2 (2000) WB Saunders, Philadelphia .
Y Roos, M Vermeulen, G Rinkel, et al., Systemic review of antifibrinolytic treatment in aneurysmal
subarachnoid haemorrhage, J Neurol Neurosurg Psychiatry 65 (1998) 942–943.
S Schwarz, S Schwab, M Bertram, et al., Effects of hypertonic saline hydroxyethyl starch solution
and mannitol in patients with increased intracranial pressure after stroke, Stroke 29 (1998)
SI Sokol, EL Portnay, JP Curtis, et al., Modulation of the renin-angiotensin-aldosterone system for
the secondary prevention of stroke, Neurology 63 (2004) 208–213.
NJ Solenski, Transient ischemic attacks. Part I: diagnosis and evaluation, Am Fam Physician 69
(2004) 1665–1674.
NJ Solenski, Transient ischemic attacks. Part II: treatment, Am Fam Physician 69 (2004)
S Warach, CS Kidwell, The redefinition of TIA: the uses and limitations of DWI in acute ischemic
cerebrovascular syndromes, Neurology 62 (2004) 359–360.
EM Wilson, Strokes, CVAs, or brain attacks: by any name they need quick attention, J Emerg Nurs
24 (1998) 251–252.
D Woo, Ischemic versus hemorrhagic stroke: rating the risk factors, J Crit Illness 18 (2003)
194–195.OO Zaidat, MJ Alexander, JI Suarez, et al., Early carotid artery stenting and angioplasty in patients
with acute ischemic stroke, Neurosurgery 55 (2004) 1237–1243.
RM Zweifler, Management of acute stroke, Southern Med J 96 (2003) 380–385.CHAPTER 2. Structural Abnormalities
Aneurysm, 442.9
Hydrocephalus, 331.4
I. Definition
A. Abnormal dilatation of an arterial wall in which the intima bulges outward
B. Usually caused by abnormal weakening
C. Usually, a sudden increase in systolic blood pressure caused by events such as straining or
sexual intercourse, which may precipitate a rupture
II. Types
A. Berry (saccular)—congenital aneurysm of a cerebral vessel
1. Tends to occur at arterial bifurcations
2. More common in adults
3. Frequently multiple
4. Usually asymptomatic
5. May be associated with polycystic kidney disease or coarctation of the aorta
B. Fusiform—aneurysm that is tapered at both ends and spindle-shaped; all walls of the blood
vessel dilate more or less equally, creating tubular swelling
C. Mycotic—caused by or infected by microorganisms (bacterial)
D. Traumatic
III. Location
A. Most intracranial aneurysms (80%-85%) are located in the anterior circulation.
1. Most commonly at the junction of the internal carotid artery and the posterior
communicating artery
2. At the anterior communicating artery complex
3. At the trifurcation of the middle cerebral artery
B. Aneurysms of the posterior circulation are most frequently located at the bifurcation of the
basilar artery or at the junction of a vertebral artery and the ipsilateral posterior inferior
cerebellar artery.
C. Multiple intracranial aneurysms, usually two or three in number, are found in 20% to 30%
of patients.
D. Rupture results in the following:
1. Subarachnoid hemorrhage (SAH)—most common (see Chapter 1)
2. Intracerebral hemorrhage (ICH)—less common (see Chapter 1)
3. Subdural hematoma (SDH)—rare (see Chapter 4)
IV. Risk factors
A. Evidence supports the association of intracranial aneurysm with heritable connective tissue
disorders (e.g., polycystic kidney disease, Ehlers-Danlos syndrome type IV, neurofibromatosis
type I, Marfan's syndrome) and their familial occurrence.
B. 7% to 20% of patients with aneurysmal SAH have a first- or second-degree relative with aconfirmed intracranial aneurysm.
C. Cigarette smoking is an environmental factor.
1. Risk of an aneurysmal SAH is about 3 to 10 times higher among smokers.
2. Risk increases with the number of cigarettes smoked.
3. Smoking decreases the effectiveness of alpha -antitrypsin, the main inhibitor of proteolytic1
enzymes (proteases) such as elactase; the imbalance between proteases in smokers may result
in the degradation of a variety of connective tissues, including the arterial wall.
D. Risk is higher among women than among men after age 50.
1. Suggests a role for hormonal factors
2. Premenopausal women have a low risk of aneurysmal SAH.
3. Postmenopausal women have a relatively high risk.
4. Postmenopausal women receiving hormone replacement therapy have an intermediate risk.
E. A moderate to high level of alcohol consumption is an independent risk factor for
aneurysmal SAH. Recent heavy use of alcohol in particular appears to increase the risk of SAH.
V. Clinical manifestations
A. Most aneurysms are asymptomatic until they rupture, at which time SAH results (see Signs
and Symptoms of SAH in Chapter 1).
B. Some focal neurologic deficits may be related to compression of adjacent structures.
C. Small amounts of blood from the aneurysm (“warning leaks”) may precede the major
hemorrhage by a few hours or days. These may cause the patient to have headaches, nausea, and
neck stiffness.
D. Ophthalmologic examination may reveal unilateral or bilateral subhyaloid hemorrhages in
approximately one fourth of patients with aneurysmal SAH. These hemorrhages are venous in
origin, are located between the retina and the vitreous membrane, and are convex at the bottom
and flat on the top.
E. Some aneurysms have a mass effect, causing the patient to become symptomatic. These
aneurysms are generally large or giant (25 mm or larger).
1. The most common symptom of mass effect is headache.
2. The most common sign is palsy of cranial nerve III (pupils).
3. Brain stem dysfunction, visual field defects, trigeminal neuralgia, cavernous sinus
syndrome, seizures, and hypothalamic-pituitary dysfunction may also occur, depending on the
location of the aneurysm.
4. These aneurysms carry a high risk of rupture (approximately 6%/year).
VI. Diagnostics
A. CT scan or magnetic resonance angiography can be performed to obtain a baseline value for
ventricular size and to rule out infarct/hemorrhage. These studies are noninvasive and carry a
lower complication rate than is associated with conventional catheter angiography.
1. CT scans are sensitive in detecting acute hemorrhage, and they show the presence of SAH
in 90% to 95% of patients who undergo scanning within the first 24 hours after hemorrhage.
2. The sensitivity of CT scanning, however, decreases to 80% at 3 days after hemorrhage,
70% at 5 days, 50% at 1 week, and 30% at 2 weeks, because blood is cleared rapidly from
the subarachnoid space.
3. CT scans are also useful in detecting any associated ICH or hydrocephalus, and the
distribution of blood may offer important clues to the location of the ruptured aneurysm.
B. Cerebral angiography can be ordered to discern the size, shape, location, and number ofaneurysms, as well as the occurrence of arterial spasm. The risk of permanent neurologic
complications is lower than was previously recognized, and cerebral angiography has a high
level of diagnostic accuracy. Angiography provides superior spatial resolution and lacks the
flow-related artifacts that may affect magnetic resonance angiography.
C. MRI angiography does not require contrast material and can be used to detect intracranial
aneurysms as small as 2 to 3 mm in diameter.
D. Standard MRI is the best method for detecting the presence of a thrombus within the
aneurysmal sac.
E. Since the late 1990s, helical CT angiography has been used to detect intracranial aneurysms,
and preliminary reports indicate that the detection rate with this technique is similar to that with
MRI angiography. Helical CT angiography has the ability to demonstrate the relation of the
aneurysm to bony structures of the skull base; it can be performed safely in patients who have
been treated with ferromagnetic clips, which are a contraindication to MRI angiography.
F. Lumbar puncture: If CT scan is negative, but a strong clinical suspicion of SAH persists, then
lumbar puncture should be performed. Herniation may occur if intracranial pressure is increased
(see Chapter 1).
G. Elevations in WBC count and sedimentation rate are indicators of a ruptured aneurysm.
VII. Management
A. Surgery
1. Choosing surgery for patients with an unruptured intracranial aneurysm involves weighing
the risk of intracranial rupture against the risks associated with brain surgery.
2. Size, location, and previous SAH are the most important features for predicting
aneurysmal rupture.
a. As was noted in the Cooperative Study of Intracranial Aneurysms and Subarachnoid
Hemorrhage, which involved 6038 ruptured aneurysms, the critical size for rupture is 7 to
10 mm. Many studies support the critical size as larger than 10 mm.
b. Major compressive symptoms (e.g., headache, neurologic signs and symptoms) should
lead to consideration of surgery.
c. Coexisting medical problems or factors that favor the need for surgery must be
considered (e.g., hypertension, poorly controlled hypertension) to prevent the risk of
3. Early (within 72 hours of the bleed) surgery is desirable for eliminating the risk of rebleed
and for allowing aggressive treatment for vasospasm, should it occur.
4. Late: after 7 days post bleed
5. Methods
a. Clipping
b. Wrapping
c. Embolization
d. Endovascular treatment is emerging. Soft metallic coils are inserted within the lumen of
the aneurysm. Goal is complete obliteration of the aneurysmal sac.
B. Medical management if surgery is not feasible, as outlined for SAH in Chapter 1, is
continued for about 6 weeks.
VIII. Possible complications
A. Vasospasm
1. Occurs several days to 3 to 4 weeks after treatment
2. Calcium channel blockers (nimodipine 60 mg every 4 hours for 21 days) have been shownto reduce the incidence of ischemic deficit from cerebral spasms.
3. Intravascular volume expansion, induced hypertension, intra-arterial papaverine infusion,
or transluminal balloon angioplasty of involved cranial vessels may also be used after the
aneurysm has been obliterated.
B. Rebleeding
1. Greatest within a few days of the first hemorrhage
2. Approximately 20% of patients will have further bleeding within 2 weeks, and 40% within
6 months.
3. Prevent hypertensive episodes (see Chapter 1)
4. Antifibrinolytic agents—Aminocaproic acid used during the first 2 weeks after hemorrhage
has been shown to reduce the risk of rebleeding. This practice is controversial, however,
because it has been associated with an increase in cerebral ischemia, and because no
significant decrease has been noted in mortality rate or in degree of disability among
C. Hydrocephalus—See Communicating Hydrocephalus.
1. Caused by interference with the flow of CSF
2. Generally occurs after at least 2 weeks
3. May be relieved by shunting
D. Seizures
E. Increased intracranial pressure (ICP)
I. Definition
A. Condition in which an excessive amount of CSF accumulates within the cerebral ventricles.
The human brain makes approximately 500 ml of CSF per day, most of which is generated by
the choroid plexus within the ventricular system. CSF circulates around the brain and spinal
cord and is reabsorbed in the venous system.
B. Hydrocephalus is a common neurosurgical problem that leads to changes in cerebral blood
flow caused by displacement, deformation, stretching, or decrease in the caliber of cerebral
vessels. Change in the vessels causes a change in vascular resistance and in cerebral perfusion
pressure, which is important for cerebral microcirculation.
C. Normal pressure hydrocephalus is an unusual cause of dementia; it occurs as a late
complication of intracerebral infection or SAH. CSF pressure in some cases may not be
elevated, but it is almost always above 100 mm H O and is usually at the upper normal limit.2
The syndrome develops subacutely over a few weeks; in some patients, no predisposing reason
is identified.
II. Etiology
A. Oversecretion/overproduction of CSF
B. Obstruction of CSF (lesions or tumors)
C. Impaired absorption
D. Normal pressure hydrocephalus may follow head injury, SAH, or meningoencephalitis.
III. Classification
A. Communicating
1. Ventricles are patent; obstruction occurs beyond the fourth ventricle.
2. Caused by impaired absorption or overproduction3. Usually occurs 4 to 20 days after aneurysmal rupture, although it may occur at any time
B. Noncommunicating
1. Obstruction occurs within or next to the ventricular system, preventing CSF made in the
lateral and third ventricles from circulating normally; thus, this fluid no longer communicates
with the subarachnoid space.
2. Related to lesions or tumors
IV. Clinical manifestations (adults)
A. Normal pressure hydrocephalus
1. Lethargy and mental failure
2. Gait disorder
3. Incontinence
4. Frequent falls and failure in the pursuit of usual activities
5. Moderate dementia
6. Language may be affected.
7. Abulic (slow to respond) but, if given time, often responds with correct answers to
8. Slow EEG
9. Enlarged ventricles
B. Posttraumatic event
1. Progressive enlargement of ventricles
2. Gait disturbances
3. Memory difficulty
4. Urinary incontinence
C. Nausea and vomiting may occur.
D. Choked discs may be found.
E. Atrophy of the optic nerve
V. Management
A. Acute: intraventricular catheter
B. Chronic: ventricular shunt
C. Endoscopic third ventriculostomy (Mixter's surgery) has been used in noncommunicating
hydrocephalus to enable the surgeon to control the condition without the need for ventricular
shunting and without long-term complications associated with shunts. The advantage of
endoscopic surgery is that, when feasible, it can be performed with minimal disruption of neural
tissue, thus frequently allowing patients to become mobilized rapidly, resulting in shorter
hospitalizations and reduced costs.
I. Definition
A. Consist of primary neoplasms (originating in the brain) or secondary neoplasms (originating
from sites other than the brain, such as the lung, the breast, the genitourinary tract, and the
gastrointestinal tract) located within the intracranial vault
B. Glioblastoma multiforme is the most common primary tumor, followed by meningioma and
C. The cause is unknown; however, genes and viruses may be associated with these lesions.II. Types and characteristics
See Table 2-1 for a description of tumor types and characteristics.
TABLE 2-1 Tumor types and characteristics
Adapted from Aminoff MJ: Nervous system. In McPhee SJ, Papadakis MA, Tierney LM, editors:
Current medical diagnosis and treatment, ed 46, New York, 2007, McGraw Hill/Appleton & Lange,
with permission.
© McGraw Hill/Appleton & Lange, with permission2007
Treatment andTumor Clinical features
Course is rapidly
progressive, with poor
Commonly, nonspecific and complaints increased prognosis. Total surgical
intracranial pressure. As the tumor grows, focal deficits removal is usually not
develop. possible, and response
to radiation therapy is
Prognosis is variable.
By the time of diagnosis,
Glioma whose presentation is similar to that of
total excision is usually
glioblastoma multiforme, but its course is more
impossible; tumor often
Astrocytoma protracted, often extending over several years.
is not radiosensitive. In
Cerebellar astrocytoma, especially in children, may have
cerebellar astrocytoma,
a more benign course.
total surgical removal is
often possible.
Glioma seen most frequently in children. Generally Treatment consists of
arises from roof of fourth ventricle and leads to surgery combined with
increased intracranial pressure accompanied by brain radiation therapy and
stem and cerebellar signs. May seed subarachnoid space. chemotherapy.
Glioma arising from the ependyma of a ventricle, Tumor is not
especially the fourth ventricle; leads early to signs of radiosensitive and is
increased intracranial pressure. Arises also from central best treated surgically if
canal of spinal cord. possible.
Slow-growing glioma. Usually arises in cerebral Treatment is surgical
Oligodendroglioma hemisphere in adults. Calcification may be visible on and is usually
skull x-ray. successful.
Tumor is inoperable;
Occurs during childhood with cranial nerve palsies and treatment is by
Brain stem glioma then with long-tract signs in the limbs. Signs of increased irradiation and shunt for
intracranial pressure occur late. increased intracranial
Presents with disequilibrium, ataxia of trunk or limbs,
Cerebellar and signs of increased intracranial pressure. Sometimes
Treatment is surgical.
hemangioblastoma familial. May be associated with retinal and spinal
vascular lesions, polycythemia, and hypernephromas.
decompression by
shunting is followed by
Manifests with increased intracranial pressure; surgical approach to
sometimes is associated with impaired upward gaze tumor; irradiation is
Pineal tumor
(Parinaud's syndrome) and other deficits indicative of indicated if tumor is
midbrain lesion. malignant. Prognosis
depends on
histopathologic findings
and extent of tumor.
Originates from remnants of Rathke's pouch above theTreatment is surgical,sella, depressing the optic chiasm. May occur at any age
Craniopharyngioma but usually in childhood, with endocrine dysfunction and but total removal may
bitemporal field deficits. not be possible.
Ipsilateral hearing loss is most common initial symptom. Treatment is excision by
Subsequent symptoms may include tinnitus, headache, translabyrinthine
vertigo, facial weakness or numbness, and long-tract surgery, craniectomy, orAcoustic neuroma
signs. (May be familial and bilateral when related to a combined approach.
neurofibromatosis.) Most sensitive screening tests are Outcome is usually
MRI and brain stem auditory evoked potential. good.
Originates from the dura mater or arachnoid; compresses
rather than invades adjacent neural structures. Treatment is surgical.
Increasingly common with advancing age. Tumor size Tumor may recur if
varies greatly. Symptoms vary with tumor site (e.g., removal is incomplete.
Meningioma unilateral exophthalmos [sphenoidal ridge], anosmia, Patients may undergo
optic nerve compression [olfactory groove]). Tumor is radiation if removal is
usually benign and is readily detected by CT scanning; incomplete, to decrease
may lead to calcification and bone erosion visible on risk of recurrence.
plain x-rays of skull.
Treatment is by whole
Associated with acquired immunodeficiency syndrome
brain irradiation;
(AIDS) and other immunodeficient states. Presentation
Primary cerebral chemotherapy may have
may occur with focal deficits or with disturbances of
lymphoma an adjunctive role.
cognition and consciousness. May be indistinguishable
Prognosis depends on
from cerebral toxoplasmosis.
CD4 count at diagnosis.
III. Clinical manifestations
A. Vary, depending on the type, location, and growth of the tumor. Most symptoms do not
develop until the tumor is well advanced.
B. Headache
C. Nausea and vomiting; vomiting may not be preceded by nausea
D. Weakness
E. Hemiparesis
F. Sensory disturbances
G. Irritability, emotional lability, forgetfulness, drowsiness, lethargy
H. Impaired gait
I. Aphasia
J. Agraphia
K. Papilledema (10%)
L. Visual disturbances
1. Amaurosis fugax (temporary blindness)
2. Diplopia
3. Diminished visual acuity
M. Generalized or focal seizure activity (30%)
IV. Diagnostics
A. MRI is the procedure of choice for imaging all types of brain tumors because of its high
sensitivity, its capacity to delineate small tumors in sites near bone, its sensitivity to tissue
edema, and its inherent multiplanar capability that allows accurate localization of tumors and
identification of their relation to normal structures.B. CT scan may be useful for screening patients with known cancers elsewhere in the body and
patients with atypical headache. Contrast medium may be needed. If CT scan is negative but
suspicion is strong, an MRI should be performed. CT scan is effective for following the
progression of a diagnosed tumor.
C. Cerebral angiography can facilitate assessment of the vascularity of lesions and/or their
proximity to blood vessels.
D. EEG can detect the presence and location of seizure activity.
E. Open brain biopsy (craniotomy) or CT- or MRI-directed stereotactic needle biopsy provides a
definitive diagnosis.
F. Metastatic workup is necessary.
1. Chest x-ray
2. Mammogram
3. Bone scan
4. Prostate examination
5. Chest/abdominal/pelvic CT
V. Management
A. Chemotherapy, depending on the type and stage of tumor. Carmustine (BCNU), lomustine
(CCNU), cisplatin, and procarbazine are the agents most commonly used for malignant glioma
in adults.
B. Radiation therapy, depending on the type of tumor. Malignant gliomas are not radiosensitive;
however, radiation increases the survival rate in affected patients.
C. Corticosteroids
1. Dexamethasone (Decadron)
a. Standard dose at initiation of therapy is 4-6 mg IV/PO 4 times a day.
b. Monitor for adverse effects.
c. Taper slowly, and discontinue if possible.
d. Patients with incompletely treated tumors may not tolerate the decrease in dosage (e.g.,
they continue to show neurologic deterioration/cerebral edema) and therefore may require
long-term steroid usage during their last months of life.
e. Prescribe a concurrent H blocker to prevent gastric irritability associated with steroid2
use: ranitidine (Zantac), 150 mg PO twice daily; cimetidine (Tagamet), 200 mg PO twice
daily; or famotidine (Pepcid), 20 mg PO twice daily.
2. Methylprednisolone (Solu-Medrol), 120 to 200 mg IV in 4 to 6 divided doses to reduce
tumor-associated edema
D. For patients with severe cerebral edema, or in situations where intracranial pressure becomes
life threatening, an osmotic diuretic may be necessary. Mannitol (Osmitrol) in the usual dose of
1 g/kg of a 20% solution IV over 3 to 5 minutes can reduce intracranial pressure.
E . In patients with recurrent seizures caused by tumor location and/or edema, anticonvulsants
may be necessary. The agent of choice for many practitioners is phenytoin (Dilantin), 1 g IV or
PO as a loading dose, followed by 300 mg/day in divided doses as a maintenance dose.
F. Brachytherapy (the stereotactic implantation of interstitial radionuclide sources [wafer]) may
have a positive effect on survival in patients with glioblastoma.
G. The modified linear accelerator used with stereotactic guidance, the gamma knife, and the
proton beam are other noninvasive stereotactic radiosurgical methods that have produced some
successful results.H. If obstructive hydrocephalus is present, surgical shunting can produce dramatic benefit.
E Bohan, Surgical management of patients with primary brain tumors, Semin Oncol Nurs 20 (2004)
C Borkowski-Benoit, Neurological problems, In: (Editor: P Logan) Principles of practice for the
acute care nurse practitioner (1999) Appleton & Lange, Stamford, Conn.
JM Clochesy, C Breu, B Dossey, AACN handbook of critical care nursing. (1997) Appleton &
Lange, Stamford, Conn .
O Devinsky, E Feldmann, HJ Weinreb, et al., The resident's neurology book. (1997) FA Davis,
Philadelphia .
FF Ferri, Practical guide to the care of the medical patient. ed 6 (2004) Mosby, St. Louis .
M Gerosa, A Nicolato, RP Foroni, The role of gamma knife radiosurgery in the treatment of primary
and metastatic brain tumors, Curr Opin Oncol 15 (2003) 188–196.
S Gilman, Medical progress: imaging the brain: first of two parts, N Engl J Med 338 (1998)
S Gilman, Medical progress: imaging the brain: second of two parts, N Engl J Med 338 (1998)
LM Hector Dunphy, Management guidelines for adult nurse practitioners. (1999) FA Davis,
Philadelphia .
MM Keiser, Neurologic disorders, In: (Editors: A Gawlinski, D Hamwi) Acute care nurse
practitioner: clinical curriculum and certification review (1999) WB Saunders, Philadelphia.
In: (Editors: SJ McPhee, MA Papadakis, LM Tierney) Current medical diagnosis and treatment ed
46 (2007) McGraw Hill/Appleton & Lange, New York.
RE Rakel, R Kersey, Saunders manual of medical practice. ed 2 (2000) WB Saunders, Philadelphia
WI Schievink, Medical progress: intracranial aneurysms, N Engl J Med 336 (1997) 28–40.
WR Shapiro, Current therapy for brain tumors: back to the future, Arch Neurol 56 (1999) 429–432.
JH Stein, Internal medicine. ed 5 (1998) Mosby, St. Louis .
JA Vanneste, Diagnosis and management of normal-pressure hydrocephalus, J Neurol 247 (2000)
M Verrees, Management of normal pressure hydrocephalus, Am Fam Physician 70 (2004)
1071–1078.CHAPTER 3. Peripheral Neuropathies
Guillain-Barré syndrome, 357.0
Myasthenia gravis, 358.00
I. Definition
A. An acute, usually rapidly progressive form of inflammatory polyneuropathy of the peripheral
B. Characterized by muscular weakness, mild distal sensory loss, and autonomic dysfunction
that, in about two thirds of cases, begins 5 days to 3 weeks after occurrence of an ordinary
infectious disorder, surgery, or immunization
C. Guillain-Barré syndrome (GBS) is the most frequently acquired demyelinating neuropathy.
II. Etiology
A. Unknown, although an autoimmune basis is probable
B. Triggered by antecedent infection; described after upper respiratory infection, infectious
mononucleosis, cytomegalovirus infection, herpes zoster, influenza A, mycoplasma,
EpsteinBarr, mumps, AIDS, Lyme disease, lymphoma (especially non-Hodgkin's), serum sickness,
surgery, and heatstroke
C. In 50% to 75% of cases, GBS is associated with Campylobacter jejuni enteritis. Culture
studies have shown that a high proportion of patients with GBS have C. jejuni in their stools at
the time of onset of neurologic symptoms.
III. Significance
A. Incidence/prevalence in the United States
1. 1.3 to 1.9 cases/100,000 annually
2. Nonseasonal, nonepidemic in nature
3. Incidence increases with age
a. 0.8 cases/100,000 at age 18
b. 3.2 cases/100,000 at age 60
B. Systems affected: nervous, endocrine/metabolic
C. Predominant age/sex
1. All ages
2. Men affected more frequently (1.25:1)
3. Bimodal peaks of occurrence in the 15- to 35-year-old group and the 50- to 75-year-old
IV. Clinical manifestations
A. Differ somewhat between subtypes of the disease
B. Symmetric, rapidly progressive distal muscle weakness and paresthesia, beginning in the legs
and ascending rapidly to the arms, face, and oropharynx. Severity of motor symptoms depends
on the nerves involved.
C. Weakness is more prominent than sensory signs and symptoms and may be more prominent
proximally; it can progress to total motor paralysis and death from respiratory failure.
D. Hypotonia; sphincters are sparedE. Reduced reflexes, followed by loss of deep tendon reflexes in 100% of patients
F. “Stocking” distribution sensory loss
1. Patient may have hyperesthesia, which may make the touch of a hand or a bed sheet very
2. Perception of joint position, vibration, and temperature may diminish.
G. Bulbar involvement: bilateral facial and oropharyngeal paresis
H. Difficulty swallowing (because of cranial nerve involvement)
I. Urine retention
J. Respiratory paralysis (involvement of intercostal muscles)
K. Autonomic dysfunction, including blood pressure fluctuations, inappropriate antidiuretic
hormone secretion, cardiac arrhythmias, and pupillary changes
V. Laboratory findings
1. Elevation in CSF protein (especially immunoglobulin [Ig]G) and lack of increased
lymphocytes strongly suggest GBS.
2. Normal values may be seen at the beginning of the illness.
3. Elevation begins a week after symptoms occur and peaks in 4 to 6 weeks.
4. Protein elevation may be very high (greater than 1000 mg/dl).
B. CBC: Early leukocytosis may be seen with a left shift that resolves during the course of
C. If diagnosis is strongly suspected, repeat lumbar puncture is indicated.
VI. Pathologic findings
A. Segmental demyelination of peripheral nerves; axonal degeneration
B. Inflammatory lesion: lymphocyte and macrophage invasion of myelin sheath
C. Special tests: electromyography—reveals slowed conduction velocities and prolonged motor,
sensory, and F-wave latencies; decreased nerve conduction related to demyelination
VII. Management
A. Severe acute polyneuropathy is a medical emergency.
B. Admit to the intensive care unit for constant monitoring and vigorous support of vital
C. Anticipate respiratory support by mechanical ventilation.
D. Measure vital capacity (VC) and arterial blood gases. If forced expiratory volume is less than
12 to 15 ml/kg, VC is less than 1000 ml, PaO (partial pressure of oxygen in arterial blood) is2
less than 70, and/or the patient is having a difficult time clearing secretions and is aspirating,
assisted ventilation may become necessary.
E. IgG
1. Therapy that has been used traditionally as an alternative to plasmapheresis (0.4 g/kg IV for
5 consecutive days)
2. Use of high-dose intravenous immune globulin G (IVIgG) may promote remyelination in
demyelinating disease.
3. This treatment has replaced plasmapheresis as the therapy of choice at many institutions.
F. Plasmapheresis
1. Perform in severe cases.1. Perform in severe cases.
2. Shortens course and reduces time on ventilator
3. Treatment of choice in those who are acutely ill; should be performed within 7 days after
4. Very beneficial in preventing paralytic complications
5. Patients reportedly improve more quickly, can be weaned from assisted ventilation earlier,
and can ambulate earlier.
6. Contraindicated in patients with cardiovascular disease (recent myocardial infarction,
unstable angina), active sepsis, and autonomic dysfunction
7. Recommendations are to use two plasma exchange treatments for mild GBS.
8. Use four or five plasma exchange treatments for severe GBS.
9. Start as soon as possible on alternating days.
G. New insights in GBS pathophysiology have emphasized the effect of cellular immune
reaction and the role of proinflammatory and anti-inflammatory cytokines (especially tumor
necrosis factor [TNF] and tumor growth factor [TGF]).
1. Research suggests the potential usefulness of interferon beta-1a (Ribif, 6 mIU
subcutaneously on alternate days) in decreasing motor deficits.
2. Effects may be related to decreased TNF production, reduced T-cell activation and
proliferation, decreased gelatinase B production, and increased TGF production.
H. Potentially interesting future treatments
1. Study suggests that CSF filtration and standard plasma exchange are equally efficacious.
2. In experimental allergic neuritis (a model of GBS), two new cyclooxygenase-2 inhibitors
were believed to be useful additional therapeutic agents in GBS because they were found to
inhibit clinical and histologic features of the disease.
I. Prevention of thrombophlebitis
1. Thromboembolic disease stockings (TEDS) and heparin (5000 units subcutaneously every
12 hours) or low molecular weight heparin
J. Pain management
1. Pain may be significant in GBS.
2. Suitable analgesics range from nonsteroidal anti-inflammatory agents to opioids.
K. Stress ulcer prevention, especially in those receiving ventilatory support.
L. Encourage fluid intake to maintain urine volume of 1 to 1.5 L/day.
M. Monitor serum and electrolytes to prevent water intoxication.
N. Maintain skin integrity. Protect skin from trauma and pressure. Reposition frequently.
O. Apply moist heat to relieve pain and to permit early physical therapy.
P. Range of motion
1. Passive range-of-motion exercises immediately
2. Active range-of-motion exercises when acute symptoms subside
3. Prevention of joint contractures is very important.
Q. Nutrition management
1. Assess pharyngeal function.
2. If patient has difficulty swallowing, initiate enteric or parental nutrition.
R. Monitor and treat patients with autonomic dysfunction as needed (bradyarrhythmias or
tachyarrhythmias, orthostatic hypotension, systemic hypertension, hypotension).S. Emotional support and social counseling
T. No drug therapy is recommended.
U. Steroids have not been shown to be of benefit in GBS.
V. Prednisone is used in the chronic form of the disease—chronic relapsing polyneuropathy.
VIII. Follow-up
A. Patient will require physical rehabilitation to regain strength.
B. Subsequent development of chronic course: chronic inflammatory demyelinating
polyradiculoneuropathy (CIDP)
1. CIDP has an insidious onset after GBS and may continue for years.
2. Plasmapheresis benefits one third of patients, as do immunosuppressive agents
IX. Expected course and prognosis
A. Weakness and paralysis progress over a 2-week period, stabilize, and then gradually improve.
Improvement over a period of months is common.
B. 10% to 23% of patients require ventilatory support.
C. 7% to 22% of patients are left with mild disability, mild weakness, or reflex loss.
D. About 10% of patients—those with a more prolonged course—have severe residual defects.
E. Axonal regeneration requires 6 to 18 months.
F. Mortality occurs at a rate of approximately 3% to 5%.
I. Definition
A. Disorder of the neuromuscular junction resulting in a pure motor syndrome characterized by
weakness and fatigue, particularly of the extraocular, pharyngeal, facial, cervical, proximal limb,
and respiratory musculature
B. Caused by an autoimmune attack on the acetylcholine receptor of the postsynaptic
neuromuscular junction, resulting in dysfunction of acetylcholine receptors and jeopardizing
normal muscular transmission
C. Onset may be sudden or severe (myasthenic crisis) but typically is mild and intermittent over
many years.
II. Significance
A. Incidence/prevalence in the United States: 2 to 5 million cases/year; 3/100,000
B. Predominant age: 20 to 40 years, but can occur at any age (1-80 years). Incidence in women
peaks in the third decade, in men in the fifth and sixth decades.
C. Predominant sex: female
III. Clinical manifestations
A. Ptosis—Ocular muscles are affected first in 40% of patients and eventually in 80%.
B. Diplopia
C. Facial weakness
D. Fatigue on chewing
E. Dysphagia
F. DysarthriaG. Dysphonia
H. Neck weakness
I. Fatigue after exercise
J. Proximal limb weakness
K. Respiratory weakness
L. Generalized weakness
M. Sensory modalities and deep tendon reflexes normal
N. Severe generalized quadriparesis may develop, especially in relapse.
IV. Diagnostics/laboratory findings
A. Acetylcholine receptor antibody (AchR-ab)
1. Generalized myasthenia—90% positive
2. Ocular myasthenia—60% positive
3. Myasthenia plus thymoma—100% positive
4. Congenital myasthenia—0% positive
5. No correlation between antibody titer and disease severity
B. Thyroid function test: Patients with myasthenia gravis (MG) have a greater incidence of
thyroid disease.
C. Vitamin B levels may be low because of associated pernicious anemia.12
D. Muscle electron microscopy: Receptor infolding and tips of the folds are lost; synaptic clefts
are widened.
E. Immunofluorescence—IgG antibodies and complement in receptor membranes
F. Antinuclear antibodies, antithyroid, and rheumatoid arthritis factor are often present.
G. Repetitive nerve stimulation: In 60% of affected patients, a decremental response occurs at 3
Hz; this is seen more frequently in the proximal, cervical, or facial muscles. The decrement is
less pronounced 30 seconds after a 30-second maximal voluntary contraction (postsynaptic
facilitation) and most pronounced 120 seconds after the contraction (post-tetanic depression).
H. Single-fiber electromyography (SFEMG): highly sensitive but less specific, technically
difficult to perform, limited availability. SFEMG assesses temporal variability between two
muscle fibers within the same motor unit (jitter). MG is a condition in which jitter is increased.
I. Edrophonium (Tensilon) test: short duration (less than 5 minutes); used in MG for
differentiating between myasthenic and cholinergic crises
1. 2 mg IV, followed in 30 seconds by 3 mg, followed in 30 seconds by 5 mg, to a maximum
dose of 10 mg
2. In MG, a sudden, brief improvement in muscle function occurs.
3. Patients in myasthenic crises improve, whereas those in cholinergic crises worsen.
4. Dangerous cardiorespiratory depression may occur, and atropine and equipment to
maintain respiration must be available during the test.
5. MRI or CT scan of the anterior mediastinum may document an associated thymoma.
V. Management
A. Typically outpatient
B. Inpatient care includes plasmapheresis, IV gamma globulin, and management of pulmonary
infections and myasthenic or cholinergic crises.C. General measures: Management is difficult and should be carried out by a neurologist who
specializes in the field.
1. Symptomatic approach
a. Reversal of weakness with cholinesterase inhibitors
b. Overdose of these agents may induce severe weakness, known as a cholinergic crisis; a
cholinergic crisis should be suspected if other signs of cholinergic overactivity are noted.
2. Immunosuppressive approach
a. Immunosuppressive therapy in some form is necessary for patients with MG.
b. Thymectomy is the treatment of choice for patients with thymoma.
c. Corticosteroids (see dosing later, under F. Medications, 2. Prednisone)
d. Plasmapheresis is consistently effective and is used for rapid improvement of severe
e. Immunosuppressive drugs such as azathioprine (Imuran), 2-3 mg/kg/day, or
cyclosporine, 5 mg/kg/day, are often used in patients with severe generalized weakness and
may reduce the need for steroids. Many require lifelong immunosuppressive therapy.
f. IVIgG has been used in myasthenic patients with severe disease and poor response to
other treatments. IVIgG therapy appears to improve strength rapidly (within 5 days of
initiation), and it lowers anti–acetylcholine receptor antibodies, but the response is
shortlived and is not uniformly observed.
3. Supportive approach
a. May include intubation
b. Tracheostomy
c. Artificial ventilation
d. Respiratory therapy
e. Antibiotic administration
f. Nasogastric tube or gastrostomy
D. Activity: as tolerated. Heat and exercise both temporarily exacerbate symptoms.
E. Diet: as tolerated
F. Medications
1. Cholinesterase inhibitors
a. Pyridostigmine bromide (Mestinon), 30-60 mg PO every 4 to 6 hours initially
i. Onset of effect is 30 minutes, duration 4 hours.
ii. Longer-acting preparation (Mestinon Timespan, 180 mg sustained-release tablets) can
be given 2 or 4 times daily.
iii. Longer-acting preparation is beneficial for those patients who have symptoms first
thing in the morning.
iv. Titrate dosage to clinical need.
v. Average requirement would be 600 mg/day.
b. Neostigmine methylsulfate (Prostigmin) 0.25, 0.5, and 1 mg/ml concentrations
i. Titrate to clinical need: 0.5-2.5 mg subcutaneously, IV, or intramuscularly (IM) every
1 to 3 hours
ii. For oral administration, usual dose is 15-375 mg/day in three to six divided doses.
c. Monitor patient for cholinergic adverse effects such as nausea and vomiting, diarrhea,
increased salivation and bronchial secretions, and cramps. These adverse effects can becontrolled with atropine and glycopyrrolate.
d. Overmedication may temporarily increase weakness, which is also enhanced by
intravenous edrophonium.
2. Prednisone should be administered to those who have responded poorly to
anticholinesterase drugs and, if indicated, have already undergone thymectomy.
a. Dose is determined on an individual basis.
b. High initial dose (60-100 mg) can gradually be tapered to a low maintenance dose.
c. Switch to every other day within 2 weeks.
d. Continue to taper very slowly, attempting to establish the minimum dosage necessary to
maintain remission.
e. Typical maintenance dosage would be 35 mg every other day, but this depends on patient
response and may range from 5 mg every other day up to 100 mg every day.
3. Azathioprine (2-3 mg/kg PO 4 times a day) is an effective treatment, given alone or in
combination with prednisone, but weakness may take several months to improve.
4. Cyclophosphamide may be used in a fashion similar to azathioprine but usually takes effect
within months.
5. Immune globulin
VI. Associated conditions
A. Thymoma
B. Thymic hyperplasia
C. Thyrotoxicosis
D. Other autoimmune disease
A Allen, S Antony, Severe Guillain-Barré syndrome associated with Campylobacter jejuni infection
with failure to respond to plasmapheresis and immunoglobulin, J Am Board Fam Pract 12
(1999) 249–252.
K Boonyapisit, H Kaminski, R Ruff, Disorders of neuromuscular junction ion channels, Am J Med
106 (1999) 97–113.
JM Clochesy, C Breu, B Dossey, AACN handbook of critical care nursing. (1997) Appleton &
Lange, Stamford, Conn .
A Creange, H Lerat, C Meyrignac, et al., Treatment of Guillain-Barré syndrome with interferon-beta,
Lancet 352 (1998) 368–369.
O Devinsky, E Feldmann, HJ Weinreb, et al., The resident's neurology book. (1997) FA Davis,
Philadelphia .
FF Ferri, Practical guide to the care of the medical patient. ed 6 (2004) Mosby, St. Louis .
A Hahn, Guillain-Barré syndrome, Lancet 352 (1998) 635–641.
H Hartung, Infections and the Guillain-Barré syndrome, J Neurol Neurosurg Psychiatry 66 (1999)
A Kaplin, C Krishnan, DM Deshpande, et al., Diagnosis and management of acute myelopathies,
Neurologist 11 (2005) 218.
J Keesey, Clinical evaluation and management of myasthenia gravis, Muscle Nerve 29 (2004)
MM Keiser, Neurologic disorders, In: (Editors: A Gawlinski, D Hamwi) Acute care nurse
practitioner: clinical curriculum and certification review (1999) WB Saunders, Philadelphia.
MJ Kothari, Myasthenia gravis, J Am Osteopath Assoc 104 (2004) 377–384; 399-400.
In: (Editors: SJ McPhee, MA Papadakis, LM Tierney) Current medical diagnosis and treatment ed46 (2007) McGraw-Hill/Appleton & Lange, New York.
DL Newswanger, Guillain-Barré syndrome, Am Fam Physician 69 (2004) 2405–2410; 2303-2305.
G Pfeiffeir, W Steffen, Guillain-Barré syndrome after heat stroke, J Neurol Neurosurg Psychiatry
66 (1999) 408.
RE Rakel, Saunders manual of medical practice. (1996) WB Saunders, Philadelphia .
RE Rakel, R Kersey, Saunders manual of medical practice. ed 2 (2000) WB Saunders, Philadelphia
DP Richman, Treatment of autoimmune myasthenia gravis, Neurology 61 (2003) 1652–1661.
V Scaioli, F Andreetta, R Mantegazza, Unusual neurophysiological and immunological findings in
myasthenia gravis: a case report, J Peripher Nerv Syst 9 (2004) 92–97.
K Scherer, DL Simel, The rational clinical examination: does this patient have myasthenia gravis?
JAMA 293 (2005) 1906–1914.
M Stangel, V Klaus, R Gold, Mechanisms of high-dose intravenous immunoglobulins in
demyelinating diseases, Arch Neurol 56 (1999) 661–663.
PA van Doorn, MP Garssen, Treatment of immune neuropathies, Curr Opin Neurol 15 (2002)
PA van Doorn, Treatment of Guillain-Barré syndrome and CIDP, J Peripher Nerv Syst 10 (2005)
R van Koningsveld, PI Schmitz, FG Meche, et al., for the Dutch GBS Study Group, Effect of
methylprednisolone when added to standard treatment with intravenous immunoglobulin for
Guillain-Barré syndrome: randomized trial, Lancet 363 (2004) 192–196.
HJ Willison, The immunobiology of Guillain-Barré syndromes, J Peripher Nerv Syst 10 (2005)
JB Winer, Treatment of Guillain-Barré syndrome, Q J Med 95 (2002) 717–721.CHAPTER 4. Neurologic Trauma
Head trauma/traumatic brain injury, 959.01
Spinal cord trauma, 952.9
I. Head trauma accounts for two thirds of all casualties of motor vehicle accidents.
A. Head trauma is the leading cause of death in all trauma cases.
B. Anatomic structures and physiologic functions of the head provide protection for the brain.
1. Scalp
2. Skull
3. Cerebral meninges (PAD—pia mater, arachnoid, dura mater)
4. CSF
C. The brain is dependent on glucose (25%) and oxygen (20%) for functioning.
II. Mechanism of injury
A. Acceleration
B. Deceleration
C. Deformation
III. Type of injury
A. Blunt trauma
B. Penetrating injury
1. High-velocity object
2. Low-velocity object
C. Coup-contrecoup injuries: brain tissue injury directly at the site of impact (coup) and at the
pole opposite the site of impact (contrecoup) that may be caused by movement of cranial
contents within the skull
IV. Categories of injury
A. Primary head injury
1. Scalp laceration
a. Most common head injury
b. May result in profuse bleeding caused by the great vascular supply to the scalp (monitor
for signs and symptoms of hypovolemia, such as increased heart rate and decreased blood
c. Apply direct pressure to control bleeding (first assess for skull fracture).
d. Suture/staple laceration after thorough examination and cleansing
i. Lidocaine 1% with epinephrine should be used on scalp lacerations to help control
ii. Do not use lidocaine with epinephrine on lacerations located on the nose or ears.
2. Skull fracture
a. Simple: no displacement of bone. Observe for scalp laceration, protect the cervical spine;
may indicate underlying brain injury
b. Depressed: bone fragment depressing the thickness of the skulli. Patients often have a scalp laceration.
ii. Patient may be asymptomatic or may have altered level of consciousness.
iii. Surgery is required to elevate and debride the wound.
iv. Prophylactic broad-spectrum antibiotics
v. Tetanus toxoid, if indicated
vi. Institute seizure precautions.
c. Basilar: fracture in the floor of the skull
i. Raccoon eyes—periorbital ecchymosis
ii. Battle's sign—mastoid ecchymosis
iii. Otorrhea and/or rhinorrhea (positive Dextrostix test result, halo or target sign, and
salty taste in mouth). Do not obstruct the flow.
iv. Prophylactic antibiotic coverage
v. Oral intubation and oral gastric tube are indicated instead of nasal intubation and
nasogastric tube.
3. Brain injury
a. Concussion: transient, reversible alteration in brain functioning
i. Brief loss of consciousness, amnesia of events
ii. Lethargy, headache, nausea, dizziness
iii. Do not give opioids. Evaluate for changes in level of consciousness.
iv. May need to admit to hospital if unconsciousness lasts longer than 2 minutes
b. Contusion: bruising to the surface of the brain with varying degrees of edema,
contrecoup injury. The skull is rough and jagged, and the brain may be damaged as it
moves across underlying structures.
i. Variable levels of consciousness and amnesia
ii. Nausea and vomiting, dizziness
iii. Visual disturbances
iv. Institute seizure precautions.
v. Brain stem contusion: posturing, variable temperature, variable vital signs
B. Hematoma
1. Epidural hematoma: collection of arterial blood between the skull and the dura mater
within the epidural space
a. Loss of consciousness, followed by a lucid interval, then rapid deterioration
b. Stupor progresses to coma.
c. Ipsilateral pupil dilatation
d. Hemiplegia
i. Obtain CT scan.
ii. Mannitol may be given to “buy time.”
iii. Immediate surgical intervention is necessary.
2. Subdural hematoma: venous bleeding between the dura mater and the brain tissue
a. Most frequently seen type of intracranial bleeding
b. Acute: develops over minutes to hours
i. Drowsiness, agitation, confusion
ii. Headacheiii. Unilateral or bilateral pupil dilatation
iv. Late hemiparesis
v. Obtain a CT scan.
vi. Surgery is required.
c. Chronic: develops over days or weeks
i. Headache
ii. Memory loss
iii. Personality changes
iv. Incontinence
v. Ataxia
vi. Obtain a CT scan.
vii. Surgery is usually required, but close monitoring may be sufficient if the hematoma
is small.
C. Infection
1. Meningitis
2. Brain abscess
D. Brain swelling or edema
V. Clinical manifestations
A. Many have been discussed previously under specific types of head injuries.
B. When the patient is beginning to decompensate, symptoms of Cushing's triad may develop.
1 . Widening pulse pressure (Systolic blood pressure will increase in attempts to maintain a
constant cerebral perfusion pressure [CPP].)
where MAP = mean arterial pressure and ICP = intracranial pressure.
2. Decreased respiratory rate
3. Decreased heart rate
C. Neurologic examination
1. AVPU—A = awake, V = responds to verbal stimuli, P = responds to painful stimuli, U =
2. Glasgow coma scale (Individuals with subdural hematoma and a score less than or equal to
8 have a poor prognosis.)
3. Posturing
a. Decorticate: flexion of upper extremities with extension of lower extremities
b. Decerebrate: extension of upper extremities and lower extremities (More of the brain
stem is involved.)
D. Laboratory findings in patients with diabetes insipidus
1. Electrolytes: increased sodium, decreased potassium, and so forth
2. Increased serum osmolality (greater than 275-285 mOsm/kg)
3. Decreased urine osmolality (N = 300-900 mOsm/kg)
4. Decreased urine specific gravity (N = 1.010-1.030)
5. CBC; hemoconcentration (hematocrit and hemoglobin may be falsely high)
VI. ManagementA. Consult a neurosurgeon.
B. Prevent hypotension and hypoxemia.
1. According to Brain Trauma Foundation guidelines, resuscitation should be aimed at
maintaining a systolic blood pressure (SBP) greater than 90 mmHg and a partial pressure of
arterial oxygen (PaO ) greater than 60 mmHg.2
2. Attempt to maintain an MAP greater than 90 mmHg.
3. If the patient is hypotensive, administer 1-2 L of isotonic crystalloid solution immediately.
Avoid overhydration as attempts are made to restore adequate blood pressure (MAP greater
than 90 mmHg).
4. The literature has increasingly recommended small-volume resuscitation with
hypertonic/hyperosmolar solutions (e.g., hypertonic saline, dextran) because of the findings
that these solutions enhance intracranial compliance, resulting in a minimal increase in ICP.
5 . Administration of blood is another way to improve tissue perfusion to the brain by
optimizing the oxygen-carrying capacity of intravascular fluid. The goal is to maintain
hematocrit at 30% to 33%.
C. Hyperventilation/hyperoxia
1. Hyperventilation (PaCO [partial pressure of carbon dioxide in arterial blood], 25-302
mmHg) has been used for decades to cause cerebral vasoconstriction and thereby lower ICP.
Cerebral vasoconstriction caused by hyperventilation has also been known to cause cerebral
2. Experts now recommend that hyperventilation should not be used routinely, especially
during the first 24 hours after injury, unless ICP is severely high or the patient requires
a. Brain Trauma Foundation guidelines specifically recommend that hyperventilation to
bring PaCO to less than 35 mmHg should be undertaken only if a measured increase in2
ICP is reported, or if increased ICP is suspected because of physical signs, while
intracranial hypertension is refractory to other interventions.
b. Other methods known to control ICP (e.g., elevating the head of the bed, sedation,
paralysis, mannitol, CSF drainage) should be instituted first.
3. Other studies support that hyperoxia during acute hyperventilation improves oxygen
delivery to the brain, as indicated by improved jugular venous bulb saturation and
arteriovenous oxygen content difference. Moderate hyperventilation to a PaCO of 30 mmHg2
in combination with a higher PaO may be beneficial in patients with head injury.2
4. Nasal intubation and a nasogastric (NG) tube have traditionally been preferred over oral
intubation, given the possibility of cervical spine injury, with the exception of basilar skull
D. Central nervous system (CNS) depressants
1. Opioid sedatives help lower ICP by reducing metabolic demand and relieving anxiety and
pain. Naloxone (Narcan) can reverse the effects of a narcotic sedative when a neurologic
assessment is conducted.
2. Short-acting opioids are the best choices.
a. IV fentanyl, 2-20 mcg/kg over 1 to 2 minutes, up to 50 mcg/kg, or sufentanil (Sufenta),
1-8 mcg/kg/minute
b. These may be supplemented with propofol (Diprivan) or benzodiazepines (diazepam
[Valium] or lorazepam [Ativan]) if the patient remains agitated or ICP remains elevated.3. Neuromuscular blocking agents
a. Vecuronium (Norcuron, 0.04-0.1 mg/kg IV) or doxacurium (Nuromax, 0.05 mg/kg)
b. Can be used to help lower ICP in patients in whom confusion, posturing, or severe
agitation is interfering with treatment or diagnostic testing
c. Patient must be sedated and intubated with an adequate set rate on the ventilator.
d. Paralytic agents also may be needed to help oxygenate and ventilate the patient.
E. Steroids
1. Corticosteroids remain controversial.
a. Theoretically, these drugs work by preventing fluid from entering the cells and by
increasing blood vessel diameter, thereby promoting cerebral blood flow.
b. However, according to Brain Trauma Foundation guidelines, the use of steroids is not
recommended for improving outcomes or reducing ICP in patients with severe head injury.
2. Many practitioners believe that the risks of steroids (e.g., compromise of immune function,
infection, delayed wound healing, gastric distress) far outweigh the benefits.
a. No significant improvement or reduction in ICP has been noted with the use of steroids.
b. A study performed on rats found that low doses of dexamethasone (Decadron) appear to
be beneficial for the treatment of cerebral trauma because they decrease brain water
F. Osmotherapy (mannitol)
1. Very useful in certain patients; drug of choice in an emergency situation when brain
herniation is pending
2. Mannitol creates an osmotic gradient across the blood–brain barrier that pulls water from
the CNS into the intravascular space.
3. Mannitol may enhance cerebral oxygen delivery via decreased blood viscosity, increased
CPP, or both.
4. Mannitol may also provide some cytoprotective effects through oxygen-free radical
5. Administer as a bolus (0.25-1 g/kg).
6. Results are quick, occurring usually within 10 to 20 minutes, and can last up to 6 hours.
7. Monitor serum osmolarity, and maintain at less than 320 mOsm. Monitor electrolytes as
well, and replace as needed.
8. Monitor blood pressure closely.
a. Hypotension is an adverse effect that results from dehydration caused by diuresis.
b. The goal is to attain beneficial effects without inducing dehydration.
9. Volume replacement may be necessary to keep the patient euvolemic and to prevent
hypotension (e.g., replace urinary output volume-for-volume each hour, or one-half
volumefor-volume each hour, with isotonic crystalloids).
10. An indwelling urinary catheter should be in place and urine output recorded each hour.
11. Some investigators are replacing mannitol with loop diuretics such as furosemide (Lasix)
and ethacrynic acid (Edecrin) to control ICP, believing that these drugs are less likely to cause
severe dehydration.
G. ICP monitoring, CSF drainage, and CPP management
1. ICP monitoring is appropriate for the following:
a. Comatose patients (Glasgow coma scale score of 3 to 8) with an abnormal CT scan
b. Comatose patients with a normal CT scan and two of the following:i. Older than 40 years of age
ii. Unilateral or bilateral motor posturing
iii. Hypotension
2. ICP monitoring is not routinely appropriate for patients with mild or moderate head injury.
3. Ventricular catheter allows the practitioner to measure ICP and to drain CSF.
4. Guideline threshold for ICP is 20 to 25 mmHg.
5. Monitoring of ICP allows the practitioner to calculate CPP (CPP = MAP − ICP).
6. Ideally, CPP should be maintained at a minimum of 60 mmHg.
H. It is recommended that anticonvulsants (phenytoin [Dilantin], carbamazepine [Mazapine])
may be used to prevent early posttraumatic seizures in those at high risk after a head injury.
Prophylactic use is not recommended for preventing late posttraumatic seizures.
I. Patient must undergo ongoing neurologic assessment for evaluation of treatment
effectiveness and the need for additional interventions.
1. Evaluation of the Glasgow coma scale score may be necessary every 30 to 60 minutes for
the first 24 hours. Note whether the patient is receiving sedation and/or paralytics because
these may lower the score.
2. Pupil size and reaction
3. Vital signs
J. It is suggested that by the seventh day after injury, 140% of resting metabolism expenditure is
replaced in nonparalyzed patients, and that 100% of resting metabolism expenditure occurs in
paralyzed patients who use enteral or parenteral formulas that contain at least 15% of calories
as protein.
K. All patients with head injury are presumed to have a cervical spine injury until proven
otherwise. Once the patient's condition has stabilized, a cervical spine series should be ordered.
L. Avoid any condition (e.g., fever, pain, shivering) that increases metabolic rate and therefore
increases the demand for O and glucose.2
M. Prospective treatment
1. Polyethylene glycol superoxide dismutase is a drug that investigators are exploring to
determine whether it can decrease toxicity to the brain associated with free radicals that are
released during trauma. This drug appears to improve clinical outcomes in head trauma
2. Lazaroids—synthetic nonglucocorticoids—constitute a group of experimental drugs that
may slow cellular membrane breakdown after head injury by inhibiting lipid peroxidation.
3. N-methyl-d-aspartates (NMDAs)
a. Potentially useful in that they inhibit harmful effects of certain excitatory amino acids
found at the site of injury that, when released during ischemia, create a hypermetabolic
state that makes the injury worse
b. Ultimate goal of NMDAs is to help minimize the extent of brain damage through
control of metabolic rate.
4. Hypothermia had been thought to possibly improve clinical outcomes through control of
a. Lowering the temperature to 89.6° F to 91.4° F has resulted in improved outcomes in
animals, and the procedure has been tested in humans.
b. Recent studies found no evidence that hypothermia is beneficial in the treatment of
patients with head injury.
5. Decompressive craniectomy has been recognized over the past few years for its use inpatients with malignant ICP caused by traumatic brain injury (TBI).
a. Treatment guidelines consider it a last resort treatment option for those who have failed
to respond to conservative therapy.
b. Studies have shown that ICP normalizes after a craniectomy.
N. Intraparenchymal brain tissue oxygenation monitoring (PbtO ): Levels lower than 15 mmHg2
during the resuscitation phase of TBI predict poor outcome.
O. Jugular venous oxygen saturation (SjvO ) provides global O saturation within the brain;2 2
normal value is 55% to 70%.
P. Transcranial cerebral oximetry: noninvasive technique for monitoring changes in cerebral
oxygen metabolism
Q. Microdialysis catheters monitor brain extracellular chemistry (e.g., glucose, lactate, pyruvate,
glutamate concentrations).
VII. Major complications
A. Posttraumatic seizures
B. Stress ulcers
C. Diabetes insipidus
D. Acute hydrocephalus
VIII. Brain death criteria
A. No spontaneous movement
B. No spontaneous respiration after 100% O is received for 10 minutes and the patient is2
tested for a period of 4 to 6 minutes, with PCO reaching 60 mmHg2
C. Absence of brain stem reflexes
1. Fixed and dilated pupils
2. No corneal reflexes
3. Absent doll's eyes
4. Absent gag reflex
5. Absent vestibular response to caloric stimulation
D. Demonstration of “no flow” state to the brain through arteriography
E. Flat EEG repeated over a 12- to 24-hour period
F. Rudimentary spinal reflexes, when present, should not influence determination of brain death.
G. Hypothermia, barbiturate poisoning, and metabolic imbalance must be ruled out as causes of
CNS lesions.
I. Mechanisms of injury
A. Motor vehicle accidents account for the largest number of spinal cord injuries (SCIs) (40%).
B. Falls or falling objects (10%-20%)
C. Acts of violence (15%)
D. Sports-related injuries (13%)
E. Penetrating wounds (12%)
II. Spinal cord injuries
A. Rapid acceleration/decelerationA. Rapid acceleration/deceleration
1. Hyperextension
a. Usually occurs as the result of a fall onto the face, forehead, or chin
b. Rear-end collisions may result in rupture of the anterior longitudinal ligament.
c. Hyperextension may cause the cord to stretch, resulting in central cord syndrome
(described hereafter at IX. Spinal cord lesions [syndromes], C, 1).
2. Hyperflexion: Greatest stress occurs at C5-C6, causing bilateral facet dislocations.
3. Vertical column loading (compression)
a. Occurs in diving accidents or falls when the patient lands on the feet or buttocks
b. Vertebral body is compressed and/or shattered, resulting in a “burst” fracture, and bone
fragments may become embedded in the cord.
c. Injuries may occur at the level of C1 with diving accidents.
4. Whiplash: sudden hyperextension of the spine that stretches the ligaments as a result of the
force of the lower body moving forward and the backward and downward movement of the
B. Distraction injuries: result from hanging
C. Penetrating trauma
1. Gunshot wound
2. Stab wound
3. Bony fragments
D. Hematoma
E. Pathologic fractures: occur in patients with osteoporosis or metastatic disease
III. Epidemiology
A. Incidence
1. 60% of SCIs involve the cervical spine.
2. Approximately 8000 SCIs occur each year, or 32.1/million.
3. Approximately 40% of patients with SCI die before they reach the hospital or during the
initial resuscitation phase.
4. Average hospital costs: $80,200 for quadriplegics and $72,000 for paraplegics
5. Average lifetime care costs of a young adult with an SCI exceed $1 million.
IV. Age
A. More common in young men (82%)
B. More common in younger persons (80% younger than 40 years, and 50% between 15 and 25
years of age)
V. Anatomy and physiology
A. 33 vertebrae
1. Cervical spine (C1-C7)
a. Highly flexible in nature, small in diameter
b. Therefore, many fractures occur here.
2. Thoracic spine (T1-T12)
a. Articulates with the ribs
b. Less common site for fracture because of its stability3. Lumbar spine (L1-L5)
a. Highly mobile, yet large in diameter
b. Requires a greater amount of force to fracture
4. Sacral spine (S1-S5)
5. Coccygeal vertebrae (3-5 coccyges)
B. Spinal cord
1. Gray matter
2. White layer
3. Meningeal layer (pia mater, arachnoid, dura mater)
VI. Assessment
A. History
1. Mechanism of injury, such as the following:
a. Speed of impact
b. Blunt versus penetrating forces
c. Flexion, extension, rotation, or distraction to the spine
d. Height of fall
e. Use of restraints or deployed airbag
f. Extent of vehicular damage
g. Position of patient in vehicle
2. Patient complaints, such as the following:
a. Back pain
b. Neck pain
c. Numbness
d. Paresthesia
3. Motor/sensory response
4. Prehospital treatment
B. Physical assessment
1. ABCs (problems with airway, breathing, and circulation) and life-threatening injuries are
treated first.
2. Pulmonary complications account for most of the early deaths that occur after acute
traumatic quadriplegia.
3. Assess respiratory ability.
a. Chest excursion
b. Use of intercostal muscles or diaphragm
c. Cervical cord injury above C3 results in respiratory arrest.
d. C5-C6 injuries spare the diaphragm, and diaphragmatic breathing occurs.
e. T1-L2 lesions cause loss of intercostal muscle use.
4. Intubation—if necessary
a. Jaw thrust maneuver
b. Apnea
c. Breathing difficultyd. Diaphragmatic fatigue
5. Arterial blood gases should be monitored closely.
6. Monitor for pneumonia, pulmonary edema, and pulmonary emboli.
C. Motor assessment
1. Inability to perform the functions listed here indicates that the lesion is above the level
a. Deltoids (C4): Apply pressure to shoulders and ask patient to shrug shoulders.
b. Biceps (C5): Have patient flex arm (gravity); then apply pressure by trying to straighten
the arm. Tell patient not to let you straighten it (resistance).
c. Wrist (C6): Have patient hyperextend the wrist (gravity) and apply pressure by trying to
straighten the wrist. Tell the patient not to let you push down (resistance).
d. Triceps (C7): Have patient extend arm (gravity) and try to pull arm up to the flexed
position. Tell patient not to let you bend arm (resistance).
e. Intrinsic (C8): Have patient abduct (fan) fingers and try to push them together.
f. Hip flexion: Have patient bend knee and apply pressure to determine resistance (L2-L4).
g. Knee extension: While hip is flexed and knee bent, have patient try to extend the knee
2. Grade strength using the following scale:
a. 5 = normal movement against gravity and full resistance
b. 4 = full range of motion against moderate resistance and gravity
c. 3 = full range of motion against gravity, not against resistance
d. 2 = extremity can move, but not against gravity (can roll but not lift)
e. 1 = muscle contracts, but extremity cannot move
f. 0 = no visible or palpable muscle contraction or movement of extremity (flaccid)
3. All motor groups must be comprehensively assessed.
4. Complete lesion
a. Patient lacks sensory function, proprioception, and voluntary motor activity below the
level of spinal cord damage.
b. Worse prognosis for recovering neurologic function
5. Incomplete lesion
a. Parts of the spinal cord at the level of the lesion are intact.
b. Sacral sparing occurs.
c. Note sensory perception and voluntary contraction of the anus around the examiner's
D. Sensory function
1. Begin at the area of no feeling and proceed to the area of feeling.
2. Assess response to pain.
a. Great toe: L4
b. Back of leg: S1-S3
c. Perianal area: S4-S5
d. Umbilicus: T10
e. Nipple line: T4
f. Ring and little fingers: C8g. Middle finger: C7
h. Thumb: C6
i. Top of shoulder: C4
3. If the patient is unable to feel pain, the lesion is at or above the spinal nerve level indicated.
E. Evaluate the patient's back.
1. Perform a well-coordinated log-roll maneuver.
2. Maintain in-line spinal stabilization.
3. Gently palpate spine for pain, tenderness, or gaps between spinous processes.
4. Observe for entrance/exit wounds, impaled objects, and other signs of injury.
VII. Key signs of various levels of injury
A. C2-C3
1. Respiratory paralysis
2. Flaccid paralysis
3. Areflexia (deep tendon reflexes [DTRs])
4. Loss of sensation below the mandible
B. C5-C6
1. Diaphragmatic breathing
2. Paralysis of intercostal and abdominal muscles
3. Quadriplegia
4. Anesthesia below the clavicle and the ulnar half of the arms
5. Areflexia (with possible exception of the biceps reflex)
6. Fecal and urinary retention
7. Priapism (spontaneous erection)
C. T12-L1
1. Paraplegia
2. Anesthesia in the legs
3. Areflexia in the legs
4. Fecal and urinary retention
5. Priapism (spontaneous erection)
D. L1-L5
1. Flaccid paralysis to partial flaccid paralysis
2. Abdominal and cremasteric reflexes present
3. Ankle and plantar reflexes absent
VIII. Multisystem impact of SCIs
A. Cardiovascular
1. Hypotension
a. Caused by loss of sympathetic tone in patients with high thoracic or cervical injury with
pooling of blood into the periphery
b. If associated with a neurologic deficit, normal or decreased heart rate, and warm,
vasodilated extremities, spinal shock is suspected.
c. Initial fluid resuscitation with 2-3 L of lactated Ringer's solution (Do not overload.
Possible loss of cardiac contractility puts the patient at risk for congestive heart failure[CHF] and pulmonary edema.)
d. Rule out hypovolemia as a cause of hypotension.
e. Vasopressors (dopamine) and hemodynamic monitoring may be indicated if patient is
unresponsive to intravenous fluids.
2. Bradycardia
a. Caused by sympathetic blockade and may lead to arrhythmia (junctional or ventricular
b. Be alert for conditions that promote bradycardia in patients with SCIs: Hypoxia,
hypothermia, and vagal stimulation.
c. Be sure the patient is well oxygenated.
d. Maintain body temperature at greater than 96.8° F.
e. Administer atropine for symptomatic bradycardia (decreased level of consciousness,
urinary output, and blood pressure).
3. Vasovagal reflex
a. Induced by straining, coughing, or bearing down
b. Frequently induced by suctioning, which leads to hypoxia, and by vagal stimulation
(bradycardia—cardiac arrest)
c. Oxygenate and hyperventilate with 100% O prior to suctioning.2
d. Limit suctioning to 10 seconds.
e. Monitor cardiac rate and rhythm.
4. Poikilothermy
a. Patient's temperature is dependent on the temperature of the environment; this
association is the result of interruption of the sympathetic pathways to the
temperatureregulating centers in the hypothalamus.
b. Maintain temperature of the environment.
5. Venous thrombosis
a. Venous stasis in the legs and pelvis resulting from decreased blood flow and flaccid
b. Administer deep venous thrombosis prophylaxis (low-dose heparin, 5000 units
subcutaneously twice daily, or low molecular weight heparin [Lovenox], 30-40 mg
subcutaneously twice daily); use antiembolic stockings, range of motion, vena cava filters.
c. Measure thighs and calves for swelling from deep venous thromboses.
6. Orthostatic hypotension
a. Occurs when patients move from supine to sitting position; related to venous pooling in
the legs and abdomen caused by loss of skeletal muscle pump and impaired sympathetic
nervous system control
b. Use thigh-high stockings and abdominal binders to promote venous return.
c. Raise the head of the bed gradually, and monitor blood pressure closely.
B. Gastrointestinal
1. Abdominal injuries resulting from trauma
a. Difficult to diagnosis in SCI because abdominal pain and muscular rigidity—telltale
signs of internal bleeding—are absent if the patient has sensory and motor deficits.
b. Assess patient for abdominal distention; monitor hematocrit and hemoglobin and blood
c. Perform diagnostic peritoneal lavage.2. Curling's ulcer
a. Patients with CNS injury may have this type of stress ulcer as a result of vagally
stimulated gastric production and/or release of adrenocorticotropic hormone.
b. Assess gastric pH, and administer antacids and H antagonists for prevention and2
c. Warm and cold water lavage may be used to treat bleeding.
d. Monitor patient for coagulation defects.
e. Vasopressin may be used.
f. Gastrectomy may be necessary in severe cases.
3. Gastric atony and ileus
a. Related to loss of central control
b. Leads to severe gastric distention that in turn can lead to respiratory compromise,
vomiting, and aspiration
c. Place an NG tube to lower wall suction. Note amount and quality of aspirate.
4. Loss of bowel function
a. Patient cannot sense when the bowel is full or cannot perform Valsalva maneuver to aid
in evacuation.
b. May lead to obstruction or autonomic dysreflexia (described immediately following
under C. Genitourinary)
c. Initiate a bowel program—suppository same time every day, am or pm
C. Genitourinary
1. Autonomic dysreflexia
a. Distended bladder is the most common cause, although it can result from any noxious
stimuli (e.g., distended bowel, wrinkled sheets, pressure ulcers, constrictive clothing,
constrictive devices such as foot splints, shoes that are tied too tightly).
b. Hypertensive crisis that may result from a noxious stimulus in injuries above T6—the
sympathetic outflow level
c. SCI may result in denervation of the bladder, which may become overdistended.
d. Noxious stimulus below the level of injury triggers the sympathetic nervous system,
causing massive release of catecholamines.
e. Result of catecholamine release is vasoconstriction.
f. Vasodilatation occurs above the site of injury—red, flushed, warm skin, as well as
headache, nasocongestion, and diaphoresis.
g. Piloerection occurs below the level of injury.
h. Place a urinary catheter to monitor urinary output and to decompress the bladder.
i. Do not drain bladder rapidly if cardiovascular system suggests autonomic dysreflexia (no
more than 600 ml at a time).
2. Urinary tract infection
a. May result from urinary retention or catheterization
b. Intermittent catheterization is recommended.
c. Early detection is essential to prevent sepsis or prolonged spinal shock.
D. Musculoskeletal
1. Impaired skin integrity related to abnormal nerve supply and poor circulation2. Paralysis
a. Muscle atony and wasting
b. Contractures
c. Perform passive range of motion and positioning, and use handsplints and boots to
prevent footdrop.
E. Psychological devastation
1. Effects on the patient
a. Disturbance of self-concept
b. Ineffective coping
c. Feelings of powerlessness
d. Denial, anger, depression
2. Practitioner's response
a. Be honest with a positive attitude.
b. Include patient in his/her care.
c. Set limits of behavior, and be consistent with care.
d. Take an interdisciplinary approach, including the following:
i. Social services
ii. Psychiatry
iii. Physical therapy
iv. Occupational therapy
v. Pastoral care
IX. Spinal cord lesions (syndromes)
A. Anterior cord syndrome
1. Probably the most devastating of the syndromes
2. Disruption of blood flow through the anterior spinal artery
3. Flexion injuries
4. Weakness or paralysis with loss of sense of pain and temperature
5. Proprioception intact
B. Posterior cord syndrome
1. Rare injury resulting from disruption of the posterior column
2. Decrease in touch proprioception and vibration
C. Central cord syndrome
1. Hyperextension injuries with stretching of the cord and subsequent hemorrhaging in the
center of the cord
2. Greater motor loss and sensation in the upper extremities than in the lower extremities
because the upper extremities are controlled by the central portion of the cord
D. Brown-Séquard syndrome
1. Stab wounds, gunshot wounds, fractures of the vertebral process, and spinal cord tumors
2. One side of the spinal cord is damaged.
3. Ipsilateral motor loss and contralateral loss of pain and temperature sensation
4. Extremities that can move have no feeling, and those that have feeling cannot move.
X. Diagnostic proceduresA. Cervical vertebrae
1. Cross-table lateral position first. All seven vertebrae must be seen. To do so, the following
may be required:
a. Firmly pulling the patient's shoulders down
b. Lateral swimmer's view
2. Obtain anteroposterior x-ray if lateral x-ray is abnormal.
3. Obtain open-mouth odontoid x-ray for conscious patient for visualization of C2.
4. Failure to obtain basic radiographic studies is the primary reason for missed diagnosis of
cervical spine injury.
B. Thoracic vertebrae
1. Lateral and anteroposterior x-rays
2. View all 12 vertebrae.
C. Lumbar vertebrae
1. Lateral and anteroposterior views
2. View all five lumbar vertebrae.
D. CT may be helpful for clear identification of normal cervical spine anatomy or the presence
of bony fragments.
E. Films in flexion/extension position or oblique films at times for further delineation of
suspected fractures
F. Myelogram detects compression of the cord by herniated disks, bone fragments, or foreign
matter, which requires surgical intervention.
G. MRI can provide further information regarding cord impingement, hematomas, and infarcts.
Cord contusion or hemorrhage cannot be visualized by any other technique.
XI. Management
A. Consult neurosurgeon.
B. Airway maintenance
1. Nasotracheal intubation or cricothyrotomy if necessary
2. Do not hyperextend or rotate the neck.
3. Administer oxygen.
C. Immobilization
1. Protective devices (e.g., cervical collar, spine board)
2. Do not remove device until x-rays have been obtained and cleared.
3. Log-roll only.
D. Intravascular fluids (limit to appropriate levels)
1. Distinguish neurogenic shock (warm, dry extremities; bradycardia) from hypovolemic
shock (cool, clammy skin; tachycardia).
E. Monitor blood pressure very closely because perfusion to the spinal cord is crucial.
1. Hypotension must be avoided to prevent ischemia caused by decreased blood flow and
perfusion to the spinal cord, which may produce neuronal injury and neurologic deficit.
2. Attempts should be made to maintain MAP at 85 to 90 mmHg.
F. Bladder catheterization
G. Nasogastric intubationH. Corticosteroids (controversial)
1. May be useful in early treatment (within the first 8 hours) of patients with spinal cord
injury, to reduce swelling
a. Reduce damage to cellular membranes that contributes to neuronal death after injury.
b. Reduce inflammation near the injury.
c. Suppress activation of immune cells that appear to contribute to neuronal damage.
2. Methylprednisolone (Solu-Medrol), 30 mg/kg as an IV bolus, followed by a maintenance
infusion of 5.4 mg/kg/hour for 23 hours
3. Improvement is noted 6 weeks to 6 months after injury.
4. Monitor patient for elevation in blood glucose levels.
5. Monitor patient for other adverse effects, such as these:
a. Immunosuppression
b. Fluid and electrolyte disturbances
c. Adrenocortical insufficiency
d. Impaired wound healing
e. Gastrointestinal disturbances
I. Preliminary clinical trials of another agent, GM-1 ganglioside
1. Useful in acute spinal cord injury for preventing secondary damage caused by the
a. Oxidative free radicals
b. Calcium-mediated damage
c. Proteases
d. Cytoskeletal dysfunction
e. Excitotoxicity
f. Immune reactions
g. Apoptosis
h. Necrosis
2. Studies suggest that it may also improve neurologic recovery from spinal cord injury
during rehabilitation.
J. Antibiotics for penetrating injuries: nafcillin, 200 mg/kg/day IV in four to six divided doses
K. Maintain room temperature; avoid poikilothermy.
L. Provide meticulous skin care: Order rotating bed for respiratory therapy (postural drainage)
and skin therapy.
M. Prepare for insertion of skeletal tongs and traction (Stryker frame, kinetic bed, or halo vest)
used to assist in restoration of the spine to a normal position (reduction).
1. At least 10 lb of weight is initially applied.
2. Weight is applied on the basis of 5 lb per interspace (i.e., a C5-C6 injury would require
2530 lb of traction).
3. Muscle relaxants are helpful.
4. Lateral x-rays are taken to assess vertebral alignment as weights are applied.
5. Too much weight can pull the spine apart, resulting in distraction injury.
6. If paralytics are needed, weight may have to be reduced.
N. Fixation: involves stabilizing vertebral fracture with wires, plates, and other types ofhardware
O. Fusion: involves attaching injured vertebrae to uninjured vertebrae with bone grafts and steel
P. Surgery may be indicated to remove bony fragments or to drain hematomas that compress the
Q. Rehabilitation begins upon admission; follow an interdisciplinary approach.
R. Electrical stimulation devices or neural prostheses were recently approved by the FDA but
are still experimental. Can be implanted in the body to allow some hand movement and
bladder/bowel control; may also assist with breathing
P Alderson, C Gadkary, DF Signorini, Therapeutic hypothermia for head injury (Cochrane review).
The Cochrane Library, Issue 1. (2005) John Wiley & Sons, Ltd, Chichester, UK .
American Association of Neurological Surgeons, Congress of Neurological Surgeons, Joint Section
on Neurotrauma and Critical Care, Guidelines for the management of severe traumatic brain
injury: cerebral perfusion pressure. (2003) Brain Trauma Foundation, Inc, New York .
JM Clochesy, C Breu, B Dossey, AACN handbook of critical care nursing. (1997) Appleton &
Lange, Stamford, Conn .
O Devinsky, E Feldmann, HJ Weinreb, et al., The resident's neurology book. (1997) FA Davis,
Philadelphia .
Z Essat, Management of autonomic dysreflexia, Nursing Standard 17 (32) (2003) 42–44.
FF Ferri, Practical guide to the care of the medical patient. ed 6 (2004) Mosby, St. Louis .
IS Grant, PJ Andrews, ABC of intensive care: neurological support, BMJ 319 (1999) 110–113.
T Gunnarsson, MG Fehlings, Acute neurosurgical management of traumatic brain injury and spinal
cord injury, Curr Opin Neurol 16 (6) (2003) 717–723.
RM Haskell, Trauma, In: (Editor: P Login) Principles of practice for the acute care nurse
practitioner (1999) Appleton & Lange, Stamford, Conn.
JA Horton III, MB Chancellor, I Labatia, Bladder management for the evolving spinal cord injury:
options and considerations, Topics in Spinal Cord Injury Rehabilitation 9 (1) (2003) 36–52.
PJ Hutchinson, PJ Kirkpatrick, Acute head injury for the neurologist, J Neurol Neurosurg
Psychiatry 73 (suppl 1) (2002) i3–i7.
H Iida, S Tachibana, T Kitahara, et al., Association of head trauma with cervical injury, spinal cord
injury or both, J Trauma 46 (1999) 450–452.
C Jastremski, Head injuries, RN 61 (1998) 40–44.
MM Keiser, Neurologic disorders, In: (Editors: A Gawlinski, D Hamwi) Acute care nurse
practitioner: clinical curriculum and certification review (1999) WB Saunders, Philadelphia.
K March, Acute head injury, In: (Editors: L Bucher, S Melander) Critical care nursing (1999) WB
Saunders, Philadelphia.
PE Marik, A Garland, Critical care review: management of head trauma, Chest 122 (2) (2002)
C Mattera, Spinal trauma: new guidelines for assessment and management in the out-of-hospital
environment, J Emerg Nurs 24 (1998) 523–538.
In: (Editors: SJ McPhee, MA Papadakis, LM Tierney) Current medical diagnosis and treatment ed
46 (2007) McGraw Hill/Appleton & Lange, New York.
National Institute of Neurology Disorders and Stroke, M Emr, S Howley, L Hudgins, et al., Spinal
cord injury: emerging concepts, www.ninds.nih.gov/health_and_medical/pubs/sci_report.htm;
Accessed February 11, 2005..
RE Rakel, R Kersey, Saunders manual of medical practice. ed 2 (2000) WB Saunders, Philadelphia
S Shackford, P Bourguignon, S Wald, et al., Hypertonic saline resuscitation of patients with headinjury: a prospective, randomized clinical trial, J Trauma 44 (1998) 50–58.
F Sheerin, Spinal cord injury: causation and pathophysiology, Emerg Nurse 12 (9) (2005) 29–38.
D Smith, Diffuse axonal injury in head trauma, J Head Trauma Rehabil 18 (4) (2003) 307–316.
RD Stevens, A Bhardwaj, JR Kirsch, et al., Critical care and perioperative management in traumatic
spinal cord injury, J Neurosurg Anesthesiol 15 (3) (2003) 215–229.
S Talbert, P Talbert, Summary of strategies for managing severe traumatic brain injury during the
early posttraumatic phase, J Emerg Nurs 24 (1998) 254–258.
A Thiagarajan, PD Goverdan, P Chari, et al., The effect of hyperventilation and hyperoxia on cerebral
venous oxygen saturations in patients with traumatic brain injury, Anesth Analg 87 (1998)
P Vespa, What is the optimal threshold for cerebral perfusion pressure following traumatic brain
injury? Neurosurg Focus 15 (6) (2003) E4.
R White, M Likavec, Spinal shock—spinal man, J Trauma 46 (1999) 979–980.CHAPTER 5. Central Nervous System Disorders
Cerebral abscess, 324.0
Encephalitis, 323.9
Encephalopathy, 348.30
Meningitis, 322.9
I. Definition
A. Inflammation of the pia mater and arachnoid of the brain or spinal cord
II. Etiology/predisposing factors
A. Predisposing factors for the development of community-acquired meningitis include
preexisting diabetes mellitus, otitis media, pneumonia, sinusitis, and alcohol abuse.
B. Bacterial meningitis
1. Profound and life threatening
2. Meninges attempt to destroy the microorganism that entered the CNS.
3. Neutrophils gather in the area and begin making exudates within the subarachnoid space.
4. Exudate causes the CSF to thicken and decreases the flow of CSF through the brain and
spinal cord.
a. Streptococcus pneumoniae (pneumococcal meningitis)
i. Most common and most serious (may cause neurologic damage ranging from deafness
to severe brain damage) bacterial meningitis
ii. Occurs frequently in infants (younger than age 2), adults with weakened immune
systems, and the elderly
iii. Rates in children younger than age 2 have decreased since the pneumococcal 7-valent
conjugate vaccine (Prevnar) has been available.
b. Neisseria meningitides (meningococcal meningitis)
i. May occur in schools, colleges, and other group settings
ii. Spread through contact with drainage of the nasopharynx or with blood
iii. High-risk groups include infants younger than age 1, people with suppressed immune
systems, travelers to foreign countries where the disease is endemic, and college
students (freshman in particular) who reside in dormitories.
c. Haemophilus influenzae
i. At one time, this was the most common cause of acute bacterial meningitis.
ii. H. influenzae B (Hib) vaccine has greatly reduced the number of cases in the US.
iii. Children most at risk are those in daycare and children who do not have access to the
d. Escherichia coli, and Enterobacter, Klebsiella, and Proteus spp
i. May occur in infants, the elderly, and immunosuppressed patients
e. Other bacterial meningitides (less common)
i. Listeria monocytogenes
ii. Staphylococci (Staphylococcus aureus and Staphylococcus epidermidis)
iii. Mycobacterium tuberculosisiv. Streptococci
f. Meningitis may follow an upper respiratory infection or head trauma.
C. Aseptic or viral meningitis
1. Pia and arachnoid space are filled with lymphocytes but not with exudate forms.
2. Much more benign and self-limited than bacterial meningitis
3. Caused by viruses
a. Mumps
b. Enterovirus
c. Influenza
d. Varicella zoster
e. Herpes simplex types 1 and 2
f. Adenovirus
g. Epstein-Barr virus
h. Human immunodeficiency virus (HIV)
4. Fungal
a. Most common in immunocompromised (particularly in patients with AIDS)
b. Candida albicans
c. Coccidioides immitis
d. Cryptococcus neoformans (most common fungal meningitis; found in bird droppings)
D. Syphilis
III. Clinical manifestations
A. Fever of 101° F to 103° F (38° C to 40° C); toxic appearance
B. Stiff neck (nuchal rigidity) related to meningeal irritation
C. Altered sensorium
D. Severe headache
E. Photophobia, may have diplopia
F. Chills, myalgias
G. Kernig's sign
1. Flex the patient's leg at the knee, then at the hip, to a 90-degree angle, and extend the knee.
2. In a patient with meningitis, this maneuver will trigger pain and spasms of the hamstring
muscles caused by inflammation of the meninges and spinal nerve roots.
H. Brudzinski's sign
1. Flex the patient's head and neck to the chest.
2. The legs will flex at the hips and at the knees in response to this movement.
I. Nausea and vomiting
J. Purpura or petechiae: may be seen with meningococcal meningitis
K. Ear, nose, and throat (ENT): may have deafness and vertigo (cranial nerve [CN] VIII)
L. Neurologic: may have exaggerated deep tendon reflexes (DTRs), seizures, unilateral or
bilateral sensory loss
IV. Laboratory findings/diagnosticsA. Lumbar puncture should be performed as soon as a diagnosis is suspected, except in
individuals with a suspected space-occupying lesion (brain abscess, subdural hematoma,
subdural abscess).
B. Lumbar puncture in bacterial meningitis
1. Appearance of CSF: cloudy
2. Opening pressure: elevated (greater than 180 mm H O)2
3. Cells: increased WBCs (1000-2000/mm; most are polymorphonuclear cells)
4. Total protein: increased (100-500 mg/dl [normal, 15-45 mg/dl])
5. Glucose: decreased (less than 40 mg/dl or 40% of glucose [normal, 60%-80%])
6. Culture: bacteria present on Gram's stain and culture
C. Lumbar puncture in viral meningitis
1. Appearance of CSF: clear, occasionally cloudy
2. Opening pressure: usually normal (less than 30 mm H O)2
33. Cells: increased WBCs (300/mm ; most are mononuclear cells)
4. Total protein: normal or slightly increased
5. Glucose: normal
6. Culture: no bacteria present; demonstration of virus requires special technique
D. CT scan of the head is indicated in patients with focal neurologic signs or diminished level of
E. In patients who have signs and symptoms and CSF findings typical of bacterial meningitis,
but in whom no organisms are found, follow-up CT scans should be obtained, even if clinical
improvement occurs, because such patients may have a brain abscess and may require
neurosurgical intervention.
F. An additional maneuver in assessing for meningitis is to elicit jolt accentuation of the
patient's headache by asking the patient to turn his or her head horizontally at a frequency of two
to three rotations per second.
1. Worsening of a baseline headache is a positive sign.
2. Include examination of the cranial nerves, motor and sensory systems, and reflexes, as well
as testing for Babinski's reflex.
G. Assess the ears, sinuses, and respiratory system.
H. Obtain blood cultures.
I. Obtain CBC, electrolytes, and liver/renal panel.
J. Chest, skull, and sinus films or chest CT scan may be necessary to facilitate detection of
primary infection.
K. Latex agglutination tests
1. Can detect antigens of encapsulated organisms such as S. pneumoniae, H. influenzae, N.
meningitides, and C. neoformans
2. Rarely used, except for detection of Cryptococcus or in partially treated patients
L. Polymerase chain reaction (PCR) testing of CSF
1. Has been employed to detect bacteria (S. pneumoniae, H. influenzae, N. meningitides, M.
tuberculosis, Borrelia burgdorferi, and Tropheryma whippelii) and viruses (herpes simplex,
varicella-zoster, cytomegalovirus, Epstein-Barr virus, and enterovirus) in patients with
meningitis2. Test results are rapid and are obtained within hours.
V. Management
A. Antibiotics must be initiated immediately in those suspected to have meningitis. Empiric
treatment includes the following:
1. Cefotaxime (Claforan), 200 mg/kg/day IV
2. Ampicillin (Ampicin), 200 mg/kg/day IV, is added for adults older than age 50 and for the
3. In those allergic to penicillin and a third-generation cephalosporin, other medications must
be considered. One drug that is excellent for infection of the CNS is chloramphenicol. It has
been found to be effective, although it has also been associated with occurrence of aplastic
anemia in approximately 1 in 40,000 patients.
B. Meningococcal meningitis: patients 18 to 60 years of age: aqueous penicillin G (3-4 million
units IV every 4 hours) or ampicillin (2 g every 6 hours); continue until 5 to 7 days after the
patient becomes afebrile
C. H. influenzae meningitis: third-generation cephalosporin (ceftriaxone [Rocephin], 50 mg/kg
IV every 12 hours) or ampicillin plus chloramphenicol (Chlorofair, 50-100 mg/kg/day IV in
divided doses)
D. Pneumococcal meningitis: aqueous penicillin IV for 12 to 15 days. Chloramphenicol is an
alternative drug.
E. Postsurgical or posttraumatic meningitis: Third-generation cephalosporin (cefotaxime,
ceftizoxime [Cefizox], ceftriaxone), with or without nafcillin (Nafcil), 2 g IV every 4 hours. If
no improvement in 24 hours, intrathecal treatment may be needed.
F. Aseptic meningitis: supportive therapy. Treat the severely ill empirically with antibiotics.
G. Tuberculosis: isoniazid (INH), 15-20 mg/kg/day (maximum, 500 mg); rifampin, 15-20
mg/kg/day (maximum, 600 mg)
H. Corticosteroids remain controversial; however, these may be prescribed when evidence
suggests cerebral edema or herniation.
I. Anticonvulsants for seizure control (phenytoin [Dilantin], 300 mg/day)
J. Acetaminophen, 325-1000 mg every 4 hours (not to exceed 4 g/day)
K. IV hydration with lactated Ringer's solution or normal saline. Avoid hypotonic solutions
such as D W (dextrose 5% in water).5
I. Definition
A. Infected space-occupying lesion in the brain
II. Etiology
A. Usually due to infection from a different primary source generally in or near the brain
1. Otitis media
2. Mastoid infection
3. Sinusitis
4. Oral surgery (rare)
B. Other sources for abscess
1. Lung infection/empyema
2. Skin infection
3. Bacterial endocarditis4. Bronchiectasis
5. Congenital heart disease
III. Clinical manifestations
A. General: ill appearance, lethargic
B. Vital signs: fever, unstable if intracranial pressure (ICP) elevated
C. Neurologic: speech and visual disturbance, hemiparesis, seizures, severe headache, stupor
progressing to coma
D. Patients go through two phases of symptoms with cerebral abscess
1. Stage I: initial formation of abscess
a. Headache, chills, fever, malaise
b. Confusion, drowsiness, speech disorder
2. Stage II: due to expanding cerebral mass
a. Vague signs and symptoms of brain tumor: recurrent headache of increased severity,
confusion, drowsy, stupor, flulike symptoms
IV. Diagnosis/treatment
A. Same as for meningitis, except that identification of the primary infectious source is key to
pathogen identification
B. Chest, skull, and sinus films may help support suspected diagnosis.
I. Definition
A. Acute inflammation of the brain caused by viral or other systemic infection, usually 2 to 12
days after primary infection, and commonly transmitted from a mosquito that carries the
II. Etiology
A. Herpes simplex virus (HSV) encephalitis
1. In the U.S., most common cause of acute sporadic viral encephalitis
B. Varicella-zoster virus
C. Possible influenza
D. Tick infestation
1. Lyme disease
2. Rocky Mountain spotted fever
3. Eastern equine encephalitis (EEE) (164 cases since 1964)
4. Japanese encephalitis (1 year after travel to Asia)
5. La Crosse encephalitis (70 cases/year)
6. St. Louis encephalitis (3000 cases/year)
7. Western equine encephalitis (19 cases/year; 639 cases since 1964)
8. West Nile virus (4008 cases in 2002 alone)
E. Toxoplasmosis
1. Commonly seen in patients with AIDS
III. Transmission of West Nile virus
A. Mosquitoes become infected when they feed on infected birds.B. The mosquito circulates the virus in the blood for several days.
C. During this time, the mosquito can infect humans and other animals by biting to take blood.
D. The virus is injected into the human or animal, where it multiplies and may cause illness.
IV. Signs and symptoms
A. General: anxious, lethargic
B. Vital signs: unstable if advanced CNS infection, fever
C. Eyes: nystagmus, ocular paralysis
D. Gastrointestinal: nausea/vomiting
E. Musculoskeletal: nuchal rigidity
F. Neurologic: severe headache, ataxia, dysphagia, hemiparesis, stupor progressing to coma,
confusion, olfactory or gustatory hallucinations, seizures
V. Diagnostic testing
A. Standard laboratory tests
1. CBC
2. Chemistry
3. Liver function tests (LFTs)
B. Lumbar puncture (LP)
1. Elevated WBC count
2. RBC count normal (elevated with HSV)
3. Protein: normal or slightly elevated
4. Glucose: normal or slightly elevated
C. Possible open brain biopsy to identify treatable causes
VI. Specific diagnostic testing
A. EEG: abnormal with slowing or epileptiform activity. Temporal lobe abnormalities suggest
HSV infection.
B. Measurement of immunoglobulin (Ig)M antibody in serum and CSF. Collect within 8 days.
Use the IgM antibody capture enzyme-linked immunosorbent assay (MAC-ELISA).
C. IgM does not cross the blood–brain barrier. If it is present in the CSF, a CNS infection
(likely, encephalitis) is suggested.
VII. Imaging diagnostics
A. CT scan
C. Brain scan
D. Usually normal initially; later, nonspecific abnormalities are identified.
E. If temporal lobe disease exists, a diagnosis of HSV infection is suggested.
VIII. Treatment for encephalitis
A. Admit to intensive care unit (ICU); most treatment is supportive.
B. IV fluids
C. Respiratory support
D. Circulatory supportE. Prevention of secondary infection
F. Anticonvulsants
G. Monitor for cerebral edema.
H. Monitor for syndrome of inappropriate antidiuretic hormone secretion (SIADH).
IX. Specific treatments
A. Acyclovir, 30 mg/kg/day for adults, is used in HSV.
B. No specific antiviral therapy is available for other causes.
C. Ribavirin in high doses and interferon alpha-2b have shown some significance for in vitro
West Nile virus, but additional research is needed.
D. Consult an infectious disease specialist.
X. Reporting encephalitis
A. The Centers for Disease Control and Prevention (CDC) has devised standards for reporting
cases of encephalitis in humans, mosquitoes, and birds.
B. Each state has specific guidelines regarding human, mosquito, and bird notification.
C. Guidelines are available for handling dead birds and mosquitoes.
D. These guidelines are available at www.cdc.com.
I. Definition
A. Dysfunction of the brain caused by a disease or disease process
II. Etiology
A. Hepatic
B. Hypertensive
C. Metabolic (lactic acidosis, metabolic acidosis)
D. Electrolytes (hyponatremia, hypoglycemia, hypercalcemia)
E. Uremic
F. Anoxic-ischemic
G. Hypercapnic
H. Endocrine (hyperparathyroidism, Cushing's disease)
J. Thiamine deficiency (Wernicke's disease)
III. Clinical manifestations
A. Depend on cause and may include the following:
1. Headache
2. Inattentiveness, impaired judgment
3. Motor incoordination
4. Drowsiness
5. Confusion
6. Stupor
7. ComaIV. Diagnosis
A. Depends on clinical event
1. Physical presentation
2. Serum laboratory analysis (ammonia)
3. CSF analysis
4. EEG activity
5. MRI
V. Management
A. ABCs of emergency care (airway, breathing, and circulation)
B. Prevention of irreversible neurologic injury
C. Anticonvulsant therapy for seizures (phenytoin, 300 mg/day)
D. Correction of underlying cause
J Attia, R Hatala, DJ Cook, et al., Does this adult patient have acute meningitis? JAMA 282 (1999)
MH Beaman, SL Wesselingh, Acute community-acquired meningitis and encephalitis, Med J Aust
176 (2002) 389–396.
Centers for Disease Control (CDC), Answers to your questions about St. Louis encephalitis (2001,
July), www.cdc.gov/ncidod/dvbid/arbor/sle_qa.htm; Accessed February 8, 2003..
Centers for Disease Control (CDC), Fact sheet: Eastern equine encephalitis (July, 2001),
www.cdc.gov/ncidod/dvbid/arbor/eeefact.htm; Accessed February 8, 2003..
Centers for Disease Control (CDC), Fact sheet: Japanese encephalitis (2001, June),
www.cdc.gov/ncidod/dvbid/jencephalitis/facts.htm; Accessed February 8, 2003..
Centers for Disease Control (CDC), Fact sheet: West Nile virus basics (2002, November 13),
www.cdc.gov/ncidod/dvbid/westnile/index.htm; Accessed February 8, 2003..
Centers for Disease Control (CDC), Fact sheet: Western encephalitis (2001, November),
www.cdc.gov/ncidod/dvbid/arbor/weefact.htm; Accessed February 8, 2003..
L Diggle, Recognition and prevention of meningitis and septicemia, Community Pract 78 (2) (2005)
M Estep, Meningococcal meningitis in critical care: An overview, new treatments/preventions and a
case study, Crit Care Nurs Q 28 (2) (2005) 111–121.
FF Ferri, Practical guide to the care of the medical patient. ed 6 (2004) Mosby, St. Louis .
L Glennie, Spotting meningitis and septicaemia early, Pract Nurs 16 (9) (2005) 426–429; 424.
RS Heyderman, HP Lambert, I O'Sullivan, et al., Early management of suspected bacterial meningitis
and meningococcal septicaemia in adults, J Infect 46 (2) (2003) 75–77.
PG Kennedy, Viral encephalitis: causes, differential diagnosis, and management, J Neurol Neurosurg
Psychiatry 75 (suppl I) (2004) i10–i15.
In: (Editors: SJ McPhee, MA Papadakis, LM Tierney) Current medical diagnosis and treatment ed
46 (2007) McGraw Hill/Appleton & Lange, New York.
RE Rakel, Saunders manual of medical practice. ed 2 (2000) WB Saunders, Philadelphia .
S Ruttimann, Clinical problem-solving: a balancing act, N Engl J Med 341 (1999) 129–130.
S Saha, S Saint, LM Tierney, A balancing act, N Engl J Med 340 (1999) 374–378.
L Smith, Management of bacterial meningitis: new guidelines from the IDSA, Am Fam Physician 71
(10) (2008) 2003–2004; 2005, 2006.
AR Tunkel, BJ Hartman, SL Kaplan, et al., Practice guidelines for the management of bacterial
meningitis, Clin Infect Dis 39 (2004) 1267–1284.CHAPTER 6. Seizure Disorders
Seizure disorders, 780.39
I. Definition
A. Transient disturbance of cerebral function caused by an abnormal paroxysmal neuronal
discharge within the brain. Epilepsy is the term used to describe recurrence of seizures.
II. Etiology
A. Cause may be unknown.
B. Metabolic disorders
1. Acidosis
2. Electrolyte imbalance (e.g., hyponatremia, hypocalcemia)
3. Hypoglycemia
4. Hypoxia
5. Alcohol or barbiturate withdrawal—most common cause of new-onset seizures in adults
C. CNS infection
D. Head trauma
E. Tumors and other space-occupying lesions
F. Vascular disease (common with advancing age and the most common cause of onset of
seizure disorder at age 60 or older)
G. Degenerative disorders, such as Alzheimer's disease in later life
H. Natural reaction to physiologic stress or transient systemic injury
I. Most common cause of seizures is noncompliance with a drug regimen on the part of a patient
in whom epilepsy has been diagnosed.
III. Clinical manifestations
A. Partial seizures: Only a restricted part of one hemisphere has been activated.
1. Simple partial seizure
a. Consciousness is preserved; rarely lasts longer than 1 minute
b. Jacksonian march movements: convulsive jerking or paresthesias/tingling that spreads to
different parts of the limb or body
c. Sensory symptoms: flashing lights, simple hallucinations, tingling, or buzzing
d. Autonomic symptoms: abnormal epigastric symptoms, pallor, sweating, flushing,
pupillary dilatation, piloerection
e. Speech arrest or vocalization
f. Nausea
g. Psychic symptoms: déjàvu; dreamy states, fear, distortion of time perception
2. Complex partial seizure
a. Any simple partial seizure onset followed by impairment of consciousness
b. Automatisms (lip smacking, chewing, swallowing, sucking, picking at clothes) may
c. May begin with a stare at the time consciousness is impaired
d. May have an auraB. Secondary generalized partial seizures: simple or complex seizures progressing to
generalized seizures, with loss of consciousness and motor activity that is often convulsive
C. Generalized seizures
1. Absence (petit mal)
a. Sudden loss of consciousness (5-30 seconds), with eye or muscle flutterings at a rate of
three per second; begins and ends so quickly that it may not be apparent
b. Common in children (ages 6-14)
c. Occasionally accompanied by mild clonic, tonic, or atonic components
d. Autonomic components (enuresis)
e. Can accompany automatisms
f. If the seizure occurs during conversation, the patient may miss a few words or may break
off for a few seconds.
g. Frequently occur several times a day, often when the patient is sitting quietly; infrequent
during exercise
2. Tonic-clonic (grand mal): Neuronal discharge spreads throughout the entire cerebral
a. Usually preceded by an aura and followed by an outcry
b. Loss of consciousness and falling
c. Respiration is arrested.
d . Tonic (muscle rigidity), then clonic (synchronous muscle jerks) contractions of the
muscles of the extremities, trunk, and head
e. Commonly with urinary incontinence
f. Usually lasts 2 to 5 minutes
g. May be preceded by a prodromal mood change and followed by a postictal state (deep
sleep, headache, muscle soreness, amnesia of events, nausea, confusion, or a combination
of these)
D. Status epilepticus: series of grand mal seizures that may occur when the patient is awake or
asleep, with the patient never gaining consciousness between attacks
1. Aggressive treatment is required for a patient with continuing seizures that last longer than
10 minutes or seizures without intervening consciousness.
2. Least common and most life threatening
IV. Diagnosis
A. Obtain a thorough history from the patient, the family, and/or observers of the event.
B. EEG is an important test for supporting the diagnosis of epilepsy, differentiating between
types of seizures, and providing a guide to prognosis.
1. Focal abnormalities indicate partial seizures.
2. Generalized abnormalities indicate primary generalized seizures.
3. A normal EEG does not rule out a seizure.
C. CT or MRI of the head—performed for all new-onset seizures, especially after age 30,
because of the possibility of an underlying neoplasm
D. Chest x-ray is also performed in patients older than age 30 with new-onset seizures because
the lungs are a common site for primary and secondary neoplasms.
E. Lumbar puncture (if indicated) is performed to assess for an infectious process after CT or
MRI has been used to rule out expanding mass that may increase ICP.F. 24-hour EEG to document seizure activity
G. Blood analysis: CBC, glucose, liver and renal function tests, Venereal Disease Research
Laboratory test (VDRL), electrolytes, magnesium, calcium, antinuclear antibody, erythrocyte
sedimentation rate, and arterial blood gases
H. Urinalysis, drug screen
I. Serum prolactin—rises to 2 to 3 times above normal for 10 to 60 minutes after occurrence of
80% of tonic-clonic or complex partial seizures
V. Management
A. Initial management is supportive.
B. Most seizures are self-limiting.
1. Maintain open airway.
2. Protect the patient from injury.
3. Administer oxygen if the patient is cyanotic.
4 . Do not force airways or objects (e.g., tongue blade) between the teeth until the muscles
have relaxed because this may cause the tongue to occlude the airway or teeth to break off
and cause a partial obstruction.
5. Start with IV normal saline.
6. Perform ECG, and monitor respiration and blood pressure.
C. For status epilepticus, follow the preceding steps plus the following:
1. 100 mg IM thiamine
2. 50-ml bolus injection of 50% glucose
3. Lorazepam (Ativan), 0.1 mg/kg at 2 mg/minute (maximum, 10 mg), or IV diazepam
(Valium), 0.2 mg/kg at 5 mg/minute (maximum, 20 mg)
4. Monitor for respiratory depression after medications are given; intubation may become
5. Increase normal saline if the patient becomes hypotensive.
6. Phenytoin (Dilantin) administered simultaneously with lorazepam or diazepam and saline
at 50 mg/minute until a loading dose of 18 mg/kg is reached.
a. In the U.S., IV Dilantin has been replaced with fosphenytoin (Cerebyx), 10–20 mg/kg IV;
this is a prodrug form of Dilantin that is rapidly and completely converted to phenytoin in
the blood.
b. Fosphenytoin does not irritate the veins, can be given with all common IV solutions, and
may be administered more quickly than Dilantin (150 mg/minute vs 50 mg/minute)
without risk of cardiovascular collapse.
c. It is also more expensive.
7. If the above measures are unsuccessful, intubate and administer phenobarbital (Luminal),
100 mg/minute IV to a maximum of 20 mg/kg, or diazepam (100 mg in 500 ml D W5
[dextrose 5% in water]), 40 ml/hour.
8. If still unsuccessful after 60 minutes, institute general anesthesia with isoflurane and
neuromuscular blockade.
D. Clinical pharmacology of the antiepileptic (Table 6-1)
TABLE 6-1 Clinical pharmacology of antiepileptic drugs
From Lehne RA: Drugs for epilepsy. In Pharmacology for nursing care, ed 5, p 191, St. Louis,
2004, WB Saunders.Drug Product Dosing Daily maintenance Target serum Induces hepatic
name schedule dosage in adults, mg level, mcg/ml ‡drug metabolism
Conventional antiepileptic drugs
3-4 times
Carbamazepine Tegretol 600-1800 6-12 Yes
Tegretol- 2 times
XR daily
2 times
Zarontin 1-2 times
Ethosuximide 750 40-100 No
(generic) daily
1-2 times
Phenobarbital 60-100 15-40 Yes
Phenytoin, 2-3 times
Phenytoin 200-300 10-20 Yes
prompt daily
Dilantin 2-3 times
Infatab daily
Dilantin 2-3 times
suspension daily
Phenytoin, 1 time
extended daily
Dilantin 1 time
Kapseals daily
3-4 times §Primidone Mysoline 500-750 Yes5-15daily
3-4 times† Depakene 750-3000 50-150 NoValproic acid daily
Depakote 2 times
ER daily
Newer antieplileptic drugs
3 timesFelbamate Felbatol 2400-3600 ND No
3 times
Gabapentin Neurontin 1200-3600 ND No
2 times †‡Lamotrigine Lamictal ND No400daily
2 times
Levetiracetam Keppra 2000-3000 ND No
2 times*Trileptal 900-2400 ND NoOxcarbazepine daily
2-4 times
Tiagabine Gabitril 16-32 ND No
2 times
Topiramate Topamax 200-400 ND No
1-2 times
Zonisamide Zonegran 200-400 ND No
To avoid serious adverse effects, all anticonvulsant medications must be tapered up or down while
drug levels and other pertinent diagnostic test results (laboratory and radiologic) are monitored.
Patients should be maintained at the lowest effective dose.
ND, Not determined.
*Oxcarbazepine does not induce enzymes that metabolize antiepileptic drugs, but it does induce
enzymes that metabolize other types of drugs.
†Dosages must be decreased in patients taking valproic acid.‡Dosages must be increased in patients taking drugs that induce hepatic drug–metabolizing enzymes.
§Target serum levels are 5 to 15 mcg/ml for primidone itself and 15 to 40 mcg/ml for phenobarbital
derived from primidone.
E. Drugs for specific types of seizures (Table 6-2)
TABLE 6-2 Drugs for specific types of seizures
From Lehne RA: Drugs for epilepsy. In Pharmacology for nursing care, ed 5, p 191, St. Louis,
2004, WB Saunders.
Drugs used for treatment
Effective and well Effective but less well *Seizure type Newer alternativestolerated tolerated
Partial seizures
Simple partial Carbamazepine Clorazepate Gabapentin
Oxcarbazepine Phenobarbital Lamotrigine
Phenytoin Primidone Levetiracetam
Valproic acid Topiramate
Same as for simple Same as for simple
Complex partial Same as for simple partial
partial partial
Secondarily Same as for simple
Phenobarbital Gabapentin
generalized partial
Primidone Lamotrigine
Primary generalized seizures
Tonic-clonic (grand
Carbamazepine Phenobarbital Lamotrigine
Oxcarbazepine Primidone Topiramate
Phenytoin Zonisamide
†Valproic acid Felbamate
Absence (petit mal) Ethosuximide Clonazepam Lamotrigine
Valproic acid Trimethadione
Myoclonic Clonazepam Lamotrigine
Valproic acid †Felbamate
Atonic Same as for myoclonic Same as for myoclonic
To avoid serious adverse effects, all anticonvulsant medications must be tapered up and down
while drug levels and other pertinent diagnostic test results (laboratory and radiologic) are carefully
monitored. Patients should be maintained at the lowest effective dose.
*These drugs appear effective for the seizures indicated. However, because experience with them is
limited, their clinical role has not been firmly established.
†Felbamate can cause aplastic anemia and liver failure. This drug should be reserved for patients
who have not responded to safer alternatives.
F. Adverse effects of newer antiepileptic drugs (Table 6-3)TABLE 6-3 Adverse effects of newer antiepileptic drugs
From Dichter M, Brodie MJ: Drug therapy: new antiepileptic drugs, N Engl J Med 334:4, 1996,
with permission. Copyright © 1996 Massachusetts Medical Society. All rights reserved.
© Massachusetts Medical Society1996
Drug Principal adverse effects Serious but rare adverse effects
Aplastic anemia
Hepatic failure
Gastrointestinal upset
Gastrointestinal upsetLamotrigine Stevens-Johnson syndrome
Gastrointestinal upset
Cognitive difficulties
Topiramate Gastrointestinal upset
Renal calculiTremor
Renal calculi
G. Interactions between newer antiepileptic drugs and conventional drugs (Table 6-4)
TABLE 6-4 Interactions between newer and conventional antiepileptic drugs
From Dichter M, Brodie MJ: Drug therapy: new antiepileptic drugs, N Engl J Med 334:4, 1996,
with permission. Copyright © 1996 Massachusetts Medical Society All rights reserved.
© Massachusetts Medical Society1996
Effect of
New drug conventional drugs Effect of new drug on conventional drugs
on new drug
Gabapentin None known None known
phenytoin, and
Lamotrigine carbamazepine Does not induce cytochrome P450
increase metabolism
by 50%
Valproic acid
When added to carbamazepine, may induce neurotoxicity
decreases metabolism
because of pharmacodynamic interactions
by 50%
Decreases metabolism of phenytoin and valproic acid
Valproic acid
Felbamate (increases serum phenytoin levels by approximately 20% and
decreases clearance
increases serum valproic acid levels by 18%-31%)
Decrease serum
Phenytoin and
carbamazepine levels
but increase serum
epoxide levels
Induces cytochrome P450, 3A isoform family (but less so than
Not affected by carbamazepine) May increase serum phenytoin and valproic
enzyme inducers acid levels by 20% to 30% if oxcarbazepine is substituted for
carbamazepine Increases metabolism of oral contraceptives
phenytoin, and
Tiagabine Does not induce cytochrome P450
enhance clearance
Does not affect serum phenytoin, carbamazepine, or valproic
acid levels
Phenytoin and
Topiramate carbamazepine Weak inducer of cytochrome P450
increase clearance
Valproic acid has no May increase serum phenytoin levels in some patients
marked effect (mechanism unknown)
Phenobarbital May increase serum phenytoin and carbamazepine levels (not
increases clearance in all studies)
H. Titrate dosages to achieve adequate serum levels. If a first drug partially controls seizures ata maximal therapeutic level, add a second drug to achieve therapeutic levels.
I. Never abruptly withdraw an anticonvulsant from a patient; these drugs should be tapered.
J. Vagus nerve stimulation (VNS): used in conjunction with medications by patients with
severe, uncontrolled seizures. Stimulation is typically applied for 30 seconds every 5 minutes.
When the vagus is stimulated, resultant impulses in some way interrupt or prevent abnormal
neuronal firing.
WT Blume, Diagnosis and management of epilepsy, Can Med Assoc J 168 (4) (2003) 441–448.
O Devinsky, Current concepts: patients with refractory seizures, N Engl J Med 340 (1999)
M Dichter, MJ Brodie, Drug therapy: new antiepileptic drugs, N Engl J Med 334 (1996)
FF Ferri, Practical guide to the care of the medical patient. ed 6 (2004) Mosby, St. Louis .
IS Grant, PJ Andrews, ABC of intensive care: neurological support, BMJ 319 (1999) 110–113.
M Lawal, Epilepsy management: management and treatment options for epilepsy, Br J Nurs 14 (16)
(2005) 854–858.
RA Lehne, Pharmacology for nursing care. ed 5 (2004) WB Saunders, St. Louis .
In: (Editors: SJ McPhee, MA Papadakis, LM Tierney) Current medical diagnosis and treatment ed
46 (2007) McGraw Hill/Appleton & Lange, New York.
S Miller, Neurological disorders, In: (Editor: VL Millonig) Adult nurse practitioner certification
review guide ed 4 (2005) Health Leadership Associates, Inc, Potomac, Md.
RE Rakel, Saunders manual of medical practice. ed 2 (2000) WB Saunders, Philadelphia .
P Ryvlin, Seizure disorders, Curr Opin Neurol 18 (2) (2005) 125–177; 198-210.
M Samuels, Update in neurology, Ann Intern Med 129 (1998) 878–885.
MR Torres, Seizures and epilepsy: an approach to diagnosis and management, J Clin Outcomes
Manage 12 (2) (2005) 103–115.
D Weaver, Epilepsy and seizures: everything you need to know (your personal health). (2001)
Firefly Books, Buffalo, NY .CHAPTER 7. Dementia
Dementia, 290.8
I. Definition
A. Broad (global) acquired impairment of intellectual function (cognition) that usually is
progressive and that interferes with normal social and occupational activities
B. Key features of dementia consist of intact arousal state and impairment of memory, intellect,
and personality.
C. Disorder characterized by one or more of the following: general decrease in level of
cognition, behavioral disturbance, and interference with daily function and independence
D. Loss of mental functions such as thinking, memory, and reasoning
E. Not a disease, but rather a group of symptoms caused by various diseases
F. Refer to Chapter 74 for ways to differentiate dementia from delirium.
II. Etiology
A. As many as 50 known causes of dementia
B. Develops when parts of the brain that are involved with learning, memory, and decision
making are affected by various infections or diseases
C. Alzheimer-type dementia (AD)
1. Most common form of dementia in the elderly
2. Accounts for 60% to 80% of dementia cases
3. Neuronal damage in AD is irreversible; therefore, the disease cannot be cured.
4. Histopathology of AD is characterized by neuritic plaques, neurofibrillary tangles, and
degeneration of cholinergic neurons in the hippocampus and cerebral cortex.
5. Beta-amyloid is present in high levels in AD; this may contribute to neuronal injury.
6. Results in cerebral atrophy
D. Diseases that cause degeneration or loss of nerve cells in the brain
1. Alzheimer's
2. Parkinson's
3. Huntington's
E. Vascular
1. Multi-infarct dementia
2. Stroke
3. Arteritis (15%-20%)
F. Infectious
1. HIV
2. Syphilis
3. Meningitis
4. Encephalitis
5. Abscess
6. Creutzfeldt-Jakob diseaseG. Postencephalitic syndrome, CNS anoxia (drug overdose, cardiac arrest)
H. Nutritional deficiencies
1. Vitamin B deficiency12
2. Folate deficiency
3. Other vitamin deficiencies
I. Toxic reactions
1. Chronic alcoholism
2. Drug toxicity
J. Subdural hematoma
K. Hydrocephalus
L. Chronic seizures
M. Illness other than in the brain
1. Kidney
2. Liver
3. CHF
4. Hypercapnia
5. Hypoxemia
6. Rhythm disturbance
7. Acute MI
8. Hypothyroidism/hyperthyroidism
N. Hearing loss
O. Blindness
P. Rule out depression
Q. Electrolyte imbalance
III. Clinical manifestations
A. Onset may be slow, continuing over a period of months or years.
B . Confusion and memory deficits (usually short term in nature: asking the same question,
repeatedly forgetting that the question was already answered)
C. Misplacing things: putting an iron in the refrigerator
D. Problems with language: forgetting simple words or using wrong words
E. Impaired abstract reasoning: unable to balance a checkbook because of forgetfulness about
what the numbers are and what to do with them
F. Higher cognitive functions may be impaired
1. Aphasia
2. Apraxia: inability to perform previously learned purposeful movements (i.e., previously
learned tasks) or to use objects properly
3. Agnosia: loss of comprehension of auditory, visual, or other sensations, although the
sensory sphere is intact; inability to recognize objects, shapes, persons, sounds, smells, and so
G. Disorientation: Patients may become easily lost, even in familiar surroundings, or may
wander.H. Patients may have difficulty with learned tasks, such as dressing or cooking.
I. Poor judgment: Patients may forget that they are watching a child and may leave the child at
J. Loss of initiative: becoming passive; not wanting to go places or see other people
K. Clouding of consciousness and orientation does not occur until the terminal stages.
L. Emotional problems such as depression, lability, or flattened affect
M. Changes in mood: fast mood swings—calm to tears to anger in minutes
N. Agitation, anxiousness, sleeplessness
O. Drastic personality changes: irritable, suspicious (paranoid ideation), fearful
P. Patients often lose insight into their deficits.
Q. Difficulty recognizing family and friends
R. Severe symptoms include the following:
1. Loss of speech
2. Loss of appetite
3. Weight loss
4. Loss of bowel and bladder control
5. Total dependence on caregiver
IV. Diagnosis
A. History
1. Preferably with family members available to give adequate history of cognitive and
behavior changes
2. Often, the spouse or other informant brings the problem to the physician's attention.
3. Self-reported memory loss does not usually correlate with dementia.
B. Physical examination
1. Neurologic examination
2. Cognitive testing
a. Attempt the Folstein Mini-Mental State Examination to screen for dementia.
i. Maximum score is 30.
ii. Score of 23 or less indicates cognitive impairment.
b. Document the progression of disease over time by repeating testing at 3- to 6-month
3. Examination should include observations of memory, thinking, concentration, attention,
judgment, insight, and behavior.
4. Mini-Cognitive Test: recall of three unrelated words, clock-drawing task
C. Screening laboratory examination
1. Glucose
2. Electrolytes
3. Magnesium
4. Calcium
5. Liver tests
6. BUN/creatinine7. Thyroid function tests
8. Vitamin B level, folate12
9. Venereal Disease Research Laboratory (VDRL) test
10. HIV (selected patients)
11. CBC with differential, clotting studies
12. Arterial blood gases
13. Cultures: blood, urine, sputum
14. Serum levels of ingested drugs
15. Illicit drugs and alcohol levels in selected patients
16. Albumin
D. Other tests, depending on patient history and findings of physical examination
1. CT of the head/MRI
Note: for tumor, subdural hematoma, infarction, hemorrhage, hydrocephalus, atrophy
2. Lumbar puncture—to rule out neurosyphilis, chronic meningitis, normal pressure
3. EEG
4. Chest x-ray—to rule out CHF, chronic lung disease, pulmonary embolus, infection
5. ECG
E. Identification of treatable causes is very important.
1. Drug-induced
2. Depression
3. Hypothyroidism/hyperthyroidism
4. Hypoglycemia
5. Vitamin B or folate deficiency12
6. Subdural hematoma
7. Liver failure
8. Normal pressure hydrocephalus
9. Stroke
10. CNS infection
11. Generalized infection
12. Cerebral neoplasm
13. Renal failure
14. Alcohol abuse
15. Hypoxia
16. Hypercalcemia
17. Vasculitis
18. Cardiopulmonary disorder
19. Anemia
F. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria
for dementia
1. Memory impairment
2. At least two of the following: aphasia, aproxia, agnosia, disturbances in executivefunctioning
3. Disturbance in 1 or 2 (above) significantly interferes with work, social activities, or
4. Disturbance does not occur exclusively during delirium.
V. Management
A. Supportive care: Consult social services.
B. Treat underlying precipitating illnesses.
C. Attempt to withdraw, reduce, or stop all nonessential medications.
D. Maintain nutrition: dietary consult
E. Avoid restraints, except for safety.
F. Speech therapy/physical therapy
G. Address safety issues: Coordinate appropriate safety measures with the patient's caregiver to
prevent injury from falls, wandering, cooking, driving, etc.
H. Because a cholinergic deficiency is present in Alzheimer's disease, cholinesterase inhibitors
modestly improve cognition, behavior, and function, and they slightly delay disease progression.
1. Donepezil (Aricept): 5-10 mg once a day at bedtime. Well tolerated with convenient
dosing; therefore, drug of choice
2. Rivastigmine (Exelon): Initial dose, 1.5 mg twice daily; maximum dose, 6 mg twice daily;
should be administered with food to enhance absorption. Similar to other cholinesterase
inhibitors, it can cause peripheral cholinergic adverse effects. Significant weight loss (7% of
initial weight) occurs in 19% to 26% of patients.
3 . Galantamine hydrobromide (Razadyne): Begin at 4 mg twice daily for a minimum of 4
weeks, after which the dosage may be increased to 8 mg twice daily. Four weeks later, the
dosage may be increased again to 12 mg twice daily. For patients with moderate renal or
hepatic impairment, the maximum dose is 16 mg daily. In those with severe renal and hepatic
impairment, this drug should be avoided.
4. Tacrine (Cognex) carries a significant risk of liver damage; therefore, it should be avoided.
I. N-methyl-d-aspartate (NMDA) receptor antagonist
1. Memantine (Namenda)
a. Used to prevent the progression of Alzheimer's disease
b. Blocks pathologic stimulation of NMDA receptors and protects against further damage
in patients with vascular dementia
c. Initiate with 5 mg once daily, increase dose by 5 mg/week over a 3-week period to target
dose of 10 mg twice daily.
J. Medications that affect serotonin have been useful in controlling aggression and agitation.
1. Lithium (Caution: Do not start lithium at a facility that cannot monitor levels.)
2. Trazodone
3. Buspirone
4. Clonazepam (Note: Atypical antipsychotics are gaining favor over Haldol, Trazodone and
K. Dopamine blockers have been used for many years to treat aggression and hyperactivity of
delirium—haloperidol (Haldol): Administer 0.5-1 mg IV/IM or PO initially, and observe
patient for 20 to 30 minutes. If the patient's condition remains unmanageable and the patient has
had no adverse reactions to haloperidol, double the dose and continue to monitor. Lorazepam
(Ativan), 1 mg IM every hour, may also be administered if needed.L. Carbamazepine (Tegretol), 100-400 mg daily; has recently been shown to reduce agitation in
patients with Alzheimer's disease
M. Emotional lability has been decreased with medication in some cases: two small doses of
imipramine (Impril), 25 mg PO 2 or 3 times daily, or fluoxetine (Prozac), 5-20 mg/day
N. Depression responds to the usual doses of antidepressants such as trazadone (Deseryl), as
well as to selective serotonin reuptake inhibitors and monoamine oxidase inhibitors, which have
the fewest anticholinergic adverse effects.
O. Other possible treatments under investigation include the following:
1. Vitamin E and selegiline (Carbex) because of their antioxidant properties
2. Nonsteroidal anti-inflammatory drugs (NSAIDs)
3. Ginkgo biloba
4. Antibiotics to treat Chlamydia pneumonia
5. In vitro studies have shown that rifampin and tetracyclines interfere with accumulation of
beta-amyloid peptide.
American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders. Fourth
edition (1994) APA Press, Washington DC .
M Boustani, B Peterson, L Hanson, et al., Screening dementia in primary care: a summary of the
evidence for the U.S. preventive service task force, Ann Intern Med 138 (2003) 927.
L Clare, Awareness in dementia: a review of assessment methods and measures, Aging Mental
Health 9 (5) (2005) 394–413.
M Eccles, J Clarke, M Livingston, et al., North of England Evidence Based Guidelines Development
Project: guideline for the primary care management of dementia, BMJ (Clinical Research Ed)
317 (1998) 802–808.
FF Ferri, Practical guide to the care of the medical patient. ed 6 (2004) Mosby, St. Louis .
GT Grossberg, AK Desai, Management of Alzheimer's disease, J Gerontol Series A Biol Med Sci 58
(4) (2003) 331–353.
L Kennedy-Malone, KR Fletcher, LM Plank, Management guidelines for gerontological nurse
practitioners. (2000) FA Davis, Philadelphia .
RA Lehne, Pharmacology for nursing care. ed 5 (2004) WB Saunders, St. Louis .
In: (Editors: SJ McPhee, MA Papadakis, LM Tierney) Current medical diagnosis and treatment ed
46 (2007) McGraw Hill/Appleton & Lange, New York.
RE Rakel, R Kersey, Saunders manual of medical practice. ed 2 (2000) WB Saunders, Philadelphia
Screening for dementia: recommendation and rationale, Ann Intern Med 138 (2003) 195.
GW Small, PV Rabins, PP Barry, et al., Diagnosis and treatment of Alzheimer's disease and related
disorders: Consensus Statement of the American Association for Geriatric Psychiatry, the
Alzheimer's Association, and the American Geriatrics Society, JAMA 278 (1998) 1363–1371.
NH Trinh, J Hoblyn, S Mohanty, et al., Efficacy of cholinesterase inhibitors in the treatment of
neuropsychiatric symptoms and functional impairment in Alzheimer disease: a meta-analysis,
JAMA 289 (2003) 210.
S Weintraub, Treatment, education, and resources for non-Alzheimer dementia: one size does not fit
all, Alzheimer's Care Q 6 (3) (2005) 201–214.
D Wilkinson, Anti-psychotic use in patients with dementia, Geriatr Med 34 (9) (2004) 49–50;
52,54-55.CHAPTER 8. Cardiovascular Assessment
Cardiovascular disorders, 302.2
I. Cardiac cycle review
A. Atrio ventricular (AV) valves close.
B. Aortic/pulmonic (semilunar) valves open.
C. Aortic/pulmonic valves close.
D. AV valves open.
E. Rapid ventricular filling (70% fill of ventricles)
F. Atrial kick (atria pushing out remaining blood to the ventricles)
I I . Auscultatory areas of the precordium—characterized by location at which valvular
activity may usually be heard best
A. Aortic—Second right intercostal space (ICS) at the right sternal border (S heart sound2
louder than S )1
B. Pulmonic—Second left ICS at the left sternal border (S louder than S )2 1
C. Erb's point—Third ICS at the left sternal border
D. Tricuspid—Left lower sternal border at the fifth ICS (closure of AV valves)
E. Mitral—Fifth ICS midclavicular line (S louder than S )1 2
III. S Heart sound1
A. Denotes closure of the mitral and tricuspid (AV) valves
B. Occurs almost simultaneously with apical and carotid impulses
C. Coincides with the R wave on ECG
D. More easily heard than S at the apex2
IV. S Heart sound2
A. Denotes closure of the aortic and pulmonic (semilunar) valves
B. Occurs at the onset of ventricular diastole (Note: Ventricular systole occurs between S and1
S .)2
C. Heard louder than S at the base of the heart1
V. Split S heart sound2
A. Normal event heard at end inspiration in some patients
B. Located in the pulmonic auscultatory area
C. If the patient holds his or her breath, the sounds will disappear.
D. Occurs approximately every fourth heartbeat
VI. S Heart sound3
A. Referred to as a ventricular gallop
B. Caused by resistance to ventricular fillingC. Occurs immediately after S (early diastole) at the left lower sternal border (apex)2
D. Occurs with such conditions as fluid overload, congestive heart failure, and cardiomyopathy
E. Normal sound associated with pregnancy (i.e., hyperdynamic state of increased volume)
F. Sounds like the word “Ken-tuc-ky”
VII. S Heart sound4
A. Referred to as an atrial or presystolic gallop
B. Caused by increased ventricular diastolic pressure
C. Occurs immediately before S (late diastole)1
D. Most clearly heard at the left lower sternal border (apex)
E. Occurs with such conditions as myocardial infarction, hypertension, and ventricular
F. Sounds like the word “Ten-nes-see”
VIII. Murmur
A. “Blowing” or “swooshing” sound that results from turbulent blood flow. Identified by the
following variables:
1. Timing—Is the murmur systolic or diastolic, pansystolic or holosystolic, pandiastolic or
2. Loudness—graded I through VI
Grade I: barely audible
Grade II: clearly audible but faint
Grade III: moderately loud, easily heard
Grade IV: loud, associated with a thrill
Grade V: very loud; heard with one corner of stethoscope off thechest wall
Grade VI: loudest; no stethoscope needed
3. Pitch—Is the pitch high, low, or medium, crescendo, decrescendo, plateau, or
4. Quality—Is the quality musical, blowing, rumbling, or harsh?
5. Location—In what area is the murmur heard best?
6. Radiation—Is the murmur heard at other auscultatory areas (e.g., neck, back, axilla)?
7. Posture—Does the murmur disappear or become louder with changes in posture?
B. Early diastolic murmurs: due to incompetent semilunar valves (e.g., aortic or pulmonic
C. Diastolic rumbling murmurs: due to mitral stenosis (low-pitched, noted at apex better in the
left lateral position, and does not radiate) and tricuspid stenosis (heard louder with inspiration)
D. Midsystolic ejection murmurs: due to forward flow through semilunar valves, namely, aortic
stenosis (loud, harsh, crescendo-decrescendo sound that radiates) and pulmonic stenosis (most
often, systolic, medium-pitched, crescendo-decrescendo sound that also radiates)
E. Pansystolic regurgitant murmurs: due to backward flow, such as with mitral regurgitation
(loud, blowing, heard best at apex, and radiates to axilla) and tricuspid regurgitation (soft,
blowing, heard best at left lower sternal border, louder with inspiration)
XI. Clicks
A. Midsystolic click: most common type; associated with mitral valve prolapseB. Aortic ejection click: related to stenosis; occurs during early systole; audible at apex and base
of the heart
C. Pulmonic ejection click: occurs during early systole; audible at the base of the heart only
X. Friction rub
A. “Scratchy,” high-pitched sound
B. Classic sound of pericarditis (inflammation)
C. Usually heard best at the apex with the patient leaning forward
XI. Peripheral pulse amplitude
A. Graded on a scale from 0 to 4
1. Bounding = +4
2. Full = +3
3. Normal = +2
4. Diminished = +1
5. Absent = 0
XII. Electrocardiographic changes associated with electrolyte disturbances
A. Hyperkalemia
1. Tall, peaked T waves
2. Widening of the QRS complex
3. Prolongation of the P wave/PR interval
4. Increased levels of K decrease ventricular depolarization and slow AV conduction.+
B. Hypokalemia
1. U waves and appearance of new or additional premature ventricular contractions
2. Less common changes include bradycardia, atrial flutter, AV block, and enhanced effects
of digitalis toxicity.
C. Hypercalcemia
1. AV blocks, bundle branch block, and bradycardia related to increased contractility of the
heart and shortening of the period of ventricular repolarization
2. Potentiated effects of digitalis toxicity
D. Hypocalcemia
1. Bradycardia to ventricular arrhythmia and asystole because low calcium levels decrease
2. Reductions in cardiac output, including hypotension and decreased effectiveness of
E. Hypermagnesemia
1. Rarely evident in the acute care setting
2. Usually related to renal failure or overadministration of magnesium during replacement
F. Hypomagnesemia
1. Changes similar to those associated with hypokalemia and hypocalcemia
a. Appearances of U wave
b. Prolonged PR/QT intervals
c. Widened QRS complexesd. Flattened T waves
e. Supraventricular tachycardia (SVT)
f. Ventricular arrhythmia
g. Torsades de pointes
2. Note: Hypomagnesemia may cause hypertension and coronary/systemic vasospasm.
3. Hypomagnesemia usually must be corrected before replacement therapy for hypokalemia
and hypocalcemia can be effective.
EG Bradley, Cardiovascular assessment, In: (Editors: L Bucher, S Melander) Critical care nursing
(1999) WB Saunders, Philadelphia.
ME Estes, Health assessment and physical examination. ed 3 (2005) Delmar Publishers, Cincinnati
AP Garrett, Assessing cardiovascular status in the older adult with cognitive impairments, J
Cardiovasc Nurs 11 (1997) 1–11.
In: (Editors: L Goldman, E Braunwald) Primary cardiology ed 2 (2003) Elsevier, Philadelphia.
C Jarvis, Physical examination and health assessment. ed 4 (2004) WB Saunders, St. Louis .
J Kelley, J Weber, Health assessment in nursing. ed 2 (2003) Lippincott Williams and Wilkins,
Philadelphia .
LM Ludwig, Cardiovascular assessment for home healthcare nurses. Part II: Assessing blood
pressure and cardiac function, Home Healthcare Nurse 16 (1998) 547–554.
LA Thelan, LD Urden, ME Lough, et al., Critical care nursing: diagnosis and management. ed 5
(2005) Mosby, St. Louis .