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Normal Pressure Hydrocephalus-2 Nursing CEs
Normal Pressure Hydrocephalus-2 Nursing CEs
Author: Kristi Hudson RN MSN CCRN

Course Description:
This course is designed to give an overview of the care and management of the patient with Normal Pressure Hydrocephalus (NPH). Statistics surrounding NPH and a description of the overall scope of the problem will be presented. The anatomy, pathophysiology, etiology, signs/symptoms and diagnosis of this syndrome will also be presented. Treatment options including the placement of a ventriculo-peritoneal shunt (VPS) and nursing care and management of the post-op VPS patient will also be presented. NANDA nursing diagnoses appropriate for the patient with NPH will be the final focus of this course.
Course Objectives:
Upon completion of this course the student will be able to:
  • List the statistics surrounding the diagnosis of NPH
  • Gain a better understanding of the scope of the problem surrounding NPH
  • Describe how CSF flows throughout the brain and spinal cord
  • Discuss the pathophysiology of NPH
  • Explain 2 possible causes for NPH
  • Describe the classic triad of symptoms found with NPH
  • Explain the diagnostic process for NPH
  • Describe the treatment option of VPS
  • Discuss the nursing care and management of the patient post VPS
  • Describe 3 possible complications of a VPS
  • List 2 appropriate NANDA nursing diagnoses for patients with NPH
Statistics and Scope of the Problem:
  • Normal Pressure Hydrocephalus (NPH) is a debilitating syndrome that affects an estimated 5% of population over the age of 65, who suffer from dementia. Some experts estimate that as many as 375,000 Americans who currently have NPH have actually been misdiagnosed with either Alzheimer’s or Parkinson’s disease.
  • Unfortunately because this syndrome is often misdiagnosed (with either Parkinson’s disease or Alzheimer’s disease); many people are forced to live with the symptoms associated with this syndrome without relief or expectation for subsequent recovery. Because NPH is one of the only forms of dementia that can be controlled and even reversed, it is imperative that an accurate diagnosis be made.
  • NPH is a brain disorder that causes blockage of the cerebral spinal fluid (CSF) which causes enlargement of the ventricles and compression of brain tissue. What is unique about this syndrome is that even with the noted enlargement of the ventricles and compression of brain tissue, the patient displays normal CSF opening pressures on lumbar puncture and normal intracranial pressures.
  •  NPH is a syndrome that begins gradually and presents with a triad of symptoms that include: gait disturbance, urinary incontinence and dementia. The onset of symptoms are insidious and often go unnoticed by the patient and/or family members, and if noted are often attributed to the “normal aging process”.
Anatomy/Pathophysiology and Etiology of NPH:
Anatomy (travel of CSF): The majority of CSF is formed in specialized areas within the ventricle which is known as the “choroid plexus”. The choroid plexus produces CSF at a rate of approximately 20ml to 25ml per hour. The CSF circulates from the two lateral ventricles through the third ventricle (a single mid-line ventricle) to the fourth ventricle which is located within the posterior fossa of the brain. After exiting the ventricular system the CSF is then circulated to the subarachnoid space surrounding the brain and spinal column (this provides a cushion or protection). From the subarachnoid space and spinal column, CSF is absorbed into the venous sinuses.
The pathophysiology for NPH is still being debated but most experts will agree that aberrations of cerebral spinal fluid (CSF) flow and absorption are central to the pathophysiology of this syndrome. The following are suggested Pathophysiologic causes of NPH:

  • One suggested mechanism is that the transmantle pressure gradient of CSF within the ventricle is greater then CSF pressure in the subarachnoid space.
  • A second mechanism suggests that the transmantle pressure impairment is at the level of the aqueduct (which would cause non-communicating NPH) or distal to the aqueduct (which would cause communicating NPH).
As with the pathophysiology of NPH, the actual cause of this syndrome is also unknown. It is estimated that approximately 50% of the cases are truly idiopathic. The following are suggested causes of NPH that can be found in the literature:

  • A history of events exists that can alter CSF flow dynamics, such as previous subarachnoid hemorrhage, trauma, meningitis, or surgery.
  • The arachnoid villi fail to maintain an adequate removal of CSF.
  • NPH often begins in infancy as benign external hydrocephalus.
  • Fibrosis and scarring of brain tissue inhibits the absorption of CSF.
  • Tumor formation inhibits the production and or absorption of CSF.
Signs and Symptoms of NPH:
One thing that is clear regarding NPH is the classic triad of symptoms that present with this syndrome. These symptoms include:

Gait Disturbance: (history of falls, gait instability, balance disturbances, decreased endurance, walking with very small steps and shuffling).

Urinary Incontinence: (Although bladder function is assessed and tested; the urinary incontinence that is associated with NPH is thought to be primarily a result of the gait and dementia components of this syndrome).

Dementia: (Although the symptoms of NPH are similar to those of other dementias; there are differences. While NPH patients often show a more severe impairment in the areas of attention, psychomotor movement and calculation; they often score higher in the areas of memory, delayed recall and overall orientation when compared to patients with other forms of dementia such as Alzheimer’s disease).

Diagnosis of NPH:
In the outpatient setting most experts agree that radiologic findings such as Computerized Tomography (CT) or Magnetic Resonance Imaging (MRI) alone are too subjective to diagnose NPH. The combination of radiologic testing with inpatient evaluation of those who are suspected of having NPH may prove to be the most successful way to accurately diagnose NPH. The following is a description of an inpatient 4 day diagnostic program:
  • Upon admission the patient is individually evaluated by physical therapy (PT), occupational therapy (OT) and speech therapy (ST) to gather baseline evaluations.
  • Once baseline assessments are complete; a Neurosurgeon places a lumbar drain and continuous CSF drainage is started (usually 4-8 ml/hr).
  • Using the same therapists and the same testing methods; PT, OT and ST evaluations are repeated once a day for each of the following three days to evaluate and document any improvement in the patient’s initial symptoms.
  • After the final set of evaluations is complete on day four, the lumbar drain is discontinued and the patient is discharged home.
  • Not until the patient is discharged from the hospital are the results of this testing evaluated (this is done post discharge to avoid any bias or pre-conceived opinions regarding improvement).
  • To determine if a patient showed significant improvement in gait, urinary incontinence and/or symptoms of dementia after continuous CSF drainage; a multi-disciplinary team consisting of physicians (Neurosurgery and Neurology), therapist (PT, OT and ST) and nurses meet to review the results.
  • When a diagnosis of NPH has been made and analysis of the data confirms improvement of symptoms after continuous CSF drainage; an internal continuous CSF drain or ventriculo-peritoneal shunt (VPS) can by offered.
  • Differential Diagnosis: Because NPH can mirror other neurological disorders, the following should be ruled out prior to diagnosing NPH with certainty:
  1. Subcortical arteriosclerotic encephalopathy (SAE)
  2. Multi-infarct encephalopathy
  3. Parkinson’s disease
  4. Chronic alcoholism
  5. Alzheimer’s’ disease
  6. Combination of several diseases (orthopedic deficits, prostate disorders, and mild dementia may present similar to NPH)
  7. Carcinomatous meningitis
  8. Intracranial infection (such as abscess, subdural empyema, meningitis)
  9. Subdural hematoma
  10. Systemic disease (Addison’s disease, hypothyroidism) or malignancy
Surgical Intervention (VPS Placement):
Surgical placement of a VPS can be offered to patients diagnosed with NPH as to an effective and permanent treatment option. The surgical procedure for placement of a VPS drain is as follows:
  • General anesthesia is administered.
  • The patient is placed on their back with head tilted to the left.
  • Hair over the scalp is clipped and shaved.
  • Two incisions are made (a small abdominal incision and a curved scalp incision). The scalp is pulled back and a burr hole is drilled through the skull.
  • The VP shunt is usually threaded first through the abdominal incision.
  • The VP shunt is then upwardly threaded under the skin through the chest, neck, behind the ear and into the enlarged ventricle.
  • After the tubing is in place a reservoir is attached and fitted into a space between the scalp and the skull.
  • The shunt can be set to remove a specified amount of CSF per hour (this amount can also adjusted externally using a magnetic device).
  • When complete the shunt is completely internal and cannot be felt or seen.
Nursing Care and Management VPS Surgery:
Nursing care and management should focus on returning the patient to a state of normal health and well being as soon as possible.
Nursing Assessment:
  • Frequent Vital Signs (Q 2 hrs initially)
  • Frequent Neuro checks (Q 2 hrs initially)
  • LOC
  • Pupillary Reaction
  • Sensory and Motor Function
  • Strict I&O
  • Assessment of Pain
  • Assessment of Surgical Incisions (head and abdomen)
Nursing care and Management:
  • Development of a Pt. Specific Nursing Care Plan
  • Turning the Pt. Q 2 Hours
  • Application of Sequential Compression Devices
  • HOB @ 30%
  • Patient/Family Teaching
  • Early Ambulation and Participation in Activities of Daily Living
  • Discharge Planning
Potential Complications Associated With VPS Surgery:
All of the following are considered to be potential post-op complications associated with ventriculo-peritoneal shunting. Identifying the onset of these complications should also be part of the nursing assessment.
  • Subdural Hematoma (Subdural hematoma is usually not apparent in the immediately post-op phase. Patients often present with a headache or progressive neurologic deficit days or even weeks after insertion of a VP shunt).  
  • Neck Hematoma (Injury to the external jugular vein or other vascular structures in the neck can result in bleeding and swelling of the neck in the post-op phase).
  • Skin Perforation (The VPS is located in the subcutaneous tunnel, just a few millimeters below the skin surface. It is in the space between the subcuticular and superficial muscule fascial layers of the head, neck, chest, and abdomen. Skin perforation is rare, but should be assessed for during routine nursing assessment).
  • Lung Injury (Because the shunt is passed below the clavicle it is possible to perforate the inner visceral region of the lung and cause a pneumothorax. Complaints of chest pain or shortness of breath should be followed up immediately).
  • Ileus (Ileus is a frequent and almost always transient complication of surgery in the abdomen. Auscultate for active bowel sounds and report hypoactive or absent bowel sounds immediately).
  • Peritonitis (Peritonitis resulting in irritation to the abdominal wall secondary to bowel rupture is an immediate post-op concern. Patients will present with a stiff, extremely sensitive abdomen and absent bowel sounds. Immediate surgical intervention to repair bowel rupture is required).
  • Infection (Infection of a VP shunt is a dreaded complication because it frequently requires revision or removal and replacement of the entire system. Patients with an infected VPS often display fever, malaise and neurological deterioration).
  • Shunt Disconnection (Shunt systems include several components in a sequence in order to provide a continuous pathway for drainage. S/S for disconnection of a VPS include headache, increased ICP, Neurophysiologic compromise).
NANDA Nursing Diagnosis for NPH:
  • Immobility r/t gait disturbance
  • Potential for skin breakdown r/t incontinence
  • Self-care deficit r/t dementia
  • Ineffective family coping
  • Ineffective individual coping
  • Potential for injury
  • Knowledge deficit
  • Potential for nutritional deficit
Dalvi, A., MD. Assistant Professor, Department of Neurology, University of Chicago (2007). Normal Pressure Hydrocephalus. Retrieved on August 28, 2009 at:

Bradley, W., Safar, F., Hurtado, C., Ord, J., & Alksne, J. Increased Intracranial Volume: A Clue to the Etiology of Idiopathic Normal-Pressure Hydrocephalus? American Journal of Neuroradiology 25:1479-1484, October 2004 Retrieved on October 28, 2006 at:

Brynes, G. (2006). Dealing with dementia: Help for relatives, friends and caregivers. Retrieved on October 20, 2006 at:
Byrd, C., RN, MSN. Normal pressure hydrocephalus: Dementia’s hidden cause. The Nurse Practitioner: The American Journal of Primary Health Care. July 2006; Vol. 31; Number 7. Pgs. 28-35. Retrieved on October 8, 2006 from ProQuest Database.
Dalvi, A., MD. (2006). Normal pressure hydrocephalus. Retrieved on March 17, 2006 at:
Hickey, J. (2003). The clinical practice of neurological and neurosurgical nursing. (5th ed.) (pp. 315-316). Lippencott, Williams and Wilkins. Philadelphia
Koop, C., E. (2006). Normal pressure hydrocephalus. Retrieved on March 15, 2006 at:
Marmarou, A., Bergsneider, M., Relkin, N., Klinge, P., & Black, P. Development of guidelines for idiopathic normal pressure hydrocephalus. Neurosurgery. 57:S2 -1-S2-3; 2005. Retrieved on October 19, 2006 at:
Neurosurgery InfoNet. (2006). Ventriculo-peritoneal (VP) shunting. Retrieved on November 11, 2006 at:
Ogino, A., Kazui, H., Miyoshi, N., Hasimoto M., Ohkawa, S., et al. Cognitive impairment in patients with idiopathic normal pressure hydrocephalus. Dementia and Geriatric Cognitive Disorders. Feb.2006; 21(2); 113-119. Retrieved on July 30, 2006 from ProQuest Database.
Verrees, M., & Selman, W., (2002). Management of normal pressure hydrocephalus. Retrieved on October 17, 2006 at:
Wilson, J. & Islam, O. (2005). Normal Pressure Hydrocephalus. Retrieved on March 17, 2006 at:

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