University of Kirkuk L -1-

College of Nursing Adult Nursing

Second Stage Lecturer
Hussein Ali

Nursing management of patients with nervous system disorder

Lecture outlines
➢ Assessment and diagnostic test
➢ Intracranial pressure
➢ Brain tumor
➢ Meningitis
➢ Brain abscess
➢ Epilepsy

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Anatomy and function of NS:
The nervous system may be categorized according to structure or function.
Structure, the nervous system is divided into the central nervous system (brain and spinal
cord) and peripheral nervous system (cranial and spinal nerves). Functional divisions include
the somatic (voluntary) and visceral (involuntary) nervous system.
The nervous system is a complex network of nerves and nerve cells (neurons) that
carry signals or messages to and from the brain and spinal cord to different parts of the body.
The nervous system is involved in receiving information about the environment around us
(sensation) and generating responses to that information (motor responses).

Diagnostic Tests for Patients with Neurological Disorders:

1. Complete medical history and physical examination.
2. A cranial computed tomography (CT): scan uses many x-rays to create pictures of the
head, including the skull, brain and sinuses. It is used primarily to rule out:

• organic disease such as a tumor or bleeding in the brain as a cause of the headache
problem. detection of a brain tumor or a blood clot.

3. Electroencephalogram (EEG) : a procedure that records the brain's continuous,

electrical activity by means of electrodes attached to the scalp.
4. Brain MRI, is a magnetic resonance imaging is performed to:

• monitor a patient's brain activity. detect brain trauma caused by accidents and also,
• detects possible occurrences of stroke and brain aneurysms as well.

5. Positron emission tomography (PET) : in nuclear medicine, a procedure that measures

the metabolic activity of cells.
6. Arteriogram (Also called an angiogram) : an x-ray of the arteries and veins to detect
blockage or narrowing of the vessels.
7. Spinal tap (Also called a lumbar puncture.) .

• a special needle is placed into the lower back, into the spinal canal. This is the area
around the spinal cord.
• The pressure in the spinal canal and brain can then be measured.
• A small amount of cerebral spinal fluid (CSF) can be removed and sent for testing
to determine if there is an infection or other problems.

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8. Neurosonography: a procedure that uses ultra-high-frequency sound waves that enable
the physician to analyze blood flow in cases of possible stroke.
9. Ultrasound (Also called sonography.): Ultrasounds are used to view internal organs as
they function, and to assess blood flow through various vessels.

Intracranial pressure:

The rigid cranial vault contains brain tissue (1400 g), blood (75 mL), and CSF (75
mL). The volume and pressure of these three components are usually in a state of equilibrium
and produce the ICP. ICP is usually measured in the lateral ventricles, with the normal
pressure being 0 to 10 mm Hg, and 15 mmHg being the upper limit of normal (normal adult
ICP is defined as 5 to 15 mm Hg)
Because of the limited space for expansion within the skull, an increase in any one of
the components causes a change in the volume of the others. Because brain tissue has limited
space to expand, compensation typically is accomplished by displacing or shifting CSF,
increasing the absorption or diminishing the production of CSF, or decreasing cerebral blood
volume. Without such changes, ICP will begin to rise.
Pathophysiology:
Increased ICP affects many patients with acute neurologic conditions. This is because
pathologic conditions alter the relationship between intracranial volume and ICP. Although
elevated ICP is most commonly associated with head injury, it also may be seen as a
secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and
toxic and viral encephalopathy. Increased ICP from any cause decreases cerebral perfusion,
stimulates further swelling (edema), and may shift brain tissue through openings in the rigid
dura, resulting in herniation, a dire and frequently fatal event.
Causes ICP:
A-Increased brain tissue volume
1- Tumor
2- Hemorrhage
3- Abscess or inflammation
4- Brain tumor

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 5- Cranial surgery
6- Ischemia and necrosis.
B-Increased cerebrospinal fluid volume
1- Obstructive.
2- Non obstructive hydrocephalus
C- Increased blood volume
1- Increased right atrial pressure.
2- Dural sinus thrombosis.
3- High atrial Paco2

Clinical Manifestations of ICP patient:

1- Lethargy is the earliest sign of increasing ICP. Slowing of speech and delay in
response to verbal suggestions are early indicators.
2- Sudden change in condition, such as restlessness, confusion, or increasing drowsiness.
3- As pressure increases, patient becomes stuporous and may react only to loud auditory
or painful stimuli. This indicates serious impairment of brain circulation, and
immediate surgical intervention may be required. With further deterioration, coma and
abnormal motor responses in the form of decortication, decerebration, or flaccidity
may occur.
4- When coma is profound, pupils are dilated and fixed, respirations are impaired, and
death is usually inevitable.
5- Decreased cerebral perfusion pressure (CPP) can result in a Cushing’s response and
Cushing’s triad (bradycardia, bradypnea, and hypertension); widening pulse pressure
is an ominous sign.
Assessment and Diagnostic Methods:
• Computed tomography (CT) and magnetic resonance imaging (MRI) most common
diagnostic tests.
• ICP monitoring provides useful information (ventriculostomy, subarachnoid bolt/screw,
epidural monitor, fiberoptic monitor).

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Complications:
• brain stem herniation, results from an excessive increase in ICP in which the
pressure builds in the cranial vault and the brain tissue presses down on the brain stem.
This increasing pressure on the brain stem results in cessation of blood flow to the
brain, leading to irreversible brain anoxia and brain death.
• Diabetes insipidus, is the result of decreased secretion of antidiuretic hormone
(ADH). The patient has excessive urine output, decreased urine osmolality
• Syndrome of inappropriate antidiuretic hormone (SIADH). is the result of
increased secretion of ADH. The patient becomes volume-overloaded, urine output
diminishes, and serum sodium concentration becomes dilute.
Medical Management:
Increased ICP is a true emergency and must be treated promptly. Immediate
management involves invasive monitoring of ICP, decreasing cerebral edema, lowering the
volume of CSF, or decreasing cerebral blood volume while maintaining cerebral perfusion.
Pharmacologic Therapy
• Osmotic diuretics and possibly corticosteroids are administered, fluid is restricted, CSF is
drained, fever is controlled (using antipyretics, hypothermia blanket, with chlorpromazine
[Thorazine] to control shivering), and cellular metabolic demands are reduced (with
barbiturates, paralyzing agents).
• If patient does not respond to conventional treatment, cellular metabolic demands may be
reduced by administering high doses of barbiturates or administering pharmacologic
paralyzing agents, such as pancuronium (Pavulon). Patient requires care in a CCU
Nursing Interventions ICP:
1- Achieving cerebral tissue perfusion
• Monitor for bradycardia and rising blood pressure.
• Keep the patient's head in midline position .
• Extreme hip flexion is avoided because this position causes an increase in intra-
abdominal and intra thoracic pressure.
• Avoid isometric muscle contractions, emotional stress.
• Enema and catheters, abdominal distension is avoided, if possible.

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2- Attaining normal respiration pattern:
• Monitor for irregular respiration.
• Paco2 should be maintained between 25-30 mmHg.
• Record a neurological observation.
3-Achieving airway clearance:
• Suction and Administer oxygen, if needed.
• Discourage coughing and straining and Elevate the head of the bed.
4-Preventing infection.
• Keep dressing set clean and dry.
• Aseptic technique is used when changing the dressing.
• Check the drainage system for loose connections, because leakage may lead to
infection.
• Monitor for signs & symptoms of meningitis, fever, chills, neck rigidity
Meningitis:
Meningitis is an inflammation of the lining around the brain and spinal cord
(inner layer is the pia mater, The middle layer is the arachnoid, outer layer is called the dura
mater) caused by bacteria or viruses. Meningitis is classified as septic or aseptic. The aseptic
form may be viral or secondary to lymphoma, leukemia, or human immunodeficiency virus
(HIV). The septic form is caused by bacteria such as Streptococcus pneumoniae and
Neisseria meningitidis.

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Pathophysiology:
The causative organism enters the bloodstream, crosses the blood–brain barrier, and
triggers an inflammatory reaction in the meninges. Independent of the causative agent,
inflammation of the subarachnoid and pia mater occurs. Increased intracranial pressure (ICP)
results. Meningeal infections generally originate in one of two ways: either through the
blood- stream from other infections (cellulitis) or by direct extension (after a traumatic injury
to the facial bones). Bacterial or meningococcal meningitis also occurs as an opportunistic
infection in patients with acquired immunodeficiency syndrome (AIDS) and as a
complication of Lyme disease.

Clinical Manifestations:
1. Headache and fever are frequently the initial symptoms. Fever tends to remain high
throughout the course of the illness. The headache is usually either steady or throbbing
and very severe as a result of meningeal irritation. Meningeal irritation results in a
number of other well-recognized signs common to all types of meningitis
2. Stiff neck: This is an early sign. Any attempts at flexion of the head are difficult
because of spasms in the muscles of the neck. Forceful flexion causes severe pain.
3. Positive Kernig's sign: When the patient is lying with the thigh flexed on the abdomen,
the leg cannot be completely extended.
4. Photophobia (extreme sensitivity to light)
5. Disorientation and memory impairment are common early in the course of the illness.
6. Seizures occur in 30% of adults with S. pneumoniae meningitis and are the result of
areas of irritability in the brain.
7. Positive Brudzinski's sign: When the patient's neck is flexed (after ruling out cervical
trauma or injury), flexion of the knees and hips is produced; when the lower extremity
of one side is passively flexed, a similar movement is seen in the opposite extremity
Brudzinski's sign is a more sensitive indicator of meningeal irritation than Kernig's
sign .

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Assessment and Diagnostic Findings:
• Computed tomography (CT) scan or magnetic resonance imaging (MRI) scan to detect a
shift in brain contents (which may lead to herniation) prior to a lumbar puncture.
• Key diagnostic tests: bacterial culture and Gram staining of CSF and blood.
Prevention:
1- Recommends that the meningococcal conjugated vaccine be given to adolescents
entering high school and to college fresh- men living in dormitories.
2- People in close contact with patients with meningococcal meningitis should be treated
with antimicrobial chemoprophylaxis using rifampin (Rifadin), ciprofloxacin
hydrochloride (Cipro), or ceftriaxone sodium (Rocephin). Therapy should be started
within 24 hours after exposure because a delay in the initiation of therapy limits the
effectiveness of the prophylaxis.

Medical Management
1. Penicillin antibiotics (eg, ampicillin, piperacillin) or one of the cephalosporins (eg,
ceftriaxone sodium, cefotaxime sodium) may be used.
2. Vancomycin hydrochloride alone or in combination with rifampin may be used if
resistant strains of bacteria are identified.
3. High doses of the appropriate antibiotic are administered IV.
4. Dexamethasone has been shown to be beneficial as adjunct therapy in the treatment of
acute bacterial meningitis and in pneumococcal meningitis if it is administered 15 to
20 minutes before the first dose of antibiotic and every 6 hours for the next 4 days.
5. Dehydration and shock are treated with fluid volume expanders.
6.Seizures, which may occur early in the course of the disease, are controlled with
phenytoin (Dilantin).

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Nursing Management:
1. Assess neurologic status and vital signs constantly. Determine oxygenation from
arterial blood gas values and pulse oximetry.
2. Insert cuffed endotracheal tube (or tracheostomy), and position patient on mechanical
ventilation as prescribed.
3. Assess blood pressure (usually monitored using an arterial line) for incipient shock,
which precedes cardiac or respiratory failure.
4. Rapid IV fluid replacement may be prescribed, but take care not to overhydrate patient
because of risk of cerebral edema.
5. Reduce high fever to decrease load on heart and brain from oxygen demands.
6. Protect the patient from injury secondary to seizure activity or altered level of
consciousness (LOC).
7. Monitor daily body weight; serum electrolytes; and urine vol- ume, specific gravity,
and osmolality, especially if syndrome of inappropriate antidiuretic hormone (SIADH)
is suspected.
8. Prevent complications associated with immobility, such as pressure ulcers and
pneumonia.
9. Institute infection control precautions until 24 hours after initiation of antibiotic
therapy (oral and nasal discharge is considered infectious).
10.Inform family about patient’s condition and permit family to see patient at appropriate
intervals.

Home work
Q/ How monitoring intracranial pressure?