The nervous system is composed of neurons with cell bodies that contain genetic material and organelles. Neurons have dendrites that receive signals and axons that transmit signals away from the cell body. There are three main types of neurons - sensory neurons that transmit peripheral signals to the central nervous system, motor neurons that carry signals from the central nervous system, and interneurons that connect sensory and motor neurons. The nervous system is protected and supported by glial cells in the central nervous system like oligodendrocytes and astrocytes, and Schwann cells and satellite cells in the peripheral nervous system. Nerve impulses are transmitted through changes in ion concentrations along the neuron membrane in a process called action potential.
The nervous system is composed of neurons with cell bodies that contain genetic material and organelles. Neurons have dendrites that receive signals and axons that transmit signals away from the cell body. There are three main types of neurons - sensory neurons that transmit peripheral signals to the central nervous system, motor neurons that carry signals from the central nervous system, and interneurons that connect sensory and motor neurons. The nervous system is protected and supported by glial cells in the central nervous system like oligodendrocytes and astrocytes, and Schwann cells and satellite cells in the peripheral nervous system. Nerve impulses are transmitted through changes in ion concentrations along the neuron membrane in a process called action potential.
The nervous system is composed of neurons with cell bodies that contain genetic material and organelles. Neurons have dendrites that receive signals and axons that transmit signals away from the cell body. There are three main types of neurons - sensory neurons that transmit peripheral signals to the central nervous system, motor neurons that carry signals from the central nervous system, and interneurons that connect sensory and motor neurons. The nervous system is protected and supported by glial cells in the central nervous system like oligodendrocytes and astrocytes, and Schwann cells and satellite cells in the peripheral nervous system. Nerve impulses are transmitted through changes in ion concentrations along the neuron membrane in a process called action potential.
COMPOSED OF: 1)Cell Body -contains large vesicular nucleus with one nucleoli and a rough endoplasmic reticulum. - contain DNA and genetic content that is present in other cells of the body. Function of procedures DNA associated with Protein Synthesis Parts: a.Mitochondria b.Organelle - lacks centrioles and centrosome which are important in cell division. 2) Dendrites- branch type structures with synapses - conduction of information is towards the body. 3) Axon- long efferent processes - projects from cell body - carries impulses away from the cell body. a. Afferent ( sensory ) neurons - transmit information from peripheral to CNS b. Efferent ( motor ) neurons - carry information away from the CNS c. Interneuron ( internutia ) - connects the sensory and motor neurons
SUPPORTING STRUCTURES OF PNS: Satellite Schwann cells Glial cells
Functions: -Protection -Provision of nutrition -Support -Conduction of impulses - Insulation 1. Schwann cells - responsible for the formation of myelin sheath for myelination PNS -covering the axon More covering C fibers (dull pain) Small covering E and B fibers (sharp and throbbing pain) 2. Nodes of Ranvier -accelerates transmission of impulses -unmyelinated Na - major component of ECF Saltatory Conduction - allowing to jump from node to node through ECF - Salthe- latin word meaning tojump - Process of jumping impulses from node to node with the used of ECF
Satellite Cells - secretes the basement membrane that protects the body from the diffusion of large molecule.
SUPPORTING STRUCTURES OF CNS: 1. Glial Cells 2. Oligodendroglial cells -produces myelin sheath in the CNS -reach out several process and from multi myelin sheath -velocity of nerve conduction 3. Astroglia -encapsulating the CNS -main source of blood brain barrier -maintain chemical environment of neurons -ex. glucose -provides transport mechanism for exchange of O2,CO2 metabolism -creates a special scar tissue called gliosis 4. Microglia cells -small phagocytic cells responsible for cleaning up debris after cellular damage, infection or cell death 5. Ependymal cells -form the living of neural tube cavity -abundant in choroids plexus-produce CSF
Metabolism Activity of the Brain: 10sec. -brain can survive 4-6 min. -cell death occur Na and K- major ions of the brain
NERVE IMPULSE Action Potential -potential of the neuron to conduct by changing ion contents -concentrates more on depolarization and repolarization
3 PHASES: a. Resting phase- undisturbed period of action potential during which nerve do not transmit impulses (+ )charge- inside (- ) charge- outside Large fibers- needs 90m volts. Smaller fibers- needs 40-60m volts. b. Threshold Potential K+ leaks out - concentration of Na should be equal to or above 60m volts or more. -if below , the gate is closed
c. Repolarization - the Na channels immediately closed but potassium channel open, not to allow Na inside but for K to go outside by itself.
3 STIMULUS: 1. Adequate stimulus -kind of physical or chemical change when the receptor is sensitive. - 90 m volts. 2. Minimal stimulus - is at least change that can excite the receptor - 40-60 m volts. 3. Subminimal stimulus -kind of physical chemical change below the threshold level that fails to excite
SYNAPTIC TRANSMISSION Synapse - point of continuity that permits transmitter or transmission of activity from one neuron to another.
2 types: Electrical Synapse - permits the passage of current carrying ions through small opening called gap junction - allow action potential to pass quickly and directly from one neuron to another Chemical Synapse - Most Common - involves special presynaptic and postsynaptic structures separated by a synaptic junction
NEUROTRANSMITTERS - communicates messages - potentiate,terminate or modulate a specific action and can either excite or inhibit cell activity. - maybe in a form of peptides. - stored and manufactured in the synaptic vesicles - small molecules that incorporate a positively charge nitrogen atoms.
THE CENTRAL NERVOUS SYSTEM Anatomy of the Brain Three major parts:
1. Cerebrum a. Frontal- the largest lobe the major functions are concentration, abstract thought, information storage and motor function. b. Parietal- a predominantly sensory lobe. The primary sensory cortex which analyze sensory informations and relays the interpretations of this information to the thalamus and other cortical areas c. temporal- contains the auditory receptive areas and also contains vital area called the interpretive area. d. occipital- the posterior lobe of the cerebral hemisphere, is responsible for visual interpretation e. Central or Insula Hipocampus essential role in the process of memory. Corpus Callosum - The thick connection of nerve fibers that connects the two hemispheres of the brain and is responsible for the transmission of information from one side of the brain to the other. Basal Ganglia - Basal ganglia are masses of nuclei located deep in the cerebral hemispheres that are responsible for control of fine motor movements, including those of the hands and lower extremities.
Diencephalon: a. Thalamus b. Hypothalamus Pituitary Gland - Pituitary gland is located in the sella turcica at the base of the brain and is connected to the hypothalamus. It is the common site for the brain tumors in adults; frequently they are detected by the physical signs and symptoms that can be traced to the pituitary, such as hormonal imbalance or visual disturbances secondary to pressure or optic chiasm.
Limbic system 2. Brain stem - The brain stem consists of the midrabrain, pons and medulla oblongata. - The midbrain connects the pons and the cerebellum with the cerebral hemispheres. - The pons is situated in front of the cerebellum between the midbrain and the medulla and is a bridge between the two halves of the cerebellum. - The medulla oblongata contains motor fibers from the brain to the spinal cord and sensory fibers from spinal cord to the brain.
Reticular formation 3. Cerebellum - Cerebellum is separated from the cerebral hemispheres by a fold of dura mater, tentorium cerebelli. The cerebellum has both the excitatory and inhibitory actions and is largely responsible for coordination of movement.
The brain is contained in the rigid skull, which protects it from injury. The major bones of the skull are the frontal, temporal, parietal, and occipital bones. These bones join at the suture lines.
Skull - is a bony structure which serves as the general framework for a head. The skull attempts to protect the brain, acting as a form of natural helmet.
2 sets of bones in the skull a. cranium - is that part of the skull that holds and protects the brain in the large cavity called the cranial vault. b. Facial bone - holds the eye in anterior position and allows facial muscles to show our feelings.
The meninges (fibrous connective tissue) - Provide protection, support and nourishment to the brain and spinal cord. The layers of the meninges are the dura, arachnoid and pia mater.
a. Dura mater-the outermost layer; covers the brain and the spinal cord. It is rough, thick, inelastic,fibrous and gray.
Layers of Dura mater: -periosteal layer- attach to the inner surface of the skull.
-meningeal layer- forms the outermost covering of the brain continues as the dura mater of the spinal cord.
Four extensions of the dura : falx cerebri tentorium falx cerebelli diaphragm sellae
Epidural space - located between the dura mater and the skull in the cranium.
b. Arachnoid - the middle membrane; an extremely thin, delicate membrane that loosely resembles a spider web. - appears white, contains choroid plexus.
Subdural space - located in between the dura mater and arachnoid layer.
c. Pia mater - the innermost membrane; a thin transparent layer that hugs the brain closely and extends into every fold of the brains surface.
Subarachnoid space - in between the arachnoid and the pia mater.
CEREBROSPINAL FLUID
- a clear and odorless fluid with a specific gravity of 1.007, is produced in the ventricles and is circulated around the brain and the spinal cord through the ventricular system. clear fluid that occupies the subarachnoid space (the space between the skull and cortex of the brain).
- It acts as a "cushion" or buffer for the cortex.
- provides a supporting and protective fluid in which the brain and the spinal cord float.
- helps maintain a constant ionic environment that serves as a medium for diffusion of nutrients, electrolytes and metabolic end products into the extracellular fluid surrounding CNS neurons and glia.
- CSF occupies the ventricular system of the brain and the spinal cord. CSF is mainly produced by the choroid plexus, but also by the epindymal lining of the brain's ventricles.
- 500 ml CSF is produced normally per day, 150 ml stays in the circulation and 350 ml is reabsorbed in the arachnoid villi.
CEREBRAL CIRCULATION - Receives approximately 15% of the cardiac output or 750ml per min. In contrast to other organs that may tolerate decreases in the blood flow because of their adequate collateral circulation,the brain lacks additional collateral blood flow result in irreversible tissue damage when blood flow is occluded for even short periods of time.
BLOOD BRAIN BARRIER - Barrier present in circulating blood and brain tissues that protects the CNS.
Function of BBB: - Primarily regulate and maintain an optimal and stable chemical environment for neurons.
There are three brain barriers, namely: 1. Blood-brain 2. Blood-CSF 3. Brain-CSF
Two types:
1. Physical Barriers- it includes tight junctions of the endothelial cells lining the capillaries, pores of the capillaries of the choroid plexuses, the basement membrane (ependymal cells) next to the choroid plexuses, and the pial-glial membrane.
2. Physiologic Process (Transport System)- Metabolic wastes, such as urea, toxins, proteins and most drugs are prevented from entering the brain tissue.
Certain events can increase the permeability of the blood-brain barrier. Dilutional hyponatremia Acute hypertension High doses of some anesthetics Vasodilation Hypercarbia
SPINAL CORD - portion of the CNS that is protected by the vertebral column and encased in the vertebral canal. - extends from foramen magnum of the skull, where it is continuous with the medulla oblongata to 2 nd lumbar vertebra; filum terminale to 1 st coccygeal vertebra.
- Average length about 42-45 cm.
The blood supply is from the anterior spinal artery and from a succession of small arteries which enter the spinal canal through the intervertebral foramina; these branches are derived.
-Consist of gray matter in form of H enclosed within white matter.
Fissures: Consist of: Ventral sulcus- divides front portion into lateral halves Dorsal sulcus- divides back portion into lateral halves Membranes of Spinal cord: 1. Pia Mater 2. Arachnoid Mater 3. Dura mater
Functions of Spinal Cord: 1. Important center of reflex for the trunk and limbs. 2. Consists of the principal conducting paths to and from the higher centers in the brain. 3. Provide neuron and synapse network to produce involuntary responses to sensory stimulation. Also allows for control of the no. of pain impulses that pass through the spinal cord on their way to the brain. 4. Carries sensory information to, and motor information from the brain.
VERTEBRAL COLUMN
- a flexible series of vertebrae, surrounds and protects the spinal cord. Ligaments hold the vertebrae together.
- The spinal cord is composed of 31 pairs of spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal. Each spinal nerve has ventral root and a dorsal root.
- The dorsal roots are sensory and transmit sensory impulses from specific areas of the body known as dermatomes to the dorsal ganglia. The sensory fiber maybe somatic, carrying information about pain, temperature, touch and position sense (proprioception) from the tendons, joints, and body surfaces; or visceral, carrying information from the internal organ.
- The ventral roots are motor and transmit impulses from the spinal cord to the body. These fibers are also either somatic or visceral. The visceral fibers include autonomic fibers that control the cardiac muscles and glandular secretions.
AUTONOMIC NERVOUS SYSTEM Part of the PNS that coordinates involuntary activities Has two division:
(1) Sympathethic Nervous System, (2) Parasympathetic Nervous System
ANS has also two neurons: (1) Preganglionic neuron- located in the brain or spinal cord and it's axon extends to the autonomic ganglia (2) Postganglionic neuron- located in the autonomic ganglia, it's axon synapses with the target tissue and innervates the effector organ. The hypothalamus is the major subcortical center for the regulation on visceral and somatic activities with an inhibitory-excitatory role in the ANS.
1. SENSORY (AFFERENT) DIVISIONS - relay messages about internal and external body environmental changes to the CNS through specific receptors.
2 Specific Receptors: a. Somatic- carry impulses from the skin, skeletal muscle joints and tendons to the CNS. b. Visceral- carry impulses involuntary muscles and glands to CNS.
2. EFFERENT (MOTOR) DIVISION - transmitted in response to the stimuli the CNS has received from the afferent division.
SENSORY SYSTEM FUNCTION Integrating Sensory Impulse The thalamus integrates all sensory impulses except olfaction. It plays a role in the conscious awareness of pain and the recognition of variation in temperature and touch. The thalamus is responsible for the sense of movement and position and the ability to recognize the size, shape, and quality of objects.
Receiving Sensory Impulses Sensory impulses enter the spinal cord by way of the posterior root. These axons convey sensations of heat, cold, and pain and enter the posterior gray column of the cord, where they make connections with the cells of secondary neurons. Pain and temperature fibers cross immediately to the opposite side of the cord and course upward to the thalamus. Fibers carrying sensations of touch, light pressure, and localization do not connect immediately with the second neuron but ascend to the cord for a variable distance before entering the gray matter and completing this connection. The axon of the secondary neuron crosses the cord and proceeds to the thalamus. Position and vibratory sensation are produced by stimuli arising muscle, joints, and bones. These stimuli are conveyed, uncrossed, all the way to the brain stem by the axon of the primary neuron. In the medulla, synaptic connections are made with cells of secondary neurons, whose axons cross the opposite side and then proceed to the thalamus.
SENSORY LOSSES Destruction of a nerve results in total loss of sensation in its area of distribution. Transection of the spinal cord yields complete anaesthesia below the level of injury. Selective destruction or degeneration of the posterior columns of the spinal cord is responsible for a loss of position and vibratory sense in segments distal to the lesion, without loss of touch, pain, or temperature perception. A lesion, such as cysts, in the center of the spinal cord causes dissociation of sensation-loss of pain at the level of lesion. this occurs because the fibers carrying pain and temperature cross within the cord immediately on entering; thus, any lesion that divides the cord longitudinally divides these fibers. Other sensory fibers ascend to the cord for variable distances, some even to the medulla , before crossing, thereby by-passing the lesion and avoiding destruction.
DIAGNOSTIC TESTS Glasgow Coma Scale Is a numeric expression of cognition, behavior and neurologic function Provides objective measurements of 3 essential components of neurologic examination: Spontaneity of eye opening Best verbal response Best motor response The total of the 3 scores ranges from 3 to 15, with 3 being the most severe and 15 being normal. A score of 8 or less indicates coma. The ff. criteria may render the GCS invalid: The client is based on the clients ability to respond and communicate. Eyes are swollen closed. The client is unable to communicate English. The client has a hearing loss. The client is blind. The client is aphasic. The client is paralyzed or hemiplegic.
Non-Invasive Test of Structure X-ray Definition A skull x-ray is a series of pictures of the bones of the skull. The nasal sinuses can also be viewed on a skull X-ray. Skull x-rays have largely been replaced by CT scans. X-ray are a form of radiation, like light or radio waves, that are focused into a beam, much like a flashlight beam. Spinal X-ray studies Show fractures, dislocations, compressions, curvature, erosion, narrowed spinal cord and degenerative process. A skull x-ray may be done to: Find fractures Find a metallic foreign object stuck in the skull Check the nasal sinuses Check problems on a babys head, such as an odd shaped skull. How to Prepare: Before the X-ray test, ask the patient if she is pregnant. If a skull X-ray is absolutely necessary, a lead apron will be placed over the abdomen to shield the baby from exposure to the X- rays. Remove any metal from the body. Some clients with neurologic disorders require nursing support through an X-ray study. Client has a suspected spinal fractures, the neck is immobilized prior to moving the client to make the X-ray films. Nurses should document thick or heavy hair. Risk A slight risk of damage to cells or tissue from being exposed to any radiation. However the risk from the X-rays is usually very low compared with the potential benefits of the test.
Computed Tomography Definition Computed tomography scanning, also called CT scan, CAT scan, or computerized axial tomography, is a diagnostic tool that provides views of internal body structures using x rays. In the field of mental health, a CT scan may be used when a patient seeks medical help for symptoms that could possibly be caused by a brain tumor. These symptoms may include headaches, emotional abnormalities, or intellectual or memory problems. In these cases, a CT scan may be performed to "rule out" a tumor, so that other tests can be performed in order to establish an accurate diagnosis. Description Computed tomography, is a combination of focused x-ray beams and the computerized production of an image. Introduced in the early 1970s, this radiologic procedure has advanced rapidly and is now widely used, sometimes in the place of standard x rays. Advantages CT completely eliminates the superimposition of images of structures outside the area of interest. Because of the inherent high-contrast resolution of CT, differences between tissues that differ in physical density by less than 1% can be distinguished. Data from a single CT imaging procedure consisting of either multiple contiguous or one helical scan can be viewed as images in the axial, coronal, or sagittal planes, depending on the diagnostic task. Patient Preparation
Before a CT Scan, make sure that the client has given informed consent. Explain that fasting usually is not required but ask whether or not the client becomes nauseated easily. Explain that a contrast agent is usually given. Because the contrast material is iodine- based, ask about any allergies to iodine or contrast dyes. If the CT Scan is of the clients head, remove any objects from hair (wigs, barrettes, earrings, hair pins) before test begins. Explain the clients role during the scan. - The client is positioned supine, and the body part to be scanned is placed into the doughnut shaped ring of the scanner. - The technician moves the table from a control room to direct the study to different areas. - The client can expect to hear mechanical noises coming from the scanner. - Emphasize that the client must remain still during the scan. - If sedation is needed, tell the client to avoid alcohol and caffeine the day of the scan, avoid eating 2 hrs prior to the scan, and avoid driving 12 hrs after the scan. After the test, assess the client for reactions to the contrast agent, hematoma, at the injection site, and the quality of pulses in the limb used for injection and contrast agent. The client may resume normal activities unless additional diagnostic tests are planned. Tell the client to expect diuresis from the dye. Encourage the intake of plenty of fluids to flush the dye and prevent nephrotoxic injury. Risks Radiation exposure from a CT scan is similar to, though higher than, that of a conventional x ray. Although this is a risk to pregnant women, the risk for other adults is minimal and should produce no effects. Severe contrast reactions are rare, but they are a risk of many CT procedures.
Magnetic Resonance Imaging Is a non-invasive test that uses powerful magnetic fields and radio frequency pulse to produce the image. It does not use ionizing radiation such as X-rays. This test involves altering hydrogen ions; the magnetic field causes the hydrogen nuclei (protons) to align small magnets in the field. Advantages It can detect disorders in white matter pathways caused by loss of myelin, as in multiple sclerosis. Can evaluate cerebral infarction within hours of event. Is the scan of choice for congenital malformations and spinal cord lesions. MRI with contrast material delineates blood flow through cerebral blood vessels in more detail than is possible with CT.
Nursing Interventions Teach the client and family about the purpose of the test, what the client will hear and feel during the examination, and the clients role during the test. Client should remove all metal-containing objects. Client may eat and may take prescribed medications before the examination. If contrast material is to be used, ask whether the client tends to become nauseated and adjust the intake of food and fluids.
Non-Invasive Test of Function Positron Emission Tomography Definition Positron emission tomography (PET) is a highly specialized imaging technique using short-lived radio labeled substances to produce extremely high resolution images of the body's biological function. Description PET is used in conjunction with compounds that closely resemble a natural substance used by the body, such as a simple sugar (glucose, for example), labeled with a radioactive atom and injected into the patient. Cancer cells are highly metabolic, so they are easily seen on the PET scan. Three Primary Uses: Determines the amount of blood flow to specific body tissues. Revealing how adequately tissues use blood or nutrients, such as oxygen. Mapping specific receptors, such as medications and neurotransmitters. Advantages It can measure the cerebral blood flow, cerebral glucose metabolism, and oxygen extraction. It can diagnose stroke, brain tumors and epilepsy and can chart the progress of Alzheimers disease, Parkinsons disease, head injury, schizophrenia, and bipolar disorder. Disadvantage PET is highly expensive. Precaution In some cases, patients may be allergic to the radioactive agents used for PET. Preparation The radiopharmaceutical is given by intravenous injection or inhaled as a gas a few minutes before the PET procedure. During the scan, the patient lies comfortably; the only discomfort involved may be the pinprick of a needle used to inject the radiopharmaceutical. Nursing Intervention Educate the client and family about the purpose of the test, what the client will hear and feel, and the clients role during the test. Instruct the patient to fast for 4 hours before the scan. If the client is diabetic, it is preferred that the blood glucose level be below 150 g/dl.
Clients who are agitated may require sedation before the scan.
Single Photon Emission Computed Tomography Definition Is a 3 dimensional imaging technique that uses radionuclides and instruments to detect single photons. It is a perfusion study that captures a moment cerebral blood flow at the time of injection of a radionuclide. Advantages Is considered experimental and investigational for all other cardiac indications and non-cardiac indications. Has a far greater sensitivity for detecting silent ischemia than ECG. Clinical studies indicate that SPECT is more accurate at detecting acute ischemia than CT scan. Has proved useful in distinguishing recurrent brain tumor from radiation necrosis. Disadvantage It cannot detect hemorrhage in order to rule out use of thrombolysis. Nursing Intervention Premenopausal women are advised to practice effective contraception before and several days after testing. Breastfeeding women are instructed to stop nursing for the period of time recommended by the nuclear medicine dept. Patients are monitored during and after the procedure for allergic reactions to the radiopharmaceutical agent. The patient is asked if he/she is claustrophobic.
Electroencephalography Definition EEG is a neurological diagnostic procedure that records the changes in electrical potentials (brain waves) in the brain. Purpose Is an important aid in the diagnosis and management of epilepsy and other seizure disorders.
Is also useful in monitoring brain wave activity and in the determination of brain death. Precautions It should be administered, monitored, and interpreted only by a specially trained health professional. It is important to recognize that diagnosis should not be based on the EEG alonethe EEG represents an adjunct to the neurological history, examination, and other specialized studies. Is an extremely sensitive instrument, and tracings can be greatly influenced by the actions and the physiologic status of the patient. It is important that the patient be properly prepared physically and psychologically in order to obtain an accurate and reliable record. Medications such as anticonvulsants, tranquilizers, stimulantsincluding coffee, tea, cola drinksand alcohol should be withheld for at least 2448 hours prior to the test. Inasmuch as hypoglycemia affects brain wave patterns, the patient is told not to withhold any meals. Nursing Interventions The patient be deprived of sleep on the night before the EEG. Antiseizure agents, tranquilizers, stimulants and depressants should be withheld 24 t0 48 hours before EEG. Coffee, tea, chocolate, and cola drinks are omitted in the meal before the tests. end Patient should be informed that the standard EEG takes 45 to 60 minutes, 12 hours for a sleep EEG.
The patient is assured that the procedure does not cause an electric shock and that the EEG is a diagnostic test, not a form of treatment.
Sedation is not advisable. The nurse needs to check the physicians prescription regarding the administration of antiseizure medication prior to testing.
Transcranial Doppler It is a noninvasive technique that is helpful in assessing vasospasm, altered cerebral blood flow found in occlusive vascular disease or stroke, and other cerebral pathology. It also uses the same noninvasive techniques as carotid flow studies except that it records the blood flow velocities of the basal artery can be measured through thin areas of the temporal and occipital bones of the skull. A hand-held Doppler probe emits a pulsed beam; the signal is reflected by the moving blood cells within the blood vessels. end Nursing Intervention The nurse should describe first the procedure to the patient. Inform the patient that this is a noninvasive test, that a hand-held transducer will be placed over the neck and the orbits of the eyes, and that some type of water-soluble jelly is used on the transducer.
Invasive Test of Function Electromyography Is obtained by inserting needle electrodes into the skeletal muscles. The electrical potentials are shown on an oscilloscope and is amplified. Advantages An EMG is useful in determining the presence of neuromuscular disorders and myopathies. It helps distinguish weakness due to neuropathy from weakness resulting from other causes. end Nursing Interventions Explain the procedure. Warn the patient to expect a sensation similar to that of an intramuscular injection.
Lumbar Puncture The insertion of a hollow needle beneath the arachnoid membrane of the spinal cord in the lumbar region to withdraw cerebrospinal fluid for diagnostic purposes or to administer medication. Advantages: to obtain CSF for examination to measure and reduce CSF pressure to determine the presence or absence of blood in the CSF to detect subarachnoid block to administer antibiotics intrathecally (into the spinal canal) in certain cases of infection. Disadvantage A Lumbar puncture may be risky in the presence of an intracranial mass lesion because intracranial pressure is decreased by the removal of CSF, and the brain may herniated downward through the tentorium and the foramen magnum. During the Procedure A lumbar puncture procedure may be performed on an outpatient basis or as part of your stay in a hospital. Procedures may vary depending on your condition and your physician's practices. Generally, a lumbar puncture follows this process: 1. Explain the procedure to the patient. 2. Tell the patient to remove any clothing, jewelry, or other objects that may interfere with the procedure. 2. Provide the gown. 3. Remind the patient to empty the bladder prior to the start of the procedure. end The patient may experience discomfort during a lumbar puncture. The physician will use all possible comfort measures and complete the procedure as quickly as possible to minimize any discomfort or pain.
Myelography Is an x-ray of the subarachnoid space taken after the injection of a contrast agent into the spinal subarachnoid space through a lumbar puncture. It helps to evaluate the spinal cord and nerve roots for suspected compression. Pressure on these delicate structures causes pain or other symptoms. DISADVANTAGES
Headache is a common complication of myelography. Rare complications of myelography include injury to the nerve roots from the needle or from bleeding into the spaces around the roots. Inflammation of the delicate covering of the spinal cord, called arachnoiditis, or infections, can also occur. Seizures are another very uncommon complication reported after myelography CLIENT PREPARATION Patients should be well-hydrated at the time they are undergoing a myelogram. All food and fluid intake should be stopped approximately four hours before the procedure. Certain medications may need to be stopped for one to two days before myelography is performed. Patients who smoke may be asked to stop the day before the test. Nursing Interventions The nurse clarifies the explanation given by the physician and answers questions. The patient is informed about what to expect during the procedure and should be aware that changes in position may be made during the procedure. The meal that normally would be eaten before the procedure is omitted. end After myelography, the patient lies in bed with the head of the bed elevated 30 to 45 degrees. The patient is encouraged to drink liberal amounts of fluid for rehydration and replacement of CSF and to decrease the incidence of post-lumbar puncture headache. The blood pressure, pulse, respiratory rate, and temperature are monitored, as well as the patients ability to void.
Cerebral Angiography Definition An angiography is an x-ray of the arteries. The arteries are not normally seen in an x-ray, so a special material, called contrast dye, is injected into one or more arteries to make them visible. It is frequently performed before craniotomy to assess the patency and adequacy of the cerebral circulation and to determine the site, size, and nature of the pathologic processes. Most cerebral angiograms are performed by threading a catheter through the femoral artery in the groin and up to the desired vessel. Alternatively, direct puncture of the carotid or vertebral artery or retrograde injection of a contrast agent into the brachial artery may be performed. Advantages Can detect aneurism, AVM, major vessel displacement vascular occlusion or thrombi. Helpful in assessing the patency and adequacy of cerebral circulation before conducting craniotomy. Disadvantage Potential complications includes temporary or permanent neurologic deficit, anaphylaxis, bleeding or hematoma at the IV site, and impaired circulation in the extremity distal to the injection site. Preprocedure Obtain an informed consent. Educate the client about the purpose of the test, what the client will experience, and the clients role in the procedure. Before the test, the client may not take anything by mouth for 4 to 6 hours but should be kept well hydrated. IV fluids may be prescribed. Encourage hydration 2 days before the test. After the groin is shaved and prepared, local anesthetic is administered. Mark the peripheral pulses. Document the neurologic status of the client. The clients should remove any metal items from the head, such as barrettes and earrings. Report allergies to iodine. Often patients with allergy to iodine also have allergies to radiopaque contrast media that may cause severe reaction. Tell the patient to expect some discomfort when the catheter is inserted. Additionally, the sensation of a warm, flushed feeling and metallic taste should be expected when the dye is injected. Caution the patient to lie still during the procedure. Postprocedure Monitor neurologic status and vital signs frequently until stable. Maintain bed rest 12 24 hours as prescribed. The extremity to which the contrast medium was injected is kept straight and immobilized for about 8 hours. Apply sandbags and a pressure dressings to the injection site as prescribed. Nursing Interventions The patient should be well hydrated, and clear liquids are usually permitted up to the time of a regular arteriogram or DSA. Before going to the x-ray department, the patient is instructed to void. The patient is instructed to remain immobile during the angiogram process and is told to expect a brief feeling of warmth in the face, behind the eyes, or in the jaw, teeth, tongue, and lips, and a metallic taste when the contrast agent is injected.
Neurologic Disorders Cerebrovascular Accident A focal neurological deficit due to a local disturbance in blood supply to the brain ( WHO ) Its onset is usually abrupt but may extend over a few hours or longer. Pathophysiology Interruption of the blood supply to the brain deprives it of oxygen and nutrients resulting in the death of brain tissues. Risks Factors for Stroke Medical Conditions Hypertension (30% to 40% risk reduction with treatment): goal BP is lower than 140/90; if renal insufficiency or heart failure, less than 130/85; if diabetic, less than 130/80 Cardiac disorderscongenital heart disease, valvular conditions, endocarditis Atrial fibrillation (risk reduction is 68% with oral anticoagulant therapy; 21% with aspirin therapy for nonvalvular causes) Diabetes mellitus (44% risk reduction in hypertensive diabetics with controlled BP) Hyperlipidemia (20% to 30% risk reduction with those with known coronary heart disease [CHD] on statin therapy): goal LDL is less than 160 mg/dL if one or no risk factor; less than 130 if two or fewer risk factors or 10-year CHD risk is less than 20%; less than 100 if two or fewer risk factors and 10-year CHD risk greater than 20% Carotid stenosis Prior history of TIA or stroke Elevated homocysteine level in blood Behaviors Cigarette smoking (50% risk reduction in 1 year; return to baseline in 5 years) Alcohol abuse Physical inactivity Cocaine use (hemorrhagic stroke)
Nonmodifiable factors Increasing age - risk doubles for each decade over age 50 Gender - men are at greater risk than women Heredity - increased risk with family history of stroke Ethnic background - Blacks and Hispanics at higher risk than Whites Types of Strokes Ischemic ( Thrombotic, Embolic ) Partial or complete occlusion of a cerebral blood flow to an area of the brain Hemorrhagic Leakage of blood from a blood vessel and hemorrhage into brain tissue, causing edema, compression of brain tissue, and spasm of adjacent blood vessels. Ischemic Stroke: Causes 1. Cerebral thrombosis atheroma where a plaque of hard fatty degenerative nature forms on the inner wall of the artery, impedes blood flow and clot forms 2. Cerebral Embolism Pieces of clot breaking off, moves to the bloodstream and lodge in a vessel blocking the passage of blood. 3. Cerebral ischemia loss of adequate blood supply due to narrowing of either the carotid or vertebral artery. Hemorrhagic Stroke ( Types ) 1. Epidural 2. Subdural 3. Subarachnoid 4. Intracerebral
Hemorrhagic stroke ( Causes ) Ruptured or leaking aneurysms Arteriovenous malformations Use of anticoagulants Hypertension Clinical Findings Internal Carotid Contralateral hemiparesis Dysphasia with dominant side involvement Blindness Agnosia(inability to recognize) Hemianopia Cranial nerve deficits Contralateral anosognosia(unaware of disability) Middle cerrebral artery Contralateral arm and leg weakness or paralysis Homonymous hemianopia Eye deviation to the opposite side Dysphagia or aphasia on dominant side Contralateral sensory impairment Apraxia with non-dominant involvement (non-purposeful movement)
Clinical findings Anterior cerebral artery Contralateral paralysis leg, foot and arm Bladder incontinence Sensory deficit Akinetic mutism( not moving and speaking ) Eye deviation towards affected side Gait impairment Mood disturbance Vertebral-basilar system Variations in LOC Hemianopia Possible quadriplegia Eye muscle paralysis Nystagmus Diplopia Dysarthria(poor articulation) Ataxia( incoordination ) Vertigo
Diagnostic Tests History and examination CT scan Arteriogram
Medical Management Close observation and monitoring of hemodynamic parameters Management of increased ICP Anticoagulant therapy heparin, thrombolytics Recombinant tissue plasminogen activator -Alteplase therapy
Nursing Management Care during the acute phase ( first 24 to 48 hours ) Maintain patent airway: O2 therapy started soon Positioning to facilitate drainage Suctioning Elevate head of bed 30 degrees Chest physiotherapy VS monitoring Respiratory pattern Decreased PR indicates increased icp Increased temperature LOC Pupil response On Mannitol drip I and O monitoring Electrolyte balance Personal hygiene Passive ROM Post Acute Care Maintain clear airway to prevent hypoxia O2 therapy humidified Tracheostomy care Deep breathing Chest physiotherapy
Preventing Falls and Other Injuries Maintain bed rest during acute phase (24 to 48 hours after onset of stroke) with head of bed slightly elevated and side rails in place. Administer oxygen as ordered during acute phase to maximize cerebral oxygenation. Frequently assess respiratory status, vital signs, heart rate and rhythm, and urine output to maintain and support vital functions. When patient becomes more alert after acute phase, maintain frequent vigilance and interactions aimed at orienting, assessing, and meeting the needs of the patient. Try to allay confusion and agitation with calm reassurance and presence. Assess patient for risk for fall status.
Surgical Management Craniotomy - surgical opening of the skull to gain access to intracranial structures to remove a tumor, relieve increased intracranial pressure (ICP), evacuate a blood clot, stop hemorrhage, or remove epileptogenic tissue. Craniotomy may be performed by means of burr holes (made with a drill or hand tools) or by making a bony flap. Craniectomy is excision of a portion of the skull. Cranioplasty is repair of a cranial defect by means of a plastic or metal plate.
Preoperative Management Diagnostic findings, surgical procedure, and expectations are reviewed with the patient. Presurgical shampoo with an antimicrobial agent may be ordered. Shave and prep are performed in the operating room. Depending on primary diagnosis, corticosteroids may be ordered preoperatively to reduce cerebral edema. Depending on the type and location of lesion, anticonvulsants may be ordered to reduce risk of seizures. The patient is prepared for the use of intraoperative antibiotics to reduce risk of infection, and urinary catheterization to assess urinary volume during operative period. If cerebral edema develops, intraoperative or postoperative osmotic diuretic (mannitol) or corticosteroids may be ordered for its treatment. Neurologic assessment is performed to evaluate and record the patient's neurologic baseline and vital signs for postoperative comparison. Family and patient are made aware of the immediate postoperative care and where the physician will contact the family after surgery. Supportive care is given as needed for neurologic deficits.
Postoperative Management Respiratory status is assessed by monitoring rate, depth, and pattern of respirations. A patent airway is maintained. Vital signs and neurologic status are monitored, using GCS; findings are documented. Arterial and central venous pressure (CVP) are monitored, possibly with a pulmonary Swan-Ganz catheter for accurate assessment of hemodynamic status. Pharmacologic agents may be prescribed to control increased ICP. Incisional and headache pain may be controlled with mild analgesic (codeine and acetaminophen) or low dose opioids (morphine sulfate or fentanyl/Duragesic), as prescribed. Monitor response to medications. Position head of bed at 15 to 30 degrees, or per clinical status of patient, to promote venous drainage. Determining appropriate position of head of bed is patient-dependent and should be adjusted based on observed changes in the patient's clinical response and ICP to positioning. A decrease in CPP is observed with raising the head of the bed to lower ICP. Turn side-to-side every 2 hours; positioning restrictions will be ordered by the physician. CT scan of the brain is performed if patient's status deteriorates. Oral fluids are provided after swallow reflex and bowel sounds have returned. Intake and output are monitored. Speech therapy may be ordered for bedside swallow study or radiographic swallow study. Signs of infection are monitored by checking craniotomy site, ventricular drainage, nuchal rigidity, or presence of CSF (fluid collection at surgical site). Periorbital edema is controlled by such measures as elevation of head of bed and cold compresses. Removal of surgical dressing and increase in activity will assist in the resolution of periorbital edema.
Autoimmune Disorders Multiple Sclerosis A demyelinating disease disease that results in the destruction of the CNS myelin. Etiology: Link between prevalence of MS and geographic location. Northern Europe, Great Britain, So. Australia, New Zealand 20-40 years old Common in women Whites / Caucasian Cause Unknown Autoimmune: associated with the dysfunctional T lymphocytes. Triggered by viral infection. Clinical Manifestation Prediliction to optic nerve, preventricular white matter, brainstem, cerebellum and spinal cord white matter. Cranial nerve dysfunction blurred central vision, faded colors, blind spots, diplopia, dysphagia, facial weakness, numbness and pain. Motor dysfunction weakness, paralysis, spasticity, abnormal gait Sensory dysfunction paresthesias, Lhermitts sign ( electric shock-like sensation radiating down the spine. Cerebellar function dysarthria, tremor, incoordination, atax ia, vertigo Bowel and bladder dysfunction fecal urgency, constipation, urinary frequency, hesitancy, nocturia Cognitive dysfunction decreased short term memory, short attention span Diagnostic Test CSF analysis increased protein, lymphocytes and IgG Evoked potentials- prolonged impulse conduction MRI demostrates white matter lesions Therapeutic Management Pharmacologic Therapy Corticosteroid Interferon beta and glatiramer acetate Diazepam, stool softeners Nursing Care Avoid precipitation of exacerbation Avoid fatigue, stress, infection, overheating, chilling. Establish regular program of exercise with rests. Provide balance diet Physical and speech therapy Promote safety Promote bladder and bowel control Provide education and emotional support
Myasthenia Gravis A disorder of transmission at the neuromuscular juncion that affects communication between the motor neuron and the innervated muscle cell. Etiology: More common in women than in men Heredofamilial disease 20-30 years old Causes Autoimmune disease caused by antibody-mediated loss of acetylcholine receptors in neuromuscular junction. Thymoma Diagnostic Tests Tensilon Test anti-cholinesterase test ( edrophonium ) Administered IV-decreases breakdown of ACh in the neuromuscular junction. (+) MG- improvement in muscle strength (-) MG no improvement or even deterioration CT on thymus Therapeutic Management Drug Therapy Anticholinesterase drugs pyridostigmine, neostigmine Corticosteroids Immunosuppresant drugs azathioprine Plasmapheresis Thymectomy Complications Myasthenia Crisis experience of a sudden exacerbation of symptoms and weakness. Occurs when muscle weakness becomes severe enough to compromise ventilation Occurs during period of infection, stress and pregnancy Medications increasing incidence: Quinidine, aminoglycosides, beta adrenergic receptor blockers, calcium channel blockers, magnesium sulfate, citrate Weakness, dyspnea, dysphagia, restlessness, difficulty speaking Cholinergic Crisis Cholinergic paralysis with sustained depolarization of motor end plates due to overmedication of Anti acetylcholinesterase Fasciculation, abdominal cramping, diarrhea, vomiting, nausea, salivation Nursing Care Monitor patient to avoid progression to complications. Administer medications as ordered. Plan short periods of activity Encourage normal ADL and divertional activities. Provide emotional and educational support. Be prepared with atropine.
Guillain-Barre Syndrome An acquired inflammatory disease that results in demyelination of the peripheral nerves with relative sparing of the axon. Progressive ascending paralysis that is usually reversible. Etiology: Altered immune response directed against a component of myelin in the peripheral nerve. Viral infection GI tract infection of camylobacter jejuni Clinical Manifestation Muscle weakness that develops in a matter of hours to 10 days. Distal lower extremities are affected first Patient may fall, develop footdrop and then be unable t walk. Paresthesias Respiratory muscle paralysis usually the last symptom. Diagnostic Tests CSF analysis increased protein level EEG slowing in motor and sensory conduction velocity. Therapeutic Management Plasma exchange IV Ig Nursing care: Monitor for respiratory paralysis Prevent complication of immobility. Nutritional support
AMYOTROPHIC LATERAL SCLEROSIS Degeneration of upper motor neurons (nerves leading from the brain to medulla or spinal cord) and lower motor neurons (nerves leading from the spinal cord to the muscles of the body). Results in progressive loss of voluntary muscle contraction and functional capacity, involving the legs, feet, arms and hands, and those that control swallowing and breathing. Cause is unknown. Usually affects men in the fifth or sixth decade of life.
Clinical Manifestations Progressive weakness and wasting of muscles of arms, trunk, and legs Fasciculations and signs of spasticity Progressive difficulty swallowing (drooling, regurgitation of liquids through nose), speaking (nasal and unintelligible), and, ultimately, breathing Cranial nerve deficits (bulbar symptoms) are present in 20% of cases (prevalence increases with age), along with dysarthria, voice deterioration, and dysphagia (Patients with bulbar presentation have poorer prognosis; these symptoms also have a profound impact on quality of life due to nutritional risk factors, aspiration, and respiratory complications.)
Diagnostic Tests Electromyography to evaluate denervation and muscle atrophy Nerve conduction study to evaluate nerve pathways Pulmonary function tests to evaluate respiratory function Barium swallow to evaluate ability to achieve various phases of swallow MRI, CT to rule out other disorders Laboratory tests: creatine kinase, heavy metal screen, thyroid function tests, CSF evaluation to rule out other causes of muscle weakness
Therapeutic Management There is no cure for ALS; nor is there a proven therapy that will prevent or reverse the course of the disorder. Riluzole (Rilutek), the first drug that has been shown to prolong the survival of ALS patients, was recently approved by the FDA, but its effects are limited. Most treatment is palliative and symptomatic. Baclofen (Lioresal) to control spasticity. Diazepam (Valium) to control fasciculations. Antidepressants, sleep medications. Feeding gastrostomy. Mechanical ventilation eventually becomes necessary. Monitor vital capacity frequently. Document pattern, and report any decrease below patient's baseline. Position patient upright, suction upper airway, and perform chest physical therapy to enhance respiratory function. Encourage use of incentive spirometer to exercise respiratory muscles. Assess for signs of hypoxia, such as tachypnea, hypopnea, restlessness, poor sleep, and excessive fatigue. Establish the wishes of the patient in terms of life-support measures; obtain copy of advance directive for chart, if applicab Provide suctioning and routine care of a patient with artificial airway and mechanical ventilation.
Degenerative Disorders Alzheimers Disease Characterized by cortical atrophy and loss of neurons, particularly in the parietal and frontal lobes. Etiology: Genetics autosomal dominant pattern Identified in familial cases on chromosome 21 which includes beta amyloid precursor protein. Age: rarely develops before age 40. Diagnostic Test No biochemical markers or tests. Confirmed only by microscopic examination of tissue obtained from biopsy. Therapeutic Management Primarily symptomatic and supportive Drug therapy For mood and sleep disorders constipation Nursing Care Counselling, planning and education of patient and family. Diet and exercise Avoid fatigue, overstimulation Enhance memory by using calendars, clocks posted schedule and notebooks Changes should be attempted slowly. Meals should not be forced and served in calm surroundings. Ensure safe environment Care for the family and caregivers
Parkinsons Disease Parkinson's disease is a chronic, progressive neurologic disease affecting the brain centers responsible for control and regulation of movement. It is characterized by tremor, bradykinesia, rigidity, and postural abnormalities. It is the second most common neurodegenerative disease. A deficiency of dopamine, due to degenerative changes in the substantia nigra of the brain, is thought to be responsible for the symptoms of Parkinson's disease. Etiology may be related to a virus; genetic susceptibility; toxicity from pesticides, herbicides, methyl-phenyl-tetrahydropyridine, or welding fumes; repeated head injuries, or other unknown cause.
Clinical Manifestations Bradykinesia (slowness of movement), loss of spontaneous movement and delay in initiating movements Resting (pill-rolling) tremor of 4 to 5 Hz. The tremor may be worse on one side of the body affecting the limbs and sometimes involves the head, neck, face, and jaw. Rigidity in performance of all movements. Rigidity is always present but increases during movement. May lead to sensations of pain, especially in the arms and shoulders. Micrographia (change in handwriting, with the script becoming smaller) Problems with speech, breathing, swallowing, and sexual function. Autonomic disorders sleeplessness, salivation, sweating, orthostatic hypotension, dizziness. Depression, dementia. Masklike facies secondary to rigidity. Gait difficulties characterized by a decreased or nonexistent arm swing; short, shuffling steps (festination); difficulty in negotiating turns; and sudden freezing spells (inability to take the next step). Poor balance when moving abruptly or suddenly changing body position. May lead to falls. Verbal fluency may be impaired. Finger tapping responses are slowed. Diagnostic tests Observation of clinical symptoms; may do imaging studies to rule out other disorders. Physical examination of upper extremity elbow flexion/extension reveals rigidity on extension. Sensorimotor assessment of grip reveals abnormally high grip forces and longer than normal to complete object lift, particularly with lighter loads. Favorable response to a single dose of levodopa helps confirm the diagnosis. Therapeutic Management Pharmacologic Anticholinergics, including trihexyphenidyl (Artane), benztropine (Cogentin), NS procyclidine (Kemadrin) to reduce transmission of cholinergic pathways, which are thought to be overactive when dopamine is deficient. These medications are most effective in controlling tremor, but are known to cause confusion and hallucinations. Amantadine (Symmetrel), originally an antiflu medication, blocks the reuptake of dopamine or increases the release of dopamine by neurons in the brain, thereby increasing the supply of dopamine in the synapses. Widely used as an early monotherapy, its effect may be augmented by drug-free days. Levodopa, a dopamine precursor, combined with carbidopa, a decarboxylase inhibitor, to inhibit destruction of L-dopa in the bloodstream, making more available to the brain. The combination of levodopa-carbidopa (Sinemet) usually is used. The addition of carbidopa prevents levodopa from being metabolized in the gut, liver, and other tissues, and allows more to get to the brain. Bromocriptine (Parlodel), pergolide (Permax), pramipexole (Mirapex), and ropinirole (Requip) are dopaminergic agonists that activate dopamine receptors in the brain. Use of the monoamine oxidase inhibitor selegiline or deprenyl (Eldepryl) boosts the effect of Sinemet when levodopa becomes less effective. Tolcapone (Tasmar) and entacapone (Comtan) are in a new drug class (COMT inhibitors) for adjunct treatment. They prolong the duration of symptom relief by blocking the action of an enzyme that breaks down levodopa before it reaches the brain. Must be taken with levodopa.
SPINAL CORD INJURIES is a traumatic injury to the spinal cord that may vary from a mild cord concussion with transient numbness to immediate and complete tetraplegia. most common sites are the cervical areas C5, C6, and C7, and the junction of the thoracic and lumbar vertebrae, T12 and L1 Mechanism are same with H.I. (causes compression, tension, and shearing) Classification 1.) COMPLETE 2.) INCOMPLETE
COMPLETE ALL MOTOR, SENSORY, AND VASOMOTOR FUNCTIONS ARE ABSENT BEVOLUNTARY LOW THE LEVEL OF INJURY LOSS OF REFLEX FUNCTION IN ISOLATED SEGMENT OF THE CORD. INCOMPLETE SOME DEGREE OF EITHER VOLUNTARY MOTOR, SENSORY, AND VASOMOTOR FUNCTIONS ARE ABSENT BELOW LEVEL OF INJURY CONDITION ASSOCIATED WITH SCI 1. SPINAL SHOCK - A CONDITION IN WHICH THERE IS AN IMMEDIATE, COMPLETE LOSS OF ALL REFLEXES , MOTOR, SENSORY AND AUTONOMIC ACTIVITY BELOW LEVEL OF INJURY - DANGER IS HYPOTENSION AND BRADYCARDIA - last few days or weeks after injury- implication?? - Signs of recovery: - what happens after spinal shock??? neurologic level - Return of anal reflex - Flaccid paralysis becoming spastic - Gradual return of autonomic function - Reflex bowel and bladder contraction 2. AUTONOMIC DYSREFLEXIA (HYPERREFLEXIA) CHARACTERIZED BY EXCESSIVE AUTONOMIC RESPONSES TO STIMULI COMMON WITH C. & HIGH T. SPINAL CORD LESION --- when will this occur? STIMULI : DISTENDED BLADDER Manifestation of hyperreflexia SEVERE HPN (300/160 mmHg) Rupture of blood vessel Severe throbbing/ pounding headache Profuse sweating above the level of the lesion Flushing of skin above level of lesion Nasal stuffiness, pilomotor spasm Blurred vision, nausea, bradycardia Management of Hyperreflexia Monitor BP Elevate HOB to a sitting position Notify AP Check possible sources of irritation (fecal impaction) topical anes. 10 15 mins. Relieve urinary obstruction (FBC) IF BP doesnt subside HYDRALAZINE (Apresoline) Nsg. Resp.: Observe AEG 3 4 hrs SURGERY (chordotomy or poudendal nerve resection) 3. SPINAL AUTOMATISM Spinal reflex activities occurring automatically after S.C. severance BP and Temp fall markedly and respond poorly to reflex stimuli 4. SPASTICITY and MUSCLE SPASM INCREASED TONE OR CONTRACTION OF MUSCLE DEVELPS 2 WEEKS SEVERAL MONTHS Flaccidity ----- SPASM May become a source of DISAPPOINTMENT This is only a REFLEX RESPONSE
DIAGNOSTICS Detailed Neuro. Exam DERMATOME & PLEXUSES X-Ray, CT SCAN, MRI ECG MEDICAL MGt Prevent further injury Keep patient in extended position Position: flat, neck immobilized with a neck collar Intubation and mechanical intubation Maintenance of vertebral alignment: Stryker turning frame, Crutchfield tongs, Halo brace DVT prophylaxis Diet: Low-calcium, high protein IV therapy GI decompression Activity: Bed rest, passive ROM exercises Laboratories Indwelling catheter AEDs High dose corticosteroids (methylprednisolone) NURSING INTERVENTION Promote adequate breathing Improve mobility Dont turn without turning frame Promote adaptation to disturbed sensory perception Maintain skin integrity Promote urinary elimination Improve bowel function Provide comfort measure Monitor and manage potential complication Promote home and community based care
INCOMPLETE SCI CENTRAL CORD SYNDROME Motor deficit more marked in the upper extremities compared to lower extremities Sensory loss more pronounced in the upper extremities Bowel/ bladder dysfunction is variable or function preserved Cause: Injury or edema to central cord ANTERIOR CORD SYNDROME Loss of pain, temperature, and motor function is noted below level of lesion Light touch, position and vibration intact Cause: Acute disk herniation or hyperflexion; injury to anterior spinal artery , which supplies the anterior 2/3 of SC BROWN-SEQUARD SYNDROME (LATERAL CORD SYNDROME) IPSILATERAL PARALYSIS OR PARESIS IS NOTED IPSILATERAL LOSS OF TOUCH, PRESSURE, & VIBRATION CONTRALATERAL LOSS OF PAIN & TEMPERATURE CAUSE: TRANSVERSE HEMISECTION OF THE CORD; USUALLY BY KNIFE OR MISSILE INJURY, UNILATERAL ARTICULAR PROCESS, ACUTE RUPTURED DISK
Trigeminal Neuralgia Tic douloureux Is sudden, excruciating, recurrent paroxysm of sharp, stabbing pains in the sensory distribution of one or more of the three branches of the 5 th cranial nerve Characterized by presence of TRIGGER ZONE Avoidance of certain acts are important clue for trigeminal Affects more women than men; middle or late life *** Unknown cause Trauma, past infections, vascular compression, neoplasm, and MS Management CARBAMAZEPINE (Tegretol) Drug of choice - reduce transmission of impulse Taken with meals - Mon. serum for toxicity (3- 14mcg/ml) GABAPENTIN (Neurontin) and Baclofen (Lioresal) Similar to GABA - derivative of GABA (SC axn) PHENYTOIN (Dilantin) *** If pain is uncontrolled - 10 20 mcg/ml ALCOHOL OR PHENOL INJECTION Temporary pain relief for months (nerve regeneration) Given before retrogasserian rhizotomy Surgical Management Microvascular Decompression (J.P.) Application of non-absorbent sponge (plastic device) in between blood vessel and T. nerve Pos.: Relieves pain & preserves normal sensation Neg.: Craniotomy Percutaneous Radiofrequency Trigeminal Gangliolysis Thermal destruction of the gasserian ganglion (partial destruction) Patient awake during the procedure Surgical procedure of choice Neg.: Loss of sensation in the affected branch Pos.: Touch and proprioceptive fxn is intact Trigeminal Rhizotomy Nursing Management Teach what to expect after surgical procedure 1 st Branch loss of corneal reflex (proper care) 2 nd & 3 rd Branch loss of sensation Teach to avoid hot and food or fluids Regular check-up with dentist Take food on the unaffected side Prevent complication of medication AEDs causes BM suppression, regular monitoring of blood count is imperative before and during TX Teach patient early indication of potential blood problem Preventing pain Identify aggravating factor Perform hygiene task during pain free moments Cotton pads and room temperature water Mouthwash instead of brushing Soft Foods and fluids at room temperature Chew on unaffected side Address anxiety, depression and insomnia ***
BELLS PALSY Most common type of peripheral facial paralysis Unilateral paralysis of the facial muscle without evidence of pathologic cause Inflammation of the 7 th cranial nerve People of increasing age and at 3 rd trimester preg. Is at high risk Possible etio are: Vascular ischemia, viral disease, autoimmune disease Manifestation Bells phenomena Drooping of the mouth Flattening of the nasolabial folds Widening of palpebral fissure Slight lag in closing the eyes Increased lacrimation Speech difficulties Painful sensation in the face, behind the ear and in the eyes **** Management Analgesics *** Corticosteroid therapy (prednisone) Physiotherapy HEAT APPLICATION GENTLE MASSAGE ELECTRICAL STIMULATION** Corneal protection Surgical Exploration Tumor is suspected Decompression of the facial nerve Surgical treatment of paralyzed face ( spinal accessory XI or hypoglossal XII) Nursing Management Reassure patient that NO STROKE has occurred (3 5 weeks) Protect involved eye ARTIFICIAL TEARS EYE PATCH EYE OINTMENT AT BEDTIME TEACH PATIENT TO MANUALLY CLOSE PARALYZED EYELID USE OF WRAP-AROUND SUNGLASSES OR GOGGLES (MAINTAIN MOISTURE)
MENIERS DISEASE Relatively common, chronic disorder in the inner ear Characterized by recurring episodes of vertigo, associated with tinnitus and deafness Exact cause is not clear but is associated with degeneration of tiny cochlear hair cells Assessment may be done through caloric testing and electronystagmography (ENG) Manifestation Severe rotational type of vertigo Nausea and vomiting Diaphoresis Tinnitus Hearing loss Feeling of pressure in the ear Brief loss of consciousness and nystagmus may occur Intervention BED REST most effective during acute episodes SQ atropine sulfate as soon as possible Diazepam IV slowly Advise AEG not to read and avoid bright light Long-term med interv.: Antihistamine (meclizine (Antivert)) Suppress vestibular system Diuretic therapy (acetazolamide (diamox) and chlorothiazide (diuril)) Dietary management Low salt & rule out allergies Relieves pressure in the endolymphatic
PERIPHERAL NERVE INJURY CARPAL TUNNEL SYNDROME Progressive medical condition in which the median nerve is compressed in the carpal tunnel ENTRAPMENT NEUROPATHY Etiology: IDIOPATHIC Risk Factor: 1. Congenital Predisposition 2. Disease or injury 3. Arm use and environmental factor Manifestation: - Paresthesia usually appears at sleep or at night - Muscle weakness - Increasing pain - Increase sweating - Muscle wasting and weakness Diagnosis: 1. History 2. P.E. 3. Diagnostic Procedure a. Phulins Maneuver b. Electrodiagnostic test Treatment: 1. Aspirin, ibuprofen, or napronex 2. Steroid injection 3. Oral prednisone 4. Vit. B 12 5. Surgery Indication: - Severe & long duration - Muscle atrophy - Progressive sensory loss in the finger Procedure: TRANSVERSE CARPAL LIGAMENT TRANSECTION
Nursing Intervention: 1. Rest hands and wrist for 2 weeks 2. Splinting of wrist and hands mild and short duration 3. Ice packs 4. Health education for prevention
NEURAL DISTURBANCE HEAD INJURY 2/3 OF DEATH FROM VEHICULAR ACCIDENT PROMPT INTERVENTION MINIMIZES DEVLP OF 2 O PROBLEMS TREATMENT OF HYPOXIA & ACID-BASE IMBALANCE DECREASES MORTALITY INTRACRANIAL MASS LESIONS MAY FOLLOW INITIAL TRAUMA SEVERE CEREBRAL SWELLING OFTEN FOLLOW BRAIN INJURY AEGS WITH H.I. OFTEN HAVE OTHER MAJOR INJURIES NECK FRACTURES ARE TO BE EXPECTED MECHANISM OF HEAD INJURY CAUSED BY SUDDEN FORCE ACCELERATION DECELERATION DERFORMATION ROTATIONAL FORCE CATEGORIES OF HEAD TRAUMA BLUNT TRAUMA Complex, with several head structures involved PENETRATING Depends on the velocity of object (low velocity and high velocity) Infection (complication) COUP INJURY COUNTRECOUP INJURY NOTE: H.I. MAY ALSO BE CLASSIFIED AS PRIMARY AND SECONDARY A.)PRIMARY HEAD INJURY SCALP INJURIES SKULL INJURIES BRAIN INJURIES FOCAL INJURY DIFFUSE INJURY SCALP INJURY SUPERFICIAL ALONE IS MINOR COVER AND APPLY PRESSURE --- EXCEPT??? SKULL INJURIES OFTEN WITH BRAIN INJURY CAUSES ABRASION AND LACERATION OF BRAIN TISSUE 3 TYPES: LINEAR no Tx needed DEPRESSED surgery BASILAR base of frontal and temporal lobes, diagnosis??? CLINICAL SIGNS INTRACRANIAL CSF FISTULA CSF OR OTHER DRAINAGE FROM EAR OR NOSE VARIOUS CRANIAL NERVE INJURIES BLOOD BEHIND THE EARDRUM PERIORBITAL ECCHYMOSIS BATTLES SIGN BRUSIE OVER THE MASTOID Mgt: DIAMOX, LUMBAR DRAIN, CRANIECTOMY, CRANIOPLASTY BRAIN INJURY FOCAL INJURY SMALL HEMORRHAGES OF THE CORTICAL SURFACES MAY CAUSE SECONDARY BRAIN DAMAGE DIFFUSE INJURY TEMPORARY LOSS OF NEUROLOGIC FUNCTION WITHOUT STRUCTURAL DAMAGE DIFFUSE AXONAL INJURY SHEARING OF AXONS IN THE W.M. IMMEDIATE COMATOSE & MAY NOT AWAKEN B.) SECONDARY HEMORRHAGE INFECTION SECONDARY BRAIN SWELLING AND EDEMA CAROTID ARTERY OCCLUSION HEMORRHAGE EPIDURAL, SUBDURAL, & INTRACEREBRAL A. EPIDURAL HEMATOMA (EXTRADURAL) - involves extracerebral blood vessels, middle meningeal artery and vein ASSESSMENT: - ACUTE MANIFESTATION? Classical Sign: 1. unconsciousness immediately after head trauma 2. Awakens & quite lucid Dx criteria 3. Later, lapses to come CONSIDERED A MEDICAL EMERGENCY!
SUBDURAL HEMATOMA (SDH) COLLECTION OF BLOOD BETWEEN DURA AND ARACHNOID BLOOD IS NOT REABSORBED BUT BECOMES ORGANIZED OR ENCAPSULATED BY THE DURA BLOOD CLOTS AND THEN LATER ON LYSES (HIGH OSMOTIC CHARACTER) --- H2o fr. SAS --- increase ICP 3 categories: ACUTE & SUBACUTE and CHRONIC Acute = 24 48 hrs Subacute = 48 2 weeks Chronic = 3 weeks months SDH MANIFESTATION Acute & Subacute SDH Changes in LOC Pupillary signs Hemiparesis Chronic SHD Seen freq. in the elderly Devlp from minor H.I. Person seems to recover, then, neurologic signs progressively develop HEADACHE prominent Symptom LOC most predominant assessment finding Focal or lateralizing symptom (hemiparesis)*** INTRACEREBRAL HEMATOMA OCCUR LESS OFTEN THAN EPIDURAL OR SDH, AND CAUSE DIRECTLY BY BRAIN TISSUE BLEEDING ASSESSMENT FINDING SAME WITH EPIDURAL AND SDH hemiplegia more common than hemiparesis Additional secondary head trauma BRAIN SWELLING AND EDEMA ASSOCIATED WITH SERIOUS HEAD INJURIES INFECTION OPEN HEAD INJURIES MENINGITIS AND BRAIN ABSCESS Classification Mild (GCS 13 to 15, with loss of consciousness to 15 minutes) Moderate (GCS 9 to 12, with loss of consciousness for up to 6 hours) Severe (GCS 3 to 8, with loss of consciousness greater than 6 hours) Diagnostic Evaluation CT scan to identify and localize lesions, edema, bleeding. Skull and cervical spine films to identify fracture, displacement. Neuropsychological tests during rehabilitation phase to determine cognitive deficits. CBC, coagulation profile, electrolyte levels, serum osmolarity, ABG values, and other laboratory tests to monitor for complications and guide treatment. MANAGEMENT/ TREATMENT EMERGENCY AND ACUTE CARE AIRWAY 100 % OXYGEN MAINTENANCE OF CIRCULATION MEASURES TO REDUCE ICP CSF DRAINAGE If disconnected, clamp nearest the head Check for leakage Avoid pressure or kinking Clamp drainage tubing when moving or turning the patient OSMOTHERAPY Dehydrate the brain; MANNITOL FBC!; I & O!; may be combined with fluid restrction STEROIDS HYPERVENTILATION HYPOTHERMIA BARBITURATES Tx FOR OTHER COMPLICATION HYPONATREMIA - < 130 Meq/L ???? FLUID RESTRICTION < 800 mL HYPERNATREMIA POLYURIA, sp. Gravity = 1.000 -1.006 HYPERMETABOLIC STATE 1 2 yrs. Prophylactic meds POST-TRAUMATIC SEIZURE STRESS ULCERS (C.U.) NURSING INTERVENTION MAINTAIN THE AIRWAY MAINTAINING FLUID AND ELECTROLYTE BALANCE POVIDING ADEQUATE NUTRITION PREVENTING INJURIES MONITOR BODY TEMPERATURE MAINTANING SKIN INTEGRITY ASSESS AL BODY SURFACE Q 8HRS TURN Q 2 4 HRS PROVIDE SKIN CARE Q 4 HRS. IMPROVE COGNITIVE FUNCTION PREVENTING SLEEP PATERN DISTURBANCE PREVENTING INJURY OBSERVE FOR RESTLESSNESS AVOID BLADDER DISTENTION PADDED SIDE RAILS, HANDS WRAPPED IN MITTS AVOID RESTRAINTS AS MUCH AS POSSIBLE AVOID USING NARCOTICS FOR RESTLESSNESS DECREASE ENVIROBNMENTAL STIMULI PROVIDE ADEQUATE LIGHTING TO PREVENT VISUAL HALLUCINATION DO NOT DISRUPT SLEEP/WAKE CYCLES
SEIZURE DISORDER epilepsy THE SACRED DISEASE fr. GREEK to take hold or seize Are paroxysmal neurologic disorders causing recurrent episodes of seizures SEIZURE a paroxysmal, uncontrolled, abnormal discharge of electrical activity in the brains gray matter. Classification of seizures General seizures Diffuse Begins bilaterally Partial seizures (focal epilepsy) Begin in one localized area A. Generalized seizures (1/3) GRAND MAL (10%) Sudden loss of consciousness Tonic phase - 30 60 seconds Clonic phase Entire grand mal = 2 5 min Post grand mal: Unresponsive Post-ictal sleep, general fatigue, depression, confusion, and headache PETIT MAL (absence) MINOR MOTOR (akinetic, myoclonic, and atonic) GRAND MAL Sudden loss of consciousness Tonic phase - 30 60 seconds Clonic phase Entire grand mal = 2 5 min Post grand mal: Unresponsive Post-ictal sleep, general fatigue, depression, confusion, and headache Petit mal (absence) seizure Usually begin during childhood and primarily limited to childhood and early adolescence Consist of brief periods of altered consciousness lasting from 5 to 30 seconds Diminish or disappear after puberty May develop grand mal or partial seizure MINOR MOTOR SEIZURES MYOCLONIC Involuntary jerking contraction of major muscles Person may be thrown to the floor AKINETIC Momentary loss of muscle movement ATONIC Total loss of muscle tone, person fall to the floor B. Partial seizures PARTIAL MOTOR SEIZURE Focus in the region of the brains motor cortex Convulsive twitching in an upper extremity (most common) Jacksonian march (central spread) PARTIAL SENSORY SEIZURES Parietal numbness and tingling Occipital bright, flashing lights Temporal difficulty with speaking/ total speech arrest PARTIAL SEIZURES WITH COMPLEX SYMPTOMATOLOGY Psychomotor seizures or partial complex seizures Frequently begins with an aura have an impairment (but not a loss) of consciousness with simple partial features, automatisms, or impairment of consciousness only. Simple partial seizures can progress to complex partial seizures, and complex partial seizures can secondarily become generalized. STATUS EPILEPTICUS IS A STATE IN WHICH A PERSON HAS CONTINUOUS SEIZURES OR SEIZURES IN RAPID SUCCESSION LASTING AT LEAST 30 MINUTES. ETIOLOGY OF SEIZURES The etiology may be unknown or due to one of the following: Trauma to head or brain resulting in scar tissue or cerebral atrophy Tumors Cranial surgery Metabolic disorders (hypocalcemia, hypoglycemia/hyperglycemia, hyponatremia, anoxia) Drug toxicity, such as theophylline (Theo-Dur), lidocaine (Xylocaine), penicillin CNS infection Circulatory disorders Drug withdrawal states (alcohol, barbiturates) Congenital neurodegenerative disorders ASSESSMENT HISTORY P.E. SKULL X-RAYS EEG CT SCAN LP MRI INTERVENTION ELIMINATING FACTORS THAT MAY CAUSE OR PRECIPITATE SEIZURES IMPROVING THE PERSONS PHYSICAL AND MENTAL HEALTH SPECIFIC MEDICAT TREATMENT SURGICAL TREATMENT MEDICAL TREATMENT Anticonvulsants or antiepileptic drugs (AEDs) Most effective method of controlling seizures that have no treatable cause High doses of a single drug are more preferred than smaller doses of several drugs SURGICAL INTERVENTION CRITERIA FAILURE OF MEDICAL APPROACH LOCALIZATION AND IDENTIFICATION OF A FOCUS OF ABNORMAL DISCHARGE THAT IS EASILY ACCESSIBLE SURGICALLY AND IS LOCATED IN DISPENSIBLE CORTEX Patient is kept awake during surgery, (alert and cooperative). temporal lobectomy, extratemporal resection, corpus callosotomy, hemispherectomy Nursing Intervention Assess neurologic and respiratory status Maintain a patent airway Monitor and record V/S, I/O, neurovital signs, and laboratory studies Administer medication as prescribed Maintain seizure precautions Protect the patient from injury during seizure activity Observe and record seizure activity Assess postictal state Encourage the patient to express feelings about powerlessness Maintain the patients diet Individualize home care instructions Know about the disorder and its implications Follow instructions for medication use and be aware of possible adverse effects Recognize signs and symptoms of seizure onset Avoid drinking alcohol Promote safe environment Wear a medical identification bracelet Identify and time seizure activity Prevent injury during seizure activity
MENINGITIS Inflammation of the meninges that surround the brain and the spinal cord. Classified as Septic and Aseptic Neisseria meningitidis (most common) Haemophilus influenzae and streptococcus pneumoniae ((causative agents) Neisseria and Streptococcus pneumoniae,most common cause ( Lippincott) Pathophysiology Infecting organism gains entry through bloodstream (2 0 infection) or direct extension Infecting organism produce an inflammatory response Meningeal vessels becomes hyperemic and increasingly permeable Blood cells (neutrophils) migrate to SAS, producing exudate Exudate formation causes meningeal irritation and increased ICP Clinical Manifestations Initial/ Classic: fever, headache Systemic infection Fever, tachycardia, chills and petechial rash Meningeal Irritation Nuchal rigidity - early sign Positive Kernigs sign Positive Brudzinskis sign Photophobia Neurologic signs Decrease in consciousness Cranial nerve palsies (ptosis, diplopia, facial weakness, tinnitus, vertigo, and deafness) Focal neurologic deficits (ataxia and motor weakness) Seizures Other Signs Petechial or purpuric rash to large area of ecchymosis from coagulopathy, especially with N. meningitidis. Disorientation and memory impairment Behavioral manifestation Other signs f Increase ICP Fulminating infection (10 % of Meningococcal meningitis) Signs of septicemia Fever Extensive purpuric lesion over face and extrinmities Shock DIC Diagnostic Evaluation LP: elevated CSF pressure; cloudy, turbid, or clear in appearance; normal or increased protein; glucose decreased or normal; culture and sensitivity test; presence of polysaccharide antigen (supports bacterial meningitis) Cultures: identify source of infection in blood, urine, and nose and throat secretions X-rays: assess for fractures, abscesses, or signs of infection in chest, skull and sinuses WBC count: elevated Prevention Vaccination: meningococcal meningitis (MCV4) Antimicrobial prophylaxis for people in close contact with meningococcal patients Rifampicin (Rifadin), Ciprofloxacin hydrochloride (Cipro), or ceftriaxone sodium (Rocephin) Vaccination as an adjunct to antibiotic (H. influenzae and S. pneumoniae) Medical Management A.) Early antibiotic therapy - Penicillin ( ampicillin and piperacillin) - Cephalosporin (ceftriaxone sodium, cefotaxime sodium) - Vancomycin hydrochloride alone or with rifampicin ** B.) Dexamethasone - given 15 to 20 minutes before 1 st dose of antibiotic (q 6 hrs for 4 days) C.) Fluid volume expanders DHN and shock D.) Phenytoin (dilantin) E.) Meaures for increased ICP F.) Diuretic, Isolation, and seizure precaution Nursing Management Provide continuous or on-going neurological assessment, monitor Vital signs Pulse oximetry and ABG is monitored Take measure to address Fever immediatey Monitor body weight, serum electrolytes, and urine volume, specific gravity, and osmolality Protect the patient from injury (seizure precaution) Prevent complication secondary to immobility Institute droplet precautions until 24 hours after the initiation of antibiotic therapy (isolation technique) Report meningococcal meningitis to local health authority
Brain Abscess Localized collection of pus within the parenchyma of the brain and spinal cord Relatively rare, complication encountered by immuno-compromised patients Pathophysiology Direct invasion from intracranial trauma or surgery Spread of infection from nearby sites (sinuses, ears, and teeth) Spread of infection from other organs(lung abscess, infective endocarditis) Clinical Manifestation HEADACHE worse in the morning (prevailing symptom) Vomiting Focal neurologic signs (depends on the location of abscess) Change in mental status Fever may or may not be present Diagnostics CT SCAN MRI Useful to obtain images of the Brain Stem and posterior fossa Medical Management Antimicrobial therapy & Surgical incision or aspiration Penicilin G (20 million U) and Chloramphenicol (4-6 g/day given IV in divided doses) Given preoperatively and postoperatively Corticosteroids Antiseizure medications (phenytoid, phenobarbital) Nursing Management Focus is on Ongoing assessment Blood laboratory test result , blood glucose and serum potassium levels Patient safety is a key nursing responsibility
Encephalitis Acute inflammatory process of the brain tissue. HERPES SIMPLEX VIRUS ENCEPHALITIS Herpes Simplex virus (HSV) is the most common cause of acute encephalitis (HSV 1) PATHO: - Infxn of buccal mucosa --- retrograde spread along trigeminal nerve --- to brain - Latent virus in brain tissue is reactivated Clinical Manifestation Inflammation and necrosis in the T F L (temporal, frontal and limbic system) Initial : FEVER, HEADACHE, CONFUSION, and BEHAVIORAL ABNORMALITIES Focal neurologic symptoms (within 7 days, last 14 21 days) Behavioral changes Focal seizures Dysphasia Hemiparesis Altered LOC Diagnostics EEG CSF High opening pressure Low glucose and high protein levels Viral cultures are almost always negative PCR (polymerase chain reaction) Identifies DNA bands of the HSV (3 rd and 10 th day of Sx onset) NEUROIMAGING MRI is the neuroimaging study of choice Medical Management ACYCLOVIR (Zovirax) medication of choice Continued for 3 weeks (prevent relapse) Slow administration (over 1 hour) Usual dose is decrease in patient with Hx of renal insufficiency FOSCARNET SODIUM (Foscavir) - in rare cases of acyclovir resistance Nursing Management ON Going Neurological Assessment Comfort measure for headache: Dimming of lights Limiting noise Administering analgesics Use opioid medication cautiously mask signs Initiate injury prevention and safety Monitor for renal complication (labs and I & O)
Fungal Encephalitis Occur rarely in healthy people COMPROMISED IMMUNE SYSTEM Common agents: Cryptococcus neoformans Histoplasma capsulatum Aspergillus Candida Albicans PATHO: - Fungal Spores enters the body via inhalation - Initially through the lungs and bloodstream - CNS --- Meningitis Encephalitis brain abscess - also causes abscess of the SC = SC compression Clinical Manifestation Common: Fever, malaise, headache, nuchal rigidity, lethargy and mental status changes Symptom of increase ICP from hydrocephalus Assessment and Diagnostics Presence of a compromised immune system and history of living or travel to certain areas Elevated WBC and ANEMIA Fungal antibodies in serum Neuroimaging CT scan and MRI CSF : Elevated WBC, and protein Culture of fungi Medical Management ANTIFUNGAL AGENTS Specific period or indefinite period (maintenance dose) AMPOTHERICIN B (Abelcet, AmBisome, Amphocin, Amphotec, Fungizone, and Fungizone IV) - standard antifungal treatment - dose high enough without causing renal toxicity FLUCONAZOLE (diflucan) or flucytosine (5-FC, 5- fluorocytosine, Ancobon) - may be administered in conjunction with ampothericin B - causes transient increase in liver enzyme - S/E: Nausea, abdominal pain, headache, dizziness, rash, reversible alopecia Nursing management On Going assessment Provide patient comfort: Administering non-opioid analgesics Limiting environmental stimuli Positioning Give diphenhydramine (Benadryl) and acetaminophen (Tylenol) approx. 30 mins before amphothericin B (fever, chills and body aches) Monitor creatinine and blood urea nitrogen Provide support to patient and family to cope up with work up ???