I.

OBJECTIVES A. General Objectives After establishing Nurse-Patient Interaction, thorough, keen and comprehensive physical assessment, providing care to the client and developing a careful study of the clients condition, the student will acquire appropriate knowledge, develop and utilize skills and enhance attitude through the proper use of nursing process as the basis of care and management of the patient with Guillain Barre Syndrome. B. Specific Objectives On completion of this case study, the student will be able to: 1. Understand what congenital Guillain Barre Syndrome is. 2. Define the terminologies used in the case study 3. Identify its clinical manifestations 4. Establish a good and therapeutic nurse-patient interaction 5. To build a trusting relationship with both the patient and significant others. 6. Trace the pathophysiology of the disease 7. Recapitulate the anatomy and physiology of the body parts involved. 8. Determine the clients health status through: a. General and Demographic Data b. History of Present Illness c. Past Medical History d. Personal and Family History

e. Physical Examination f. Course in the ward 9. Utilize skills in performing physical examination to the patient. 10. Analyze laboratory results and correlate it with patients condition 11. Familiarize self to some medical and diagnostic procedures related to the patients present condition. 12. Determine the relevance of the drugs or medication to the patient. 13. Formulate nursing diagnosis and provide necessary nursing

management and interventions 14. Determine the rationale behind the applied nursing interventions 15. Render quality-nursing care through implementation of the Nursing Care Plan 16. Evaluate effectiveness of Nursing Care Plan and medical management 17. Provide continuity of care by giving health teachings not only to patient but also as well the Significant Others

II.

INTRODUCTION Most people will make a full recovery within a few weeks or months, with no further trouble. Some cases take longer We have nerves that live outside the central nervous system (the brain and spinal cord), and deal with our body's senses and movements. These are called our peripheral nerves. Guillain-Barre syndrome (also known as acute inflammatory or post infective polyradiculoneuropathy) is a rare but serious disease of the peripheral

nervous system. It makes the bodys own immune system attack the nerves, causing widespread inflammation that leads to a tingly, numbing sensation in the arms and legs. This can eventually result in a short-term loss of feeling and movement (temporary paralysis).It is slightly more common in men than women, and can affect people of any age, even children. What exactly causes the condition is unclear and there is no way to pinpoint who may be most at risk. However, in most cases of Guillain-Barre syndrome the person had a virus or bacterial infection in the last four weeks. The nervous system is divided into the:

peripheral nervous system (PNS) central nervous system (CNS) The PNS consists of:

sensory neurons running from stimulus receptors that inform the CNS of the stimuli

motor neurons running from the CNS to the muscles and glands - called effectors - that take action. The CNS consists of the:

spinal cord and the brain

THE PERIPHERAL NERVOUS SYSTEM IN FOCUS In the peripheral nervous system, neurons can be functionally divided in three ways:

1. Sensory (afferent) - carry information INTO the central nervous system from sense organs or motor (efferent) - carry information away from the central nervous system (for muscle control). 2. Cranial - connects the brain with the periphery or spinal - connects the spinal cord with the periphery. 3. Somatic - connects the skin or muscle with the central nervous system or visceral - connects the internal organs with the central nervous system

The peripheral nervous system is subdivided into the

sensory-somatic nervous system and the autonomic nervous system

The Spinal Nerves All of the spinal nerves are "mixed"; that is, they contain both sensory and motor neurons. All our conscious awareness of the external environment and all our motor activity to cope with it operate through the sensory-somatic division of the PNS. The Autonomic Nervous System The autonomic nervous system consists of sensory neurons and motor neurons that run between the central nervous system (especially the hypothalamus and medulla oblongata) and various internal organs such as the:

heart lungs

viscera glands (both exocrine and endocrine)

It is responsible for monitoring conditions in the internal environment and bringing about appropriate changes in them. The contraction of both smooth muscle and cardiac muscle is controlled by motor neurons of the autonomic system. The actions of the autonomic nervous system are largely involuntary (in contrast to those of the sensory-somatic system). It also differs from the sensory-somatic system is using two groups of motor neurons to stimulate the effectors instead of one.

The first, the preganglionic neurons, arise in the CNS and run to a ganglion in the body. Here they synapse with

postganglionic neurons, which run to the effector organ (cardiac muscle, smooth muscle, or a gland).

The autonomic nervous system has two subdivisions, the

sympathetic nervous system and the parasympathetic nervous system.

The Sympathetic Nervous System The preganglionic motor neurons of the sympathetic system arise in the spinal cord. They pass into sympathetic ganglia which are organized into two chains that run parallel to and on either side of the spinal cord.

The preganglionic neuron may do one of three things in the sympathetic ganglion:

synapse with postganglionic neurons which then reenter the spinal nerve and ultimately pass out to the sweat glands and the walls of blood vessels near the surface of the body.

pass up or down the sympathetic chain and finally synapse with postganglionic neurons in a higher or lower ganglion

leave the ganglion by way of a cord leading to special ganglia (e.g. the solar plexus) in the viscera. Here it may synapse with postganglionic sympathetic neurons running to the smooth muscular walls of the viscera. However, some of these preganglionic neurons pass right on through this second ganglion and into the adrenal medulla. Here they synapse with the highly-modified postganglionic cells that make up the secretory portion of the adrenal medulla.

The neurotransmitter of the preganglionic sympathetic neurons is acetylcholine (ACh). It stimulates action potentials in the postganglionic neurons.

The neurotransmitter released by the postganglionic neurons is noradrenaline (also called norepinephrine).

The action of noradrenaline on a particular gland or muscle is excitatory is some cases, inhibitory in others. (At excitatory terminals, ATP may be released along with noradrenaline.)

The release of noradrenaline

stimulates heartbeat

raises blood pressure dilates the pupils dilates the trachea and bronchi stimulates the conversion of liver glycogen into glucose shunts blood away from the skin and viscera to the skeletal muscles, brain, and heart

inhibits peristalsis in the gastrointestinal (GI) tract inhibits contraction of the bladder and rectum and, at least in rats and mice, increases the number of AMPA receptors in the hippocampus and thus increases long-term potentiation (LTP).

In short, stimulation of the sympathetic branch of the autonomic nervous system prepares the body for emergencies: for "fight or flight" (and, perhaps, enhances the memory of the event that triggered the response).

Activation of the sympathetic system is quite general because

a single preganglionic neuron usually synapses with many postganglionic neurons;

The release of adrenaline from the adrenal medulla into the blood ensures that all the cells of the body will be exposed to sympathetic stimulation even if no postganglionic neurons reach them directly.

The Parasympathetic Nervous System

The main nerves of the parasympathetic system are the tenth cranial nerves, the vagus nerves. They originate in the medulla oblongata. Other preganglionic parasympathetic neurons also extend from the brain as well as from the lower tip of the spinal cord.

Each preganglionic parasympathetic neuron synapses with just a few postganglionic neurons, which are located near - or in - the effector organ, a muscle or gland. Acetylcholine (ACh) is the neurotransmitter at all the pre- and many of the postganglionic neurons of the parasympathetic system. However, some of the postganglionic neurons release nitric oxide (NO) as their neurotransmitter.

Parasympathetic stimulation causes

slowing down of the heartbeat lowering of blood pressure constriction of the pupils increased blood flow to the skin and viscera peristalsis of the GI tract

In short, the parasympathetic system returns the body functions to normal after they have been altered by sympathetic stimulation. In times of danger, the sympathetic system prepares the body for violent activity. The parasympathetic system reverses these changes when the danger is over.

The vagus nerves also help keep inflammation under control. Inflammation stimulates nearby sensory neurons of the vagus. When these nerve impulses reach the medulla oblongata, they are relayed back along motor fibers to the inflamed area. The acetylcholine from the motor neurons suppresses the release of inflammatory cytokines, e.g., tumor necrosis factor (TNF), from macrophages in the inflamed tissue.

Although the autonomic nervous system is considered to be involuntary, this is not entirely true. A certain amount of conscious control can be exerted over it as has long been demonstrated by practitioners of Yoga and Zen Buddhism. During their periods of meditation, these people are clearly able to alter a number of autonomic functions including heart rate and the rate of oxygen consumption. These changes are not simply a reflection of decreased physical activity because they exceed the amount of change occurring during sleep or hypnosis.

IMMUNE SYSTEM

The immune system is composed of many interdependent cell types that collectively protect the body from bacterial, parasitic, fungal, viral infections and from the growth of tumor cells. Many of these cell types have specialized functions. The cells of the immune system can engulf bacteria, kill parasites or tumor cells, or kill viral-infected cells. Often, these cells depend on the T helper subset for activation signals in the form of secretions formally known as cytokines, lymphokines, or more specifically interleukins.

The Organs of the Immune System

Bone Marrow -- All the cells of the immune system are initially derived from the bone marrow. They form through a process called hematopoiesis. During hematopoiesis, bone marrow-derived stem cells differentiate into either mature cells of the immune system or into precursors of cells that migrate out of the bone marrow to continue their maturation elsewhere. The bone marrow produces B cells, natural killer cells, granulocytes and immature thymocytes, in addition to red blood cells and platelets.

Thymus -- The function of the thymus is to produce mature T cells. Immature thymocytes, also known as prothymocytes, leave the bone marrow and migrate into the thymus. Through a remarkable maturation process sometimes referred to as thymic education, T cells that are beneficial to the immune system are spared, while those T cells that might evoke a detrimental autoimmune response are eliminated. The mature T cells are then released into the bloodstream.

Spleen -- The spleen is an immunologic filter of the blood. It is made up of B cells, T cells, macrophages, dendritic cells, natural killer cells and red blood cells. In addition to capturing foreign materials (antigens) from the blood that passes through the spleen, migratory macrophages and dendritic cells bring antigens to the spleen via the bloodstream. An immune response is initiated when the macrophage or dendritic cells present the antigen to the appropriate B or T cells. This organ can be thought of as an immunological conference center. In the

spleen, B cells become activated and produce large amounts of antibody. Also, old red blood cells are destroyed in the spleen.

Lymph Nodes -- The lymph nodes function as an immunologic filter for the bodily fluid known as lymph. Lymph nodes are found throughout the body. Composed mostly of T cells, B cells, dendritic cells and macrophages, the nodes drain fluid from most of our tissues. Antigens are filtered out of the lymph in the lymph node before returning the lymph to the circulation. In a similar fashion as the spleen, the macrophages and dendritic cells that capture antigens present these foreign materials to T and B cells, consequently initiating an immune response.

The Cells of the Immune System

T-Cells -- T lymphocytes are usually divided into two major subsets that are functionally and phenotypically (identifiably) different. The T helper subset, also called the CD4+ T cell, is a pertinent coordinator of immune regulation. The main function of the T helper cell is to augment or potentiate immune responses by the secretion of specialized factors that activate other white blood cells to fight off infection.

Another important type of T cell is called the T killer/suppressor subset or CD8+ T cell. These cells are important in directly killing certain tumor cells, viralinfected cells and sometimes parasites. The CD8+ T cells are also important in down-regulation of immune responses. Both types of T cells can be found throughout the body. They often depend on the secondary lymphoid organs (the

lymph nodes and spleen) as sites where activation occurs, but they are also found in other tissues of the body, most conspicuously the liver, lung, blood, and intestinal and reproductive tracts.

Natural Killer Cells -- Natural killer cells, often referred to as NK cells, are similar to the killer T cell subset (CD8+ T cells). They function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. NK cells, unlike the CD8+ (killer) T cells, kill their targets without a prior "conference" in the lymphoid organs. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively.

B Cells -- The major function of B lymphocytes is the production of antibodies in response to foreign proteins of bacteria, viruses, and tumor cells. Antibodies are specialized proteins that specifically recognize and bind to one particular protein that specifically recognize and bind to one particular protein. Antibody production and binding to a foreign substance or antigen, often is critical as a means of signaling other cells to engulf, kill or remove that substance from the body.

Granulocytes or Polymorphonuclear (PMN) Leukocytes -- Another group of white blood cells is collectively referred to as granulocytes or polymorphonuclear leukocytes (PMNs). Granulocytes are composed of three cell types identified as neutrophils, eosinophils and basophils, based on their staining characteristics with certain dyes. These cells are predominantly important in the removal of bacteria

and parasites from the body. They engulf these foreign bodies and degrade them using their powerful enzymes.

Macrophages -- Macrophages are important in the regulation of immune responses. They are often referred to as scavengers or antigen-presenting cells (APC) because they pick up and ingest foreign materials and present these antigens to other cells of the immune system such as T cells and B cells. This is one of the important first steps in the initiation of an immune response. Stimulated macrophages exhibit increased levels of phagocytosis and are also secretory.

Dendritic Cells -- Another cell type, addressed only recently, is the dendritic cell. Dendritic cells, which also originate in the bone marrow, function as antigen presenting cells (APC). In fact, the dendritic cells are more efficient apcs than macrophages. These cells are usually found in the structural compartment of the lymphoid organs such as the thymus, lymph nodes and spleen. However, they are also found in the bloodstream and other tissues of the body. It is believed that they capture antigen or bring it to the lymphoid organs where an immune response is initiated. Unfortunately, one reason we know so little about dendritic cells is that they are extremely hard to isolate, which is often a prerequisite for the study of the functional qualities of specific cell types. Of particular issue here is the recent finding that dendritic cells bind high amount of HIV, and may be a reservoir of virus that is transmitted to CD4+ T cells during an activation event.

IV. OVERVIEW OF THE DISEASE A. Description Guillaine Barre (ghee-yan-ba-ray) Syndrome is a disorder in which the bodys immune system attacts part of the peripheral nervous system. Most patients, however recover from even the most severe causes of GBS, although some continue to have degree of the weaness. Guillaine Barre Syndrome can affect anybody. It can strike at any age and both sexes. It is a serious disorder that occurs when the bodys defense system mistakenly attacks part of the nervous system. This leads to nerve inflammation taht causes msucle weakness. B.Causes, Incidence and the Risk Factors Guillaine Barre Syndrome is an autoimmune disorder ( the bodys immune system attack itself). Exactly waht triggers Guillain-Barre syndrome is unknown. The syndrome may occur at any age, but is most common in people of both sexes between ages 30 and 50. It often follows after: Minor infections such as Lung infection or gastrointestinal infection Swine flu vaccination ( during 1976)

It may occur along with viral infections such as: AIDS Herpes Simplex Mononucleosis Systemic Lupus erythematosus

Hodgkins Disease

Some may get GBS often bactetial infection. A similar syndrome may occur often surgery or when someone is critically ill. C. Signs and Symptoms Symptoms of GBS can get worse very quickly. It may take only a few hours to reach the most severe symptoms, but weakness that increases over severeal days is also common. Typical symptoms include: Loss of reflexes in the arms and legs Low blood pressure or poor blodd pressure control Muscle weakness or loss of muscle function ( paralysis often starting from the legs Ascending paralysis) Numbness Sensation changes Muscle pain Uncordinated movement

Other symptoms include: Blured vision Clumsiness Difficulty moving face muscle Palpitations

Emergency Symptoms (seek immediate helps) Breathing temporarily stops Difficulty of breathing Difficulty of swallowing Drooling Fainting Feeling of light-headedness when standing

D. Diagnostic Tests A history of increasing muscle weakness and paralysis may be a sign of GBS, especially if there was a recent illness. A medical exam may show muscle weakness and problems with involuntary bdy functions, such as blood pressure and heartbeat. The ecamination may also show that reflexes, such as the ankle or knee jerk are decresing or missing There may be sgns of decreased breathing caused by paralysis of the breathing muscles. The following test may be ordered: Cerebrispinal fluid sample (spinal tap) to show if theres a presence of infection. ECG for heart functon Electromyography (EMG) to test electrical activity in muscles Nerve condution velocity test

Pulmonary function tests to determine of the disorder affects the lung function

E. Treatment There is no cure for GBS. However, many treatments are available to reduce symptoms, treat complications and speed up recovery. When symptoms are severe, the patient will need to go to the hospital for treatment, whch inlcude artificial breathing support. In early stages of the illness treatments that remove or block the patients that attack the nerve cells, called antibodies, may reduce the severity and duration of GBS. These methods include: Plasmopheresis used to remove the antibodies from the blood. The process involves taking blood from the body, usually from the arm, pumping it into a machine that removes the antibodies, then sending it back into the body. Blocking antibodies using high dose immunoglobulin thereapy (IMG). In this case, the immunoglobulins are added to the blood in large quantities, blocking the antibodies that cause inflammation. Other treatments are directed at preventing complications: Blood thinners to prevent blood clots Breathing support or breathing tube and ventilator Pain is treated with anti inflammatory drugs and narcotics. Proper body positioning or a feeding tube may be used to prevent chocking if the muscle used for swallowing are weak.

F. Prognosis Most people survive and recover completely. About 30% of patients still have same weakness after 3 years. A patients outcome is most likely to be very good when the symptoms go away within 3 weeks after they first started. G. Complications Respiratory failure Contractures of joints Deep vein thrombosis Infections Low or unstable blood pressure Permanent paralysis Pneumonia Pressure ulcer

V. CASE STUDY PROPER A. General Data NAME: Patient X ADDRESS: Leseb Bauko, Mountain Province, Kalinga Province BIRTHDAY: March 21, 2007 AGE: 5 years old SEX: Female BIRTHPLACE: Kalinga Province RELIGION: Roman Catholic FATHERS NAME: James Bocot

MOTHERS MAIDEN NAME: Mrs. Conception ADMISSION DATE: Feb 28, 2012 ADMISSION TIME: 4:20 PM CHIEF COMPLAINT: weakness of both upper anf lower extremities ADMITTING DIAGNOSIS: Guillain Barre Syndrome B. History of present Illness Eleven months prior to admission, Patient X fell on the pavement.

Immediately after the incident there was weakness noted on both extremities. She prefers to sleep most of the time. There was no pain. No bladder and bowel problems noted. Three days after, there was no improvement and the parents decided to bring her to Lorma General Hospital in San Fernando, La Union. There, she was diagnosed with Spinal Cord Contussion C3 T1 secondary to fall and Pneumonia. Also signs of atelectasis of left Hemithorax was seen, thus, an emergency tracheostomy was done. Ten months prior to admission, she was discharged and still unable to move both shoulders as well as Lower extremities. But she was reffered to Philippine Orthopedic Center for more observations. C. Past medical History Last april 2011, she was hospitalized and diagnosed with Spinal Cord Contussion C3 T1 secondary to fall and Pneumonia. Aside from that, no further hospitalizations were noted. She experienced coughs, colds and fever but commonly relieved through self medication.

D. Family Health History There was no trace of PTB, Cancer, Blood disorders, and diabetes mellitus in the family. But hypertension exist in her paternal side. E. Physical Exam General Condition Conscious, unresponsive to questions Afebrile; T = 36.5 C Not in respiratory distress; R= 25 breaths/min Unable to ambulate

Vital Signs Head Eyes With whitish sclera and slightly pale conjunctiva With pupils equally reactive to light accomodation With intact eyelids Symmetrical; hair equally distributed No lessions noted on scalp T=36.5 C P=87bpm RR=25 breaths/min BP= 80/60 mmHg

Ears Nose Mouth Neck with Tracheostomy Tube; dry and intact with secretions draining from the Tracheostomy, whitish in color, moderate in amount Chest with symmetrical expansion upon breathing with wheezing sound heard on both lung fields upon auscultation no redness around tracheostomy with slightly pale and moist Lips with productive cough noted; draining through Tracheostomy Tube no lesions noted With intact nasal septum Symmetrical and properly aligned no nasal discharges noted no nasal flaring noted Symmetrical; aligned with the outer canthus of the eyes No discharges noted

Abdomen with soft and non-tender abdomen upon palpation with normoactive bowel sounds, 18 bowel sounds auscultated

Upper Extremities able to sway the right arm but unable to lift it unable to move the left arm with capillary refill time of 2 secs with pale nailbeds

Lower Extremities Skin with good skin turgor no lesions noted unable to move both lower extremities no sensations on both lower extremities upon touching or pinching with pale nailbeds with capillary refill time of 1-2secs

VI. DIAGNOSTIC AND LABORATORY EXAMS TYPE OF EXAM: Complete Blood Count Date: Feb. 28, 2012 Component Hgb Hct Segmenters Leukocytes Normal 9.5-11.4 g/dl 30%-40% 50%-70% 500010000 Lymphocytes 20%-40% Monocytes Eosinophils Platelets 2%-8% 1%-4% 150000400000 MCV MCH MCHC 82-92 fl 28-32 pg 32%-38% 87fl 27 pg 31% Normal Normal Normal 42% 9% 4% 546000 Elevated Elevated Normal Elevated Result 11.6g/dl 37% 45% 10900 Interpretation Normal Normal Decreased Elevated Nursing Responsibilities Assess for signs of infection Monitor vital signs such as Temp. Instruct to perform proper and frequent handwashing techniques Instruct to increase oral fluid intake Observe for signs of abnormal clots Refer to physician

TYPE OF EXAM: Complete Blood Count Date: March 5, 2012 Component Hgb Hct Normal 9.5-11.4 g/dl 30%-40% Result 13.1g/dl 39% Interpretation Elevated Normal Nursing Responsibilities Assess for signs of

Segmenters Lymphocytes Monocytes Eosinophils Platelets

50%-70% 20%-40% 2%-8% 1%-4% 150000-400000

55% 55% 39% 6% 359000

Normal Elevated Elevated Elevated Normal

infection Monitor vital signs such as Temp. Instruct to perform proper and frequent handwashing

MCV MCH MCHC

82-92 fl 28-32 pg 32%-38%

89fl 30 pg 34%

Normal Normal Normal

techniques Instruct to increase oral fluid intake Encourage to eat Vit. C rich foods like oranges

TYPE OF EXAM: Complete Blood Count Date: April 7, 2012 Component Hgb Hct Segmenters Normal 9.5-11.4 g/dl 30%-40% 50%-70% Result 11.4g/dl 35% 52% 38% 6% 4% 349000 Interpretation Normal Normal Normal Normal Normal Normal Normal Nursing Responsibilities Instruct to continue performing handwashing Reinstruct to increase intake of Vit. C rich foods such as oranges Encourage more to increase OFI

Lymphocytes 20%-40% Monocytes Eosinophils Platelets 2%-8% 1%-4% 150000400000

MCV MCH MCHC

82-92 fl 28-32 pg 32%-38%

87fl 29 pg 33%

Normal Normal Normal

TYPE OF EXAM: Urinalysis Date: March 2, 2012 Component Color Normal Straw/ amber Result yellow clear 7.5 1.015 Interpretation Normal Normal Elevated Normal Nursing Responsibilities Instruct to eat acidic foods such as oranges and cranberry juice Instruct to increase OFI

Transparency clear Reaction Specific gravity 4-6.8 1.005-1.030

TYPE OF EXAM: Urinalysis Date: April 11, 2012 Component Color Normal Straw/ amber Result yellow hazy 6.0 1.030 Interpretation Normal Abnormal Normal Normal Nursing Responsibilities Instruct to drink fresh buko juice Instruct to increase OFI

Transparency clear Reaction Specific gravity 4-6.8 1.005-1.030

TYPE OF EXAM: Fecalysis Date: March 2, 2012 Component Color Normal Yellowbrown Consistency Well formed Well formed Normal Result Brown Interpretation Normal Nursing Responsibilities Instruct on proper perineal care Instruct to increase OFI

TYPE OF EXAM: Blood Chemistry Date: March 23, 2012 Component Normal Result Interpretation Nursing Responsibilities BUN Creatinine 5-18mg/dl 0.3-0.7mg/dl 2.86mg/dl 4.6mg/dl Decreased Elevated Monitor for signs of renal failure Instruct to increase OFI Encourage to avoid foods high in preservatives

TYPE OF EXAM: Blood Chemistry Date: April 10, 2012 Component Normal Result Interpretation Nursing Responsibilities SGOT SGPT Na 0-35U/L 4-36U/L 136-145 mEq/L K Ca Cl 3.5-5 mEq/L 9-10.5 mg/dl 98-106mEq/L 4.5 mEq/L 2.35mg/dl 101mEq/L Normal Below Normal Normal 32.21U/L 16.73U/L 138mEq/L Normal Normal Normal Monitor for muscle weakness and signs of fracture Instruct to eat calcium rich foods like milk and eggs Instruct to perform passive ROM exercises

TYPE OF EXAM: MRI Date: March 26, 2012 IMPRESSION: Significant internal resolution of intrinsic signal abnormality of C3 to C7 Currently, within ventral cord from C4-5 to C6. Localized atrophy at C6-7 Myelomalacia Chiari I malformation

VIII. COURSE IN THE WARD Feb. 28, 2012 Admitted to childrens ward under the service of Dr. Garcia, Dr. Sanchez, Dr. Ballestre, and Dr. Villarosa with orders made such as secure consent, pneumonia and pressure sore precautions, turn side to side q2, proper bed positioning, and apply footboard 4 in. Also, the following lab exams were ordered: CBC with ESR, BUN, crea, Na, K, Cl, Ca, SGPT, SGOT, UA, FA, and MRI of cervical spine. Only CBC was done. No meds ordered. Additional orders were given such as suction tracheostomy PRN. Referred to PT with orders of deep breathing and coughing exercises. Involved in play therapy. Late evening, the client became febrile. The physician ordered Paracetamol 250mg/5ml, 3ml every 4 hours and TSB. The fever subsided. Feb. 31, 2012 The client was referred to Pedia and co-managed regarding CBC and X-ray results. March 1, 2012 The doctor ordered to carry out all Pedia orders about CBC and X-ray results. The client was still with cough and referred due to bronchitis of right lung field. March 2, 2012 The client was sent to PT with orders of diaphraghmatic strengthening exercises. UA and FA were facilitated. March 3, 2012 The physician ordered to continue suctioning.

March 4, 2012 The physician ordered repeat CBC in morning but not facilitated due to lack of finances. March 5, 2012 Repeat CBC was facilitated. March 12, 2012 The client had no bowel movement for 5 days. Physical exam revealed impacted fecal material. The doctor ordered manual stool extraction then insert Glycerine supp per rectum after or Bisacodyl pediatric supp 5mg/ supp per rectum if glycerine NA. March 23, 2012 BUN and crea were facilitated. March 28, 2012 Client was brought to PT. March 29, 2012 The client vomited 3 times and had no bowel movement for 3 days. Bisacodyl was inserted and put on NPO for 3 hours, then soft diet after 3 hours. At afternoon, (-) vomiting. The doctor ordered STAT plain x-ray of abdomen and facilitated. Further observations were made and no vomiting reported. DAT was ordered. March 31, 2012 The client was transferred under the service of Dr. Garcia, Dr. Aggrano, Dr. Suarez, and Dr. Dacanez. April 1, 2012 The client undergone PT with cryotherapy and play therapy.

April 6, 2012 The client was improving. The physician ordered repeat UA, CBC with ESR, serum electrolytes, SGOT, SGPT, calcium. April 7, 2012 CBC was facilitated. April 10, 2012 SGOT, SGPT, Na, K, Ca, and Cl were facilitated. April 11, 2012 UA was repeated.

VII. PATHOPHYSIOLOGY Modifiable History of trauma Presence of medical condition Non modifiable Age

Infectious microorganisms in an amino acid mimics peripheral nerve myelin proteins

Immune system cannot distinguish the difference between two proteins

Attacks and destroys all peripheral nerve myelins

Influx of macrophages and other immune mediated agents that attacks myelins

Inflammation and destruction of nerve myelins Axon is unable to support nerve conduction

Demyelination of nerves at the diaphragm and muscles Respiratory failure

Nerve demyelination Muscle weakness and diminished reflexes

Pharyngeal and vagus nerve affection

Inability to swallow and clear secretions

Emergency tracheostomy Instability of BP and heart rate

XI. EVALUATION Currently, the client was still admitted at Philippine Orthopedic Center in childrens ward. During the third day of handling the client, the student was able to build a trusting relationship that leads to the provision of the aimed nursing care. The client was still unable to move lower extremities. The student witnessed the complication of GBS and was able to provide proper care to the client. Aside from difficulty of breathing and paralysis, no more further complaints noted. As a result of good nurse-patient interaction, the planned goals were achieved and the desired nursing interventions were rendered therapeutically.