Rajiv Gandhi University of Health Science, Karnataka
Curriculum Development Cell
CONFIRMATION FOR REGISTRATION FOR SUBJECTS FOR DISSERTATION
Registration No. :
Name of the candidate : Ms. REMYA HARIDAS
Address : #160, CHELIKERE,BANASWADI OUTER
ROAD, BEHIND BTS BUS DEPOT,
KALYAN NAGAR, BANGLORE 43
Name of the Institution : Banglore city college of Nursing
Course of Study and Subject : MSc Nursing in MSN
Date of submission :
Title of study : “A STUDY TO EVALUATE THE EFFECTIVENESS OF STRUCTURED TEACHING PROGRAMME ON KNOWLEDGE REGARDING THE IMPORTANCE OF PUPILLARY CHANGES IN NEUROLOGICAL CLIENTS AMONG STAFF NURSES IN SELECTED HOSPITALS AT BANGALORE”
Brief resume of intended work : Attached
Signature of the Student :
Guide Name : Mrs. VIJAYA LAKSHMI
Remarks of the guide :
Signature of the guide :
Co-Guide Name : Mrs. VIJAYA LAKSHMI
Signature of Co-Guide :
HOD Name :
Signature of the HOD :
Principal name :
Principal mobile No. :
Principal E-mail ID :
Principal signature :
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES. BANGALORE, KARNATAKA.
“A STUDY TO EVALUATE THE EFFECTIVENESS OF STRUCTURED TEACHING PROGRAMME ON KNOWLEDGE REGARDING THE IMPORTANCE OF PUPILLARY CHANGES IN NEUROLOGICAL CLIENTS AMONG STAFF NURSES IN SELECTED HOSPITALS AT BANGALORE”
SYNOPSIS PROFORMA FOR REGISTRATION OF SUBJECT FOR DISSERTATION
Miss. REMYA HARIDAS
BANGALORE CITY COLLEGE OF NURSING
BANGALORE -43, KARNATAKA
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE, KARNATAKA.
SYNOPSIS PROFORMA FOR REGISTRATION OF SUBJECT FOR DISSERTATION
1
/NAME OF THE CANDIDATE AND ADDRESS
/Miss. Remyaharidas
1st year M.sc Nursing.
Bangalore City College of Nursing
Bangalore-560043
KARNATAKA2
/NAME OF THE INSTITUTION
/Bangalore City College of Nursing
Banglore3
/COURSES OF THE STUDY AND SUBJECT
/ M.Sc(N) 1st yearMEDICAL SURGICAL NURSING
4
/DATE OF ADMISSION
5
/TITLE OF THE SUBJECT
/ A STUDY TO EVALUATE THE EFFECTIVENESS OF STRUCTURED TEACHING PROGRAMME ON KNOWLEDGE REGARDING THE IMPORTANCE OF PUPILLARY CHANGES IN NEUROLOGICAL CLIENTS AMONG STAFF NURSES IN SELECTED HOSPITALS AT BANGALORE6. BRIEF RESUME OF INTENTED WORK
INTRODUCTION:
HEALTH CAN BE DEFINED AS A CONDITION OF BEING SOUND IN BODY, MIND OR SPIRIT ESPECIALLY FREEDOM FROM PHYSICAL DISEASE OR PAIN.
To be in good health its important that each and every in our body should function properly. Eyes is an important organ which most of us take it for granted. It’s a highly specialized sense organ which unlike most organ of body, is available to external examination .One of its external structure include pupils. The pupil is the space that dilates and constricts in response to light. Normal pupils are round and constrict symmetrically when a bright light shines on them. About 20% of population have pupils that are slightly unequal in size that respond equally to light.[1]
Different neuroanatomical pathways are involved in the control of pupil , the integrity and the functionality of these neurological pathways can be often be ascertained through the analysis and interpretation of pupillary behavior .This makes the pupil size and the pupillary light reflex an important factor to be considered in many clinical conditions. More specifically , the location of the pupillomotor nuclie and efferent occulomotor nerve is important for assessing the onset of descending transtentorial herniation and brainstem compression ,its has also been shown through blood flow imaging the pupillary changes in neurological patients in ICU are highly correlated with brainstem oxygenated and perfusion or ischemia[2] . High intracranial pressure in a brain injured patient result more frequently in poor neurological outcomes and death. High intracranial pressure are associated with pupillary abnormalities of brain injured patient.
The signs of pupil problems can be noted by change in pupil size, which can occur as a result of medications drugs and toxins. Some neurological conditions such as stroke, brain tumor and injury to the brain can also cause change in pupil size on both eyes. The pupillary mechanism can also be characterized by different neuronal and mechanical nonlinearitis.
Pupillary evaluation in the clinical settings in often performed in very subjective manner with a pen flash light for reactivity and a pupil gauge for pupil size. Pupil reaction to light should be brish and after removal of light source the pupil should return to its original size. There
should also be a consensual reaction to the light source that is the opposite pupil also constricts when the light source is applied to one eye.
In addition to controlling the amount of light that enters the eye, the pupillary light reflex provides a useful diagnostic tool. It allows for testing the integrity of the sensoryandmotorfunctions of the eye. Under normal conditions, the pupils of both eyes respond identically to a light stimulus, regardless of which eye is being stimulated. Light entering one eye produces a constriction of the pupil of that eye, the direct response, as well as a constriction of the pupil of the unstimulated eye; theconsensual response Comparing these two responses in both eyes is helpful in locating a lesion.
For example, a direct response in the right pupil without a consensual response in the left pupil suggests a problem with the motor connection to the left pupil (perhaps as a result of damage to thenerve or Edinger-Westphal nucleusof the brainstem[3]). Lack of response to light stimulation of the right eye if both eyes respond normally to stimulation of the left eye indicates damage to the sensory input from the right eye (perhaps to the right retina oroptic nerve.
6.1 NEED FOR STUDY:
Medical caregivers examine pupil size because they can be directly correlated to health conditions. In this case, it isn’t only the size of the pupils that are noted but their reactivity and equality too. In normal circumstances, pupils should be neither large nor small, but average. If extra light is supplied, both pupils should constrict and if surroundings become darker, both pupils should dilate, equally. What happens in one eye should also happen in the other, giving a bilateral reaction.
Since nurse is also one of the important personality in the medical field, the nurse practitioners should have a fair knowledge about pupillary changes among the neurological clients. The pupillary evaluation in the clinical settings is ofen performed in very subjective manner with a pen flash light for reactivity and a pupil gauge for pupil size , which can be used by the nurse practitioner also.
Traumatic brain injuries (TBIs) affect more than 1.4 million Americans annually[4] Nurses caring for these patients routinely perform serial neurologic assessments, including pupillary examinations. While nurses are likely familiar with basic components of the pupillary examination, some confusion about more specific aspects of the examination and the physiologic basis of the pupillary response may still remain. Therefore, it is important to identify the key components of a pupillary examination and its associated physiologic response. So once they know how to perform this pupillary examination, it will be a great help to the patients.
The pupillary changes can be mostly seen in the cases such as brain injury, stroke ,brain tumer, thired nerve palsy. Horner’s syndrome some of the medications such as atropine steroids contraceptives etc and early detection of these changes may save the life of the patients. Appropriate training and ongoing professional development in this field of study are essential for optimised clinical outcomes. Therefore the identification of pupillary changes among the critically ill patient may prevent further detoriation of their health condition. Thepupillary light reflexis areflexthat controls the diameter of thepupil, in response to the intensity (luminance) of light that falls on theretinaof theeye, thereby assisting inadaptationto various levels of darkness and light, in addition toretinalsensitivity.[5] Greater intensity light causes the pupil to become smaller (allowing less light in), whereas lower intensity light causes the pupil to become larger (allowing more light in). Thus, the pupillary light reflex regulates the intensity of light entering the eye.
Twenty-two patients with acute optic neuritis were studied by the techniques of infrared pupillometry and visual evoked responses (VER) to pattern reversal. A relative afferent pupillary defect was found in all cases and the magnitude of this defect was found to be related to the amplitude, but not to the latency, of the VER. During follow-up the afferent defect was found to remain persistently abnormal while other methods of clinical evaluation could not demonstrate abnormality reliably. The amplitude of the VER also remained low.[6]
Emergency roomphysicians routinely assess the pupillary reflex because it is useful for gaugingbrain stem function. Normally, pupils react (i.e. constrict) equally. Lack of the pupillary reflex or an abnormal pupillary reflex can be caused by optic nerve damage, oculomotor nerve damage,brain stem deathand depressant drugs, such as barbiturates. Therefore involvement of nurses in assessment of pupillary reflexes among the neurological clients is considered as a vital , to detect the changes in brain stem function..
Early detection of brain death can also be done using the pupillary reflexes to external stimuli, as such organ transplantation can also be promoted by using this as a tool ,after confirming the brain death with additional scanning method such as CT Scan ,MRI etc ..
The focus of this study is mainly to evaluate the knowledge among the staff nurses who come in direct contact with the neurological clients of importance of pupillary reflexes and also to improve their care by providing knowledge regarding management of pupillary changes in these patients…
6.2 REVIEW OF LITERATURE:
Review of literature is the key step in the research process. It improves the systematic identification, location, and summary of the written material that contains information of research problem.
The overall purpose of the review of literature is to develop a strong knowledge base to carry out research and other scholarly education.
Pupillographic findings in 39 consecutive cases of harlequin syndrome was done In this, a consecutive series of 39patientswith harlequin syndrome who were referred to a tertiary autonomic function laboratory underwent slit-lamp examinations. Results were compared with a meta-analysis of all previously reported cases of harlequin syndrome. From this the following conclusions were made .The frequent coexistence of harlequin and Horner syndromes without other neurologic deficits suggest pathologicchanges affecting the superior cervical ganglion. Because either syndrome may occur alone, damage is apparently selective. Among thepatientswith harlequin syndrome who also have tonic pupils and tendon areflexia (Holmes-Adie syndrome), we postulate a ganglionopathy affecting not merely the (sympathetic) superior cervical ganglion, but also the (parasympathetic) ciliary and dorsal root ganglia. Because we found that more than 10% of patientshad an undisclosed mass lesion in the chest or neck or a generalized autonomic neuropathy, we recommend a targeted evaluation in selectedpatientswith harlequin syndrome.[7]
A study related to Neurological features of congenital fibrosis of the extraocular muscles type 2 with mutations in PHOX2A was done .Congenital fibrosis of the extraocular muscles type 2 (CFEOM2) is a complex strabismus syndrome that results from mutations in the homeodomain transcription factor PHOX2A. To define the clinical and neuroimaging features ofpatientswith this autosomal recessive syndrome, the study included 15 patientswith genetically defined CFEOM2. Allpatientsunderwent full neurological,neuro-ophthalmological and orthoptic assessments.[8]
Twelvepatientshadpupillarypharmacological testing and nine had 3.0 tesla MRI of the brain, brainstem and orbits. They concluded the CFEOM2 phenotype and neuroimaging are both consistent with the congenital absence of CNs 3 and 4. Additional features included presence of most central ocular motility reflexes, a central lack ofpupillaryresponsiveness of uncertain aetiology and modest phenotypic variability that does not correlate with specific PHOX2A mutations. Clinical presentation, neuroimaging and Phox2a-/- animal models all support the concept that CFEOM2 is a primary neurogenic abnormality with secondary myopathicchanges.[9]
Prehospital status and treatment among severe traumatic brain injury was conducted. In this collected data sets from 396patientswith severe TBI (Glasgow Coma Scale score < 9) included by 5 Austrian hospitals were available. The analysis focused on incidence and/or degree of severity of typical clinical signs, frequency of use of different management options, and association with outcomes for both. The following outcome was find out ,the majority ofpatientswere male (72%), mean age was 49 +/- 21 years, mean injury severity score (ISS) was 27 +/- 17, mean first GCS score was 5.6 +/- 2.9, and expected hospital survival was 63 +/- 30%. ICU mortality was 32%, 90-day mortality was 37%, and final outcome was favorable in 35%, unfavorable in 53%, unknown in 12%. They found that age > 60 years, ISS > 50 points, GCS score < 4, bilateralchangesinpupil size and reactivity, respiratory rate < 10/min, systolic blood pressure (SBP) < 90 mm Hg, and heart rate < 60/min were associated with significantly higher ICU and 90-day mortality rates, and lower rates of favorable outcome.[10]
A study on False negative apraclonidine test in twopatientswith Horner syndrome in this two women aged 34 and 46 years with a cocaine-confirmed oculosympathetic defect (Horner syndrome) were tested with 1 % topical apraclonidine on separate days. Neither patient demonstrated a reversal of anisocoria, the current criterion for diagnosing a Horner syndrome using apraclonidine. Thus, these twopatientswith an established oculosympathetic defect were said to have a "negative test" for Horner syndrome. Yet both women showed subtlepupiland/or lidchangesin response to apraclonidine that were consistent with sympathetic denervation supersensitivity. Reversal of anisocoria following topical apraclonidine does not occur in allpatientswith a unilateral oculosympathetic defect and more specific parameters for defining a positive test result might optimize apraclonidine's utility as a diagnostic test for Horner syndrome.[11]
Evaluation of visual functions inpatientson ethambutol therapy for tuberculosis was done to study the incidence of clinical and subclinical optic nerve toxicity with ethambutol therapy inpatientswith tuberculosis and to evaluate the reversibility of its side effects after cessation of therapy. This prospective randomized controlled study included 60 newly diagnosed adult cases of tuberculosis, who were randomly assigned into two groups. The study group included 30patients(60 eyes) who received ethambutol as a part of their anti-tubercular treatment and the control group included 30patients(60eyes) who did not receive ethambutol. Thepatientswere examined on monthly basis. The visual parameters studied were best corrected visual acuity,pupillaryreactions, optic discchanges, color vision, contrast sensitivity,pupilcycle time, visual field charting and visual evoked potential. Ethambutol was stopped in thosepatientsin whom toxicity was detected and they were followed more frequently ethambutol induced ocular toxicity was seen in threepatients(10%) in this study. The maximum visual recovery occurred in first six to eight weeks after stopping ethambutol. The visual recovery was complete in only one patient, but it was partial in twopatientsi.e. visual fields, contrast sensitivity and visual evoked potential remained abnormal.[12]