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A
CASE STUDY OF
GUILLAIN-BARRE
SYNDROME GBS
SUBMITTED ON
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CASE STUDY
PATIENT INFORMATION :
Patient’s Name : Mr. Sunil Yalwande
Age : 16 years Sex : Male
Address :
Admission Date : 20/11/14
Ward : ICU
Indoor NO : 639969
Education : 10th standard
Occupation : farmer
Religion : Hindu
Blood group : O +ve
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Discharge Date : ------
Diagnosis : Guillain-Barre Syndrome GBS
Income per month : 9000 Rs./ month(family)
Weight : 35 kg Height : 152 cm
Health Habits :
- Smoking : No
- Tobacco chewing : No
- Alcohol Consumption : No
Vegetarian : Yes
Non-vegetarian : 2-3 Times/week
Chief complaints with duration : Complaint of throat pain since 5 days
Complaint of fever since 5 days
Complaint of Difficulty in Swallowing since 5 days
Complaint of Regurgitation since 2 days,
Complaint of Loss of Motor power since 2days.
1) Family history :
Age Relationsh
Illness in
Sr. Name of Family in ip Occupation
Family Education
No. Members Yea With
Members
r Patient
1 Pravinji Yalwande 53 Father TB Illiterate Farmer
2 Sunita Yalwande 50 Mother No 9th std. Housewife
3 Gopal Yalwande 22 Brother No 12th std. Shop keeper
4 Radha Yalwande 20 Sister in No 10h std. Housewife
law
5 Sonal Yalwande 18 Sister No 8th std Student
6 Sunil Yalwande 16 Self Recently 10th std. Student
GBS
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Sunil was very healthy.He didn’t had any illness and didn’t took any regular
medicine. He had no other major illness like TB, HT, DM or any congenital
abnormalities etc.
Sunil had complaint of throat pain ,fever, Difficulty in swallowing since 5 days.
So he came on date 20-11-11 and he was seen by Dr N.M.Kadri. At that time, he was
diagnosed as a tonsillitis and admitted in ward general ward. Treatment was started
but gradually patient lost his motor power of four limb and also Paletal muscles
were involved on date19-11-11. Also nasal regurgitation occurred on date 22-10-11.
Respiratory muscles were involved and there was a need to put patient on ventilator
and he was shifted to ICU. Then he was finally diagnosed as Guillain-Barre
Syndrome GBS.
4) Personal history :
Sunil looks well nourished, his skin colour is brown. He has no bad habit. He
eats non-vegetarian food .In the routine food he takes dal, roti, rice and sabji 2
times in a day. He would like to take tea, he takes tea 5-6 times in a day. Some
times in the food he likes veg. biriyani, sher Khurma, samosa, idali sambhar etc. he
does not like any soup and salad.
i) Personal hygiene :
- Oral hygiene : once a time with tooth brush.
- Bath : once in a day daily
- Sleep and Rest : 7 hours/ day and 1 hour rest in afternoon time daily
ii) Elimination :
- Bowel per day : Regular per day, once in morning time daily.
- Urine frequency : 1500 ml/ day
iii) Mobility and Exercise :
- Moderate : Moderate exercise he has doing.
- Joint pain during walking. Restricted movement of the leg.
iv) Sexual and Marital history :
He is not married.
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There are some clinics near his home where primary care can be provided.
Transport facility is available in the form of Government bus services as well as
private vehicles are also available for transportation.
6) Housing :
Sunil has his own pakka house in Vishrantwadi. The house is having 2 rooms, 1
kitchen and facilities of toilet and bathroom are also available in house. There is also
facilitiy of electricity and drinking water from the borewell.
NURSING ASSESSMENT :
a) General observation :
Sensorium : he is conscious and well oriented
Foul body odour : no any bad odour from his body
Foul breath : no
Posture : normal
Hair : black and shiny hair, Clean no any dandruff.
b) Vital sign :
Temperature : 98.4 F.
Pulse : 88 /min. Regular high volume Tachycardia (some time)
Respiration : 26 /min. Tachypnea
BP : 120/80 mm of Hg.
c) Subjective data :
Patient is on ventilator so he can not speak but by sign language indicates
Restlessness, fatigue, psychologically disturbance
d) Objective Data :
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Assessment of Cardiovascular system :
Heart rate : 88 beats/min.
Rhythm : Regular
Apical Pulse : 88 beats/min.
Jugular vein distention : No.
Spo2: 94%.
Respiratory System :
Respiration rate : 26 breaths /minwith help of ventilator
Breath sound : normal
Dysponea : Present.
Pulmonary effusion : No.
Cough: Productive cough.
Abdomen :
Hepatomegaly : No.
Skin :
Color of mucous membrane : Pink
Peripheral Cyanosis : No. Clubbing: No.
Ecchymosis : No
Urinary system :
Urine output : 1700 ml/24hrs.
Extremities :
Edema : No
Color and Temperature of Skin : Cold and clammy.
DIAGNOSTIC TESTS :
i) Biochemical Test:
2. Sr. Electrolytes
- Bl. Urea 33.0 mg / dl 13- 40 mg / dl
- Sr. Creatinine 0.7 mg / dl 0.8- 1.4 mg / dl
- Sr. Na+ 136m Eq/ L 135 – 149 m Eq/ L
- Sr. K+ 3.5m Eq/ L 3.5 – 5.5 m Eq/ L
- Sr. Cl- 104 m Eq/ L 98 – 108 m Eq/ L
- Sr. Bil. Total : 0.8 mg % 0.0 – 1.0 mg %
Direct : - 0.0 – 0.25 mg %
Indirect : - 0.0 – 0.75 mg %
- S. G. P. T 14.0 IU/L 0 – 40 U/L
- Sr. Alkaline Phosphate 200.5 U/L 124 – 341 U/L
- Total Proteins : 6.36 G/L 6.6 – 8.3 G/L
Albumin : 4.42 G/L 3.5 – 5.0 G/L
Globulin : 1.94 G/L 2.3 – 3.3 G/L
A/G ratio : 2.22 1.0 – 4.0
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INTRODUCTION OF GBS
Anatomy & Physiology
The nervous system consists of two divisions: the central nervous system (CNS),
including the brain and spinal cord, and the peripheral nervous system, made up of
the cranial and spinal nerves. The peripheral nervous system can be further divided
into the somatic, or voluntary, nervous system, and the autonomic, or involuntary,
nervous system. The function of the nervous system is to control all motor, sensory,
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autonomic, cognitive, and behavioral activities. The nervous system has
approximately 10 million sensory neurons that send information about the internal
and external environment to the brain and 500,000 motor neurons that control the
muscles and glands. The brain itself contains more than 20 billion nerve cells that
link the motor and sensory pathways, monitor the body’s processes, respond to the
internal and external environment, maintain homeostasis, and direct all
psychological, biologic, and physical activity through complex chemical and electrical
messages.The brain is divided into three major areas: the cerebrum, the brain stem,
and the cerebellum. The cerebrum is composed of two hemispheres, the thalamus,
the hypothalamus, and the basal ganglia. Additionally, connections for the olfactory
(cranial nerve I) and optic (cranial nerve III) nerves are found in the cerebrum. The
brain stem includes the midbrain, pons, medulla, and connections for cranial nerves
II and IV through XII. The cerebellum is located under the cerebrum and behind the
brain stem. The brain accounts for approximately 2% of the total body weight; it
weighs approximately 1,400 g in an average young adult.
DEFINITION
Guillain-Barre syndrome (GBS) is an acute, rapidly progressing, ascending
inflammatory demyelinating polyneuropathy of the peripheral sensory and motor
nerves and nerve roots. GBS is most often, but not always, characterized by
muscular weakness and distal sensory loss or dysesthesias. GBS is the most
frequently acquired demyelinating neuropathy. It affects one in 100,000 people and
must be identified quickly to initiate treatment and decrease life-threatening
complications. Usually GBS occurs a few days or weeks following symptoms of a
respiratory or GI viral infection. Occasionally, surgery or vaccinations will trigger the
syndrome. The disorder can develop over the course of hours, days, or weeks.
Maximum weakness usually occurs within the first 2 weeks after symptoms appear,
and by the third week of the illness 90% of all patients are at their weakest. About
30% of those with GBS have residual weakness after 3 years and the recurrence rate
is approximately 3%.
Mortality results form respiratory failure, autonomic disturbances, sepsis, and
complications of immobility and occurs at a rate of about 5% despite intensive
medical care.
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In most patients, the syndrome is preceded by an infection (respiratory or
gastrointestinal) 1 to 4 weeks before the onset of neurologic deficits.
In some instances, it has occurred after vaccination or surgery It may be due
to a primary viral infection, an immune reaction, some other process, or a
combination of processes.
One hypothesis is that a viral infection induces an autoimmune reaction that
attacks the myelin of the peripheral nerves.
Proximal portions of the nerves tend to be affected most often, and the nerve
roots within the subarachnoid space are commonly involved. Autopsy findings
have shown inflammatory edema and demyelination with some lympho-cytic
infiltration that is especially prominent in the spinal nerve roots.
CLINICAL MANIFESTATIONS
MANAGEMENT :
SPECIAL MANAGEMENT
Plasmapheresis
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Done in patient on date 23-11-11
NURSING MANAGEMENT :
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NURSING CARE PLAN
Patient Name : Sunil Yalwande Age : 16Yrs Wt : 35kg Diagnosis : GBS Date : 21-11-11
Patient Name : Popatji P Thakor Age : 13 Years Wt : 35 kg Diagnosis : GBS Date : 20-11-11.
Advise patient and family that acute phase lasts 1 to 4 weeks, then patient
stabilizes and rehabilitation can begin; however, convalescence may be
lengthy, from 3 months to 2 years.
Instruct patient in breathing exercises or use of incentive spirometer to
reestablish normal patterns.
Teach patient to wear good supportive and protective shoes while out of bed
to prevent injuries due to weakness and paresthesia.
Instruct patient to check feet routinely for injuries because trauma may go
unnoticed due to sensory changes.
Reinforce maintenance of normal weight; additional weight will further stress
the motor abilities.
Encourage the use of scheduled rest periods to avoid over-fatigue.
Be aware that GBS is a significant cause of new long-term disability for at least
1,000 persons per year in the United States, necessitating long-term
rehabilitation and community reintegration. Outcome can range from mild
paresthesias to death. The chance of recovery is significantly affected by age,
antecedent gastroenteritis, disability, electrophysiologic signs of axonal
degeneration, latency to nadir, and duration of active disease.
Given the young age at which GBS sometimes occurs, the patient and family
care must be treated as an integral unit, assessing family communication,
knowledge, adjustment, and use of support systems.
Include in caregiver training strategies the need for exercise, positioning, and
activity to prevent secondary complications, such as contractures, deep vein
thrombosis (DVT), hypercalcemia, and pressure ulcers.
RESEARCH
Abstract
Guillain Barré syndrome is one of the best examples of a post infectious immune
disease and offers insights into the mechanism of tissue damage in other more
common autoimmune diseases. Controlled epidemiological studies have linked it to
infection withCampylobacter jejuni in addition to other viruses including
cytomegalovirus and Epstein Barr virus. The syndrome includes several pathological
subtypes, of which the most common is a multifocal demyelinating disorder of the
peripheral nerves in close association with macrophages. Evidence from histological
examination of peripheral nerve biopsy and postmortem samples suggests that both
cell mediated and humoral mechanisms are involved in the pathogenesis.
Immunological studies suggest that at least one third of patients have antibodies
against nerve gangliosides, which in some cases also react with constituents of the
liposaccharide of C jejuni. In the Miller Fisher variant of the disease, these
antiganglioside antibodies have been shown to produce neuromuscular block, and
may in part explain the clinical signs of that disorder. Treatment with both
intravenous immunoglobulin and plasma exchange reduces the time taken for
recovery to occur, although mortality remains around 8%, with about 20% of
patients remaining disabled.
Abstract
Guillain-Barré syndrome consists of at least four subtypes of acute peripheral
neuropathy. Major advances have been made in understanding the mechanisms of
some of the subtypes. The histological appearance of the acute inflammatory
demyelinating polyradiculoneuropathy (AIDP) subtype resembles experimental
autoimmune neuritis, which is predominantly caused by T cells directed against
peptides from the myelin proteins P0, P2, and PMP22. The role of T-cell-mediated
immunity in AIDP remains unclear and there is evidence for the involvement of
antibodies and complement. Strong evidence now exists that axonal subtypes of
Guillain-Barré syndrome, acute motor axonal neuropathy (AMAN), and acute motor
and sensory axonal neuropathy (AMSAN), are caused by antibodies to gangliosides
on the axolemma that target macrophages to invade the axon at the node of
Ranvier. About a quarter of patients with Guillain-Barré syndrome have had a
recent Campylobacter jejuni infection, and axonal forms of the disease are especially
common in these people. The lipo-oligosaccharide from the C jejuni bacterial wall
contains ganglioside-like structures and its injection into rabbits induces a
neuropathy that resembles acute motor axonal neuropathy. Antibodies to GM1,
GM1b, GD1a, and GalNac-GD1a are in particular implicated in acute motor axonal
neuropathy and, with the exception of GalNacGD1a, in acute motor and sensory
axonal neuropathy. The Fisher's syndrome subtype is especially associated with
antibodies to GQ1b, and similar cross-reactivity with ganglioside structures in the
wall of C jejuni has been discovered. Anti-GQ1b antibodies have been shown to
damage the motor nerve terminal in vitro by a complement-mediated mechanism.
Results of international randomised trials have shown equivalent efficacy of both
plasma exchange and intravenous immunoglobulin, but not corticosteroids, in
hastening recovery from Guillain-Barré syndrome. Further research is needed to
discover treatments to prevent 20% of patients from being left with persistent and
significant disability.
The Lancet, Volume 366, Issue 9497, Pages 1653 - 1666, 5 November 2005
doi:10.1016/S0140-6736(05)67665-9
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WEBSITES:
http://mp.bmjjournals.com/content/54/6/381.abstract
http://www.thelancet.com/journals/lancet/article/PIIS0140-
6736(05)67665-9/fulltext
http://www.thelancet.com/journals/lancet/article/PIIS0140-
6736(97)12308-X/fulltext
http://www.thelancet.com/journals/lancet/article/PIIS0140-
6736(97)12308-X/fulltext