Running head: COMPREHENSIVE CLINICAL CASE STUDY
Comprehensive Clinical Case Study
Neeta Monteiro, RN, BSN, CNRN
Wright State University-Miami Valley College of Nursing and Health
NUR 7202
Dr. Kristine Scordo
October 15, 2013
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COMPREHENSIVE CLINICAL CASE STUDY
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History and Physical
Source of Information
Information is gained from the patient and his adult son. The patient is alert and oriented.
The information obtained from the patient and son is dependable and consistent. Primary
language of communication is English. The patient gives consent for his son to participate in his
care.
Chief Complaint
Bilateral lower extremity weakness
History and Physical
Mr. Z. K. is a 59 year old Caucasian male who presents to the emergency department
with his son, with the complaints of numbness and tingling in his toes since the past 3 days. Over
the past two days he has had an unsteady gait and has been having difficulty walking. The patient
states he couldn’t get out of bed this morning due to lower extremity weakness. The weakness is
progressively getting worse and now he is unable to move his lower extremities. He is also
having difficulty articulating his words, and chewing and swallowing his food. He states he is
starting to feel tingling sensation in his hands and is experiencing some difficulty in breathing.
The patient denies any bowel or bladder involvement. He denies any associated fevers, but states
a couple of weeks ago he had an episode of upper respiratory illness with cough. He complains
of some lower back pain, but denies any injury to his back or any recent falls. He denies having
similar symptoms in the past. He denies any history of neuromuscular weakness in his immediate
family. He has history of hypertension, diabetes, and hyperlipidemia. He denies any recent
travels, tick bites, camping, eating tinned food, drug or alcohol use, or exposure to any sick
COMPREHENSIVE CLINICAL CASE STUDY
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contacts. He reports to be in relatively good health otherwise. He denies trying any mediation for
his present situation. He denies any relieving or exacerbating factors.
Medical History
Childhood Illnesses. He had measles at age 6 years, and asthma as a child. He fell off his
bicycle and sustained a left elbow fracture when he was 10 years old. No other significant
childhood illnesses.
Adult Illnesses. History of diabetes, hypertension, and hypercholesterolemia. He takes
all of his medications regularly and his blood pressure, blood sugars and cholesterol levels are
well controlled per his primary care physicians report one month ago.
Surgical History. Cholecystectomy at age 40 years and appendectomy at age 25 years.
No other significant surgical history is reported by the patient.
Medications. His home medications include lisinopril 10 mg once a day orally,
hydrochlorothiazide 5 mg once a day orally, lipitor 80 mg orally at bedtime and metformin 500
mg twice a day orally.
Allergies. He is allergic to penicillin and bee stings.
Immunization. Patient has received the flu shot last fall. He received his tetanus shot 2
years ago. He is up-to-date with all of the childhood immunizations.
Personal and Social History. The patient is divorced and has a son. He lives
independently. He works as a college professor. He does not smoke, or drink alcohol. He
exercises at least five times a week for 45 minutes per day. He does not use any recreational
drugs and reports to eating a healthy diet most of the time.
Family History. The patient’s parents are both alive and healthy. His dad (80 years) has
history of diabetes and prostate cancer. His mom (78 years) has history of hypertension and
COMPREHENSIVE CLINICAL CASE STUDY
stroke. He has only one sibling who is 55 years old. She is reportedly in good health and has no
significant health history. His maternal and paternal grandparents are deceased. Patient does not
have information regarding their health history.
Review of Systems
General. Patient reports to be in relatively good health. He goes to the primary care
physician for an annual checkup regularly. He takes all of his medications as prescribed. Patient
denies any recent significant weight gain or weight loss.
Skin/Hair/Nails. Denies any hair loss, skin rash, or changes in nail color.
HEENT. Patient denies any head injury, vision problems, photophobia, hearing loss,
nose bleeds, throat pain, or swelling in his throat or neck. He states he is having difficulty
chewing and swallowing his food. He also complaints of difficulty articulating his words. He
goes for regular dental visits and denies any dental issues.
Neck. Denies any pain in his neck, neck stiffness, or swelling in his neck.
Chest. Patient had history of asthma as a child but denies any respiratory problems as an
adult. Complains of some breathing difficulty. No cough, no chest pain, no chest tightness. He
has never smoked.
Cardiovascular. Denies chest pain, chest tightness, shortness of breath. Has history of
hypertension for the past two years.
Gastrointestinal. Denies nausea, vomiting, abdominal pain, loss of appetite, gastro
esophageal reflux disease, constipation, and diarrhea. Last bowel movement was yesterday.
Genitourinary. Patient denies difficulty urinating, increased frequency, burning
micturition, or dysuria. Has voided three times today over the past six hours.
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Musculoskeletal. Denies any musculoskeletal pain, joint stiffness, redness, and recent
falls. Patient states he started having numbness and tingling in his feet, with unsteady gait since
the past three days. He had difficulty getting out of bed this morning due to weakness in his
lower extremities. Denies similar issues in the past. He is now starting to feel tingling in his
upper extremities.
Neurological. Denies history of head injury, strokes, loss of consciousness, headache,
visual deficits, and dizziness. Per patient he has been experiencing difficulty with moving his
lower extremities since this morning. He has difficulty articulating his words, chewing and
swallowing food. No vision deficits. Complaints of numbness and tingling in his lower
extremities and hands.
Psychological. Patient denies history of depression, insomnia, anxiety, or suicidal
ideations in the past. Patient states he is getting very stressed due to not being able to move his
lower extremities. He is normally psychologically very stable and has a good group of supportive
friends and family. He has a stable job, good health insurance, economically stable, and denies
being under excessive physical or emotional stress on a regular basis.
Physical Examination
Vitals. Temperature 98.6o F, BP 118/68 mmHg, pulse 98/minute, RR 20/min, SpO2 95%
on 2 liters nasal cannula. Height 5’10”, weight 175 pounds.
General. Patient is pleasant, alert, well groomed, and interactive. Appears younger that
stated age. Well nourished, lying in stretcher. Appears to be in mild discomfort due to back pain.
Patient is also having mild respiratory distress at this time. Has 2 liters of oxygen per nasal
cannula. Oxygen saturation is 95 percent. Able to answers questions appropriately.
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Skin/Hair/Nails. Skin is pink, smooth, free of rash, discoloration, or bruises. No edema.
Hair is shiny, well distributed and soft to touch. Scalp is clean. Finger nails are clean and
trimmed. Nail beds are pink, no clubbing. Has good capillary refill.
Head. Head is normocephalic with no bruising or tenderness. Patient unable to raise his
eyebrows. Smile is symmetric.
Eyes. Vision is intact bilaterally. Extra ocular movements are intact, no nystagmus. No
ptosis, lid lag, or eye drainage.
Ears. Pinna is intact without any lesion or masses. Tympanic membrane is pearly gray
and intact. No exudate or ear wax noted. Whispered words are heard accurately in bilateral ears.
Nose. No drainage. Nares patent. No deviation in nasal septum. Nasal mucosa pink and
moist. No sinus sensitivity.
Mouth. Mouth is pink and moist. No ulcers noted. Good dentition. No missing teeth.
Tongue is pink and in midline. Uvula is midline on phonation. Moderate cough and gag. Patient
started coughing with swallow evaluation. No tonsillar swelling, exudate, or redness.
Neck. Neck is flexible with normal flexion, extension, and rotation. No tracheal
deviation. No masses, tenderness, warmth, redness, or swelling. No palpable lymph nodes.
Thyroid nonpalpable.
Spine and Back. Spinous processes are vertically aligned, no scoliosis. Has reproducible
tenderness on the lumbar and sacral region. No costovertebral tenderness noted. No erythema,
induration, or swelling noted on the back.
Thorax and Lungs. Symmetrical chest rise and fall. Bilateral lungs fields are clear to
auscultation. Resonance noted in bilateral lung fields.
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Heart. S1, S2 normal. No S3 or S4. No rubs, murmurs, gallops, or clicks noted. No
heaves or thrills. Point of maximum impulse in the mid clavicular line, left fifth intercostal space.
Abdomen. Abdomen is flat and even. Skin smooth without lesions or redness. Bowel
sounds are regular. No masses or tenderness noted on palpation. Liver nonpalpable. Tympany
noted on percussion. No palpable lymphadenopathy.
Extremities. Upper extremities within normal range of motion. No swelling, rash or
redness in all four extremities. Strength 4/5 in bilateral upper extremities. Radial pulses 2+
bilaterally. Lower extremities no edema, or calf tenderness. Sensation is dull in bilateral lower
extremities. Strength equally weak in bilateral lower extremities 2/5. Unable to perform flexion
and extension of ankles and toes bilaterally. The biceps, brachioradialis, and triceps reflexes are
2+. The knee jerk reflex and the plantar reflexes are absent.
Neurological. Alert and oriented. Speech slightly slurred but appropriate. Follows
commands applicably. Pupils are equal, round and reactive to light. Extraocular movements are
intact. Has difficulty raising his eyebrows. Tongue is midline, smile symmetric. Sensory pinprick
and light touch deficits in bilateral lower extremities. Finger to nose is smooth and intact; unable
to perform heel to shin due to muscle weakness. Gait not tested since patient unable to stand.
Deep tendon reflexes are absent in the lower extremities.
Genitalia. Genitalia without rash, ulcers, redness, discharge or swelling. Urethral meatus
is centrally located. Scrotal sac with no edema. Bilateral testes are firm, rubbery, smooth, equal,
and move freely. No bulging noted in the inguinal region on straining.
Psychiatric. No history of depression, anxiety and suicidal ideations. Appears slightly
anxious that is appropriate to the given situation.
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Laboratory Test Results
Table 1 Complete Blood Count (CBC)
CBC
Result
CBC
6.0
4.79
Segmented
Neutrophils %
Lymphocytes %
14.0
41.4
252
MCV
Normal
Range
3.8-10.8
K/mm3
3.90-5.20
m/mm3
12.0-15.6 g/dL
35.0-46.0 %
130-400
k/mm3
80-100 FL
86.5
MCH
27-33 PG
29.2
MCHC
32-36 g/dL
33
RDW
9.0 -15.0 %
14.1
WBC count
RBC Count
Hemoglobin
Hematocrit
Platelet count
Normal
Range
40.0-75.0
Result
18.0-47.0
20.0
Monocytes %
Eosinophils %
Basophils %
0-14
0-7
0.0-2.0
3.5
1.2
0.1
Absolute
segmented
neutrophils
Absolute
lymphocyte
Absolute
monocyte
Absolute
Eosinophil
1.5-7.8
K/mm3
6.8
0.9-4.1
k/mm3
0.2-1.1
k/mm3
0.0-0.6
k/mm3
1.3
BMP
Total protein
Albumin
A/G ratio
Bilirubin,
total
Alkaline
phosphate
AST
ALT
Bilirubin
Direct
Bilirubin,
indirect
GFR
Normal Range
6.0-8.3 gm/dL
3.5-5.2 gm/dL
0.8-2.6
0.0-1.2 mg/dL
Result
8.1
4.5
1.3
2.2
23-144 U/L
120
0-46 U/L
0-60 U/L
0.0-0.4 mg/dL
24
35
0.2
0.0-1.2 mg/dL
1.0
67
0.5
0.2
(Normal values from Dugdale, 2012)
Table 2 Basic Metabolic Panel (BMP)
BMP
Sodium
Potassium
Chloride
Carbondioxide
Normal Range
135-148 mEq/L
3.4-5.3 mEq/L
96-110 mEq/L
19-32 mEq/L
Result
146
3.7
104
28
Anion Gap
10-20
18
Glucose
BUN
Creatinine
70-100 mg/dL
3-29 mg/dL
0.5-1.2 mg/dL
138
19
0.8
BUN/creat
7.0-25.0 (calc)
ratio
Calcium
8.5-10.5 mg/dL
(Normal values from Dugdale, 2012)
24
9.4
82
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The results of the cerebrospinal fluid analysis, computed tomography (CT) of the head,
magnetic resonance imaging (MRI) of the spine, nerve conduction study (NCS), and
electromyography (EMG) results are pending. The results of these tests will be revealed as the
case study progresses.
Differential Diagnosis
Differential diagnosis for a patient presenting with flaccid paralysis of the lower
extremities can be practically complex. There are several medical conditions that can present
with flaccid paralysis of the lower extremities including Guillain-Barre syndrome (acute
inflammatory demyelinating polyneuropathy), tick paralysis, botulism, spinal cord lesion,
myasthenia gravis, poliomyelitis, acute transverse myelitis. Considering the patient’s medical
history, review of systems, physical examination, and results of the laboratory tests, it is
important to rule out conditions that can cause similar symptoms and come to a final diagnosis
(Amato & Hauser, 2012).
Guillain-Barre Syndrome (GBS). GBS is an autoimmune disorder that affects the
myelin sheath of the peripheral nerves disrupting the signaling process, usually causing
symmetrical ascending paralysis. The signs and symptoms of GBS include weakness and sensory
deficits such as numbness and tingling typically initiating in the toes and feet, unstable gait,
difficulty walking, difficulty with extraocular movement, facial expression, speech, mastication,
or swallowing, severe lower back pain, difficulty with bowel and bladder function, tachycardia,
and labile blood pressure. The weakness can then rapidly or gradually propagate upwards,
ultimately causing paralysis of the entire body, including the respiratory muscles causing
respiratory distress requiring intubation. Symptoms of GBS usually worsen over a period of four
weeks, and in some cases more rapidly over few hours or days (Amato & Hauser, 2012). .
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Literature has included varying forms of GBS that are well-established such as the acute
inflammatory demyelinating polyradiculo neuropathy (AIDP), acute motor axonal neuropathy,
acute motor sensory axonal neuropathy, Miller-Fisher variant and acute pan autonomic
neuropathy. Differentiating between these variants may however be quite challenging. In the
western world including the United States, the most common form of GBS is the AIDP which is
distinguished by mild sensory symptoms followed by progressive areflexic ascending motor
paralysis, usually climaxing within a month (Ramachandran, 2012).
There is no clear-cut etiology for GBS. Researchers consider the disorder to be
autoimmune, with more than fifty percent preceded by a respiratory or gastrointestinal infection.
Some cases of GBS are also associated with pregnancy and vaccination, while others are not
associated with any causative agents. The risk factors for GBS include the young and the old,
infection with campylobacter, mycoplasma pneumonia, surgery, Epstein-Barr virus, influenza
virus, Hodgkin’s disease, mononucleosis, HIV, rabies and vaccination (Amato & Hauser, 2012).
Work-up for GBS usually includes a thorough history and physical examination,
supported with laboratory studies such as complete blood count (CBC) and basic metabolic panel
(BMP) to rule out other underlying conditions such as electrolyte imbalance, infection, and
anemia. Confirmation of the diagnosis is mainly based on lumbar puncture, electromyography,
and nerve conduction test. Cerebrospinal fluid (CSF) in GBS usually reveals an elevated CSF
protein which is greater than 0.55 grams per liter devoid of elevation in the CSF white blood cell
count. Nerve conduction test is a sensitive test for the diagnosis of GBS and displays a delay in
F-waves indicating demyelination of the nerve roots. Severe paralysis will show slow response
of the motor nerves and conduction interference. Magnetic resonance imaging (MRI) and
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computed tomography (CT) of the spine may be beneficial in excluding other causes of
weakness such as transverse myelitis and spinal cord lesions (Ramachandran, 2012).
The patient’s history and presenting signs and symptoms are most consistent with acute
inflammatory demyelinating polyradiculo neuropathy, the most common variant of GBS. The
patient presents with numbness and tingling in his toes since the past 3 days. Over the past two
days he has had an unsteady gait and has been having difficulty walking. He had difficulty
getting out of bed this morning due to lower extremity weakness. The weakness is also
progressively getting worse and he is unable to move his lower extremities. Additionally, he is
having difficulty articulating his words, and chewing and swallowing his food. He is also having
some tingling in his hands and is experiencing difficulty in breathing. Two weeks prior to the
onset of symptoms the patient experienced an episode of upper respiratory illness with cough. He
also acknowledges some lower back pain, but denies any injury to his back or falls. All of these
factors are consistent with the symptoms and etiology of GBS, making GBS the most likely
diagnosis in the patient. The diagnosis will be confirmed after obtaining the results of the CSF
examination and the nerve conduction study (Amato & Hauser, 2012).
Acute Transverse Myelitis (ATM). ATM is a serious inflammatory condition affecting
the width of the spinal cord that causes impairment in the myelin sheath. In ATM there is an
interference with the signaling between the nerves in the spinal cord and the receptor organs. The
signs and symptoms of ATM include abrupt occurrence of pain in the lower back, sensory
deficits such as numbness, tingling, or burning, increased sensitivity, and paresthesias in the toes
and feet. The disorder can quickly advance to further worsening symptoms such as motor
weakness, urinary retention, and bowel dysfunction. Hyperreflexia is one of the typical features
of ATM. The level of the spinal cord involvement demarcates the symptoms, which disrupts the
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activity at that spinal level and the levels inferior to it. The most common area of demyelination
is at the thoracic level causing lower extremity paralysis and bowel and bladder dysfunction.
ATM is considered to be an autoimmune disorder that is usually preceded by a viral or bacterial
infection. However the exact cause of the disease is unknown. Treatment of ATM includes
intravenous steroids, plasma exchange, pain medications, supportive care, and rehabilitative
therapy (Greenberg, Aminoff, & Simon, 2012).
Diagnosis of ATM is based on magnetic resonance imaging which reveals inflammation
of the spinal cord, spinal cord compression, or blood vessel malformation. Performing a spinal
tap and examination of the cerebrospinal fluid (CSF) usually displays increased number of white
blood cells and normal to marginally higher proteins. An MRI of the spine that was performed
on the patient did not reveal any areas of inflammation, or edema. Moreover, the patient is
experiencing areflexia rather than hyperreflexia. Besides, ATM normally does not involve the
cranial nerves and bulbar symptoms. All these characteristics make ATM a very unlikely
diagnosis in the patient (Greenberg, Aminoff, & Simon, 2012).
Myasthenia Gravis (MG). MG is an autoimmune disorder where the antibodies destroy
the acetylcholine receptors at the neuromuscular junction. This causes an interruption in the
transmission of impulses at the skeletal muscles producing weakness and extreme exhaustion.
There is worsening of symptoms with monotonous usage of the same muscle, with improvement
witnessed after relaxing and resting the muscle. The weakness usually begins with the cranial
nerve involvement such as the ocular muscles followed by the bulbar muscles causing difficulty
with vision, eyelid drooping, diplopia, chewing, and swallowing. Progression of the disease
usually involves extremity weakness which is more proximal rather than distal. MG may also
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rarely progress to respiratory muscle involvement causing respiratory distress. Deep tendon
reflexes as well as sensory function are usually normal (Drachman, 2012).
MG is usually activated by conditions such as upper respiratory tract infection, operative
procedures, gestation, and certain medications. Diagnosis of MG is made by obtaining a
thorough history and clinical manifestations of symptoms. The key element that directs the
practitioner towards the diagnosis of MG is the improvement in muscle weakness following
periods of rest. The diagnosis is confirmed by discovering acetylcholine receptors antibodies in
the serum which is seen in approximately 85 percent of the patients affected with MG.
Electromyogram (EMG) reveals a gradual decrease in reaction to repetitive nerve stimulation.
Another test that is used to aid in the diagnosis of MS is the Tensilon test. The Tensilon test is
used to differentiate between a myasthenic crisis and a cholinergic crisis. Tensilon
(endophonium chloride) is an anticholinergic when administered causes a rapid improvement in
muscle strength that lasts briefly for about five minutes. If symptoms worsen it is considered to
be due to cholinergic crisis. Tensilon administration can cause bradycardia which may require
atropine administration (Drachman, 2012).
Treatment of MG includes the use of acetylcholinesterase inhibitors such as
pyridostigmine, corticosteroids such as prednisone, and immunosuppressants such as
cyclosporine. Severe cases may necessitate plasmapheresis and administration of
immunoglobulin. Disabling ocular MG may require excision of the thymus gland (Drachman,
2012).
The patient does not have any ocular movement involvement, eyelid drooping, or
diplopia. The patient’s symptoms are more consistent with ascending weakness, sensory deficits,
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and loss of DTRs. Moreover, acetylcholine receptor antibodies were not detected in the serum
making MG an unlikely diagnosis (Drachman, 2012).
Spinal Cord Compression (SCC). SCC is caused due to compression of the spinal cord
from tumors, granulomas, abscesses, or bony deformities. SCC usually causes severe pain at the
level of involvement and has associated symptoms such as sensory deficits, flaccid paralysis,
bowel and bladder incontinence, urinary retention, and loss of reflexes below the level of
involvement. SCC is a medical emergency and should be ruled out promptly. Diagnosis of SCC
is confirmed by obtaining an MRI with and without contrast of the spine. In conditions where a
MRI is unobtainable, a CT myelogram is indicated. Treatment of SCC includes administration of
corticosteroids to reduce swelling around the spinal cord. Surgery and radiation may be
necessary depending on the etiology of the SCC (Cornett & Dea, 2013).
Although the patient is presenting with flaccid paralysis, he also has some cranial nerve
involvement. Moreover, the patient also does not have bowel or bladder dysfunction. An MRI of
the spine performed on the patient did not reveal any abnormal pathologic involvement making
SCC an extremely unlikely diagnosis in the patient (Cornett & Dea, 2013).
Final Diagnosis
The results of the cerebrospinal fluid analysis, computed tomography of the head,
magnetic resonance imaging of the spine, nerve conduction velocity test, and electromyography
results were obtained and are displayed in Table 3 and Table 4.
Table 3 Cerebrospinal Fluid (CSF) Analysis
CSF
Normal Range
Pressure (cm H2O)
9-18
Appearance
Clear
Total Protein
15-40 mg/dL
Glucose
50-75 mg/dL
White blood cell count
0-5 lymphocytes
(Normal values from Sabatine, 2013)
Results
10
Clear
180 mg/dL
60 mg/dL
3
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Table 4 CT head, MRI Spine, Nerve conduction study (NCS), Electromyography (EMG)
Test
Computed Tomography (CT) of
the head without contrast
Magnetic Resonance Imaging
(MRI) with and without contrast
of the whole spine
Nerve conduction study
Electromyography
Results
No acute hemorrhage, mass or hydrocephalus. Normal study.
The vertebral bodies are normal in height. The spinal cord and
conus is normal in signal and morphology. There is no
abnormal pre or paraspinal tissue. No spinal cord
compression. MRI images did not reveal any fracture.
Nerve conduction study displayed decreased nerve conduction
velocity. There is a prolongation of the F wave and absent H
reflex, indicating damage to the myelin sheath at the nerve
bases. Sensory nerve conduction is diminished.
The electromyography examination of affected muscles
displays diminished conduction and mobilization. EMG study
display acquired demyelinating form of neuropathy consistent
with GBS.
Taking into consideration the patient’s history, physical examination findings, results of
the MRI Spine, CT head, CBC, BMP, CSF results, NCS, and EMG results the patient is
diagnosed with acute inflammatory demyelinating polyneuropathy (AIDP). The MRI with and
without contrast did not reveal any offending spinal cord compression pathology. The CBC and
BMP results were within normal range. The CSF studies revealed a protein level of 180 mg per
liter and normal WBC count. The high levels of protein in the CSF may be attributed to a
disruption in the blood brain barrier permeability at the junction of the base of the nerve roots
typically seen in GBS. The nerve conduction test displayed a delay in F-waves and absent H
reflex, indicating demyelination of the nerve roots. The EMG displayed acquired demyelinating
form of neuropathy consistent with AIDP. Therefore, the patient was diagnosed with GBS and
was treated appropriately (Amato & Hauser, 2012).
Diagnostic Tests
Diagnostic tests are the backbone of medical therapy that aids the practitioner in
narrowing down to the final diagnosis. Making an accurate diagnosis is crucial so as to be able to
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provide the appropriate treatment for the disorder, thereby stimulating healing and promoting
health for the patients. Neurological disorders can be very challenging to diagnose and treat, and
are the number one cause of long term disability. Diagnostic tests for GBS are aimed at not only
supporting the diagnosis of GBS, but also tests that will help rule out the differential diagnosis.
Table 5 displays the most widely used diagnostic tests to confirm the diagnosis of GBS and rule
out the differential diagnosis (Sharma, Sood, & Sharma, 2013).
Table 5 Diagnostic Tests and Rationale
Diagnostic Test
Cerebrospinal Fluid
(CSF)
Electromyography
(EMG)
Nerve Conduction
Velocity Studies
Serum Antibodies
Rationale
The CSF will reveal a high protein concentration of 100 to 1000
mg/dL along with normal white blood cell level (< 5 cells/mm3)
which is seen in up to 60 percent of the patients presenting with
GBS within seven days and more than 75 percent of the patients by
twenty one days, since the presentation of symptoms. The high
levels of protein in the CSF may be attributed to a disruption in the
blood brain barrier permeability at the junction of the base of the
nerve roots. In patients co-infected with other disorders such as HIV,
elevated levels of WBC may be noted in the CSF.
EMG assists in analyzing the adequacy of electrical activity among
the peripheral nerves and the muscle fibers. In AIDP the
electromyography examination of affected muscles displays
diminished conduction and mobilization. Patients that display more
than 80% loss of motor activity are expected to have worse
outcomes. EMG studies display demyelinating form of neuropathy.
The study is done to diagnose nerve damage or destruction. It
measures how fast electrical signals move through the nerve. These
studies are beneficial not only for the confirmation of the diagnosis
of GBS but also to distinguish between the different variants. In
GBS there is decreased nerve conduction velocity. In AIDP there is
a prolongation or non-existence of the F wave and absent H reflex,
indicating damage to the myelin sheath at the nerve bases. The speed
and amplitude with which nerve conduction takes place is also
diminished around the third to fourth week in the peroneal, tibial,
median and ulnar nerves. Sensory nerve conduction is either lost or
diminished.
Antibodies against GQ1b, a ganglioside component of nerve are
found in up to 90 % of the patients with Miller Fisher syndrome.
Antibodies to GM1, GD1a, GaINac-GD1a, and GD1b are mostly
associated with axonal variants of GBS. Antibodies to GT1 are
associated with swallowing dysfunction. Antibodies to GD1b are
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associated with pure sensory GBS.
Basic Metabolic Panel
To rule out electrolyte imbalance, hypoglycemia, hyperglycemia,
assess kidney function
Complete Blood Count
To rule out infection, anemia, thrombocytopenia
Head CT
To rule out intracranial involvement such as tumors, intracranial
hemorrhage, aneurysmal malformation, and infarcts
MRI with and without
To rule out spinal cord compression, spinal cord inflammation,
contrast of spine
cauda equine syndrome, transverse myelitis, spinal tumors
Pulmonary Function Test PFT measures the ability of the lungs to participate in gas exchange.
(PFT)
In patients presenting with respiratory muscle weakness, monitoring
respiratory vitals such as the vital capacity and negative inspiratory
force is extremely important. A forced vital capacity of less than 20
ml per kilogram, maximum inspiratory pressure of less than 30
cmH2O and maximum expiratory pressure of less than 40 cmH2O
are warnings for approaching respiratory arrest necessitating
intubation.
Electrocardiogram
Approximately two thirds of the patients presenting with GBS
display signs of autonomic dysfunction such as tachycardia,
bradycardia, dysrhythmias, and labile blood pressure necessitating
vigilant monitoring of the patients cardiac status.
(Sharma, Sood, & Sharma, 2013)
Prioritized Plan
Disease Modifying Treatment
The American Academy of Neurology (AAN) recommends treating patients with GBS
with plasma exchange (PE) or intravenous immunoglobulin (IVIG). Other than plasma exchange
and IVIG, no other treatment modalities have displayed effectiveness in the treatment of GBS.
Patients not treated with PE or IVIG, continue to have worsening of symptoms for up to 14 days
and thereafter symptoms continue to persist for another 14 days before they gradually start to
improve over a matter of months. Both PE and IVIG have revealed to be equally beneficial and
shorten the recovery phase by up to 50 percent. A combination of PE and IVIG has not displayed
any added benefit (Patwa, Chaudhry, Katzberg, Rae-Grant, & So, 2012).
Plasma Exchange. Plasma exchange (PE) rapidly removes the disease causing
autoantibodies, complement bodies, and cytokines from the circulation thereby speeding
COMPREHENSIVE CLINICAL CASE STUDY
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recovery and improvement in symptoms by half the time. PE is most beneficial when started as
early as possible usually within a week. AAN endorses PE for adult patients confined to bed
within four weeks of onset of symptoms. For patients who are mobile, PE is recommended
within 14 days of initiation of symptoms. PE requires the placement of a central venous catheter
and is executed for approximately ten days providing four to six exchanges. The adverse
reactions include low blood pressure, infection, and problems with central venous access (Patwa,
Chaudhry, Katzberg, Rae-Grant, & So, 2012).
In a meta-analysis conducted by Raphael and colleagues in 2012, comparing PE and
supportive care, the authors concluded that PE significantly amplified the percentage of patients
who regained the capability to ambulate with support after four weeks (RR 1.60, 95% CI, 1.19 to
2.15). Moreover, within 12 months the probability of full muscle strength regain was
considerably superior with PE than without (95% CI, 1.07 to 1.45).
Intravenous Immunoglobulin (IVIG). The mechanism of action of IVIG in Guillain
Barre is unidentified, but is thought to offer supplement anti-idiotypic antibodies, controlling the
task of the receptors, disturbing the instigation of complement, T and B cells, and formation of
cytokines. Treatment with IVIG is given for up to five days, at 0.4 gram/kilogram daily. Severe
cases of GBS may necessitate longer duration of treatment. Adverse reactions of IVIG include
inflammation of the meninges, urticaria, kidney injury, and rarely ischemic cerebral infarcts. The
benefit of IVIG is the ease with which it can be administered, and is considered to be safer than
PE (Patwa, Chaudhry, Katzberg, Rae-Grant, & So, 2012).
In a systematic review conducted by Hughes, Swan and Van Doorn in 2012, comparing
PE and IVIG in 632 severely affected patients, the authors concluded that IVIG initiated within
14 days from the start of symptoms accelerated restoration of muscle strength equivalent to PE.
COMPREHENSIVE CLINICAL CASE STUDY
19
Adverse reactions were considerably uncommon with both the therapies. However, the
probability of completing the full course of treatment was much more probable with IVIG than
PE (95% CI 0.25 to -0.20).
The choice of treatment between PE and IVIG depends on the availability and
accessibility, safety, suitability, and preference of the practitioner. When IVIG and PE are both
obtainable and if there are no known contraindications to their usage, the recommendation is to
use IVIG due to the ease with which it can be administered. Treatment with corticosteroids did
not substantiate improvement in primary outcome measures and did not display any overall
benefits. Therefore, corticosteroids are no longer recommended as the mainstay of treatment for
GBS (Patwa, Chaudhry, Katzberg, Rae-Grant, & So, 2012).
Supportive Care. The management of patients with GBS depends on the extent of
muscular weakness and involvement of respiratory muscles. Approximately one third of the
patients affected with GBS have respiratory involvement requiring ventilator support. Patients on
ventilator should have ventilator associated pneumonia prevention measures. Due to involvement
of the autonomic nervous system, most patients require intensive care monitoring. Supportive
measures for patients with GBS include deep vein thrombosis prophylaxis such as compression
stockings and sleeves, unfractionated heparin, bowel and bladder training, physical and
occupational rehabilitation and training, and emotional support and psychotherapy. Patients with
pain issues should have adequate pain management measures (Amato & Hauser, 2012).
Respiratory Failure. Patients with GBS can decline rather quickly due to the
progression of muscle weakness and involvement of the respiratory muscles. Due to bulbar
involvement, they may develop swallowing deficits and are at high risk for aspiration. Therefore,
it is extremely important to primarily monitor their respiratory vitals such as the vital capacity
COMPREHENSIVE CLINICAL CASE STUDY
20
and negative inspiratory force. Patients with a forced vital capacity of less than 20 ml per
kilogram, maximum inspiratory pressure of less than 30 cmH2O and maximum expiratory
pressure of less than 40 cmH2O are warnings for approaching respiratory arrest necessitating
intubation. The other predictors for respiratory failure include rapid progression of symptoms
less than seven days, difficulty coughing and swallowing, facial weakness, inability to raise the
head, immobility, and elevated liver enzymes. Criteria for discontinuation from ventilator
support incorporate improving muscle strength and sequential progress in pulmonary function
tests (PFTs). Patients requiring mechanical ventilation for more than two weeks and those who
display poor PFT results qualify for a tracheostomy (Amato & Hauser, 2012).
Autonomic Dysfunction (AD). Autonomic dysfunction is a frequently appreciated
phenomenon and is noted in approximately two thirds of the patients presenting with GBS.
Patients with AD may present with an inconsistent heart rate, dysrhythmias, urinary retention,
labile blood pressures, gastroparesis, and loss of perspiration. Therefore vigilant monitoring of
the patients cardiac status, electrocardiogram, blood pressure, heart rate, hydration status, bowel
sounds, and urine output is critical (Rinaldi, 2013).
Pain. Somatosensory or neuropathic pain is commonly seen in at least half of the patients
with GBS. Gabapentin 300 mg three times a day with a maximum dose of 1800 mg per day, and
Carbamazepine 100 mg twice a day are appropriate for pain management during the initial stages
of GBS. For chronic neuropathic pain management pregabalin 75 mg twice a day and
amitriptyline 25 to 100 mg per day may be added (Rinaldi, 2013).
Rehabilitation. Rehabilitation is extremely important in patients with GBS who develop
resolute motor weakness. Therapy should be tailored to the individual patient’s needs to improve
muscle strength, incorporating isometric and resistive exercises. In the acute phase, performing
COMPREHENSIVE CLINICAL CASE STUDY
21
daily range of motion exercises and proper body alignment is beneficial in preventing
contractures. Rehabilitation should focus on correct foot and extremity positioning, good posture,
and healthy diet. Some patients may also need assistance with communication. A
multidisciplinary team approach is ideal when caring for patients with GBS (Rinaldi, 2013).
Prognostic Factors. Recovery from GBS may be unfavorable if the patient is older in
age, the onset of symptoms was rapid, severe extremity weakness on arrival, respiratory paralysis
requiring mechanical ventilation, distal motor response amplitude was less than 20 percent, and
diarrhea was associated with the preceding illness (Rinaldi, 2013).
Long-Term Outcomes. Approximately 80 percent of the patients with GBS are able to
walk independently in about six months. In twelve months complete regaining of muscle strength
is seen in approximately 60 percent of the patients while 14 percent of the patients continue to
have severe muscle weakness. About five percent of the patients diagnosed with GBS die within
one year although adequately treated and managed in the intensive care unit. Relapses may be
seen in about ten percent of the patients, and are treated similarly as a primary attack of GBS
(Rinaldi, 2013).
APN Authority to Prescribe. According to the Ohio Board of Nursing, 2013, treatment
with intravenous immunoglobulin should be physician initiated or physician consulted. Plasma
exchange is ordered by specialized physicians. The medications for the management of
neuropathic pain such as Gabapentin, Carbamazepine, pregabalin, and tricyclic antidepressants
may be prescribed by an APN with a valid certificate to prescribe in the state of Ohio as
authorized by the Ohio Board of Nursing (Ohio Board of Nursing, 2013).
COMPREHENSIVE CLINICAL CASE STUDY
22
Follow up
Patients treated for GBS should be closely monitored for progression of the symptoms,
respiratory status and overall recovery. Patients should be monitored in the intensive care unit
during the acute phase due to autonomic dysfunction. Patients on ventilator should have
prophylaxis for prevention of ventilator associated pneumonia. Patients requiring prolonged
ventilatory support will require a tracheostomy. Assessing respiratory vitals such as the forced
vital capacity and negative inspiratory flow help determine risk for respiratory failure or if
already intubated assesses adequacy for weaning and extubation. Gastrointestinal and
Gastrourinary monitoring should be continued. Patients with appropriate gastric motility should
be started on supplemental nutrition. Patients confined to bed should be assessed for DVTs and
pressure ulcers. Rehabilitation, physical therapy and occupational therapy are crucial for the
prevention of contractures and overall recovery and long term prognosis of the patient.
Neuropathic pain should be adequately controlled with anticonvulsants and antidepressants.
Patients should be provided with emotional and psychological support during the initial phase
and through the course of the illness and rehabilitation phase until complete recovery, and
thereafter should be assessed for relapse (Rinaldi, 2013).
Health Promotion Activities
The patient should be encouraged to continue with regular follow-ups with his primary
care physician. Once his condition improves he should be encouraged to participate in physical
activity as much as he can tolerate. He should continue to take all of his home medication as
prescribed to control his blood pressure, cholesterol, and diabetes. The patient does not smoke,
drink alcohol and does not use illegal drugs. The patient should be complimented for not making
unhealthy behavioral choices, and should be encouraged to continue to make good behavior
COMPREHENSIVE CLINICAL CASE STUDY
23
choices in the future. Educating the patient in making healthy dietary choices is extremely
important since the patient is hypertensive, diabetic, and has hypercholesterolemia. Including
family members in health education, rehabilitation training, and overall care of the patient will
improve their knowledge and interest and alleviate fear and anxiety. Family participation also
enhances overall positive outcomes and improves long-term prognosis (Rinaldi, 2013).
Literature updates include some cases of GBS that have transpired following
vaccinations, although vaccine-associated GBS is unclear. Literature suggests not administering
vaccines during an acute period of GBS and for up to a period of 12 months following the
occurrence of GBS. After the initial one year post GBS, recommendations for vaccinations
should be considered on an individualized approach. In situation where GBS occurred within six
weeks following a specific vaccine, future deterring of the vaccine is recommended. For most
patients who are predisposed to severe attacks of the influenza, the annual influenza vaccine is
recommended unless the patient developed GBS subsequent to the influenza vaccine (Rinaldi,
2013).
Relapses can occur in up to ten percent of the patients with GBS. The patient and family
should be provided education regarding GBS and encouraged to seek medical attention if similar
symptoms occur in the future (Rinaldi, 2013).
The patient in the case study required intubation for respiratory support. He was admitted
in the intensive care unit and remained on the ventilator for a week. As part of his treatment he
received IVIG for five days, following which his symptoms started to gradually improve. He was
subsequently moved out of the ICU to a step down unit and thereafter to inpatient rehabilitation
for further therapy.
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24
References
Amato, A. A., & Hauser, S. L. (2012). Chapter 385. Guillain-Barré Syndrome and other
immune-mediated neuropathies. In D. L. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser,
J. L. Jameson, & J. Loscalzo (Eds), Harrison's Principles of Internal Medicine, 18e.
Retrieved October 23, 2013 from http://www.accessmedicine.com
Chiang, S., & Ubogu, E. (2013). The role of chemokines in Guillain-Barre syndrome. Muscle
and Nerve, 48(3), 320-333. Retrieved from
http://www.onlinelibrary.wiley.com.ezproxy.libraries.wright.edu
Cornett, P. A., & Dea, T. O. (2013). Chapter 39. Cancer. In M. A. Papadakis, S. J. McPhee, M.
W. Rabow, & T. G. Berger (Eds), CURRENT Medical Diagnosis & Treatment 2014.
Retrieved October 24, 2013 from http://www.accessmedicine.com
Drachman, D. B. (2012). Chapter 386. Myasthenia Gravis and other diseases of the
neuromuscular junction. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L.
Jameson, & J. Loscalzo (Eds), Harrison's Principles of Internal Medicine, 18e. Retrieved
October 23, 2013 from http://www.accessmedicine.com
Dugdale, D. C. (2012). Complete blood count and basic metabolic panel. Medline Plus.
Bethesda, MD: National Library of Medicine. Retrieved from http://www.nlm.nih.gov
Greenberg, D. A., Aminoff, M. J., & Simon, R. P. (2012). Chapter 9. Motor disorders. In D.A.
Greenberg, M. J. Aminoff, & R. P. Simon (Eds), Clinical Neurology, 8e. Retrieved
October 23, 2013 from http://www.accessmedicine.com
Hughes, R., Swan, A., & Van Doorn, P. (2012). Intravenous immunoglobulin for Guillain-Barre
syndrome. Cochrane Database of Systematic Reviews, 7, 1-60. Retrieved from
http://www.onlinelibrary.wiley.com.ezproxy.libraries.wright.edu.
COMPREHENSIVE CLINICAL CASE STUDY
25
Ohio Board of Nursing. (2013). The formulary developed by the committee on prescriptive
governance. Retrieved from http://www.nursing .ohio.gov
Patwa, H. S., Chaudhry, V., Katzberg, H., Rae-Grant, A. D., & So, Y. T. (2012). Evidence-based
guideline: Intravenous immunoglobulin in the treatment of neuromuscular disorders.
Report of the therapeutics and technology assessment subcommittee of the American
Academy of Neurology. Neurology. 78(13), 1009-1015. Retrieved from
http://www.neurology.org
Raphael, J. C., Chevrer, S., Hughes, R., & Annane, D. (2012). Plasma exchange for GuillainBarre syndrome. The Cochrane Database of Systematic Reviews, 7, 1-47. Retrieved from
http;//www.onlinelibrary.wiley.com.ezproxy.libraries.wright.edu
Rinaldi, S. (2013). Update on Guillain-Barre syndrome. Journal of the Peripheral Nervous
System, 18(2), 99-112. Retrieved from
http://www.onlinelibrary.wiley.com.ezproxy.libraries.wight.edu.
Sabatine, M. S. (2013). The Massachusetts General Hospital Handbook of Internal Medicine.
Philadelphia, PA: Lippincott Williams & Wilkins.
Sharma, G., Sood, S., & Sharma, S. (2013). Early electro diagnostic findings of Guillain Barre
syndrome. Neurology and Neurophysiology, 4(142). Retrieved from
http://www.omicsonline.org