Republic of the Philippines

Mariano Marcos State University

COLLEGE OF HEALTH SCIENCES
City of Batac 2906, Ilocos Norte Philippines
Tel/Fax No. (63) (077) 670-1920 E-mail: mmsu_chs_2009@yahoo.com

In partial fulfillment of the requirements in the subject

RLE 104A

Report

REYES SYNDROME
GUILLAIN-BARR SYNDROME
Presented by:
Tagata, Ana Mae P.
BSN III-B, Group 3

Presented to:

Prof. Norma L. Eclarin

Clinical Instructor

December 1, 2015

Description of the Disorder

Reyes syndrome was first described in 1963 in Australia by RDK Reye and described a
few months later in the United States by GM Johnson.
The said syndrome is a rare, acute, and potentially life-threatening condition that affects
all bodily organs but is most harmful to the brain primarily the central nervous system (causing
an acute, non-inflammatory encephalopathy) and the liver (causing elevations in ammonia levels
and liver enzymes, but no jaundice); it is noncontagious, and too often misdiagnosed as
encephalitis, meningitis, diabetes, poisoning, drug overdose, or sudden infant death. It occurs
primarily among children who are recovering from a viral infection, such as chicken pox or the
flu. It usually develops a week after the onset of the viral illness but can also occur a few days
after onset.
The cause and cure of Reye's syndrome is unknown. According to the National Reye's
Syndrome Foundation, "the National Reye's Syndrome Foundation (NRSF), the U.S. Surgeon
General, the Food and Drug Administration, the Centers for Disease Control, and the American
Academy of Pediatrics recommend that aspirin and combination products containing aspirin not
be taken by anyone under 19 years of age during fever-causing illnesses."
In the United States, the syndrome became a reportable disease in 1973. Peak incidence
was reported in 1979-80. Moreover, percentage of patients with a previous diagnosis of it is
0.4% while the percentage of patients who have a sibling with a Reyes syndrome history is
2.9%. In terms of racial distribution, 93% for White, 5% for African American, and with the
remaining percentage for Asian, American Indian, and Native Alaskan.
Risk Factors
Taking aspirin to treat a viral illness or infection
Children between the ages of 4 and 12, although it can occur at any age
After common viral infections such as influenza or chickenpox, an ordinary upper
respiratory infection such as a cold
Children with undiagnosed metabolic disorders may also be at risk, though this is not
completely clear.
Manifestations
The stages used in the CDC classification of Reye syndrome are as follows:

Stage 0 - alert, abnormal history and laboratory findings (elevated liver enzymes,
elevated ammonia levels, and low serum glucose levels) consistent with Reyes
syndrome, and no clinical manifestations
Stage 1 - vomiting, sleepiness, and lethargy
Stage 2 - restlessness, irritability, combativeness, disorientation, delirium, tachycardia,
hyperventilation, dilated pupils with sluggish response, hyperreflexia, (+) Babinski
reflex, and appropriate response to noxious stimuli

Stage 3 - obtunded, comatose, decorticate rigidity, and inappropriate response to noxious

stimuli
Stage 4 - deep coma, decerebrate rigidity, fixed and dilated pupils, loss of oculovestibular
reflexes, and dysconjugate gaze with caloric stimulation
Stage 5 - seizures, flaccid paralysis, (-) DTR, no pupillary response, and respiratory arrest

The primary symptoms of Reyes syndrome include persistent vomiting and mental status
changes. These symptoms are generally the result of increased intracranial pressure and brain
swelling. Also, the causes of symptoms associated with Reye's syndrome related to dysfunction
of the liver and a resultant increase in serum ammonia levels and other toxins. These toxins cause
increased pressure in the brain and swelling, leading to brain dysfunction and can progress to
death.
The onset of Reye syndrome can be rapid, and signs and symptoms may worsen within
hours.
Complications
Cardiovascular
Cardiac arrhythmias
Cardiovascular collapse
Respiratory
Respiratory failure
Renal
Ammonia toxicity
Diabetes Insipidus
Acute renal failure
Neurological
Residual or acute mental impairment
Cerebral edema
Coma
Brain herniation
Seizures
Increased intracranial pressure
Infective
Aspiration pneumonia
Sepsis
Gastrointestinal
Gastrointestinal bleeding

Pathophysiology
The pathogenesis is unclear, but a preceding viral infection seems to be an initial factor
involved in most cases. In certain genetically predisposed individuals, this infection then disrupts
mitochondrial function and lipid metabolism in numerous organs, particularly the liver, kidneys,
brain, and in skeletal muscle tissues. Damaged cells release cytokines and other mediators that
facilitate metabolic changes, and possibly sensitize tissues for further injury by exogenous
factors.
In the liver specifically, this metabolic failure leads to decreased gluconeogenesis with
increased fatty acid and ammonia production. This process may then be aggravated by the
introduction of additional environmental factors, or by an underlying metabolic disorder. In the
CNS, the resultant hypoglycemia and hyperammonemia may lead to cerebral edema and
increased intracranial pressure.
Medical Management
Diagnostic Procedures
1) History Taking
2) Physical Exam
3) Ammonia Test
- It is primarily used to help investigate the cause of changes in behavior and
consciousness. It may be ordered to help support the diagnosis of Reye's
syndrome or hepatic encephalopathy caused by various liver diseases.
- Result: ammonia level will be elevated, and is directly related to consciousness
and survival.
* Normal ranges for ammonia levels are: newborns - 170-340 mcg/dL or 100-200
mcmol/L; children - 70-135 mcg/dL or 41-80 mcmol/L; and adults - 15-60 mcg/dL or
21-50 mcmol/L.
4) Liver Function Tests
-

Used to determine if the liver has been damaged or its function impaired.
Elevations of certain liver tests in relation to others assist in that determination.

Alanine aminotransferase (ALT), also called serum glutamate pyruvate

transaminase (SGPT), is an enzyme necessary for energy production. It is present
in a number of tissues, including the liver, heart and skeletal muscles, but is found
in the highest concentration in the liver. Because of this, it is used in conjunction
with other liver enzymes to detect liver disease. Additionally, in conjunction with
the aspartate aminotransferase test (AST), it helps to distinguish between heart
damage and liver tissue damage. For Reyes syndrome, this test will be elevated
to usually 200 IU/L or more in the absence of jaundice.

Aspartate aminotransferase (AST), also called serum glutamic-oxaloacetic

transaminase (SGOT), is another enzyme necessary for energy production. It also
may be elevated in liver and heart disease. In liver disease, the AST increase is
usually less than the ALT increase.

5) Liver Biopsy
-

The definitive test for Reyes syndrome with examination of the mitochondria
under an electron microscope. This test will show the fat accumulation in the
liver, where large vacuoles of triglyceride fat accumulate in liver cells via the
process of steatosis (i.e., abnormal retention of lipids within a cell).
6) Skin Biopsy
- May be needed to test for fatty acid oxidation disorders or metabolic disorders.
During a skin biopsy, a health care provider takes a small skin sample for
analysis.
7) Spinal tap, also known as lumbar puncture
- Help the health care provider identify or rule out other diseases with similar signs
and symptoms. During a spinal tap, needle is inserted through the lower back. A
small sample of CSF is removed.
- Result: low white blood cell count
8) CT Scan or MRI
- Can identify or rule out other causes of behavior changes or decreased alertness.
A CT Scan uses an imaging machine linked to a computer. It creates detailed
images of the brain. An MRI scan uses a strong magnetic field and radio waves to
generate images of the brain.
- CT scans in patients with severe cases of Reyes syndrome will show diffuse
cerebral edema with compression of the ventricles.
9) Electroencephalogram (EEG)
A procedure that records the brain's continuous, electrical activity by means of
electrodes attached to the scalp.
- Result: Early stage - slow wave activity revealed
Advanced stage - flattened wave activity revealed
10) Hemodialysis
- In some cases of progressive and resistant Reye's syndrome, hemodialysis has
also been used to remove toxins believed to be partly responsible for the brain
swelling.
11) Intracranial Pressure Monitoring (ICP)
- Measures the pressure inside of the child's head.
Therapeutic Management
No specific treatment exists for Reyes syndrome; supportive care is based on the
stage of the syndrome with aggressive treatment provided to correct or prevent metabolic
abnormalities, particularly hypoglycemia and hyperammonemia, promoting effective
cerebral perfusion, and controlling intracranial pressure.

1) Admission to the intensive care unit (ICU) is warranted for continued monitoring and
treatment.
2) Establish and maintain the patients airway, breathing, and circulation.
3) Avoid giving aspirin or medications that contain aspirin to treat viral illnesses unless
specifically instructed to do so by doctor. Do not give aspirin to anyone younger than
19.
- Other names for aspirin include: acetylsalicylic acid, acetylsalicylate, salicylic
acid, and salicylate. If child or teenager has the flu or chickenpox, use other
medications such as acetaminophen, ibuprofen, or naproxen sodium to reduce
fever or relieve pain.
Stages 0-1
-

Keep the patient quiet.

Frequently monitor vital signs and laboratory values.

Maintain electrolytes, serum pH, albumin, serum osmolality, glucose, and urine
output in normal ranges. Consider restricting fluids to two thirds of maintenance.
Overhydration may precipitate cerebral edema. Use colloids (e.g., albumin) as
necessary to maintain intravascular volume. Dehydration may compromise
cardiovascular volume and reduce cerebral perfusion. Glucose should be
maintained in the 100-125 mg/dL range; this will require administration of D10 or
D20. Place a Foley catheter to monitor urine output.

Correct fluid and electrolyte abnormalities, hypoglycemia, and acidosis. If the

patient is hypoglycemic, administer dextrose 25% as an intravenous (IV) bolus in
a dose of 1-2 mL/kg.

Avoid rapid correction or overcorrection. Recognize that administration of sodium

bicarbonate results in a significant sodium load.

Consider giving ondansetron 1-2 mg IV every 8 hours to decrease vomiting.

Antacids may also be administered for GI protection.

Stage 2
-

Continuous cardiorespiratory monitoring

Elevate the head to 30, keep the head in a midline orientation

Use isotonic rather than hypotonic fluids

Endotracheal intubation may be required at this stage to maintain the airway,

control ventilation, and prevent increased ICP

Place a nasogastric tube to decompress the abdomen.

Avoid overhydration, and administer furosemide 1 mg/kg as often as every 4-6

hours to control fluid overload.

Administer Sodium phenylacetatesodium benzoate which is FDA-approved for

the treatment of acute hyperammonemia and associated encephalopathy in
patients with deficiencies in enzymes of the urea cycle. During the first 15
minutes of the initial dose of sodium phenylacetatesodium benzoate, administer
ondansetron 1-2 mg IV. If the ammonia level is higher than 500 g/dL or if the
patients condition fails to respond to the initial dose of sodium phenylacetate
sodium benzoate, start dialysis, preferably hemodialysis.

Stages 3-5
-

Continuously monitor ICP, central venous pressure, arterial pressure, or end-tidal

carbon dioxide.

Perform endotracheal intubation if the patient is not already intubated.

Treat increased ICP by following standard guidelines, which, in addition to

correction of hyperammonemia, proper positioning of the head, and appropriate
fluid management, include the following:

Ventilation to maintain the partial pressure of carbon dioxide in the normal

range
Aggressive management of fever to prevent the increased cerebral metabolism
and increased cerebral blood flow resulting from hyperpyrexia
Analgesia and sedation to alleviate agitation or prepare for painful
interventions
Paralytic agents to control shivering
If other measures fail, mannitol 20% solution dosed at 0.25-0.5 g/kg IV
infused over 10-20 minutes as often as every 6-8 hours, or hypertonic saline
3% dosed at 3-5 mL/kg over 3-30

Treat seizures with phenytoin 10-20 mg/kg IV as a loading dose, followed by 5

mg/kg/day IV divided every 6 hours or fosphenytoin dosed as 10-20 mg/kg
phenytoin equivalents

Correct coagulopathy (prothrombin time >16 seconds). Options include fresh

frozen plasma (FFP), cryoprecipitate, platelets, vitamin K, and exchange
transfusion. FFP 10-15 mL/kg every 12-24 hours provides rapid correction and
volume expansion and should be administered, particularly if active bleeding is
present or if invasive procedures (e.g., ICP monitoring device placement or liver
biopsy) are required. If the fibrinogen level is lower than 100 mg/dL,
cryoprecipitate 10 mL/kg every 6 hours should be considered instead of FFP
because cryoprecipitate has a higher concentration of fibrinogen. If invasive
procedures are to be performed, platelets should also be given as needed to restore
the platelet count to a value higher than 50,000/L. Vitamin K 1-10 mg IV may be
administered instead of FFP or cryoprecipitate if the need for correction is not an
emergency.

Pharmacologic Management
1) Drug: Urea Cycle Disorder Treatment Agents
Indication: Ammonia detoxicants are used for treatment of hyperammonemia; they
enhance elimination of nitrogen.
- Sodium phenylacetate and sodium benzoate (Ammonul)
2) Drug: Antiemetic agents
Indication: Antiemetic agents are administered to decrease vomiting and during the
initiation of sodium phenylacetatesodium benzoate therapy.
- Ondansetron (Zofran, Zuplenz)
3) Drug: Diuretics
Indication: Decrease pressure on the brain. They also increase fluid loss through
urination.

Nursing Diagnoses and Possible Interventions

Potential Nursing Diagnoses for Reyes Syndrome
- Ineffective breathing pattern
- Impaired gas exchange
- Impaired physical mobility
- Risk for ineffective cerebral tissue perfusion
- Risk of injury from convulsions
- Risk for impaired skin integrity and infection related to impaired mobility (possibly
from coma)
Possible Nursing Interventions for Reyes Syndrome
- Maintain hydration by administering fluids intravenously

Institute and maintain seizure precautions

Preventing skin breakdown from immobility: pad bony prominences, range of motion
exercises, turning and position changes
Monitor intake and output, as the patient may be taking diuretics and may experience
renal impairment from the condition
Maintain nothing-by-mouth status of ordered
Provide care for endotracheal tube and mechanical ventilator; ensure patency
Initiate intravenous access and ensure patency
Administer medications as ordered; such as glucose, vitamin K, diuretics, and
paralytics
Care for intracranial pressure monitoring device
Provide a quiet environment to reduce risks of increasing the intracranial pressure
Position the head at midline and raise the head of the bed to 30 degrees
Administer blood products as ordered Administer vitamin K, fresh frozen plasma, and
platelets as necessary to reduce the risk of bleeding; institute bleeding precautions
Obtain specimens for laboratory testing (such as serum glucose levels, hepatic
enzyme levels, and ammonium levels) for changes.
Support the patient and family and provide teaching for coping mechanisms related to
situational crises

Description of the Disorder

Guillain-Barr syndrome (GBS) is a disorder in which an autoimmune attacks the
peripheral nerve myelin. The result is acute, rapid segmental demyelination of peripheral nerves
and some cranial nerves, producing ascending weakness and progress up the body over a few
days or weeks. The disorder can be mild, moderate or severe, with life support needed in the
worst cases. Most people spontaneously recover, although some will be left with permanent
disabilities.
In these cases the disorder is life threatening - potentially interfering with breathing and,
at times, with blood pressure or heart rate - and is considered a medical emergency.
Moreover, it's not possible for GBS to be transmitted from one person to another and it's
not inherited.
Other names for Guillain-Barr syndrome include acute idiopathic polyneuritis, acute
idiopathic polyradiculoneuritis and Landry's ascending paralysis.
Subtypes of Guillain-Barr syndrome

Acute inflammatory demyelinating polyneuropathy

The acute inflammatory demyelinating polyneuropathy (AIDP) subtype is the
most commonly identified form in the United States. It is generally preceded by a
bacterial or viral infection.
Nearly 40% of patients with AIDP are seropositive for C jejuni. Lymphocytic
infiltration and macrophage-mediated peripheral nerve demyelination is present.
Symptoms generally resolve with remyelination.

Acute motor axonal neuropathy

The acute motor axonal neuropathy (AMAN) subtype is a purely motor disorder
that is more prevalent in pediatric age groups. AMAN is generally characterized by
rapidly progressive symmetrical weakness and ensuing respiratory failure.
Nearly 70-75% of patients with AMAN are seropositive for Campylobacter, with
the majority of cases of AMAN being associated with preceding C jejuni diarrhea.
Patients typically have high titers of antibodies to gangliosides. Inflammation of the
spinal anterior roots may lead to disruption of the blood-CNS barrier. Biopsies show
wallerian-like degeneration without significant lymphocytic inflammation.

Acute motor-sensory axonal neuropathy

Acute motor-sensory axonal neuropathy (AMSAN) is a severe acute illness
differing from AMAN in that it also affects sensory nerves and roots. Patients are

typically adults. AMSAN often presents as rapid and severe motor and sensory
dysfunction. Marked muscle wasting is characteristic, and recovery is poorer than it is
from electro physiologically similar cases of AMAN.
As with AMAN, AMSAN is often associated with preceding C jejuni diarrhea.
Pathologic findings show severe axonal degeneration of motor and sensory nerve fibers
with little demyelination.

Miller-Fisher syndrome
Miller-Fisher syndrome (MFS), which is observed in about 5% of all cases of
GBS, classically presents as a triad of ataxia, areflexia, and ophthalmoplegia. Acute onset
of external ophthalmoplegia is a cardinal feature. Ataxia tends to be out of proportion to
the degree of sensory loss. Patients may also have mild limb weakness, ptosis, facial
palsy, or bulbar palsy. Patients have reduced or absent sensory nerve action potentials and
absent tibial H reflex.

Acute pan autonomic neuropathy

Acute pan autonomic neuropathy, the rarest GBS variant, involves the
sympathetic and parasympathetic nervous systems. Patients have severe postural
hypotension, bowel and bladder retention, anhidrosis, decreased salivation and
lacrimation, and pupillary abnormalities. Cardiovascular involvement is common, and
dysrhythmias are a significant source of mortality. Significant motor or sensory
involvement is lacking. Recovery is gradual and often incomplete.

Pure sensory GBS

A pure sensory variant of GBS has been described in the literature. It is typified
by a rapid onset of sensory loss, sensory ataxia, and areflexia in a symmetrical and
widespread pattern.

Other variants
The pharyngeal-cervical-brachial variant of GBS is distinguished by isolated
facial, oropharyngeal, cervical and upper limb weakness without lower limb involvement.
There can be combinations of any of the above subtypes, and virtually any combination
of nerve injury.

The annual incidence of GBS is 1 to 2 cases per 100,000 people. Results of studies on
recovery rates differ, but most indicate that 60% to 75% of patients recover completely. On the
other hand, death occurs in 3% to 10% cases (Lugg, 2010).
Risk Factors
Any gender or age, however, it is more frequent in males between 16 and 25 years of age
and those older than 55 years (Bader & Littlejohns, 2010).
Infectious agents that may trigger the immune system to attack nerve roots and peripheral
nerves.
- Campylobacter jejuni, which can cause a type of food poisoning; Mycoplasma, which
can cause pneumonia; Cytomegalovirus (CMV), which can cause fever, chills, sore
throat, swollen glands, body aches, and fatigue; Epstein-Barr virus (EBV), which can
cause mononucleosis (mono);
Varicella-zoster
virus,
which
can
cause chickenpox and shingles; and HIV.
Occasionally surgery will trigger the syndrome.
In rare instances vaccinations may increase the risk of GBS.
Manifestations (ascending)

Initial (dyskinesia inability to execute voluntary movements; hyporeflexia; and

paresthesia a sensation of numbness, tingling, or a pins and needles; weakness of the
lower limbs which may progress to the upper extremities, trunk and facial muscles)

Respiratory distress

Diminished/absent DTRs

Inability to swallow and talk

Inability to close the eyes

Inability to move

Severe and persistent pain in the back and calves of the legs

Complications

Respiratory failure
Cardiac dysrhythmias
Immobility complications

Pathophysiology
The body's immune system begins to attack the body itself, causing what is known as an
autoimmune disease. Usually the cells of the immune system attack only foreign material and
invading organisms. In Guillain-Barr syndrome, however, the immune system starts to destroy
the myelin sheath that surrounds the axons of many peripheral nerves, or even the axons
themselves (axons are long, thin extensions of the nerve cells; they carry nerve signals). The
myelin sheath surrounding the axon speeds up the transmission of nerve signals and allows the
transmission of signals over long distances.
In diseases in which the peripheral nerves' myelin sheaths are injured or degraded, the
nerves cannot transmit signals efficiently. That is why the muscles begin to lose their ability to
respond to the brain's commands, commands that must be carried through the nerve network. The
brain also receives fewer sensory signals from the rest of the body, resulting in an inability to feel
textures, heat, pain, and other sensations. Alternately, the brain may receive inappropriate signals
that result in tingling, "crawling-skin," or painful sensations. Because the signals to and from the
arms and legs must travel the longest distances they are most vulnerable to interruption.
Therefore, muscle weakness and tingling sensations usually first appear in the hands and feet and
progress upwards.
When GBS is preceded by a viral or bacterial infection, it is possible that the virus has
changed the nature of cells in the nervous system so that the immune system treats them as
foreign cells. It is also possible that the virus makes the immune system itself less discriminating
about what cells it recognizes as its own, allowing some of the immune cells, such as certain
kinds of lymphocytes and macrophages, to attack the myelin. Sensitized T lymphocytes
cooperate with B lymphocytes to produce antibodies against components of the myelin sheath
and may contribute to destruction of the myelin, such as gangliosides GM1 and GD1b,
distributed throughout the myelin in the peripheral nervous system. Most of the pathogens that
are known to cause GBS gain entry to the body through mucosal or gut epithelium. The innate
immune response results in the uptake of the pathogens by immature antigen presenting cells
(APCs). After migration to lymph nodes, a mature, differentiated APC can present peptides in
MHC class II molecules and activate CD4 T cells that recognize antigens from the infectious
pathogen.
In the case of C. jejuni infection, antibodies are produced, leading to activation of the
complement system, and phagocytosis of the bacteria takes place. However, in rare cases the
antibodies produced against certain C. jejuni antigens will also bind to gangliosides of the
nervous tissue, causing complement activation and damage by phagocytes. This results in
damage to peripheral nervous tissues, which leads to demyelination and axonal damage. The
most commonly proposed mechanism for the development of autoimmune disease is molecular
mimicry. Molecular mimicry refers to the situation where the pathogen and host share nearly

identical antigens, which induces an antibody and T-cell immune response that is cross reactive.
There is more than one way in which an immune response can become cross-reactive. The
pathogen and host can have homologous or identical amino acid sequences, or the host B cell
receptors and T cell receptors can recognize non-homologous peptides. The strongest evidence
for the molecular mimicry hypothesis has come from discoveries in research with C. jejuni
strains, the most common pathogen associated with GBS (specifically AMAN).
Medical Management
Diagnostic Procedures
1) Medical History
- For any unusual symptoms experiencing and any recent past illnesses or
infections.
2) Physical Examination
- Muscle Strength and Activity Tests
- Reflex Tests, such as the knee-jerk reaction
3) Spinal Tap/Lumbar Puncture
- Spinal tap, a procedure in which a needle is inserted into the patient's lower back
and a small amount of CSF from the spinal column is withdrawn for study to
check for higher than expected levels of protein in the CSF.
- Result: higher-than-normal levels of protein in their CSF.
4) Electromyography
- A nerve function test that reads electrical activity from the muscles to help the
doctor learn if the muscle weakness is caused by nerve damage or muscle
damage.
- To test the muscles, a needle electrode is inserted into the muscle to give an
electrical recording of muscle activity. This helps determine whether the muscles
respond when certain nerves are stimulated. In GBS, the muscles may not respond
due to nerve damage.
- To test the nerves, a surface electrode (a small, metal disc) is stuck to the skin to
stimulate the nerves with a small electric shock. The response from the nerves
(how quickly the nerves conduct electric signals) is measured. In GBS,
nerve responses may be slower than normal, although the changes may be minor
in the early stages.
Therapeutic Management
There is no known cure for GBS. However, there are therapies that lessen the
severity of the illness and accelerate the recovery in most patients. There are also a
number of ways to treat the complications of the disease.
1) Plasma Exchange (also called Plasmapheresis)
- A method by which whole blood is removed from the body and processed so that
the red and white blood cells are separated from the plasma, or liquid portion of
the blood. The blood cells are then returned to the patient without the plasma,
which the body quickly replaces. The technique seems to reduce the severity and

2)

3)

4)

5)

6)

duration of the GBS episode. This may be because plasmapheresis can remove
antibodies and other immune cell-derived factors that could contribute to nerve
damage.
High-dose Immunoglobulin Therapy
Doctors give intravenous injections of the proteins that, in small quantities, the
immune system uses naturally to attack invading organisms. Investigators have
found that giving high doses of these immunoglobulins, derived from a pool of
thousands of normal donors, to GBS patients can lessen the immune attack on the
nervous system. IVIG is given by infusion into a vein, usually every day for five
days. Each infusion takes about two hours.
Physical Therapy
- Addressing upright tolerance and endurance may be a significant issue during the
early part of physical rehabilitation. Active muscle strengthening can then be
slowly introduced and may include isometric, isotonic, isokinetic, or progressive
resistive exercises to help keep the muscles flexible and strong and to prevent
venous sludging (the buildup of red blood cells in veins, which could lead to
reduced blood flow) in the limbs which could result in deep vein thrombosis
Occupational Therapy
- To promote positioning, posture, upper body strengthening, range of motion
(ROM), and activities that aid functional self-care.
Speech Therapy
- Is aimed at promoting speech and safe swallowing skills for patients who have
significant oropharyngeal weakness with resultant dysphagia and dysarthria.
Respiratory therapy
-

Monitoring for respiratory failure, bulbar weakness, and difficulties with

swallowing help to anticipate complications. Proper positioning of the patient to
optimize lung expansion and secretion management for airway clearance is
required to minimize respiratory complications. Serial assessment of ventilatory
status is needed, including measurements of vital capacity and pulse oximetric
monitoring. Respiratory assistance should be considered when the expiratory vital
capacity decreases to less than 18 mL/kg or when a decrease in oxygen saturation
is noted (arterial PO2 < 70 mm Hg). Tracheotomy may be required in a patient
with prolonged respiratory failure, especially if mechanical ventilation is required
for more than 2 weeks.

7) Nutrition
-

Enteral or parenteral feedings are required for patients on mechanical ventilation

to ensure that adequate caloric needs are met when the metabolic demand is high.

Pharmacologic Management
1) Drug: Immunomodulatory Agents
Indication: These medications are used to improve the clinical and immunologic
aspects of GBS. They may decrease autoantibody production and increase the
solubilization and removal of immune complexes.
-

Intravenous immunoglobulin (Bivigam, Carimune NF, Gammagard S/D,

Gamunex-C, Hizentra, Octagam, Privigen)

2) Drug: Analgesics
Indication: Used for relief of mild to moderate pain and inflammation
-

Acetaminophen (Tylenol, Aspirin Free Anacin, Cetafen, Feverall, Mapap Extra

Strength); Ibuprofen (Motrin, Advil, Neoprofen, Provil); Indomethacin (Indocin);
Naproxen (Naprosyn, Naprelan, Aleve, Anaprox); Diclofenac (Voltaren-XR,
Cataflam, Zipsor, Cambia); Ketoprofen; Celecoxib (Celebrex)

3) Drug: Low Molecular Weight Hepari

Indication: Used in the prophylaxis of deep venous thrombosis (DVT).
- Enoxaparin (Lovenox); Dalteparin (Fragmin); Tinzaparin
4) Drug: Anticonvulsants
Indication: Used to alleviate painful dysesthesias, which frequently accompany
peripheral neuropathies. Although they have many different mechanisms of action,
their use for alleviating neuropathic pain probably depends on their general tendency
to reduce neuronal excitability.
- Gabapentin (Gralise, Neurontin) and Carbamazepine (Carbatrol, Equetro, Epitol,
Tegretol, Tegretol-XR)
Nursing Diagnoses and Possible Interventions
Ineffective breathing pattern related to weakness or paralysis of the respiratory muscles.
Disturbed Sensory perception related to changes in reception and transmission.
Ineffective Tissue perfusion related to autonomic nervous system dysfunction that causes
vascular buildup with decreased venous return.
Impaired physical mobility related to neuromuscular damage.
Imbalanced nutrition less than body requirements related to damage affecting
neuromuscular reflex swallowing and GI function.
Anxiety related to situational crisis.
Pain Acute/Chronic related to neuromuscular damage (paresthesias, disestesia)
Knowledge Deficit related to less remembering, cognitive limitations.

Nursing Interventions:
1. Monitor respiratory status through vital capacity measurements, rate and depth of
respirations, and breath sounds.
2. Monitor level of muscle weakness as it ascends toward respiratory muscles. Watch for
breathlessness while talking which is a sign of respiratory fatigue.
3. Monitor the patient for signs of impending respiratory failure.
4. Monitor gag reflex and swallowing ability.
5. Position patient with the head of bed elevated to provide for maximum chest excursion.
6. Avoid giving opioids and sedatives that may depress respirations.
7. Position patient correctly and provide range-of-motion exercises.
8. Provide good body alignment, range-of-motion exercises, and change of position to
prevent complications such as contractures, pressure sores, and dependent edema.
9. Ensure adequate nutrition without the risk of aspiration.
10. Encourage physical and occupational therapy exercises to help the patient regain strength
during rehabilitation phase.
11. Provide assistive devices as needed (cane or wheelchair) to maximize independence and
activity.
12. If verbal communication is possible, discuss the patients fears and concerns.
13. Provide choices in care to give the patient a sense of control.
14. Teach patient about breathing exercises or use of an incentive spirometer to reestablish
normal breathing patterns.
15. Instruct patient to wear good supportive and protective shoes while out of bed to prevent
injuries due to weakness and paresthesia.
16. Instruct patient to check feet routinely for injuries because trauma may go unnoticed due
to sensory changes.
17. Urge the patient to maintain normal weight because additional weight will further stress
monitor function.
18. Encourage scheduled rest periods to avoid fatigue.

REFERENCES
Book
Hinkle, J.L. and Cheever, K.H. (2014). Brunner & suddarths textbook of medical-surgical
nursing, 13th Edition. Philippines: Lipincott Williams & Wilkins. (pp. 2043-2046).
Timby, B.K. and Smith, N.E. (2005). Essentials of nursing: Care of adults and children.
Philadelphia: Lippincott Williams & Wilkins. (p. 140-141, 521-522).
Internet
Centers for Disease Control and Prevention (October, 2015). Guillain-Barr
syndrome
and
Flu
Vaccine.
Retrieved
November
22,
http://www.cdc.gov/flu/protect/vaccine/guillainbarre.htm.

2015

from

Marquez, C. (November, 2013). Guillain-Barr Syndrome: How Nurses Should Manage.

Retrieved November 22, 2015 from http://rnspeak.com/medical-and-surgicalnursing/guillain-barre-syndrome-nurses-manage/.
NCP Nanda (2012). 10 Nursing Diagnosis for Guillain-Barre Syndrome. Retrieved November
22, 2015 from http://www.ncpnanda.top/2012/10/10-nursing-diagnosis-for-guillainbarre.html.
Nursing Care Plan (2014). Guillain-Barre Syndrome Care Plan Nursing. Retrieved November 22,
2015 from http://nursing-care-plan.blogspot.com/2014/07/guillain-barre-syndrome-careplan.html.
Patient Education Institute (2015). Reye Syndrome. Retrieved November 22, 2015 from
http://www.kaahe.org/en/ArabicSampleModules/modules/infectd/idgo01a1/idgo0101/idg
o0101.pdf.
Weiner, D. L. ( April, 2015). Reye Syndrome. Retrieved November 22, 2015 from
http://emedicine.medscape.com/article/803683-overview.