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Running head: DUNBAR CASE STUDIES
Dunbar: Case Study Three and Four
Whitney L. Dunbar
Wright State University
Nursing 7202
November 18, 2013
Dr. Kristine Scordo
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Dunbar: Case Study Three and Four
Case Study Three
1. Which of the following processes can produce postoperative hypotension? Explain your
rationale. Bold the correct answer.
A. Hypovolemia secondary to blood or fluid loss
B. Sepsis
C. Adrenal insufficiency
D. Perioperative myocardial infarction
E. All of the above
All of the above processes can produce postoperative hypotension and should be
considered for this patient. Each process will be discussed why it is a potential cause for this
patient.
Hypovolemia secondary to blood or fluid loss is a potential cause for this patient’s
hypotension due to her recent intrabdominal surgery. Fluid therapy during perioperative consists
of replenishing maintenance necessities, replacing preexistent fluid deficits, and replacing fluid
loss from the surgical wound. Also, it is important to estimate blood loss from surgery and to
replace deficits with crystalloids or colloids unless a transfusion is necessary for severe anemia.
Also, evaporative loss in intrabdominal surgery is substantial due to the size of the wound and
exposure of the surface area. The length of the surgical procedure is comparative to the
evaporative losses and why it is important for the duration of the surgery to be documented.
Significant intravascular reduction and substantial fluids shifts can be caused from internal
redistribution of fluids, third-spacing. Third-spacing from traumatized, inflamed, or infected
tissue can separate a great amount of fluid in the interstitial space and move the fluid through the
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serosal surfaces or into bowel lumen. Clinical manifestations of hypovolemia consist of poor
skin turgor, dehydration of mucous membranes, weak peripheral pulses, tachycardia and low
blood pressure, and decreased urine output (Butterworth, Mackey, & Wasnick, 2013). This
patient does exhibit sinus tachycardia with low blood pressure and her hypovolemia could be
caused from receiving inadequate intraoperative fluid replacement.
Sepsis is a possible cause for hypotension in this patient. Sepsis entails the incidence of
an infection and the systemic inflammatory response. The criteria for sepsis includes a
temperature above 38 degrees Celsius or below 36 degrees Celsius, heart rate greater than 90
beats per minute, respiratory rate more than 24 breaths per minute, white blood cell count greater
than 12,000 mm3, less than 4,000 mm3, or more than 10% bands. A patient needs to exhibit two
or more of the previous conditions and has a source of infection. Additional clinical
manifestations are hypotension, altered mental status, hot and flushed skin, edema, and a
decrease in urinary output. Surgical wounds, central venous catheters, pneumonia, and foley
catheters are all potential sources for postoperative infections for surgical patients (Brunicardi et
al., 2010; Longo et al., 2012).
Adrenal insufficiency is a potential cause for hypotension in this patient. Adrenal
insufficiency can be primary or secondary from trauma, surgery, or infection from acute stress.
It is described as no myocardial or vascular response to catecholamines with hypovolemic shock.
Adrenal insufficiency lacks cortisol and cortisol sustains homeostasis of the cardiovascular
system, particularly when there is stress on the body. A deficiency of cortisol leads to a decrease
in myocardial contractility and systemic vascular resistance. The diagnosis can be missed
postoperatively because there are no specific signs and symptoms for secondary adrenal
insufficiency. Treatment typically includes the administration of intravenous corticosteroids and
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multiple liters of isotonic saline. An adrenocorticotropic hormone stimulation test can aid in
confirming the diagnosis of adrenal insufficiency. This is a potential diagnosis for this patient
since she had recent surgery and currently has hypotension (Miller & Pardo, 2011).
Perioperative myocardial infarction should be considered as a possible cause for this
patient’s hypotension. Patients can acquire acute coronary syndrome from a separation of plaque
due to physiologic stress and increased levels of catecholamines from surgery. Also, an inequity
between myocardial oxygen supply and demand from an increased heart rate, low or high blood
pressure, anemia, or hypoxemia can cause subendocardial ischemia in patients with coronary
disease. Anesthesia can be a causative influence because it can lead to hypotension and
decreased cardiac output. Clinical manifestations can include low blood pressure, dyspnea, or
signs of congestive heart failure (McKean, Ross, Dressler, Brotman, & Ginsberg, 2012). A
preoperative cardiac assessment should be completed prior to surgery for patients who will be
having noncardiac surgery in order for proper intraoperative treatment. A patient with cardiac
risk factors should be placed on a cardiac monitor postoperatively to monitor for
electrocardiogram changes (Miller & Pardo, 2011).
2. Which of the following is the most appropriate method to diagnose BMAH? Explain
your answer.
A Cortrosyn stimulation test
B. CT scan of adrenal glands
C. CT scan of adrenal glands and Cortrosyn stimulation test
D. Random plasma cortisol level
A cortrosyn stimulation test and a computed tomography (CT) scan of the adrenal glands
are the most appropriate methods to diagnose a bilateral massive adrenal hemorrhage (BMAH).
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A cortrosyn stimulation test is an appropriate method to assess for primary adrenal insufficiency.
The test starts with obtaining a baseline serum cortisol level. Then cosyntropin, a synthetic
adrenocorticotropic hormone (ACTH), 250 mcg intravenous (IV) is administered to the patient.
A serum cortisol level should be drawn thirty and sixty minutes after the administration of IV
cosyntropin. It is considered a normal response if the serum cortisol level doubles the baseline
serum cortisol value or increases in an increment of 7 mcg/dL to a peak level above 18 mcg/dL.
A peak serum cortisol level below 18 mcg/dL, a poor cortisol response to cosyntropin, is
indicative of adrenal insufficiency (Nicoll, Mark Lu, McPhee, & Pignone, 2012). An ACTH
level should be obtained to distinguish primary adrenal insufficiency from secondary adrenal
insufficiency. An elevated ACTH level indicates primary adrenal insufficiency and a normal or
decreased ACTH level indicates secondary adrenal insufficiency (McKean et al., 2012).
Patients with primary adrenal insufficiency should have a CT of the adrenal glands
implemented to assess for potential hemorrhage, BMAH. The most frequent imaging test
acquired for adrenal hemorrhage is a CT of the adrenal glands. An adrenal hematoma can vary
in appearance on a CT due to age of the patient and the hematoma. A round or oval mass at the
location of the adrenal gland illustrates an adrenal hemorrhage on the CT scan. Periadrenal
stranding is frequently observed on the CT scan. Also, high attenuation is seen on the CT scan
with acute and subacute hematomas (Simon & Palese, 2009).
A random plasma cortisol level is not an appropriate method to diagnose a patient with
BMAH. This value is limited because baseline serum cortisol levels can be inadvertently
decreased from physiological diurnal rhythm of cortisol secretion (Longo et al., 2012).
3. Which of the following can occur in patients with primary adrenal insufficiency?
Explain your answer.
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A. Electrolyte abnormalities
B. Hypotension
C. Mental status changes
D. Abdominal pain
E. All of the above
Electrolytes abnormalities, hypotension, mental status changes, and abdominal pain can
all occur in patients with primary adrenal insufficiency. Electrolyte abnormalities include
hyponatremia and hyperkalemia due to mineralocorticoid deficiency. The primary
mineralocorticoid produced is aldosterone. The role of aldosterone is to escalate sodium
reabsorption and potassium elimination in the distal tubule and the collecting duct in the kidney.
This is important in regulating the overall Na+ mass and continuing blood pressure. Therefore,
when there is a deficiency in aldosterone it leads to a decrease in potassium secretion and causes
hyperkalemia. Also, a deficiency in aldosterone leads to salt wasting and causes hyponatremia
since there is no increase in sodium reabsorption. Hypotension is due to a glucocorticoid and
mineralocorticoid deficiency. These deficiencies result in a decrease in myocardial contractility,
decreased responsiveness to catecholamines, and hypovolemia with hyponatremia. Mental status
changes occur from hyponatremia and hypotension. Abdominal pain occurs from glucocorticoid
deficiency. Patients with primary adrenal insufficiency may present with anorexia, weight loss,
nausea, vomiting, and salt craving (McKean et al., 2012; Molina, 2013).
4. Which of the following is not a risk factor for developing BMAH? Explain your
rationale.
A. Postoperative state
B. Coagulopathy
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C. Thromboembolic disease
D. Diabetes
E. Sepsis
Diabetes is not a risk factor for developing BMAH. Postoperative state, coagulopathy,
thromboembolic disease, and sepsis are all risk factors for the development of BMAH (Simon &
Palese, 2009).
Sepsis and the postoperative state increase the risk for the development of BMAH due to
the stress on the patients body. Other stressful situations related to adrenal hemorrhage consist
of hypotension, pregnancy, burns, and giving exogenous steroids or ACTH. The pituitary gland
secretes ACTH when the body is enduring stress and an elevated ACTH level stimulates the
expulsion of catecholamines. There is an escalation of blood flow to the adrenal gland due to the
increase levels of catecholamines and this leads to a rising secretion of glucocorticoids.
Increased pressure inside the adrenal vein during stress is an outcome from the combination of
elevated arterial flow and vasoconstriction of the adrenal vein caused by the increase in
catecholamines. The increase pressure of the adrenal vein can potentially result in adrenal
hemorrhage. Specifically, Waterhouse-Friderichsen syndrome is correlated with adrenal
hemorrhage. Other organisms associated with sepsis and adrenal hemorrhage consist of
Pseudomonas infection, Proteus bacteremia, Escherichia coli, Staphylococcus aureus, and
Klebsiella species. Septic patients have a greater risk by six-fold for developing adrenal
hemorrhage. Also, patients who are septic with low blood pressure or disseminated intravascular
coagulation have a greater risk for developing adrenal hemorrhage (Simon & Palese, 2009).
Coagulopathies are risk factors for developing BMAH. BMAH is frequently linked to
the use of anticoagulants, for example, heparin. The administration of an anticoagulant in the
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acute illness setting can increase the risk for bleeding and possibly lead to BMAH. Also, BMAH
has been observed in situations with heparin-induced thrombocytopenia (HIT). A patient
diagnosed with HIT has an increased risk for developing a thromboembolism and a decrease in
platelet count because the stimulation of heparin factor four antibodies causes platelet
accumulation and activation. Therefore, a thrombus could evolve in the central adrenal vein with
the presence of HIT and lead to BMAH. Patients who are administered heparin for more than six
days have an increased risk for developing BMAH compared to patients who do not receive
heparin. Also, patients with thrombocytopenia have a 15 times increased risk for developing
BMAH compared to patients without thrombocytopenia (Simon & Palese, 2009).
Thromboembolic disease is a risk factor for the development of BMAH in a patient.
Particularly, patients who have existing antiphospholipid antibodies or lupus anticoagulant have
an increase risk for BMAH. It is believed these patients have an increase likelihood for
developing an adrenal vein thrombosis and then leads to BMAH. Patients who endure high
stressful conditions or receive anticoagulant medication and have existing antiphospholipid
antibodies or lupus anticoagulant have a higher risk for BMAH (Simon & Palese, 2009).
5. Which of the following statements regarding the long-term management of patients with
BMAH is correct? Explain your answer.
A. Glucocorticoid therapy is needed only during acute illnesses
B. Patients should be discharged on maintenance doses of oral glucocorticoids and
mineralocorticoids
C. Patients do not need mineralocorticoid therapy
D. Adrenal function is likely to recover over four to six months with no further need for
glucocorticoids
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Oral glucocorticoids and mineralocorticoids should be continued for long-term
management when a patient with primary adrenal insufficiency secondary to BMAH is
discharged. Typically, these patients do not regain complete adrenal function and need steroids
for life. Classically, glucocorticoid replacement therapy is 10 to15 mg of oral hydrocortisone
administered after waking up in the morning and 5 to 10 mg administered six to eight hours later
in the evening. The treatment is ordered to imitate the circadian cortisol secretion. The diurnal
cortisol production of 8 to 12 mg/m2 is comparable to the total everyday dose of 15 to 25 mg oral
of hydrocortisone. Prednisolone and dexamethasone are both long-acting glucocorticoids and
can be prescribed for patients who experience fatigue in the afternoon or who are inefficiently
adherent to the hydrocortisone regimen. Healthcare providers assess a patient clinically for the
sufficiency of glucocorticoid treatment. A patient with adequate glucocorticoid replacement
treatment will exhibit a sense of well-being and a satisfactory appetite. A diminished sense of
well-being will display under treatment. Extreme weight gain, characteristics of Cushing
syndrome, and osteoporosis are clinical manifestations of over treatment of glucocorticoids.
Also, mineralocorticoids need to be replaced in patients with primary adrenal insufficiency.
Fludrocortisone is an effective synthetic mineralocorticoid and is usually initiated at 0.1 mg
orally a day. The dose range is 0.05 to 0.2 mg a day orally and is administered in the morning.
Edema, hypertension, and hypokalemia are signs a patient displays when too much
mineralocorticoid therapy is replaced. The healthcare provider can evaluate the adequacy of
mineralocorticoid replacement therapy by monitoring and assessing the patients blood pressure
and serum electrolyte composition (Gardner, Shoback, & Greenspan, 2011; McKean et al.,
2012).
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Case Study Four
A 52 year old male presents to the emergency department (ED) by emergency medical
service (EMS) with a five day history of progressive limb weakness, numbness and tingling, and
diffuse aching pain. The feelings of pins and needles began in his toes and fingertips of both
hands and feet and have progressed to his wrists and ankles over the last five days. The aching
pain and limb weakness started in his hands and feet four days ago but have advanced to his hips,
back, and shoulders. This morning he was unable to get out of bed without assistance from his
wife and unable to hold a fork to feed himself. His wife tried to feed him breakfast but he could
only chew a couple bites because he was having trouble swallowing. His wife called 911. Upon
arrival he denies fever, chills, dizziness, vitiligo, diarrhea, constipation, chest pain, shortness of
breath. He did state the last time he urinated he felt a sense of incomplete voiding and hesitancy.
He has no past medical history except two weeks ago he was diagnosed with an upper respiratory
tract infection by his primary care physician. His upper respiratory tract infection symptoms
were resolved one week prior to neurological changes.
Physical examination reveals a body temperature of 99.8 degrees Fahrenheit, heart rate of
112 beats per minute, blood pressure of 152/72 mmHg, respiratory rate of 22 breaths per minute,
and pulse oximetry of 97% on room air. He is in no acute distress. He has S1 and S2 present
with a regular rhythm and without murmurs, gallops, rubs, or clicks. Lungs are clear to
auscultation bilaterally with symmetrical expansion. Pulses are two plus in all extremities.
Abdomen has hypoactive bowel sounds without palpable organomegaly or masses. Skin warm,
dry, and intact without rashes or lesions. Muscle strength 3/5 in bilateral lower and upper
extremities. Right and left Achilles reflexes are graded a zero. Bilateral patellar, bicep,
brachioradialis, and tricep reflexes are all graded one. Pupils are equal, round, and reactive to
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light with both pupils at 4 mm. Right eyebrow and right corner of mouth have a slight droop
with smoothing of the forehead. The basic metabolic panel, arterial blood gas, and complete
blood cell count are unremarkable. A non-contrast head CT scan reveals no acute process. The
electrocardiogram displays normal sinus tachycardia rhythm without ST-T wave abnormalities.
1. What are the differential diagnoses? Explain.
First, Guillain-Barre Syndrome (GBS) is a highly suspected diagnosis for this patient.
Typically, GBS is a monophasic immune-mediated illness of the peripheral nervous system with
a critical onset. Usually, a gastrointestinal or upper respiratory infection precedes the start of
GBS by 14 days. Also, immunization and surgery have been linked to GBS. This patient had an
upper respiratory tract infection two weeks before the start of his neurological symptoms. The
symptoms of GBS start quickly with distal and comparatively symmetrical paraesthesias and
trailed by progressive weakness of the limbs. A classic clinical manifestation of GBS includes
ascending paralysis. Ascending paralysis is where the weakness begins in the hands and feet,
travels towards the trunk, and is symmetrical. Facial or pharyngeal weakness can be observed in
patients with GBS. The phrenic nerve can be affected in patients with GBS and can cause
diaphragmatic weakness. Mechanical ventilation is needed in around one-third of hospitalized
patients with GBS because of oropharyngeal or respiratory weakness. About half of the patients
with GBS experience pain. A usual autonomic nervous system dysfunction a patient with GBS
experiences is tachycardia. A patient with GBS may experience hypertension, arrhythmias,
hypotension, gastrointestinal dysmotility, and urinary retention. Patients can have areflexia or
hyporeflexia on physical examination. Approximately, 90% of patients with GBS advance to
clinical nadir by four weeks and become non-ambulatory during the ailment. This patient
presents with a five-day history of progressive limb weakness, numbness and tingling, and
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diffuse aching pain. His symptoms began distally and progressed symmetrically and ascending.
He has dysphagia, facial weakness, urinary retention, inability to ambulate without assistance,
sinus tachycardia, and hypertension. His clinical manifestations correlate with GBS (Meena,
Khadilkar, & Murthy, 2011; Ropper & Samuels, 2009).
Myasthenia gravis (MG) is a potential diagnosis for this patient. MG is an autoimmune
neuromuscular disorder described by variable muscle weakness and fatigability. An antibodymediated autoimmune attack reduces the amount of accessible acetylcholine receptors at
neuromuscular junctions. There is an increase incidence in women in their twenties and thirties
and men in their fifties and sixties. The muscle weakness enhances late in the day or with
recurrent use. The weakness can improve after sleep or rest. Systemic disorders or infections
can cause augmented myasthenic weakness and can precipitate crisis. Clinical manifestations
include dysphagia, dysarthria, and pins and needles sensation. Limb weakness occurs proximal
to distal and can be asymmetrical. Deep tendon reflexes are present even with muscle weakness.
Patients with MG may have weakness of the eyelid and extraocular muscles. These patients may
present with diplopia and ptosis. Crisis occurs when the patient needs mechanical ventilation
due to the severity of respiratory muscle. Crisis can happen suddenly to a patient with MG. This
patient did have an upper respiratory tract infection preceding his neurological symptoms.
Corresponding clinical manifestations of MG include the patient being a male in his fifties and
presents with muscle weakness, dysphagia, and pins and needles sensation. He could have MG
leading to myasthenic crisis. However, his symptoms are symmetrical and start distally. Also,
he currently has no visual complaints and there were no abnormalities on eye examination
(Longo et al., 2012).
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Another potential diagnosis for this patient is botulism. Botulism is a food-borne ailment
produced by the exotoxin Clostridium botulinum. Botulism usually occurs from the ingestion of
bacteria from in home-preserved canned products, vegetables, and home-cured ham. Clinical
manifestations evolve over two to four days and begin 12 to 36 hours after ingestion of the
contaminated food. At the neuromuscular synapse from the peripheral nervous system the toxin
inhibits the release of acetylcholine. Clinical manifestations of botulism can include nausea,
anorexia, vomiting, diplopia, blurred vision, hoarseness, dysphagia, nasality of voice, failure to
phonate, and dysarthria. Pupils can be unreactive to light and accommodation is usually absent.
After this clinical manifestations patients with botulism experience progressive weakness of the
muscles of the neck, limbs, and face. This progressive muscle weakness can lead to respiratory
failure. Deep tendon reflexes can be absent in patients with severe generalized weakness.
However, the gag reflex is still intact. Also, sensation stays intact. A patient can stay awake and
alert during the illness unless severe anoxia acquires from respiratory failure (Ropper &
Samuels, 2009). This patient has some correlating clinical manifestations associated with
botulism and his symptoms occurred over five days. However, he denies gastrointestinal
symptoms and there are no eye abnormalities.
Cervical myelopathy is a possible diagnosis for this patient and is an outcome from
pathologic degeneration of the cervical spine. The degeneration begins at the intervertebral disc.
Eventually, it can lead to compression of spinal components at the root or cord level. Typically,
patients present with subtle complaints. Patients usually experience an expected step-wise
progression over weeks to years. A patient may report clumsiness of their hands and having a
difficult time feeding themself or getting dressed. Also, the patient may struggle with balance
and gait. Physical examination can detect hyperreflexia and pathologic reflexes indicating an
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upper motor neuron lesion, distal muscle weakness, and motor weakness. This patient presents
with distal muscle weakness and is unable to feed himself. However, his clinical manifestations
began and progressed in less than a week (McKean et al., 2012).
2. What tests should the healthcare provider order to diagnose Guillain-Barre Syndrome?
Explain your rationale.
A lumbar puncture for cerebral spinal fluid (CSF) examination and electrodiagnostic
(EDX) testing should be implemented to diagnose GBS. The CSF protein concentration is
elevated without a rise in white blood cells in over 90% of patients with GBS at the peak of the
ailment. However, these abnormal findings of the CSF analysis are only found in 50% of GBS
patients in the first few days of illness. The CSF protein level is more than 50 mg/dL. It is
believed the rise in CSF protein reflects the widespread inflammatory condition of the nerve
roots. The CSF is either acellular or has a small amount of lymphocytes. The CSF has a normal
opening pressure. A different or an additional disease process should be considered if there is
persistent pleocytosis in CSF examinations. The EDX testing consists of an electromyogram and
nerve conduction studies. EDX testing will usually display temporal dispersion, slowed
conduction velocity, conduction block, a decrease in the amplitude of muscle action potentials,
prolonged distal and F-wave latencies in patients with GBS. Prolonged distal muscle action
potential latencies and temporal dispersion are more frequently observed in the beginning of
GBS. Also, the H reflex is usually absent or very delayed. Another EDX finding for GBS is a
sural sparing pattern. Sural sparing occurs when there is a normal sural sensory nerve reaction
when there are atypical upper extremity sensory nerve outcomes. The sural sparing pattern is
very rare in other neuropathies (Meena et al., 2011; Ropper & Samuels, 2009).
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Along with these two tests, clinical assessment is a requirement for the diagnosis of GBS.
A patient should display progressive weakness of lower and uppers limbs in four weeks with
areflexia or hyporeflexia. A basic metabolic panel, complete blood counts, CT scan of the spine
may be completed to rule out other differential diagnoses. Magnetic resonance imaging may
display enhancement of the cauda equina nerve roots from gadolinium (Ropper & Samuels,
2009).
3. What electrolyte should be closely monitored in GBS patients? Explain your rationale.
Hyponatremia is the usual electrolyte abnormality in patients with GBS and should be
closely monitored. Clinical manifestations of hyponatremia include lethargy, nausea, headache,
and disorientation. Serious clinical manifestations can occur if hyponatremia is left untreated
and include seizure, respiratory arrest, coma, brainstem herniation, permanent brain damage, and
death. A percentage of GBS patients develop hyponatremia after the first week of neurological
symptoms. Hyponatremia is usually due to syndrome of inappropriate antidiuretic hormone
(SIADH) but can be attributed to natriuresis. Central nervous system disorders, including GBS,
are the main causes of SIADH. It is more predominant in GBS patients who are receiving
mechanical ventilation because positive end expiratory pressure can also cause SIADH. SIADH
and natriuresis receive different treatment. Therefore, a central venous pressure should be
measured since it is the best way to distinguish the two conditions. A GBS patient with SIADH
requires sodium replacement and fluid restriction. A GBS patient with natriuresis needs sodium
replacement and intravascular volume expansion (Meena et al., 2011; Papadakis, McPhee, &
Rabow, 2013; Ropper & Samuels, 2009).
4. What is the appropriate therapy for a patient diagnosed with GBS? Include all types of
therapy and rationale for your choices.
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The appropriate therapy for patients with GBS patients can vary. It depends on the
progression of the disease, when GBS is recognized, and when the patient receives treatment for
GBS. Patients who are able to walk five meters without assistance can be managed at outlying
centers. GBS patients who are in the first week of onset of neurological symptoms need to be
closely monitored for progression of the disease. GBS patients should be transferred to the
intensive care unit at specialized centers if a patient displays signs of respiratory failure, ileus, or
heart rate and blood pressure variations. These patients need to be placed on a continuous
cardiac monitored. GBS patients should be monitored for urinary tract infections, pneumonia,
and septicemia. This patient should be admitted to the intensive care unit at a specialized center.
Therapies for patients with GBS include management of respiratory failure, dysautonomia, deep
vein thrombosis prophylaxis, analegesia, nutrition, immunotherapy, and other therapies (Meena
et al., 2011).
Management of respiratory failure is vital since one third of GBS patients require
mechanical ventilation. Respiratory failure can be anticipated when the GBS patient has an
increase heart and respiratory rate, asynchronous actions of abdomen and chest, maximal
inspiratory pressure less than 30 mm H2O, vital capacity less than 20 mL/kg, and a maximal
expiratory pressure less than 40 cm H2O. Additional factors associated with respiratory failure
Respiratory failure is likely to occur when bulbar paresis, neck weakness, and facial weakness
present within a week of onset neurological symptoms. Typically, weaning from ventilator
support takes two to six weeks. A tracheostomy should be considered at two week after oral
intubation. A healthcare provider can wait an additional week to wean from the ventilator if the
patient has improvement in pulmonary function (Meena et al., 2011).
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Management of dysautonomia is important because acute dysautonomia is a significant
reason for death in GBS patients. Patients may display hypertension, tachycardia, and postural
hypotension from too much sympathetic over activity and parasympathetic under activity. Most
GBS patients experience tachycardia with a heart rate of 100 to 120 beats per minute. One third
of GBS patients have hypertension and if the mean arterial pressure is more than 125 mmHg an
antihypertensive with a short half-life should be administered since GBS patients can have labile
blood pressures. Labetalol, nitroprusside, or esmolol infusions are examples of an
antihypertensive with a short half-life. Sustaining intravascular volume with intravenous
infusions of 0.9 sodium chloride and vasopressors for short durations and not administering
diuretics are recommended to manage hypotension. The healthcare provider should explore for
other causes if the patient continues to have persistent hypotension. Approximately, 15% of
GBS patients develop gastrointestinal disorders. Nasogastric suctioning, neostigmine or
erythromycin, and stopping enteral feeds can efficiently manage dysmotility (Meena et al.,
2011). Also, bladder dysfunction may occur in GBS patients and should initially be managed to
prevent over-distention. A foley catheter may be inserted if the GBS patient is hemodynamically
unstable to monitor urine output (Ropper & Samuels, 2009).
Deep vein thrombosis prophylaxis management is important to implement in GBS
patients until they are able to walk independently. Patients should be administered subcutaneous
unfractionated or fractionated heparin and support stockings. Coumadin should be initiated in
patients who are anticipated to be bedridden for an extended period of time and has already
received a tracheostomy (Meena et al., 2011).
Pain management is important to implement since many GBS patients experience pain
during the disease process. Opioid analogues are effective for GBS patients experiencing pain.
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Gabapentin, tricyclic antidepressants, non-steroidal anti-inflammatory drugs, and carbamazepime
are other drugs that could be useful for GBS patients. Decrease in bowel motility and sedation
should be monitored (Meena et al., 2011).
Managing nutrition is important in GBS patients. Gastric or nasogastric tube feeding
should be started early and at a lower rate. It is recommended to place these patients on a high
energy and high protein diet to decrease muscle wasting and help with respiratory weaning.
GBS patients tolerate continuous enteral feeding better than bolus feeding (Meena et al., 2011).
Immunotherapy is effective in GBS patients when it is administered within the first few
weeks of illness. Plasmapheresis and intravenous immunoglobulins (IVIg) are both effective
immunotherapies. Immunotherapy should definitely be given to patients if treated within the
first two weeks from beginning of weakness and who are incapable to independently walk.
Plasma exchange has been observed to decrease the risk of progressing respiratory failure. There
is no establishment on the number of plasma exchanges and volume of plasma removed for GBS
patients. Typically, 200 to 250 mL/kg of plasma is exchanged over seven to ten days. In order
to greatly decrease the circulating immunoglobulin complexes more than two plasma exchanges
are needed. Patients with GBS benefit more from continuous flow plasma exchange and
albumin as the exchange fluid than intermittent flow exchanges and fresh frozen plasma. IVIg
has been observed to be just as efficient as plasma exchange in GBS patients. IVIg has become
the preferred immunotherapy in several medical centers because it has a greater convenience and
availability. The regimen for IVIg is 0.4 g/kg bodyweight daily for five days in a row (Meena et
al., 2011).
There are other therapies and interdisciplinary team members that need to be involved in
patients with GBS. Speech therapy needs to evaluate patients who have dysphagia. Physical and
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occupational therapy can assist with range of motion exercises, proper positioning, mobility
skills, and active muscle strengthening. Patients may need to be transferred to a rehabilitation
center after being discharged from the hospital. Also, a social worker and care coordinator can
collaborate with the healthcare provider and family with discharging the patient to a suitable
facility (Longo et al., 2012).
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