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 antibody-

mediated 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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DUNBAR CASE STUDIES

Ropper, A., & Samuels, M. (2009). Adams and victor’s principles of neurology (9th ed.). New

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Simon, D., & Palese, M. (2009). Clinical update on the management of adrenal hemorrhage.

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