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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 1 DUNBAR CASE STUDIES 2 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 DUNBAR CASE STUDIES 3 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 DUNBAR CASE STUDIES 4 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). DUNBAR CASE STUDIES 5 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. DUNBAR CASE STUDIES 6 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 DUNBAR CASE STUDIES 7 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 DUNBAR CASE STUDIES 8 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 DUNBAR CASE STUDIES 9 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). DUNBAR CASE STUDIES 10 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 DUNBAR CASE STUDIES 11 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 DUNBAR CASE STUDIES 12 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). DUNBAR CASE STUDIES 13 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 DUNBAR CASE STUDIES 14 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). DUNBAR CASE STUDIES 15 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. DUNBAR CASE STUDIES 16 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). DUNBAR CASE STUDIES 17 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. DUNBAR CASE STUDIES 18 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 DUNBAR CASE STUDIES 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). 19 DUNBAR CASE STUDIES 20 References Brunicardi, C., Anderson, D., Billiar, T., Dunn, D., Hunter, J., Matthews, J., & Pollock, R. (2010). Schwartz’s principles of surgery (9th ed.). New York, NY: McGraw Hill Companies. Butterworth, J., Mackey, D., & Wasnick, J. (2013). 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Pocket guide to diagnostic tests (6th ed.). New York, NY: McGraw Hill Companies. Papadakis, M., McPhee, S., & Rabow, M. (2013). Current medical diagnosis and treatment (52nd ed.). New York, NY: McGraw Hill Medical. DUNBAR CASE STUDIES Ropper, A., & Samuels, M. (2009). Adams and victor’s principles of neurology (9th ed.). New York, NY: McGraw-Hill Companies. Simon, D., & Palese, M. (2009). Clinical update on the management of adrenal hemorrhage. Current Urology Reports, 10, 78-83. doi: 10.1007/s11934-009-0014-y 21