Winter 2014 Adult Acute Care Bulletin

Winter 2014 Adult Acute Care Bulletin

Keith Lamb, RRT-ACCS
Adult Critical Care Supervisor
UnityPoint Health System
Des Moines, IA

Joe Hylton, RRT-NPS, CPFT

Brady Scott, MS, RRT-ACCS
Clinical Education Coordinator and Assistant Professor
Department of Respiratory Care
Rush University Medical Center
Chicago, IL

Specialty Practitioner of the Year: Tom Gillin, BS, RRT

Keith Lamb, RRT-ACCS

The section was pleased to present its 2013 Specialty Practitioner of the Year award to Tom Gillin, BS, RRT. Tom received the award at AARC Congress 2013 in Anaheim last November.

A respiratory therapist with Christiana Care Health System since 1999, Tom has taken a leadership role within the department, focusing most of his energy on critical care, most recently surgical critical care. As a surgical critical care specialist, he spends the majority of his time at the bedside taking care of some of the sickest patients in Delaware and the surrounding areas. According to his fellow therapists, he has certainly impacted outcomes and the community owes him thanks.

They also believe Tom exemplifies what it means to be a respiratory therapist. He never avoids an opportunity to teach or learn, and is respected by all. He has led a team of critical care professionals to rewrite the meaning of autonomy and therapist-led respiratory critical care.

Twice named Trauma Practitioner of the Year by the department of trauma and surgical critical care, Tom is a true leader at the bedside and beyond, and we congratulate him on being named our 2013 Specialty Practitioner of the Year.


Neurally Adjusted Ventilatory Assist: A Brief Overview

Hana Alsomali, Respiratory Care Graduate Student, and J. Brady Scott, MSc, RRT-ACCS, Rush University, Chicago, IL

Patient-ventilator asynchrony is a very common issue in patients who are spontaneously breathing with assisted ventilation. New ventilator modes and features focusing on the patient-ventilator interaction aim to improve synchronization. Neurally adjusted ventilatory assist (NAVA) is an example of a mode designed to address asynchrony. NAVA improves synchronization by improving how quickly the ventilator detects and responds to the patient’s spontaneous efforts.1,2

Principle of operation

NAVA improves patient-ventilator synchrony by optimizing ventilator response time. Instead of responding to airway pressure or flow changes in the circuit, NAVA responds to the electromyography activity of the diaphragm. The electrical activity of the diaphragm (EAdi) is sensed through the use of a special nasogastric tube designed with several electromyography (EMG) electrodes located near its distal end. Transmitting the signal directly from the diaphragm to the ventilator reduces the ventilator’s response time and thus improves patient-ventilator synchrony.1

The mechanical inflation with NAVA is triggered when the electrical activity of the diaphragm  signal is more than the set threshold, which often is 0.5 microvolts.3 The clinician sets the NAVA level, which is the amount of pressure delivered per microvolt of diaphragm EMG activity. The pressure delivered during inspiration is the product of the preset NAVA level (cm H2O/microvolt) and the EAdi signal (microvolt) exerted by the patient.1,3 Therefore, by using NAVA the ventilator provides a portion of the ventilatory effort while the patient provides the remainder.

During inspiration, as the diaphragm EMG activity increases, the delivered pressure also increases, and as the diaphragm relaxes and its EMG activity decreases, pressure decreases.1 Thus, the mechanically-assisted breath delivered is proportional to the neural activity as detected by the EAdi signal. The delivered tidal volume varies according to the EAdi signal changes. This pattern results in a breath volume and duration that are consistent with the volume and duration of the neural respiratory cycle. During NAVA, the mechanically assisted breath cycles into exhalation and the expiratory valve opens when 40-70% of the peak EAdi signal is reached.3

In addition to the EAdi as a trigger mechanism during NAVA, the ventilator’s conventional pneumatic triggering mechanisms are still functional; thus triggering is by a first-come, first-served principle. If an EAdi signal is not sensed due to dislocation of the nasogastric tube, the ventilator switches to a pressure support mode as a backup strategy. Additionally, if the patient stops exerting spontaneous breathing efforts the ventilator will switch to a pressure controlled ventilation mode as a second backup strategy.3

Setting the NAVA level: the empirical titration method

As mentioned previously, the clinician sets the NAVA level, which is the amount of pressure delivered per microvolt of diaphragm EMG activity.1,3 In order to set an appropriate NAVA level, the clinician may perform an empirical titration procedure by gradually increasing the amount of ventilator assist. There are three different phases in the empirical titration method: under-assist, adequate assist, and over-assist. This is where the clinician’s knowledge and experience becomes important; by recognizing these different phases an appropriate level of support will be selected.3

Patients with respiratory insufficiency who are ventilated with an inappropriately low NAVA level causing an inadequate pressure increase will result in respiratory demand not being met. These patients will demonstrate a rapid shallow breathing pattern clinically. The respiratory center will increase the intensity of the neural output, causing high EAdi signals, which implies respiratory distress.3

When the clinician increases the NAVA level progressively, the delivered inspiratory pressure increases and the amplitude of the EAdi signal gradually decreases until it reaches a plateau and results in a constant tidal volume. This has been termed the comfort zone, which suggests the delivered minute volume meets the patient’s respiratory demand and the respiratory muscles are maximally unloaded.3

When the NAVA level is increased above the comfort zone, the inspiratory pressure excessively increases and the amplitude of the EAdi decreases further below the plateau level reached in the comfort zone. There will also be an increase in the tidal volume. This occurrence has been termed the zone of overcompensation. The resulting high pressures in this zone could create over distention of the lungs and ventilator-induced lung injury.3

While this method is described in the literature, it is not the only one used clinically. At this time, the perfect method to set NAVA is not known.

NAVA versus conventional gas delivery

In volume control ventilation (VCV), when the patient is not exerting any effort a certain amount of pressure is exerted when the tidal volume is delivered. As the patient increases his inspiratory effort, the ventilator pressure will decrease. In VCV, despite the inspiratory effort exerted by the patient, a fixed flow and volume will be delivered.

The airway pressure remains constant in pressure modes of ventilation regardless of the patient’s effort. The volume and flow delivered during pressure modes depends upon the patient’s airway resistance and compliance. An increased effort results in increased volume delivery.

In comparison to the aforementioned modes, when using NAVA the delivered ventilator pressure and volume vary directly with patient effort. As the patient effort increases, the delivered ventilator pressure and volume will increase; conversely, as the patient effort decreases the ventilator pressure and volume will decrease.1,4

NAVA versus pressure support

Unlike NAVA, pressure support ventilation (PSV) requires the clinician to manually set and frequently assess the level of support, inspiratory rise time, and point of cycling. Even though this has advantages, such as control of the breathing pattern, it can lead to over or under assisting of the patient as the ventilatory demand, muscle strength, and other physiological factors change.5

Piquilloud et al. conducted a prospective, interventional study in 22 intubated spontaneously breathing patients with acute respiratory failure. The study compared NAVA and PSV. Results showed that NAVA reduced trigger delay time, excess inspiratory time, and incidence of asynchronies compared to PSV.6

Futier et al. also compared NAVA to PSV during noninvasive ventilation (NIV) in 16 consecutive patients with acute respiratory failure and found that NAVA reduced severe patient ventilator asynchrony and yielded a comparable gas exchange improvement.7

Noninvasive applications

NIV is broadly used to manage patients with impending respiratory failure and it is also used to prevent reintubation in patients with high risk to develop post extubation respiratory failure. Patient-ventilator asynchrony is common when pressure support is used with noninvasive ventilation (PS-NIV). This may be due to the presence of leaks around the patient-ventilator interface, which affects the triggering and cycling mechanisms.8 The use of the EAdi signal instead of airway pressure and flow changes to trigger, cycle, and deliver appropriate amounts of pressure may improve patient-ventilator synchrony during NIV.7,8

Piquilloud et al. found that the use of NAVA during NIV when compared to PS-NIV improved patient ventilator synchrony by decreasing trigger delay time and severe asynchronies. Their study also showed the ability of NAVA to eliminate ineffective efforts and delayed cycling.8

Bertrand et al. conducted a study comparing NAVA with PSV during NIV in patients with acute respiratory failure. They found that NAVA reduced severe patient-ventilator asynchrony and yielded comparable gas exchange improvements when compared to PS-NIV.9 Studies are still needed in this area to determine if the use of NAVA with NIV improves patient outcome.7,8

NAVA in neonates

Premature neonates seem to determine their ventilator demands better than clinicians. NAVA has the capability to provide patients the ability to use electrical activity of the diaphragm as a feedback to regulate ventilation.9 Studies conducted in the neonatal population have shown that NAVA improves synchrony and the patient-ventilator interaction. It has also been noted that neonatal patients on NAVA have lower tidal volumes and peak airway pressures and their respiratory rates are higher when compared to PSV.9 NAVA appears to function well in neonates, but improvement in clinical outcomes, when used invasively or noninvasively in this population, remains unknown.9

Clinical use

NAVA can be used safely in patients with an undamaged ventilatory drive. It is still unclear if using NAVA has benefits over conventional modes of ventilation. However, limited available data shows that NAVA would be useful in patients with ventilator asynchrony. Also, NAVA has the ability to compensate for leaks, so it may be beneficial in neonatal and pediatric patients who have uncuffed tubes. Lastly, patients with chronic respiratory failure might benefit from NAVA.1

NAVA may not have any particular benefit in patients only needing short-term ventilation. There is no available data on the use of NAVA in surgical patients, most likely because they usually require short-term, uncomplicated ventilation. NAVA would not be appropriate for heavily sedated patients or those with significant hemodynamic compromise.1 Further investigation is needed to better identify when to apply NAVA, the appropriate patient populations, and whether or not the mode affects outcomes.10

NAVA and future research

There is a need for studies evaluating the optimal time to begin the weaning process with NAVA. More research is also required to determine proper NAVA settings, or a system that can be used by both expert and novice clinicians to apply the mode. So far, empirical titration of NAVA level is a method suggested in the literature, but this technique is not simple to perform.11

That said, neurally adjusted ventilatory assist improves patient ventilator synchronization and response time by responding directly to the electrical activity of the diaphragm. The amount and duration of the ventilator assist in NAVA is consistent with the amount and duration of the neural respiratory cycle. NAVA, when compared to PSV, improves patient ventilator synchronization.

NAVA is still considered a newer mode of ventilation and more investigation is needed to clearly identify its role.1,3


  1. Kacmarek RM. Proportional assist ventilation and neurally adjusted ventilatory assist. Respir Care 2011;56(2):140-148; discussion 149-152.
  2. Stewart NI, Jagelman TA, Webster NR. Emerging modes of ventilation in the intensive care unit. Br J Anaesth 2011;107(1):74-82.
  3. Verbrugghe W, Jorens PG. Neurally adjusted ventilatory assist: a ventilation tool or a ventilation toy? Respir Care 2011;56(3):327-335.
  4. Haas CF, Bauser KA. Advanced ventilator modes and techniques. Crit Care Nurs Q 2012;35(1):27-38.
  5. Sinderby C, Beck J. Proportional assist ventilation and neurally adjusted ventilatory assist-better approaches to patient ventilator synchrony? Clin Chest Med 2008;29(2):329-342, vii.
  6. Piquilloud L, Vignaux L, Bialais E, Roeseler J, Sottiaux T, Laterre PF, et al. Neurally adjusted ventilatory assist improves patient-ventilator interaction. Intensive Care Med 2011;37(2):263-271.
  7. Bertrand PM, Futier E, Coisel Y, Matecki S, Jaber S, Constantin JM. Neurally adjusted ventilatory assist vs. pressure support ventilation for noninvasive ventilation during acute respiratory failure: a crossover physiologic study. Chest 2013;143(1):30-36.
  8. Piquilloud L, Tassaux D, Bialais E, Lambermont B, Sottiaux T, Roeseler J, et al. Neurally adjusted ventilatory assist (NAVA) improves patient-ventilator interaction during non-invasive ventilation delivered by face mask. Intensive Care Med 2012;38(10):1624-1631.
  9. Stein H, Firestone K, Rimensberger PC. Synchronized mechanical ventilation using electrical activity of the diaphragm in neonates. Clin Perinatol 2012;39(3):525-542.
  10. Moerer O. Effort-adapted modes of assisted breathing. Curr Opin Crit Care 2012;18(1):61-69.
  11. Terzi N, Piquilloud L, Roze H, Mercat A, Lofaso F, Delisle S, et al. Clinical review: Update on neurally adjusted ventilatory assist – report of a round-table conference. Crit Care 2012;16(3):225.


Common Endocrine Disorders/Emergencies: Part 2

Jeff McCall, RRT, NREMT-P
Carolinas Healthcare System/MedCenter Air Critical Care Transport, Charlotte, NC

In Part 1 of this two-part series I covered the anatomy of the endocrine system, plus three common endocrine disorders/emergencies (type 1 and 2 diabetes, and diabetic ketoacidosis and hyperosmolar hyperglycemic state). In this edition I’ll take a look at several other common endocrine problems respiratory therapists may encounter in the clinical setting.

Adrenal crisis1,2

Adrenal crisis and severe acute adrenocortical insufficiency are often elusive diagnoses that may result in severe morbidity and mortality when undiagnosed or ineffectively treated. Although it is thought by experts that more than 50 steroids are produced within the adrenal cortex, cortisol and aldosterone are by far the most abundant and physiologically active.

In primary adrenocortical insufficiency, glucocorticoid and mineralocorticoid properties are lost; however, in secondary adrenocortical insufficiency (i.e., secondary to disease or suppression of the hypothalamic-pituitary axis), mineralocorticoid function is preserved. Although suppression of the hypothalamic-pituitary axis from chronic exogenous steroid use is the most common cause of secondary adrenal insufficiency, the possibility of hypopituitarism due to hypothalamic-pituitary disease must be considered.

With acute hypopituitarism, other hormone deficiencies must be identified and treated in addition to treating adrenal insufficiency with corticosteroids. For instance, if a patient with panhypopituitarism due to Sheehan syndrome (postpartum pituitary infarction) is only treated for adrenal crisis, severe cardiovascular compromise from the untreated associated hypothyroidism likely occurs. Death can result if the hypothyroid state is not diagnosed.

Patients experiencing adrenal insufficiency or an adrenal crisis will often present with weakness (99%), pigmentation of skin (98%), weight loss (97%), abdominal pain (34%), salt craving (22%), diarrhea (20%), constipation (19%), syncope (16%), and vitiligo (9%).

Treatment will consist of:

  • Maintaining airway, breathing, and circulation
  • If coma is present, consider glucose, thiamine, or naloxone
  • Use aggressive volume replacement therapy (dextrose 5% in normal saline solution)
  • Correction (if required) of specific electrolyte abnormalities: hypoglycemia, hyponatremia, hyperkalemia, hypercalcemia.

Addison’s disease 3,4

When Thomas Addison described the disease that now bears his name, bilateral adrenal destruction by tuberculosis was its most common cause. Now tuberculosis accounts for only 7- 20% of cases; autoimmune disease is responsible for 70-90%, with the remainder being caused by other infectious diseases, replacement by metastatic cancer or lymphoma, adrenal hemorrhage or infarction, or drugs.

Disseminated tuberculosis or fungal infections are still a major cause of adrenal insufficiency in populations with a high prevalence of these diseases, but as tuberculosis has been better controlled, the overall incidence of Addison’s disease has decreased. The prevalence of Addison’s disease in Western countries has been estimated at 35–60 per million, but three studies indicate it may be as high as 144 per million.


In acute presentations of Addison’s disease, prominent nausea, vomiting, and vascular collapse can be seen. Abdominal symptoms may take on features of an acute abdomen. Hyperpyrexia may be present, with temperatures reaching 105° F or higher, and the patient may be comatose.

In chronic presentations of Addison’s disease, hyperpigmentation, progressive weakness or fatigue, joint pain, nausea, vomiting, and occasionally diarrhea can be present. Dizziness with orthostasis may be present, due to hypotension. Myalgia and flaccid muscle paralysis may occur due to hyperkalemia. Impotence and decreased libido may occur in male patients. Female patients may have a history of amenorrhea due to the combined effect of weight loss and chronic ill health or secondary to premature autoimmune ovarian failure.


In stress situations, the normal adrenal gland output of cortisol is approximately 250-300 mg in 24 hours. This amount of hydrocortisone in soluble form (hydrocortisone sodium succinate or phosphate) should be given, preferably by continuous infusion. Clinical improvement, especially blood pressure response, should be evident within 4–6 hours of hydrocortisone infusion. Otherwise, the diagnosis of adrenal insufficiency would be questionable.

After 2–3 days, the stress hydrocortisone dose should be reduced to 100-150 mg, infused over a 24-hour period, irrespective of the patient’s clinical status. This is to avoid stress gastrointestinal bleeding. As the patient improves and as the clinical situation allows, the hydrocortisone infusion can be gradually tapered over the next 4–5 days to daily replacement doses of approximately 3 mg/h (72–75 mg over 24 h) and eventually to daily oral replacement doses, when oral intake is possible.

As long as the patient is receiving 100 mg or more of hydrocortisone in 24 hours, no mineralocorticoid replacement is necessary. The mineralocorticoid activity of hydrocortisone in this dosage is sufficient. Thereafter, as the hydrocortisone dose is weaned further, mineralocorticoid replacement should be instituted in doses equivalent to the daily adrenal gland aldosterone output of 0.05–0.20 mg every 24 hours. The usual mineralocorticoid used for this purpose is 9-alpha-fludrocortisone, usually in doses of 0.05–0.10 mg per day or every other day. Patients may need to be advised to increase salt intake in hot weather.


A pheochromocytoma is a benign adrenal gland tumor that secretes epinephrine and norepinephrine hormones. The most common symptom is high blood pressure, which sometimes can be extreme. Other symptoms are usually nonexistent, unless the person experiences pressure from the tumor, emotional stress, changes in posture, or is taking beta-blocker drugs for a heart disorder. Each individual may experience symptoms differently. Other symptoms may include rapid pulse, palpitations, headache, nausea, vomiting, and clammy skin.


Treatment for pheochromocytoma usually includes removing the tumor. Before removing the tumor, however, hypertension should be controlled with the use of alpha-adrenergic and beta-adrenergic blockades. Rarely pheochromocytomas can be malignant and may metastasize to other organs. Chemotherapy following resection of the primary tumor is the treatment of choice for malignant pheochromocytomas.


Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction of the mineralocorticoid hormone aldosterone by the adrenal glands when not a result of excessive renin secretion. Aldosterone causes increased sodium and water retention, as well as potassium excretion, leading to an increase in arterial blood pressure. As a result the most common clinical features of aldosteronism are hypertension and hypokalemia.


The treatment for hyperaldosteronism depends on the underlying cause. In patients with a single benign tumor (adenoma), surgical removal (adrenalectomy) may be curative. This is usually performed laparoscopically, through several very small incisions. For patients with hyperplasia of both glands, successful treatment is often achieved with spironolactone or eplerenone, drugs that block the effect of aldosterone.8


This is a condition in which the thyroid gland produces and secretes excessive amounts of the free (not protein bound, and circulating in the blood) thyroid hormones, triiodothryonine (T3) and orthyroxine (T4). Hyperthyroidism occurs when the thyroid releases too much of its hormones over a short (acute) or long (chronic) period of time.

Many diseases and conditions can cause this problem, including:

  • Getting too much iodine
  • Graves disease (accounts for most cases of hyperthyroidism)
  • Inflammation (thyroiditis) of the thyroid due to viral infections or other causes
  • Noncancerous growths of the thyroid gland or pituitary gland
  • Some tumors of the testes or ovaries
  • Taking large amounts of thyroid hormone


Treatment depends on the cause and the severity of symptoms.

Hyperthyroidism is usually treated with one or more of the following:

  • Antithyroid medications
  • Radioactive iodine (which destroys the thyroid gland and stops the excess production of hormones)
  • Surgery to remove the thyroid

If the thyroid must be removed with surgery or destroyed with radiation, thyroid hormone replacement pills will be prescribed. Beta-blockers such as propranolol are used to treat some of the symptoms, including rapid heart rate, sweating, and anxiety until the hyperthyroidism can be controlled.


This is a condition in which the thyroid gland doesn’t produce enough of certain important hormones. It an autoimmune disease. Individuals who develop a particular inflammatory disorder known as Hashimoto’s thyroiditis suffer from the most common cause of hypothyroidism. Autoimmune disorders occur when the immune system produces antibodies that attack a person’s own tissues. This process may involve the thyroid gland. Scientists aren’t sure why the body produces antibodies against itself. Some think a virus or bacterium might trigger the response, while others believe a genetic flaw may be involved. Most likely, autoimmune diseases result from more than one factor. However it happens, these antibodies affect the thyroid’s ability to produce hormones.

Removing all or a large portion of the thyroid gland can diminish or halt hormone production. In that case, the patient will need to take thyroid hormone for life. Radiation used to treat cancers of the head and neck can affect the thyroid gland and may lead to hypothyroidism. Also, a number of medications can contribute to hypothyroidism. One such medication is lithium, which is used to treat certain psychiatric disorders.

Patients suffering from hypothyroidism may present with fatigue, increased sensitivity to cold, constipation, dry skin, unexplained weight gain, puffy face, hoarseness, muscle weakness, elevated blood cholesterol level, muscle aches/tenderness/stiffness, joint pain/stiffness/swelling, heavier than normal or irregular menstrual periods, thinning hair, slowed heart rate, depression, and impaired memory.


The goal of therapy is restoration of the euthyroid state, which can be readily accomplished in almost all patients by oral administration of synthetic thyroxine (T4). Appropriate treatment reverses all the clinical manifestations of hypothyroidism.

Myxedema coma11

Myxedema coma is defined as severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs. It is a medical emergency with a high mortality rate. Fortunately, it is now a rare presentation of hypothyroidism, likely due to earlier diagnosis as a result of the widespread availability of thyrotropin (TSH) assays. Patients can present with generalized fatigue, cold intolerance, constipation, and dry skin. Common features of long-standing hypothyroidism are usually present as well. These features slowly progress to lethargy, delirium, or coma.


Myxedema crisis/coma is a life-threatening condition; therefore, patients with this disorder must be stabilized in an ICU. The first 24-48 hours are critical. If the diagnosis is considered likely, immediate and aggressive administration of multiple interventions is necessary to lower an otherwise high rate of mortality.

Metabolic syndrome12

Metabolic syndrome is a complex risk factor that arises from insulin resistance accompanying abnormal adipose deposition and function. It is a risk factor for coronary heart disease, as well as for diabetes, fatty liver, and several cancers. Metabolic syndrome is thought to be caused by adipose tissue dysfunction and insulin resistance. Dysfunctional adipose tissue also plays an important role in the pathogenesis of obesity-related insulin resistance.

Both adipose cell enlargement and infiltration of macrophages into adipose tissue result in the release of proinflammatory cytokines and promote insulin resistance. Insulin resistance appears to be the primary mediator of metabolic syndrome. Insulin promotes glucose uptake in muscle, fat, and liver cells and can influence lipolysis and the production of glucose by hepatocytes.

Risk factors for metabolic syndrome include family history, poor diet, and inadequate exercise. Patients may present with hypertension, hyperglycemia, hypertriglyceridemia, reduced high-density lipoprotein cholesterol, and abdominal obesity. Chest pains or shortness of breath may manifest, suggesting the rise of cardiovascular complications. In patients with insulin resistance and hyperglycemia, or with diabetes mellitus, acanthosis nigricans, hirsutism, peripheral neuropathy, and retinopathy may be present. In patients with severe dyslipidemia, xanthomas or xanthelasmas may be present.


The initial management of metabolic syndrome involves lifestyle modifications, including changes in diet and exercise habits. Indeed, evidence exists to support the notion that diet, exercise, and pharmacologic interventions may inhibit the progression of metabolic syndrome to diabetes mellitus.

Treatment of hypertension should proceed to achieve a goal blood pressure of less than 140/90 mm Hg or, in patients meeting diagnostic criteria for diabetes mellitus, less than 130/80 mm Hg.


  1. Nieman LK. Clinical manifestations of adrenal insufficiency in adults.
  2. Klauer KM. Adrenal crisis in emergency medicine.
  3. Nieman LK. Causes of primary adrenal insufficiency (Addison’s disease).
  4. Griffing GT. Addison disease treatment & management.
  5. Adrenal tumors.
  6. Young WF, Kaplan NM, Burton RD. Clinical features of primary aldosteronism.
  7. Conn JW, Louis LH. Primary aldosteronism: a new clinical entity. Trans Assoc Am Physicians 1955;68:215–31; discussion, 231–233.
  8. Williams Textbook of Endocrinology. (11th edition). Philadelphia: Saunders/Elsevier. 2008.
  9. Hyperthyroidism.
  10. Hypothyroidism.
  11. Myxedema coma or crisis.
  12. Metabolic syndrome treatment & management.


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