Critical Lab Values in Dysphagia?

Critical Lab Values to Monitor in Dysphagia

Evaluations and Treatments

When we review the medical record, we need to gather the numbers that are potentially valid markers of decreased host resistance and infection.

by Karen Sheffler, MS, CCC-SLP, BCS-S of SwallowStudy.com

Perfect numbers like perfect men (and women) are very rare.”

(by René Descartes, French philosopher and mathematician, with “and women” added to be fair)

Show me the numbers! What numbers may be markers of aspiration, dysphagia, decreased host resistance, frailty and infection?

We want quick and easy answers, but unfortunately, it is just not that easy.

On one side, when the Speech-Language Pathologist integrates lab assessments into her comprehensive dysphagia evaluation, she is appropriately gathering the many puzzle pieces that form the patient’s complex picture. On the other side, some numbers can lie and have complexities far greater than our master’s degree prepared us for.

This blog only skims the surface of lab values and patient data (for the adult population), and it is not in our scope of practice to translate them into a diagnosis. This blog is inspired by Mills & Ashford (2008) and their concept of holistic dysphagia. When we evaluate the whole patient, we attempt to gauge not only the patient’s overall level of dysphagia and aspiration risk, but also the risk of getting sick with pneumonia. The patient, family and medical team want to know our best clinical judgement on how long will it take to get better. What is the patient’s rehabilitation prognosis? What are the risks for a downward slide into sarcopenia, readmissions, morbidity, and mortality? This is not an exact science. The perceived level of risk may even vary within that patient from one day to the next.

A host of information awaits in the electronic medical record. Picture the medical resident in the back computer room, gathering numbers and data while wolfing down lunch without yet laying hands on the patient. Pneumonia may already be high in her differential diagnosis if the computer reports: a new infiltrate on the chest x-ray, leukocytosis (an elevated White Blood Cell count of >12.0), a fever of >38 degrees Celsius for >24 hours, and a medley of symptoms that correlate with pneumonia (i.e., cough, change in mental status, increased respiratory rate, shortness of breath and sputum production). Leukocytosis is typical with pneumonia; however, what if the number is elevated due to steroids like Prednisone, a traumatic accident, inflammation, or a bone marrow problem. Leukocytosis is one example of the incredible complexity of the human body, which is why we as therapists need to ask the medical team questions, no matter how many years of experience we have. For example, “Are there reasons, other than a developing aspiration pneumonia, that could be causing an elevation in the patient’s WBC count?” See this quick blog by Catherine Shaker, MS, CCC-SLP, BCS-S on asking questions.

Again, we are not diagnosing the disease, but integrating information on the whole patient will help guide our impressions and recommendations.

So here are 9 sets of numbers to consider:

(Click here for a handy chart/pdf: Lab values for dysphagia)

1) Body Mass Index (BMI):

We love our dietitians. Let them carry the calculators and do the math or use the myriad of BMI calculators online.

Bottom line: refer to the registered dietitians (RD) and collaborate with them when you are worried about your patient’s baseline frailty, cachexia, poor intake, weight loss, ability to meet caloric and hydration needs, and more.

a. BMI for the USA, because we like to be stubbornly different:

Weight in pounds (lbs) times 703, divided by height (inches) squared.

Equation: lbs x 703 / in2

For example, a 6 foot (72 inches) tall man weighing 180 pounds would have the following formula:

180 x 703 = 126,540 / 72 x 72 = 5,184; so 126,540 / 5,184 = 24

BMI = 24

b. BMI for the rest of the world & the Metric system:

Weight (kilograms) divided by height (meters) squared.

Equation: kg / m2

According to WHO Classifications, our gentleman above is normal weight. Here are the typical ranges, whether using the metric system or not:

Underweight……..<18.5

Normal……………..18.5 – 24.9

Overweight ……….25 – 29.9

Medically Obese…30 – 39.9

Morbidly Obese…..>40

2) Albumin and Prealbumin:

These are not necessarily good nutrition markers, as studies have shown that a decreased intake does not always equal a decrease in these lab values. Additionally, an increase in intake is not equal to an increase in values. Albumin and Prealbumin are influenced by many factors other than intake. Albumin is “the most flawed marker,” per Bahn’s (2006) review.

I noticed in Mills & Ashford’s (2008) review of laboratory assessments, they stated: “nutritional status has been closely tied to the strength of the immune system (p. 132).” However, they potentially incorrectly used only albumin as the marker of nutritional status. They noted that an aspirating patient who is normally hydrated, but has an albumin of 2.0, may have a weakened immune response and could develop infection faster than a similar patient with normal albumin. This is likely true and acknowledges that albumin is artificially elevated in a dehydrated patient, but it leaves out a host of other factors that can influence albumin and even prealbumin. Here are the normal values, half-lives, and some more of the factors that influence results:

Normative reference ranges (vary slightly depending on lab):

Serum Albumin (Alb):  

>3 years old: 3.5 – 5.0 g/dL

<3 years old: 2.9 – 5.5

Half-life: about 12-21 days

Prealbumin (PAB):      

18-45 mg/dL, but I have seen normal range also reported as 15-40 mg/dL

<11 mg/dL would be a significant nutritional risk

Half-life: 2-3 days

Influenced by (Banh, 2006; Bernstein, et al., 2014):

  • Hydration status (dehydration artificially elevates Alb, especially, as the overall plasma volume is decreased)
  • Medications, like corticosteroids, can artificially elevate PAB and lower Alb
  • Medical conditions, like CHF, can increase the plasma volume and artificially lower Alb and PAB
  • Renal dysfunction can cause kidneys to leak albumin into the urine and lower albumin.
  • Severe renal disease can artificially elevate PAB
  • Pregnancy can lower Alb and PAB
  • Bedridden state can lower Alb
  • Liver disease and Hepatic failure can cause lower Alb, as the protein is produced in the liver
  • Medical interventions, like intravenous fluid, can dilute plasma volume and lower the Alb (this can also happen with blood transfusions, overhydration and ascites).
  • Inflammatory processes (i.e., acute and chronic issues, such as: metabolic stress, infection, trauma, surgery, cancer, autoimmune process, burns, Crohn’s disease) can lower Alb and PAB. To detect for the influence of inflammation, it is sometimes suggested to measure CRP (C-Reactive Protein), which has a half-life of 19 hours. However, CRP does not always elevate in an acute phase response to inflammation. The following severe chronic inflammatory conditions do not show elevation of CRP: leukemia, ulcerative colitis, systemic lupus. In general during critical illness, patients with “prolonged elevations of CRP, along with consistently low serum PAB and Alb, appeared sicker and more resistant to treatment” (Banh, 2006, page 57).

A Nutrition Support Specialist, Le Banh, M.S., R.D., CNSD, wrote a clear review of these issues. I’m partial to this since she mentioned speech therapy (and rehabilitation in general). Banh (2006, p. 63) concluded this:

“Until better data is available, perhaps we should focus on other aspects of their nutrition care, such as ensuring that the patient actually receives what is prescribed, and whether or not the patient is clinically improving based on parameters such as ventilator weaning, wound healing, or participation in physical, occupational, or speech therapy. It is important to realize that an increase in PAB or Alb level may be the result of improvement in overall clinical status, and not necessarily due to improved nutritional status.”

3) Red Blood Cell Indices: Red Blood Cell (RBC), Hematocrit (HCT) and Hemoglobin (Hgb)

Hematocrit is the percentage of red blood cells in the total blood volume. Hemoglobin is attached to red blood cells and carries oxygen molecules throughout the body. Most of the iron in the body is found in hemoglobin. When red blood cells are lost, like in a gastrointestinal (GI) bleed, then less oxygen is transported. Low lab values in this area may indicate a type of anemia. Iron deficiency anemia is one type that is common in the geriatric population. This may be due to blood loss, protein-energy malnutrition and nutrition deficiencies, chronic disease, and B12 and Folate deficiencies. Per the review by Mills and Ashford (2008), anemia is associated with a risks for cognitive decline and mortality, and the following are potential symptoms of anemia:

  • Fatigue
  • Loss of energy
  • Shortness of breath
  • Difficulty concentrating
  • Dizziness

Note: If the geriatric patient has a poor intake plus memory loss and forgetfulness, a Vitamin B12 is also checked to catch a deficiency, before the cognitive deficits become permanent. Vitamin B12 values of less than 350 pg/mL (258 pmol/L) are considered at least a mild deficiency, but folate supplementation can mask a B12 deficiency (Berstein, et al., 2014).

Normative reference ranges (vary slightly depending on lab and populations served):

RBC…..4.7 – 6.1 million cells/μL (microliter) for men; 4.2 – 5.4 for women

Hgb……14 – 17 g/dL (men); 12 – 16 g/dL (women)

HCT….. 41 – 51% (men); 36 – 47% (women)

 

4) Immune System & White Blood Cells (WBC)

The WBC count is the total number of leukocytes in a sample of blood. There are 5 types of leukocytes: neutrophils, eosinophils, basophils, lymphocytes, and monocytes. An elevated WBC count (leukocytosis) may indicate the body is reacting to an inflammatory response, if one can mount a response. The white blood cells (leukocytes) are just one component of a complex immune defense. The complete blood count (CBC) panel will show a percentage of neutrophils in the white blood cell count (which is typically 60-70%) and an Absolute Neutrophil Count (ANC). Per Mills & Ashford (2008), the dysphagia clinician should pay attention to the neutrophils, as these are the first responders to the site of a microbial infection. For example, neutrophils are present in the oral cavity, maintaining a homeostasis by trapping and destroying pathogens. However, in times of stress, injury and critical illness, the host’s immune defenses are depressed and so are the neutrophils. The protective chemistry of the oral cavity is altered. Then the mouth becomes over-colonized with pathogenic bacteria, which when aspirated along with food, liquid and secretions could readily turn into an infection. It is fascinating that back in 1975, Bartlett & Gorbach already used the term: “Triple Threat of Aspiration Pneumonia,” to describe the combination of: stress of critical illness, temporary neutropenia, and aspiration of colonized oropharyngeal bacteria. Langmore and team reinforced this in 1998 and 2002. The field still needs to reinforce this issue of colonization of the oral cavity by respiratory pathogens (Ortega, et al, 2015).

Normative reference ranges (vary slightly depending on lab and populations served):

WBC……………4.8 – 10.8 K/mm3 (total number of leukocytes in sample)

Neut %………..40 – 70 % of the WBC (>70% could indicate acute bacterial infection)

Lymph %……..25 – 33 % (how prepared is the host’s baseline immune defense)

ANC (normal)…>1500/mm3

ANC (mild neutropenia)…500 – 1500/mm3

ANC (mod-severe neutropenia)…<500/mm3

ANC (neutrophilia)…>7500/mm3 (indicating acute bacterial infection)

Elevations in WBC count could be the body’s reaction to an inflammatory process (i.e., an injury, a traumatic brain head injury, stroke, cancer, etc); however, if the ANC is also elevated, then maybe there is a bacterial infection (Mills & Ashford, 2008). The other side of this is when a patient is on neutropenic precautions and cannot fight off infections; therefore, staff and visitors have to wear masks and gloves to protect the patient from the bugs that they may carry into the room.

 

5) Hydration & Electrolytes: Blood/Urea Nitrogen (BUN), Creatine (Creat) and Sodium (Na)

Fluid and electrolyte disorders (i.e., dehydration) were the most common dysphagia-associated major disease comorbidity per a survey done by Altman, et al (2010). This 2005-2006 sample of 77,540,204 short-stay hospitalizations (<30 days) is from the National Hospital Discharge Survey conducted annually by the Nation Center for Health Statistics of the Centers for Disease Control and Prevention. Unfortunately, dysphagia was solely identified if the ICD-9-CM code (787.2) was listed in the top 7 codes assigned to each patient’s record. Certainly, this method severely underestimated the rate of dysphagia; however, the finding of dehydration as the number one dysphagia-related disease and/or symptom is crucial to our work. Identifying dysphagia early is important. Altman, et al (2010) noted that the presence of dysphagia was associated with a 40% increase in length of stay. Dysphagia is present with a greater number of co-morbidities, leading to sicker and more debilitated patients. When these patients with dysphagia required rehabilitation (showing a potentially more involved patient), they had a 13-fold increase in mortality.

Hydration status is a critical value to check first, as dehydration can artificially increase values of albumin, RBC, potassium and chloride.

Some electrolytes may be particularly associated with dysphagia. I will not attempt to address them all. A level that is frequently checked in cases of significant mental status changes is ammonia. I have seen ammonia levels severely high in patients with hepatic encephalopathy, where the liver is not removing toxins from the blood. These patients can certainly become dysphagic due to the significant cognitive and neurological changes that occur. Low potassium (Hypokalemia) can cause weakness and fatigue that could contribute to dysphagia. Low calcium (Hypocalcemia) can cause many issues, but those that may relate to dysphagia could be: mental status changes, depression, extrapyramidal symptoms, neuromuscular irritability (i.e., paresthesias and numbness around the mouth, twitching, spasms, muscle cramps). The population of patients with head and neck cancers who require radical resections (particularly those affecting the parathyroid glands) and those on chemotherapy may be particularly at risk for hypocalcemia.

Lastly, Mills & Ashford (2008) reviewed how elevated BUN and creatine are indicators of renal impairment. Complications that relate to dysphagia are: decreased urine output, dry mouth, loss of appetite, nausea, vomiting and dehydration (Mills & Ashford, 2008).

Normative reference ranges (vary slightly depending on lab and populations served):

BUN……………5mg/dl – 25 mg/dL (have seen tighter range: 8 – 20 mg/dL)

Creat…………..0.7 – 1.3 mg/dL

Sodium……….135 – 145 mmol/L

Ammonia…….15 – 50 µmol/L

Potassium…..3.5 – 5.0 mmo/L

Chloride……..98 – 107 mmol/L

Ionized Calcium…4.4 – 5.4 mg/dL or 1.1 – 1.35 mmo/L

 

6) Peripheral Oxygen Saturation (SpO2)

In the past, people have assumed that an aspiration will cause an automatic drop in peripheral oxygen saturation. It has been mentioned in articles, like Marik and Kaplan (2003), stating that pulse oximetry may be performed during a clinical assessment. Collins & Bakheit, (1997) stated that the use of SpO2 was a reliable “method of diagnosis of aspiration” and could be used routinely during clinical assessment. However, their study confirmed aspiration in only 22 out of 54 consecutive inpatient and outpatient stroke patients, so their numbers were small. A drop of 2% or more was considered significant, which may be too tiny to be clinically important, as other research has suggested a change of 4%.

The selection of the 2% criterion by Collins and Bakheit is arbitrary and may have been chosen to fit their data. No empirical basis exists outside their study to indicate that pulse oximetry can accurately predict aspiration. (Colodny, 2000, p. 71).”

Collins & Bakheit indicated that the males had significant desaturation; however, it was “significant” only at two minutes after the aspiration with an average drop of 3.1%. At the actual time of aspiration, there was only an average difference of 1.3%. The maximum desaturation by females who aspirated was only 1.6% change at the time of aspiration, which was not deemed significant.

Stephen Leder (2000) and Nancy Colodny (2000) gave great reviews of the problems with the research up until 2000. Leder concluded that oxygen saturation does not correlate with aspiration, stating: “Although SpO2 has theoretical clinical importance in dysphagia management, it does not appear to be a clinically relevant indirect marker of aspiration status (page 204).” The research by Colodny (2000) showed similar findings that there is no relationship between aspiration on a FEES exam and SpO2 levels. Aspirators tended to have lower levels in general, indicating patients with dysphagia may have compromised respiratory systems. Again, this supports Leder’s point that there is general clinical importance in overall dysphagia management. Interestingly, the heart rate (HR) became elevated during feeding for all subjects, even for the healthy controls without dysphagia, so that should not necessarily be a marker for distress either. Similarly, a drop in oxygen saturation during a swallowing evaluation could be due to the physical exertion of eating the meal, feeding themselves, the positioning, underlining disease processes, and more.

Experts in the dysphagia field continue to question the use of this marker of aspiration. At the European Society for Swallowing Disorders in Barcelona, Spain (See #ESSD2015 on Twitter), Dr Ianessa Humbert and Dr Maggie-Lee Huckabee moderated a panel where a presenter (Marian, T.), shared her research on monitoring peripheral oxygen saturation (SpO2) in stroke patients who were undergoing FEES assessments. The research noted that only 10% of stroke patients had a drop in SpO2 when aspiration was detected. There was no correlation between the extent of desaturation and the severity of aspiration or the quality of the cough reflex. Marian concluded that this marker is not useful to screen for aspiration when assessing adult stroke patients during a bedside assessment. 

2017 Updates: 

See Marian, T., et al. (2017) publication titled: Measurement of Oxygen Desaturation Is Not Useful for the Detection of Aspiration in Dysphagic Stroke Patients. An oxygen saturation decline of 2% or more was only seen in 5 out of the 50 study participants. Again this is using a cut-off of 2% rather than the 4% difference suggested. 

This hot topic was also addressed at the Dysphagia Research Society in 2017 in Portland, Oregon. A systematic review was presented in a poster format by Britton, Deanna, of Portland State University, who studied this with Amy Lederle, Stephanie Ennis, Joshua O Bandit, Cassie Quinn and Donna Graville. They did not focus solely on stroke patients. They noted that the majority of the studies did not support the use of pulse oximetry monitoring  to detect aspiration. They found that only one study by Wang, et al. in 2005 used a control group along with adequate criteria of over 3%, and these researchers also found no correlation between an aspiration event and desaturation. 

7) Respiratory Rate (RR)

Normal resting RR for adults: 16 – 20 breaths/minute

Baseline resting respiratory rates higher than 25 breaths/minute have been found to be associated with aspiration in patients with COPD (Cvejic, et al., 2011). Steele & Cichero (2014) noted: “It is worthwhile to measure resting respiratory rate during swallowing evaluation (p. 301).” I think of the ICU patient puffing away at 30-40 breaths per minute and requiring a face mask. I say to myself: if I can’t even get to the mouth and if there is no break between breaths, than we should not be feeding the patient. This is a good time to ask the ICU nurse and respiratory therapist what they think. Maybe the doctor’s order went in yesterday for you to evaluate, but that patient at 8:30 am today is a whole different story.

 

8) Arterial Blood Gas (ABG)

This is a simplification of ABGs and addressing only a fraction of the critical values. Again, ask questions. Here is one example of a typical patient seen by SLPs:

Let’s say your patient recently weaned off the ventilator and has been making good progress. When he progresses to wearing a Passy-Muir Valve on his trach tube for a couple of hours at a time, the team draws an ABG during that time. The team is checking for hypoventilation, which could cause abnormal CO2 retention and acidosis. A decrease in pH to the acid side and an increase in PaCO2 could indicate respiratory acidosis. The team may need to ensure adequate ventilation to “blow off” the excess CO2. The ABG also gives a more accurate SaO2 percentage than the peripheral oxygen saturation.

Normal ABG Values

pH…………….7.35 – 7.45 (<7.35: Acidosis)

PaCO2………35 – 45 mmHg (>45: Acidosis)

PaO2………..80 – 100 mmHg

HCO3…………..22 – 26 mEq/L

SaO2……………> 95%

Base Excess: +/–  2 (amount of hydrogen ions needed to return blood pH to 7.35)

 

9) International Normalized Ration (INR) therapeutic range:

Normal INR therapeutic range: 2.0 – 3.0

A high INR means that the blood does not clot quickly, and there could be a bleeding risk. A low INR means that the blood may clot too quickly. However, for surgery the INR needs to be <1.5.

If you are performing a procedure on a patient that is invasive and could potentially cause bleeding (i.e., Flexible/Fiberoptic Endoscopic Evaluation of Swallowing or FEES), then it is crucial to review medications that could increase the risk of bleeding (Coumadin/warfarin), as well as to be aware of the INR. Warfarin does not have to be stopped prior to our FEES procedure, as the risk for bleeding should be low. The most common issue may be a nose bleed. However, if the patient is on warfarin and had a recent high INR, it would be crucial to speak directly with the doctor prior to scheduling the exam. 

 

Summary:

We do not evaluate the patient’s swallowing function in isolation (see this prior blog by Dr Samantha Shune for more reading), just as we do not make quick judgements based on the patient’s age or any one lab value. The lab values discussed in this blog are only one piece of the patient’s puzzle.

Puzzle not completed of an elderly man. A comprehensive dysphagia evaluation attempts to complete a complex picture of the patient.

Laboratory assessments, blood tests and other patient data can “shed light” on the patient’s underlying health status and ability to fight off infections (Mills & Ashford, 2008). Of course, we also listen to our patient, the family and caregivers, the aides who feed the patient, the nurses and the doctors. We consider goals from the patient and medical team. We analyze the person’s medical record, past medical history, functional baseline, current medical condition, and current functional status. We synthesize all these little puzzle pieces into a holistic approach to evaluating our patients. As I have advocated for in the past, this initial Clinical Bedside Swallowing Evaluation is more than a screen.

With this level of critical thinking and analysis (See Dysphagiaramblings.net for reviews of Humbert’s & Plowman’s Critical Thinking in Dysphagia Management), you and your bedside examination will:

  • Develop a rapport with the patient, family, caregivers, and team to better serve them ongoingly.
  • Assess the patients cognitive-linguistic status, especially orientation and ability to follow commands. Deficits in these areas have been shown to increase the odds of liquid and puree aspiration (Leder, et al, 2009).
  • Assess oral motor status, especially lingual strength and range of motion. Leder, Suiter, Murray & Rademaker (2013) found patients with decreased lingual range of motion had a higher aspiration risk.
  • Analyze the speech and voice. Dysarthria and dysphonia correlate strongly with aspiration, especially after stroke (Daniels, et al., 1998; Horner, et al., 1988).
  • Identify patients who may have aspiration and dysphagia, and may be at risk for developing an aspiration pneumonia.
  • Develop a hypothesis regarding the patient’s ability to take in food, liquid and medications effectively and safely.
  • Make good judgements as to when a patient requires an instrumental examination (i.e., MBSS or FEES).
  • Train, educate and counsel the patient, family, caregivers and medical team regarding the safest interventions to take prior to instrumental testing. If the patient refuses further testing, and especially in instances of palliative care, you may be able to help them “aspirate more safely.” (per Coyle in Suiter, Coyle & Sterling, 2014, November).
  • Trial interventions. Train and prepare the patient for the next steps (i.e., prepare them for the instrumental testing).

All that and more is a holistic approach to dysphagia. Please also see my Part 1 and Part 2 of Good Dysphagia Evaluations Guide Treatment.

Please share your experience and knowledge regarding lab values that may help and those that may lie a bit!

 

References:

Altman, K.W., Gou-Pei, Y. & Schaefer, S.D. (2010). Consequence of Dysphagia in the Hospitalized Patient: Impact on Prognosis and Hospital Resources. Archives of Otolaryngology Head and Neck Surgery, 136 (8), 784-789.

Banh, L. (2006). Serum proteins as markers of nutrition: What are we treating? Nutrition Issues in Gastroenterology, Series #43, 46-64. Retrieved on 10/1/15 from: http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/BanhArticle.pdf

Bartlett, J.G., & Gorbach, S.L. (1975). The triple threat of aspiration pneumonia. Chest, 68, 560-566.

Bernstein, M., Kreutzer, C. & Steffen, L.M. (2014). Nutritional Assessment for the Older Adult. In M. Bernstein & N. Munoz (Ed.), Nutrition for the Older Adult: Second Edition (pp. 153-181). Burlington, MA: Jones & Bartlett Learning.

Collins, M.J. & Bakheit, A.M.O. (1997). Does pulse oximetry reliably detect aspiration in dysphagic patients? Stroke, 28, 1773–1775. http://stroke.ahajournals.org/content/28/9/1773.long

Colodny, N. (2000). Comparison of dysphagics and nondysphagics on pulse oximetry during oral feeding. Dysphagia, 15 (2), 68-73.

Cvejic, L., Harding, R., Churchward, T., Turton, A., Finlay, P., Massey, D., Bardin, P.G., Guy, P. (2011). Laryngeal penetration and aspiration in individuals with stable COPD. Respirology, 16, 269–75.

Daniels, S., Brailey, K., Priestly, D., Herrington, L., Weisberg, L., Foundas, A. (1998). Aspiration in patients with acute stroke. Archives of Physical Medicine and Rehabilitation, 79, 14–19.

Horner, J., Massey, W., Riski, J., Lathrop, M., Chase, K. (1988). Aspiration following stroke: Clinical correlates and outcome. Neurology, 38, 1359–1362.

Langmore, S.E, et al. (1998). Predictors of aspiration pneumonia: How important is dysphagia? Dysphagia, 13, 69-81.

Langmore, S.E, et al. (2002). Predictors of aspiration pneumonia in nursing home residents. Dysphagia, 17 (4), 298-307.

Leder, S.B. (2000). Use of arterial oxygen saturation, heart rate, and blood pressure as indirect objective physiologic markers to predict aspiration. Dysphagia, 15 (4), 201-205. DOI: 10.1007/s004550000028. http://www.ncbi.nlm.nih.gov/pubmed/11014882

Leder, S.B., Suiter, D.M. & Lisitano Warner, H. (2009). Answering orientation questions and following single-step verbal commands: Effects on aspiration status. Dysphagia, 24 (3), 290-295. http://www.ncbi.nlm.nih.gov/pubmed/19263106

Leder, S.B., Suiter, D.M., Murray, J. & Rademaker, A.W. (2013). Can an oral mechanism examination contribute to the assessment of odds of aspiration? Dysphagia, 28 (3), 370-374. http://www.ncbi.nlm.nih.gov/pubmed/23292501

Marik, P.E. & Kaplan, D. (2003). Aspiration pneumonia and dysphagia in the elderly. Chest, 124 (1), 328-336.

Marian, T. et al. (2017). Measurement of oxygen desaturation is not useful for the detection of aspiration in dysphagic stroke patients. Cerebrovasc Dis Extra, 7(1), 44-50. doi: 10.1159/000453083.

Mills, R.H. & Ashford, J.R. (2008). A Methodology for the Inclusion of Laboratory Assessment in the Evaluation of Dysphagia. Perspectives on Swallowing and Swallowing disorders, 17 (4), 128-134. doi:10.1044/sasd17.4.128 http://sig13perspectives.pubs.asha.org/article.aspx?articleid=1783521&resultClick=1

Murray, J. (2010). Frailty, nutrition, sarcopenia in the geriatric patient with dysphagia. SIG 15 Perspectives on Gerontology, 15, 35-41. doi:10.1044/gero15.2.35 http://sig15perspectives.pubs.asha.org/article.aspx?articleid=1761309&resultClick=1

Ortega, O., Sakwinska, O., Combremonth, S., Berger, B., Sauser, J., Parra, C., Zarcero, S., Nart, J., Carrión & Clavé, P. (2015). High prevalence of colonization of oral cavity by respiratory pathogens in frail older patients with oropharyngeal dysphagia. Neurogastroenterology & Motility, 1-11. doi:10.111/nmo.12690.

Suiter, D., Coyle, J. & Sterling, L. (2014, November). 1135: Bedside Swallow Examinations: What they can do & what they can’t. Seminar presented at the annual convention of American Speech-Language-Hearing Association, Orlando, FL.

Steele, C.M. & Cichero, J.A.Y. (2014). Physiological factors related to aspiration risk: A systematic review. Dysphagia, 29, 295-304.

 

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