There is no magic pill to cure dysphagia.
There are plenty of medications that can cause difficulties eating and swallowing.
When we evaluate a person’s eating and swallowing function, we have to put on our critical thinking caps, be detectives, and collaborate with the team. To determine if there may be a drug-induced dysphagia, we discuss symptoms and medications with the patient/family/caregivers, medical team, psychiatrists, pharmacists, and nurses. Lethargy, cognitive impairment, inattention, distractibility, tremors, dry mouth, discoordination, oral and pharyngeal delays in swallowing, food getting stuck, burning sensation and odynophagia, drooling, dysphonia, weak cough, aspiration, and inability to manage secretions could all potentially be “blamed” on medications.
In this blog, I will cover some medications that Speech-Language Pathologists (SLPs) working with adults should have in their radar. First, I will discuss how Sinemet could relieve symptoms of dysphagia in patients with Parkinson’s Disease when used correctly. Second, I will cover three groups of medications that could cause side effects which could elevate risks for dysphagia and aspiration, particularly in geriatrics (keep in mind the mnemonic of ABA).
1. A medication that can relieve symptoms that lead to dysphagia:
In the case of Parkinson’s Disease, there are case studies to show that the delivery of Levodopa (L-dopa is the agonist in Sinemet, which is Carbidopa/Levodopa) on an empty stomach one hour prior to a meal can significantly improve swallow function. Fonda, et al. (1995) noted the following: reduction in oral tremor, reduction in laryngeal tremor during swallow, improvements in total swallow time, reduction in laryngeal penetration with solids/liquids, and reduction in aspiration with liquids. I recall testing a patient with Parkinson’s Disease with a Modified Barium Swallow and noting significant dysphagia and aspiration. She commented during the study that the team had kept her completely NPO for the study, including not giving her the morning Sinemet dose. Fortunately, we were able to abort the study, call the nurse in the ICU and have her come down and administer the Sinemet. Not surprisingly, when the study resumed after one hour, the patient’s swallow function returned to within functional limits.
We should pay close attention to medications during our evaluation. We can use our electronic medical record systems to track administrations and timing. The Sinemet especially needs to be on an empty stomach at least 30 minutes before a meal, as it is absorbed in the small bowel. The rate of absorption can be affected by delayed gastric emptying and competition with food in the stomach (particularly amino acids). We should also keep in mind that Sinemet can cause dry mouth, so the clinician and team can monitor for this issue.
2. ABA = Anticholinergics, Benzodiazepines, and Antipsychotics:
Maybe you have heard the medical team talking about Anticholinergics, “Benzos,” “typical” and “atypical” antipsychotics. SLPs need to be ready to discuss these medications with the medical team.
A. What do the doctors mean by Anticholinergic effects?
Anticholinergics work by blocking the neurotransmitter acetylcholine and interrupting the “parasympathetic nerve impulses in the central and autonomic nervous system” (per Priff & Harold, 2005, in Pharmacology: A 2-in-1 Resource for Nurses, pg 36). They can be used to treat spastic conditions of the GI tract or urinary tract, motion sickness, extrapyramidal symptoms caused by other drugs, sinus bradycardia, and more. The main issue related to swallowing function is that many anticholinergics are antimuscarinic agents. This effect can cause decreased mucous and saliva production in the nose, mouth and throat, causing a dry mouth that could also elevate risk for dental caries.
Examples of common anticholinergics with antimuscarinic action:
Benzatropine (Cogentin – counteract the parkinsonian features caused by antipsychotic medications)
Diphenhydramine (Benadryl, Advil PM, Unisom, Sominex)
Doxylamine (Restavit, for insomnia)
However, the side-effects are much greater than simply a dry mouth, and many can affect a patient’s ability to safely consume meals. For example, other potential side effects include: decreased coordination, memory loss, confusion, disorientation, inability to sustain attention, illogical thinking, visual disturbances and more. The elderly are at greater risk for falls with anticholingergics due to sudden drops in blood pressure upon standing (orthostatic hypotension). Geriatrics with long-term use of anticholinergics have shown to be at risk for mental and physical decline, with increased risk for death.
Wikipedia reported on this mnemonic for the cluster of common side-effects (From “Anticholinergic Toxidrome” in Life in the Fast Lane):
- Blind as a bat (dilated pupils)
- Red as a beet (vasodilation/flushing)
- Hot as a hare (hyperthermia)
- Dry as a bone (dry skin and mouth)
- Mad as a hatter (hallucinations/agitation)
- Bloated as a Toad (ileus or urinary retention)
- And the heart runs alone (heart racing, tachycardia)
B. What’s up with the Benzos?
Benzodiazepines (i.e., Lorazepam, aka Ativan) may lead to potentially fatal respiratory depression, per drug label warnings. They are generally used as anticonvulsants, anxiolytic (reduce anxiety), muscle relaxants, and sedative-hypnotics. Benzodiazepines have been noted to significantly increase the elderly’s risk for cognitive impairment, delirium, falls, fractures, motor vehicle accidents, and amnesia, per a lecture by Cheryl Marks, MSN, RN-BC, FNP-BC (2015, November). With our heightened awareness of delirium prevention recently, I find that Ativan is almost never used in acute care treatment for the elderly. Benzos are listed on the BEERS list of inappropriate medications for older adults, due to the short-term and long-term adverse side-effects. Priff & Harold (2005) noted that in geriatric patients with liver disease and/or low serum albumin tend to experience the neurological side-effects to a greater degree, such as: drowsiness, confusion, dizziness, nystagmus, vertigo, dysarthria, tremor, and more. One can see how those CNS adverse reactions complicate a stroke eval significantly if the patient received Ativan in the ED for agitation. These CNS side effects can affect the patient’s ability to feed himself and eat/swallow safely.
A. Antipsychotics/Neuroleptics/Major Tranquilizers:
This class of medication is used to treat psychotic symptoms (such as those in schizophrenia), bipolar, major depressive disorders, delusions, hallucinations, agitation, movement disorders seen in Tourette’s Syndrome and Huntington’s Chorea, and even intractable hiccups (Priff & Harold, 2005).
The “conventional” or “typical” antipsychotics are the first generation of antipsychotic medications and tend to cause a higher risk for adverse side-effects, such as tardive dyskinesia and extrapyramidal symptoms. Examples of typical antipsychotics:
- Chlorpromazine (Thorazine)
- Haloperidol (Haldol)
The newer, “novel” or “atypical” antipsychotics supposedly cause less adverse reactions. Examples of atypical antipsychotics include:
- Lurasidone (Latuda)
- Olanzapine (Zyprexa)
- Quetiapine (Seroquel)
- Aripiprazole (Abilify)
Sokoloff & Pavlakovic (1997) compared two typical antipsychotics, noting that chlorpromazine may frequently cause sedation, orthostatic hypotension and anticholinergic effects (dry mouth and blurred vision). Whereas, Haldol and Loxapine may increase the risk for:
- Extrapyramidal symptoms
- Neuroleptic Malignant Syndrome (NMS)
- Drug-induced dysphagia
Neuroleptics block dopamine receptors in the basal ganglia. Examples of extrapyramidal or parkinsonian signs are: akathisia (restlessness), dystonia, tremors, rigidity, bradykinesia, masked face, lack of automatic body movements. Neuroleptic-induced parkinsonism, occurs in 12-45% of patients, especially in elderly, per Casey (1993). The bradykinesia and muscle rigidity may be the cause of the oropharyngeal dysphagia and aspiration, speculated Sokoloff & Pavlakovic (1997). The side-effects may occur at very low doses but become more severe at higher doses.
There are many case reports in the literature of neuroleptics causing dysphagia. Sokoloff & Pavlakovic (1997) presented a case of a patient with dementia whose symptoms of agitation were not controlled by his baseline Haldol and Thioridazine, and he was changed to Loxapine, which was increased to 5mg two times a day. After a week, the patient started choking and became congested. The Modified Barium Swallow Study (MBSS or videofluoroscopy) showed: reduced mastication, tongue pumping, reduced tongue range of motion, reduced tongue base movement (likely due to rigidity), reduced bolus control, delayed initiation of pharyngeal swallow, reduced laryngeal movement, residue in valleculae and pyriforms after the swallow with penetration on this residue, and silent aspiration on thin liquids. The repeat study over 2 weeks after medication was discontinued showed significant improvements.
Sliwa & Lis (1993), Dziewas, et al. (2007), and Hughes, et al. (1994) showed similar issues with Haldol, with dysphagia complicated by aspiration pneumonia and weight loss. Hughes (1994) also noted that haloperidol produced a bradykinesia of the swallowing process. The MBSS showed: poor bolus control, reduced laryngeal elevation, decreased epiglottic inversion, reduced cricopharyngeal opening, residue in the pyriforms, and aspiration with liquids. Similar to many case reports, the repeat MBSS two weeks after the removal of Haloperidol showed a resolution of the dysphagia.
Unfortunately, many studies regarding neuroleptic drug-induced dysphagia are case studies only. As noted by Aldridge & Taylor’s systematic review in 2012, when excluding commentaries and single case reports, most studies do not use instrumental assessments to determine the frequency of dysphagia in this population of adults with mental illness. Only one study in 1969 by Hussar, et al. used “cineradiographic evaluation of swallowing with thin barium mixture,” and they found 46% of patients with schizophrenia had dysphagia (Aldridge & Taylor, 2012, page 128). Many other studies, using only interviews and retrospective analysis of medical records, of course found lower incidences of dysphagia (17-19%).
What do you think of when you hear Haldol?
I heard a nurse describe it as “Vitamin H”!
It is perceived as a quick and effective fix for that patient who is climbing out of bed and at risk for self-injury. What is needed is a multidisciplinary approach to think critically about this medication’s risks and benefits.
When I think about Haldol, I recall my own case reports of patients who have acutely developed slurred speech, pooling and drooling of secretions, and difficulty swallowing. I have seen patients who have received too much Haldol end up intubated in the ICU. I have also performed Modified Barium Swallow Studies, showing severe dysphagia in the presence of Haldol, only to resolve after two weeks off of Haldol.
I also recall how Haldol, invented in the 1950’s, seemed to go out of favor in the late 1990’s. It is interesting how many papers on the topic are from that time. However, Haldol seems to be enjoying a recent resurgence within the last 5-10 years. These trends may be due to the increased focus on delirium prevention in the last 10 years.
Prophylactics and Prevention of Delirium:
I often hear physicians discussing the use of Haldol as the pharmacologic intervention of choice to control agitation in patients with delirium, in order to avoid benzodiazepines and other sedative hypnotics. At times it is the drug of choice due to its reduced anticholinergic side-effects (Sevris, 1996). Other times it is chosen for its ease of availability and administration in oral, IV and IM forms.
Haldol is not only being used to control agitation in a patient who already has delirium, it is also being used prophylactically to prevent post-op delirium in geriatric surgery patients (e.g., Kalisvaart, et al., 2005; Wang, et al., 2012). However, the doses are very low and for a very short duration. Kalisvaart, et al., used 1.5mg/day preoperatively and continued this for only 3 days postoperatively. They found no significant reduction in the incidence of delirium, only in the duration of the delirium and the length of stay. Wang, et al., only administered 0.5mg, followed by 0.1mg/hour for only 12 hours, for a total of 1.7mg. They noted the incidence of delirium during the first 7 days was 15.3% in the Haldol group and 23.2% in the placebo group. It should be noted that some of their measures reported as significant were of minimal functional difference (i.e., mean length of ICU stay at 21.3 hours for Haldol group versus 23 hours for control group).
The take-home message here is that these doses were very small and not in combination with a cocktail of other sedating medications. This is not the neurologically impaired agitated patient in the ICU receiving Clozapine, Zyprexa and Haldol. This is not that patient who receives 15 mg a day of Haldol who shows an inability to manage secretions.
Do Atypical/Novel Antipsychotics Cause Less Side Effects?
I recall a neurologist comparing Haldol to Zyprexa, as he said: “Haldol is like banging your head into a brick wall, and Zyprexa is just using one brick.” Atypical antipsychotics are thought to cause less EPS side effects, but it is not so simple, as the medications may have other side effects that need to be avoided. One major issue with atypical antipsychotics is that they can cause cardiovascular side effects of QT interval prolongation and life-threatening arrhythmias (Priff & Harold, 2005).
Zyprexa is also used for its convenient orally dissolvable tab, called Zydis. (Zyprexa is also known as Olanzapine, which is in the category of “atypical,” “novel”, or 2nd generation antipsychotics.) Prolonged use of Zyprexa can cause similar side-effects of EPS and dysphagia. I recall a patient who was on newly taken off Cymbalta and placed on Zyprexa and he showed severe oropharyngeal dysphagia on a Modified Barium Swallow, with silent aspiration and poor sensation of his diffuse bilateral pharyngeal residue that did not clear after 4 swallows. When retested after 3 weeks off Zyprexa and onto Seroquel (another atypical antipsychotic), he had at least a functional swallow with slight modifications and strategies. Larsen, et al. (2010) found that one 5mg dose of Zyprexa pre-operatively and one 5mg dose post-operatively reduced the incidence of delirium, but the delirium lasted longer and was more severe in the Zyprex group when compared to the placebo.
Sico & Patwa (2011) reported a case of Risperidone-induced dysphagia with bulbar palsy characteristics in a 58 year old male with a psychotic disorder, but intact mental status. The only change in medications was the addition of Risperidone 2 weeks prior to his dysphagia onset. All other laboratory and neurological examinations ruled-out other causes. His modified barium swallow study showed severe oropharyngeal dysphagia with hypomotility, oropharyngeal residue after the swallow and aspiration. Additionally, his voice was dysphonic; he had facial diplegia with weakness of eye closure; he had minimal palatal elevation with an absent gag reflex; but he did not have extrapyramidal symptoms such as bradykinesia, rigidity or tremor. His prolactin levels were found to be high and he developed gynecomastia. During a hospitalization, only his risperidone was discontinued (his baseline medications of methadone and clonazepam were continued). Within 9 days off risperidone, his gag reflex returned, and he was started on a soft diet. After 1 month his dysphagia and other bulbar symptoms completely resolved, and he started to gain weight. After 3 months, his gynecomastia resolved, and prolactin levels returned to normal.
Even information released by the drug Seroquel (aka, Quetiapin fumarate, which is another “atypical” antipsychotic used to treat major depressive disorder, bipolar, and schizophrenia) states that it is not approved for use in psychotic conditions related to dementia, and it may increase the risk of death in older adults with dementia-related conditions.
Is the Focus on Delirium Prevention Leading to Overuse of Neuroleptics?
Are we preventing delirium while increasing the risk for neuroleptic malignant syndrome (NMS), Tardive Dyskinesia (TD), extrapyramidal symptoms, dysphagia, pneumonia and death due to pneumonia?
Nagamine (2008) compared the typical antipsychotic, Haloperidol, versus an atypical antipsychotic, Risperidone, and found that patients on Haloperidol had a reduced production of Substance P, which was correlated with an inhibition of the swallow and cough reflexes. Nagamine concluded that patients on haloperidol are at increased risk for aspiration, aspiration pneumonia and mortality, especially among elderly patients with dementia and neuropsychiatric illness.
Fortunately, others are noticing the overuse of antipsychotics too. See this quick article on Drugs.com.
Please also see this more in depth FDA warning regarding “increased mortality in elderly patients with dementia-related psychosis,” regarding Haldol injection (for immediate release) and Haldol Decanoate injection (IM).
There seems to be a lack of consistency in recommendations for Haldol’s usage. One can read warnings on the drug label and from the FDA that this drug is not recommended for the elderly, especially in treating dementia-related psychosis. However, I was at a talk on delirium last year, and Haldol was listed first in a chart of medications that can be used to manage agitation in the elderly with delirium, especially when the behavior is threatening to self or others. The textbook, Pharmacology: A 2-in-1 Reference for Nurses, specifically reports that conventional antipsychotics are used to calm agitated geriatric patients.
When using Haldol to control acute agitation related to delirium, neurological disease or dementia-related psychosis, the risks are elevated. Because Haldol takes 30-90 minutes to work, there is a significant risk of giving additional doses within that time. There is a risk of using additional medications if the Haldol is perceived as not effective (i.e., combinations with Zyprexa or Ativan can elevate the risk for adverse reactions from Haldol). One of the side-effects of Haldol at high doses is akathisia (restlessness), but agitation and restlessness are often symptoms trying to be treated with Haldol. What symptoms are we treating and what have we caused?
Does the “benefit” of Haldol outweigh the risks? We have to ask:
- Do we need a quick medication fix due to a lack of available non-pharmacological interventions (i.e., delirium prevention strategies, staff availability to be a sitter, and calming/relaxation techniques)?
- Can the patient tolerate the elevated risk for prolonged lethargy, aspiration on secretions, dysphagia, and poor oral intake?
The medical team frequently looks to Cogentin (Benzotropine) as an antiparkinsonian medication to alleviate the parkinsonian symptoms. However, this has significant anticholinergic side-effects as noted above.
Discontinuation of the offending medications can lead to resolution of the dysphagia, but it may take days to clear out of the body and weeks for full resolution of the symptoms of the drug-induced dysphagia. Haldol stays in the system after the medication has been discontinued, with a half-life of 14-26 hours in IV form and 14-37 hours when given orally in healthy individuals. It is metabolized in the liver and excreted in the feces and urine. The elderly and/or those with liver and kidney disease may have an even greater issue with slow clearance of the medications.
Unfortunately, tardive dyskinesias (TD) can be persistent and even irreversible, as the antiparkinsonian medications do not resolve them. Per the FDA report above: “The risk (for persistent TD) appears to be greater in elderly patients on high-dose therapy, especially females.”
The speech-language pathologist can have a big impact in this area of adverse drug reactions and drug-induced dysphagia.
In closing, I want to stress the fact that it may not be just one medication that is the culprit for your patient’s difficulty eating and swallowing. The medical team also needs to consider the issue of polypharmacy. Regarding the issue of polypharmacy, check out this interview with Dr Holly Holmes, from University of Texas, Houston. She spoke on the implications of polypharmacy in the elderly at the SIOG 2015 (International Society of Geriatric Oncology). She notes that polypharmacy may be taking over 5-10 medications, but the main issue is that the patient may be “taking more drugs than is indicated.” She notes that polypharmacy can cause falls, cognitive impairment, and delirium.
Hospitalized elderly patients, especially those who are critically ill, have an elevated risk for developing delirium (up to 56% during hospitalization and up to 87% during ICU stay per Dr Kennedy, 2015, October). Per Kennedy’s talk, hospitalized patients over the age of 65 with delirium have increased risks for complications within the hospitalization, such as:
- prolonged length of stay (which often means prolonged bedridden status),
- 3-times greater risk for functional decline, and
- 3 times greater risk for nursing home placement after hospitalization (Kennedy, 2015, October).
Add to this the side effects of medications like anticholinergics, benzos and antipsychotics. Then you have significantly increased the risk for adverse consequences, such as a drug-induced-dysphagia-related aspiration pneumonia.
During the post-operative course for an elderly patient, the risk is also high for cognitive impairments, increased pain, anxiety and medical complications, per Marks (2015, October). Marks advised to avoid the following medications in older adults:
- Muscle relaxants (i.e., Flexeril)
- Antihistamines (i.e., Diphenydramine, aka, Benedryl has a long half-life and should be avoided in the elderly)
- Tricyclic Antidepressants or TCAs (due to anticholinergic effects, orthostatic hypotension, and sedation). Wilson & Mottram (2004) noted the following common side effects with TCAs: dry mouth, drowsiness, dizziness and lethargy. TCAs have been replaced now by SSRIs (Selective serotonin reuptake inhibitors, like Celexa and Prozac). However, SSRIs may still cause nausea, vomiting, dizziness and drowsiness in some elderly, per Wilson & Mottram (2004).
Holmes reminds: “The pharmacist is a vastly underutilized resource.” The pharmacist can help the team play “which came first?” Did an increase/change in a medication(s) lead to the dysphagia and result in a pneumonia? Was the dysphagia caused by side-effects of confusion, inattention, dry mouth, and/or parkinsonian symptoms?
Further research is needed to foster a multidisciplinary approach to minimize adverse effects of medications, especially in developing non-pharmacological interventions to reduce agitation and delirium. If pharmacological interventions are necessary, then “start low and go slow,” per Marks (2015, October). Close monitoring of the patient is necessary when adding medications, and many hospitals are now using pharmacists assigned to the inpatient floors. Patients and families need to be adequately informed of the risks and potential benefits of the medications. The speech-language pathologist contributes to the team by investigating all potential root causes of the dysphagia. We need more studies to delineate the true incidence of dysphagia in the population of patients taking typical and atypical antipsychotics.
Thank you for reading. I look forward to comments.
FREE pdf of a handy Medications Side-effects Chart that I created. This is not a complete list of medications that could cause dysphagia-related side-effects. The chart is meant to be a resource or guide for the medical speech-language pathologist or other healthcare professional. It cannot substitute consultation with appropriate healthcare professionals. The chart covers medications that may cause dysphagia, including esophageal dysphagia and gastroesophageal complications, dry mouth, and central nervous system depression.
See also the FDA search tool for quick access to most drug labels on FDA approved drug products.
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