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Akathisia: “Ants in the Pants”
Potentially poor outcome if untreated
Case
The patient is a 65-year-old female with increasing anxiety and agitation. She completed cycle 2 of chemotherapy for breast cancer several hours ago. Her premedication was Reglan (metoclopramide); her only other medication is tamoxifen. Other than breast cancer, she suffers only from osteoarthritis.
She is found pacing about the ward – almost uncontrollably. She feels she must move, only to have to stop and, shortly afterwards, feels the urge to move again. This has never happened to her before. She must move despite being fatigued. She also complains of an odd overall feeling; something akin to “ant in the pants.” She is nervous and exhausted. What is her diagnosis and what clues to it are in her presentation?
Background
The word “akathisia” is derived from the Greek language and means “unable to sit.” It is thought to occur as a consequence of dopaminergic blockade in the midbrain region. The decrease in dopaminergic activity leads to a subsequent decrease in inhibitory motor control which, in turn, manifests as involuntary movements.
In this malady, the patient is seen as perpetually in motion. The patient feels the need to move until they must stop. But once static, they have the urge to move again. They pace, they rock and they ‘fidget’ – they just cannot sit still. This feeling has been likened to having “ants in the pants.” Patients become anxious, agitated, and suffer from insomnia. They cannot rest.
If left unresolved akathisia can torment patients to sheer exhaustion. For some it serves as a harbinger of suicide. This toxicity is more commonly seen in the psychiatric pharmacy with the most common offender being haloperidol. The causative agents of the least notoriety are the non-antipsychotics.
Diagnosis and treatment
Akathisia is an extrapyramidal symptom found largely but NOT exclusively with psychiatric medications. There are drugs in the non-psychiatric field that can also cause it, including antiemetics (e.g., metoclopramide), antihypertensives (e.g., diltiazem), and narcotics (e.g., cocaine). Metoclopramide is given under circumstances ranging from diabetic gastroparesis to premedicating chemotherapy. It is a peripheral and centrally acting dopamine antagonist. There are no lab tests or radiographic workups to diagnose akathisia. Its manifestations are erratic and disturbing, and the prognosis is doleful if unresolved.
The primary intervention for the treatment of akathisia is its recognition and the discontinuation of the offending drug. Beyond this, for symptomatic care, there is a compendium of case reports and small studies supporting many drugs, but only a few have received consistent recommendation. Beta-adrenergic antagonists, such as propranolol, are considered the gold standard, the first choice for the treatment of akathisia. Their toxicities include orthostatic hypotension and bradycardia. Additionally, they are contraindicated in the setting of asthma.
Anticholinergics, such as benztropine (cogentin) and trihexylphenidyl (artane) are considered in the literature as 2nd line treatments, behind beta-blockers. However, the data advocating their use is limited. They have multiple side-effects including sedation, memory impairment, visual impairment, and urinary retention. They are also contraindicated in patients with closed-angle glaucoma.
An equivalent alternative to beta-blockers could also be the 5HT2a receptor antagonists such as mirtazapine (remeron) and cyproheptadine (periactin). This class of medications is thought to act by an inhibitory control of dopaminergic neurons. Sedation and weight gain are the primary toxicities, and they are contraindicated in patients who are breastfeeding.
Benzodiazepines, such as clonazepam (klonopin), have shown some efficacy in improving symptoms but the data is very limited. The risk of tolerance and dependence, coupled with the problems of sedation impacting the elderly, prompts their placement in reserve. Vitamin B6 (pyridoxine), when given in a high dose format, causes significant improvement in akathisia. However, it can cause headache and nausea. Chronic administration of high doses has also been found to cause a severe and irreversible sensory neuropathy as well as lead to seizures. Many other agents have been studied, but the data are too small to warrant recommendation.
Conclusion
Akathisia remains an extreme reaction to drugs not always in the psychotropic class. The hospitalist will likely deal with the acute onset, a dramatic form, and a potentially poor outcome if untreated. The patient’s only true defense is the physician’s clinical acumen and their ability to recognize it.
Dr. Killeen is a physician in Tampa, Fla. He practices internal medicine, hematology, and oncology, and has worked in hospice and hospital medicine.
Recommended reading
Van Gool AR, Doorduijn JK, Sevnaeve C. Severe akathisia as a side effect of metoclopramide. Pharm World Sci. 2010; 32(6):704-706.
Loonen AJM, Stahl SM. The mechanism of drug-induced akathisia. CNS Spectr. 2010;15(11):491-494.
Forcen FE, Matsoukas K, Alici Y. Antipsychotic-induced akathisia in delirium: A systemic review. Palliat Support Care. 2016;14(1):77-84.
Sethuram K, Gedzior J. Akathisia: Case presentation and review of newer treatment agents. Psychiatric Annals. 2014;44(8):391-396.
Pringsheim T, et al. The assessment and treatment of antipsychotic-induced akathisia. Can J Psychiatry. 2018;63(11): 719-729.
Tachere RO, Mandana M. Beyond anxiety and agitation: A clinical approach to akathisia. Royal Australian Coll Gen Practitioners. 2017;46(5): 296-298.
Key points
- Although associated more with psychiatric medications, akathisia can occur with non-psychotropics as well.
- To recognize the illness, the clinician must notice the repetitive involuntary movements and pacing as well as the “ants in the pants” fidgeting involved.
- Primary treatment consists of medication discontinuation with pharmaceutical intervention as a backup.
- Recognition is the key to successful treatment.
Classic signs of akathisia
- Fidgeting – “ants in the pants”
- Swinging the legs while seated
- Rocking from foot to foot
- Walking while in a static position
- Inability to sit or stand still – pacing
- Onset appears with the initiation or dose adjustment of an offending drug
Quiz
1. Which of the following findings occur in Akathisia?
A. Fidgeting
B. Pacing
C. Swinging the legs while seated
D. All the above
Answer: D
Akathisia is manifest as involuntary hyperactivity of the extremities, particularly the lower extremities. People feel the urge to move, to continue endlessly in motion, stopping only when fatigue sets in. The fidgeting has been described by patients as feeling like “ants in the pants.”
2. Which of the following interventions are used to treat akathisia?
A. Drug discontinuation
B. Propranolol
C. Mirtazapine
D. All the above
Answer: D
All the interventions mentioned are used to treat akathisia. The foremost is to stop the offending drug. Failing this, propranolol is the “gold standard” while 5HT2a antagonists, such as mirtazapine, are favored when beta-blockers either fail or are contraindicated.
3. The use of pyridoxine (Vitamin B6) in the treatment of akathisia is associated with what toxicities?
A. Headache
B. Nausea
C. Seizures
D. All the above
Answer: D
The use of Vitamin B6 in the treatment of akathisia has several drawbacks. Its administration is associated with headache and nausea, and high dose usage increases the risk of seizure.
4. If unresolved, akathisia can lead to which of the following?
A. Insomnia
B. Suicide
C. Physical exhaustion
D. All the above
Answer: D
Akathisia, left unrecognized and untreated, can eventually lead to physical exhaustion, and is compounded by difficulties in trying to rest, hence insomnia. The physical and mental torment of this malady can lead to suicide.
Potentially poor outcome if untreated
Potentially poor outcome if untreated
Case
The patient is a 65-year-old female with increasing anxiety and agitation. She completed cycle 2 of chemotherapy for breast cancer several hours ago. Her premedication was Reglan (metoclopramide); her only other medication is tamoxifen. Other than breast cancer, she suffers only from osteoarthritis.
She is found pacing about the ward – almost uncontrollably. She feels she must move, only to have to stop and, shortly afterwards, feels the urge to move again. This has never happened to her before. She must move despite being fatigued. She also complains of an odd overall feeling; something akin to “ant in the pants.” She is nervous and exhausted. What is her diagnosis and what clues to it are in her presentation?
Background
The word “akathisia” is derived from the Greek language and means “unable to sit.” It is thought to occur as a consequence of dopaminergic blockade in the midbrain region. The decrease in dopaminergic activity leads to a subsequent decrease in inhibitory motor control which, in turn, manifests as involuntary movements.
In this malady, the patient is seen as perpetually in motion. The patient feels the need to move until they must stop. But once static, they have the urge to move again. They pace, they rock and they ‘fidget’ – they just cannot sit still. This feeling has been likened to having “ants in the pants.” Patients become anxious, agitated, and suffer from insomnia. They cannot rest.
If left unresolved akathisia can torment patients to sheer exhaustion. For some it serves as a harbinger of suicide. This toxicity is more commonly seen in the psychiatric pharmacy with the most common offender being haloperidol. The causative agents of the least notoriety are the non-antipsychotics.
Diagnosis and treatment
Akathisia is an extrapyramidal symptom found largely but NOT exclusively with psychiatric medications. There are drugs in the non-psychiatric field that can also cause it, including antiemetics (e.g., metoclopramide), antihypertensives (e.g., diltiazem), and narcotics (e.g., cocaine). Metoclopramide is given under circumstances ranging from diabetic gastroparesis to premedicating chemotherapy. It is a peripheral and centrally acting dopamine antagonist. There are no lab tests or radiographic workups to diagnose akathisia. Its manifestations are erratic and disturbing, and the prognosis is doleful if unresolved.
The primary intervention for the treatment of akathisia is its recognition and the discontinuation of the offending drug. Beyond this, for symptomatic care, there is a compendium of case reports and small studies supporting many drugs, but only a few have received consistent recommendation. Beta-adrenergic antagonists, such as propranolol, are considered the gold standard, the first choice for the treatment of akathisia. Their toxicities include orthostatic hypotension and bradycardia. Additionally, they are contraindicated in the setting of asthma.
Anticholinergics, such as benztropine (cogentin) and trihexylphenidyl (artane) are considered in the literature as 2nd line treatments, behind beta-blockers. However, the data advocating their use is limited. They have multiple side-effects including sedation, memory impairment, visual impairment, and urinary retention. They are also contraindicated in patients with closed-angle glaucoma.
An equivalent alternative to beta-blockers could also be the 5HT2a receptor antagonists such as mirtazapine (remeron) and cyproheptadine (periactin). This class of medications is thought to act by an inhibitory control of dopaminergic neurons. Sedation and weight gain are the primary toxicities, and they are contraindicated in patients who are breastfeeding.
Benzodiazepines, such as clonazepam (klonopin), have shown some efficacy in improving symptoms but the data is very limited. The risk of tolerance and dependence, coupled with the problems of sedation impacting the elderly, prompts their placement in reserve. Vitamin B6 (pyridoxine), when given in a high dose format, causes significant improvement in akathisia. However, it can cause headache and nausea. Chronic administration of high doses has also been found to cause a severe and irreversible sensory neuropathy as well as lead to seizures. Many other agents have been studied, but the data are too small to warrant recommendation.
Conclusion
Akathisia remains an extreme reaction to drugs not always in the psychotropic class. The hospitalist will likely deal with the acute onset, a dramatic form, and a potentially poor outcome if untreated. The patient’s only true defense is the physician’s clinical acumen and their ability to recognize it.
Dr. Killeen is a physician in Tampa, Fla. He practices internal medicine, hematology, and oncology, and has worked in hospice and hospital medicine.
Recommended reading
Van Gool AR, Doorduijn JK, Sevnaeve C. Severe akathisia as a side effect of metoclopramide. Pharm World Sci. 2010; 32(6):704-706.
Loonen AJM, Stahl SM. The mechanism of drug-induced akathisia. CNS Spectr. 2010;15(11):491-494.
Forcen FE, Matsoukas K, Alici Y. Antipsychotic-induced akathisia in delirium: A systemic review. Palliat Support Care. 2016;14(1):77-84.
Sethuram K, Gedzior J. Akathisia: Case presentation and review of newer treatment agents. Psychiatric Annals. 2014;44(8):391-396.
Pringsheim T, et al. The assessment and treatment of antipsychotic-induced akathisia. Can J Psychiatry. 2018;63(11): 719-729.
Tachere RO, Mandana M. Beyond anxiety and agitation: A clinical approach to akathisia. Royal Australian Coll Gen Practitioners. 2017;46(5): 296-298.
Key points
- Although associated more with psychiatric medications, akathisia can occur with non-psychotropics as well.
- To recognize the illness, the clinician must notice the repetitive involuntary movements and pacing as well as the “ants in the pants” fidgeting involved.
- Primary treatment consists of medication discontinuation with pharmaceutical intervention as a backup.
- Recognition is the key to successful treatment.
Classic signs of akathisia
- Fidgeting – “ants in the pants”
- Swinging the legs while seated
- Rocking from foot to foot
- Walking while in a static position
- Inability to sit or stand still – pacing
- Onset appears with the initiation or dose adjustment of an offending drug
Quiz
1. Which of the following findings occur in Akathisia?
A. Fidgeting
B. Pacing
C. Swinging the legs while seated
D. All the above
Answer: D
Akathisia is manifest as involuntary hyperactivity of the extremities, particularly the lower extremities. People feel the urge to move, to continue endlessly in motion, stopping only when fatigue sets in. The fidgeting has been described by patients as feeling like “ants in the pants.”
2. Which of the following interventions are used to treat akathisia?
A. Drug discontinuation
B. Propranolol
C. Mirtazapine
D. All the above
Answer: D
All the interventions mentioned are used to treat akathisia. The foremost is to stop the offending drug. Failing this, propranolol is the “gold standard” while 5HT2a antagonists, such as mirtazapine, are favored when beta-blockers either fail or are contraindicated.
3. The use of pyridoxine (Vitamin B6) in the treatment of akathisia is associated with what toxicities?
A. Headache
B. Nausea
C. Seizures
D. All the above
Answer: D
The use of Vitamin B6 in the treatment of akathisia has several drawbacks. Its administration is associated with headache and nausea, and high dose usage increases the risk of seizure.
4. If unresolved, akathisia can lead to which of the following?
A. Insomnia
B. Suicide
C. Physical exhaustion
D. All the above
Answer: D
Akathisia, left unrecognized and untreated, can eventually lead to physical exhaustion, and is compounded by difficulties in trying to rest, hence insomnia. The physical and mental torment of this malady can lead to suicide.
Case
The patient is a 65-year-old female with increasing anxiety and agitation. She completed cycle 2 of chemotherapy for breast cancer several hours ago. Her premedication was Reglan (metoclopramide); her only other medication is tamoxifen. Other than breast cancer, she suffers only from osteoarthritis.
She is found pacing about the ward – almost uncontrollably. She feels she must move, only to have to stop and, shortly afterwards, feels the urge to move again. This has never happened to her before. She must move despite being fatigued. She also complains of an odd overall feeling; something akin to “ant in the pants.” She is nervous and exhausted. What is her diagnosis and what clues to it are in her presentation?
Background
The word “akathisia” is derived from the Greek language and means “unable to sit.” It is thought to occur as a consequence of dopaminergic blockade in the midbrain region. The decrease in dopaminergic activity leads to a subsequent decrease in inhibitory motor control which, in turn, manifests as involuntary movements.
In this malady, the patient is seen as perpetually in motion. The patient feels the need to move until they must stop. But once static, they have the urge to move again. They pace, they rock and they ‘fidget’ – they just cannot sit still. This feeling has been likened to having “ants in the pants.” Patients become anxious, agitated, and suffer from insomnia. They cannot rest.
If left unresolved akathisia can torment patients to sheer exhaustion. For some it serves as a harbinger of suicide. This toxicity is more commonly seen in the psychiatric pharmacy with the most common offender being haloperidol. The causative agents of the least notoriety are the non-antipsychotics.
Diagnosis and treatment
Akathisia is an extrapyramidal symptom found largely but NOT exclusively with psychiatric medications. There are drugs in the non-psychiatric field that can also cause it, including antiemetics (e.g., metoclopramide), antihypertensives (e.g., diltiazem), and narcotics (e.g., cocaine). Metoclopramide is given under circumstances ranging from diabetic gastroparesis to premedicating chemotherapy. It is a peripheral and centrally acting dopamine antagonist. There are no lab tests or radiographic workups to diagnose akathisia. Its manifestations are erratic and disturbing, and the prognosis is doleful if unresolved.
The primary intervention for the treatment of akathisia is its recognition and the discontinuation of the offending drug. Beyond this, for symptomatic care, there is a compendium of case reports and small studies supporting many drugs, but only a few have received consistent recommendation. Beta-adrenergic antagonists, such as propranolol, are considered the gold standard, the first choice for the treatment of akathisia. Their toxicities include orthostatic hypotension and bradycardia. Additionally, they are contraindicated in the setting of asthma.
Anticholinergics, such as benztropine (cogentin) and trihexylphenidyl (artane) are considered in the literature as 2nd line treatments, behind beta-blockers. However, the data advocating their use is limited. They have multiple side-effects including sedation, memory impairment, visual impairment, and urinary retention. They are also contraindicated in patients with closed-angle glaucoma.
An equivalent alternative to beta-blockers could also be the 5HT2a receptor antagonists such as mirtazapine (remeron) and cyproheptadine (periactin). This class of medications is thought to act by an inhibitory control of dopaminergic neurons. Sedation and weight gain are the primary toxicities, and they are contraindicated in patients who are breastfeeding.
Benzodiazepines, such as clonazepam (klonopin), have shown some efficacy in improving symptoms but the data is very limited. The risk of tolerance and dependence, coupled with the problems of sedation impacting the elderly, prompts their placement in reserve. Vitamin B6 (pyridoxine), when given in a high dose format, causes significant improvement in akathisia. However, it can cause headache and nausea. Chronic administration of high doses has also been found to cause a severe and irreversible sensory neuropathy as well as lead to seizures. Many other agents have been studied, but the data are too small to warrant recommendation.
Conclusion
Akathisia remains an extreme reaction to drugs not always in the psychotropic class. The hospitalist will likely deal with the acute onset, a dramatic form, and a potentially poor outcome if untreated. The patient’s only true defense is the physician’s clinical acumen and their ability to recognize it.
Dr. Killeen is a physician in Tampa, Fla. He practices internal medicine, hematology, and oncology, and has worked in hospice and hospital medicine.
Recommended reading
Van Gool AR, Doorduijn JK, Sevnaeve C. Severe akathisia as a side effect of metoclopramide. Pharm World Sci. 2010; 32(6):704-706.
Loonen AJM, Stahl SM. The mechanism of drug-induced akathisia. CNS Spectr. 2010;15(11):491-494.
Forcen FE, Matsoukas K, Alici Y. Antipsychotic-induced akathisia in delirium: A systemic review. Palliat Support Care. 2016;14(1):77-84.
Sethuram K, Gedzior J. Akathisia: Case presentation and review of newer treatment agents. Psychiatric Annals. 2014;44(8):391-396.
Pringsheim T, et al. The assessment and treatment of antipsychotic-induced akathisia. Can J Psychiatry. 2018;63(11): 719-729.
Tachere RO, Mandana M. Beyond anxiety and agitation: A clinical approach to akathisia. Royal Australian Coll Gen Practitioners. 2017;46(5): 296-298.
Key points
- Although associated more with psychiatric medications, akathisia can occur with non-psychotropics as well.
- To recognize the illness, the clinician must notice the repetitive involuntary movements and pacing as well as the “ants in the pants” fidgeting involved.
- Primary treatment consists of medication discontinuation with pharmaceutical intervention as a backup.
- Recognition is the key to successful treatment.
Classic signs of akathisia
- Fidgeting – “ants in the pants”
- Swinging the legs while seated
- Rocking from foot to foot
- Walking while in a static position
- Inability to sit or stand still – pacing
- Onset appears with the initiation or dose adjustment of an offending drug
Quiz
1. Which of the following findings occur in Akathisia?
A. Fidgeting
B. Pacing
C. Swinging the legs while seated
D. All the above
Answer: D
Akathisia is manifest as involuntary hyperactivity of the extremities, particularly the lower extremities. People feel the urge to move, to continue endlessly in motion, stopping only when fatigue sets in. The fidgeting has been described by patients as feeling like “ants in the pants.”
2. Which of the following interventions are used to treat akathisia?
A. Drug discontinuation
B. Propranolol
C. Mirtazapine
D. All the above
Answer: D
All the interventions mentioned are used to treat akathisia. The foremost is to stop the offending drug. Failing this, propranolol is the “gold standard” while 5HT2a antagonists, such as mirtazapine, are favored when beta-blockers either fail or are contraindicated.
3. The use of pyridoxine (Vitamin B6) in the treatment of akathisia is associated with what toxicities?
A. Headache
B. Nausea
C. Seizures
D. All the above
Answer: D
The use of Vitamin B6 in the treatment of akathisia has several drawbacks. Its administration is associated with headache and nausea, and high dose usage increases the risk of seizure.
4. If unresolved, akathisia can lead to which of the following?
A. Insomnia
B. Suicide
C. Physical exhaustion
D. All the above
Answer: D
Akathisia, left unrecognized and untreated, can eventually lead to physical exhaustion, and is compounded by difficulties in trying to rest, hence insomnia. The physical and mental torment of this malady can lead to suicide.
Sarcopenic obesity: The wasting within
Case
The patient is a 65-year-old white female who recently was discovered to have a 2-cm spiculated lung mass in the right upper lobe. She is undergoing an evaluation at present but her main complaint today is that of profound weakness and fatigue. Her appetite and energy level are noticeably less; her family ascribes this to anxiety and depression. Her other medical problems include diabetes, hypertension, osteoporosis, and obesity. The patient believes that she’s lost about 20-25 pounds recently, though her family is skeptical, adding that “she’s been heavy all her life.” Her body mass index is 40. What additional interventions would you add to her workup?
Background
Sarcopenic obesity occurs as a natural consequence of aging. As a general rule, as many as half the women and a quarter of the men over age 80 years are affected. A total of about 18 million people are involved.
One thought as to etiology is that as one ages, proteolysis outdoes protein synthesis. Fat then replaces the body’s muscle, permeates the viscera, and becomes the prominent body form. Chronic lipodeposition leads to chronic inflammation which, in turn, augments protein catabolism. The elderly become less energetic and less active, and the muscle mass decreases further. A vicious cycle develops. Concurrently with obesity, patients suffer with the onset of dyslipidemia, osteoarthritis, osteoporosis (due to vitamin D deficiency), insulin resistance, and an overall increase in frailty.
Sarcopenic obesity also plays a prognostic role in the management of cancer patients where the presence of sarcopenia correlates with earlier death and decreased capacity for therapy. Patients seen as obese are less likely to receive the intensive care (particularly nutritional support) that patients seen as a higher risk receive. The cancer cachexia is less pronounced. The obesity seen externally masks the wasting within.
Diagnosis and treatment
Sarcopenic obesity suffers from an inexact definition. According to the World Health Organization, obesity is defined, officially, as a body mass index of greater than 30 kg/m2. Muscle mass is an important part of this entity, too, but the inclusion of muscle function in this definition brings, seemingly, a point of conjecture. Is muscle function necessary? By what scale do you measure it? This imprecision makes comparative research in the field somewhat more difficult.
As clinical acumen remains the major diagnostic approach to this disease, confirmatory testing for sarcopenic obesity comprises MRIs/CTs and dual energy x-ray absorptiometry (DXA) scans. Presently DXA is used to assess bone density in the diagnosis of osteoporosis. It also reveals the decreased lean appendicular (extremity) muscle mass which, along with the increased BMI, forms the basic diagnosis of sarcopenic obesity. DXA scans are favored over CTs for the assessment of appendicular lean muscle mass. DXA scans provide a relatively inexpensive method of estimating fat, muscle, and additionally, bone density. CTs are less favored because of their radiation exposure as well as their high cost. Assessing muscle strength, using handgrip dynomometry, is available though not widely advocated.
Of the myriad modalities tried in sarcopenic obesity, many have shortcomings. No particular diet format can be advocated. Hypocaloric diets, with or without protein supplementation, offer little advantage to a good physical exercise program. The administration of vitamin D, with calcium, can be of benefit to those sarcopenically obese patients suffering with osteoporosis. Other medications, as exemplified by testosterone, vitamin K, myostatin inhibitors, or mesenchymal stem cells, are either anecdotal or dubious in nature. More research is definitely needed.
The key component for the treatment of sarcopenic obesity is exercise, both aerobic and resistant. Physical exercise recruits muscle satellite cells into the muscle fibers strengthening their composition. Growth factors are also released that stimulate the production of muscle satellite cells. Muscle mass becomes augmented and fortified. Aerobic exercise counteracts the negative metabolic effects of lipids. Resistance training is felt to improve strength when in combination with aerobic exercise, compared with aerobic exercise alone. Research has shown that high-speed resistance training, over a 12-week period, had shown a greater improvement in muscle power and capacity when compared to low-speed training. It was also recommended that patients exercise only until fatigued, not until “failure,” as a stopping point. Programs must be customized to fit the individual.
Sarcopenic obesity is a form of deconditioning that occurs naturally with age but is compounded by cancer. Research into this disease is confounded by a lack of accepted definitions. Radiographic workup and lifestyle changes are the mainstay of medical management. The foremost diagnostic tool remains, as always, clinical suspicion.
Dr. Killeen is a physician in Tampa, Fla. He practices internal medicine, hematology, and oncology, and has worked in hospice and hospital medicine.
Recommended reading
Gruber ES et al. Sarcopenia and Sarcopenic Obesity are independent adverse prognostic factors in resectable pancreatic ductal adenocarcinoma. PLoS One. 2019;14(5): e02115915.10.1371/journal.pone.0215915 [PMID 31059520].
Lombardo M et al. Sarcopenic Obesity: Etiology and lifestyle therapy. Eur Rev Med Pharmacol Sci. 2019; 23: 7152-62.
Petroni M et al. Prevention and treatment of Sarcopenic Obesity in women. Nutrients. 2019; Jun 8.10.3390/nu1161302 [PMID 31181771].
Barcos VE, Arribas L. Sarcopenic Obesity: Hidden muscle wasting and its impact for survival and complications of cancer therapy. Ann Oncol. 2018;29(suppl. 2):ii1-ii9.
Zhang X et al. Association of Sarcopenic Obesity with the risk of all-cause mortality among adults over a broad range of different settings: An update meta-analysis. BMC Geriatr. 2018;19:183-97.
Key points
- • In sarcopenic obesity a patient’s muscle loss in mass can be clouded, overshadowed by the obese body habitus. The major diagnostic tool initially is clinical suspicion.
- • The diagnostic tests for sarcopenic obesity are DXA and CT scans.
- • The best treatment for sarcopenic obesity is a good exercise plan.
Quiz
1. What is the best treatment for sarcopenic obesity?
A. Testosterone
B. Vitamin K
C. Myostatin inhibitors
D. None of the above
Answer: D
There is no particular pharmaceutical treatment, to date, for sarcopenic obesity. Only an exercise program has proved to be of benefit. Those for whom fatigue might be problematic could benefit perhaps by doing “energy banking” or taking programmed naps/rest periods prior to exercise.
2. DXA scans are favored over CT scans because of which of the following?
A. Less cost
B. Capacity to diagnose osteoporosis
C. Less radiation exposure
D. All of the above
Answer: D
DXA scans offer all of the above advantages over CT scans. Also, patients with sarcopenic obesity found to be osteoporotic could be started on vitamin D and calcium supplementation.
3. Which of the following hamper the diagnosis and treatment of sarcopenic obesity?
A. The issue of muscle function
B. Difficulties in comparative research studies
C. Remembering that muscle wasting can occur without external evidence of cachexia
D. All of the above
Answer: D
Obtaining a precise definition of sarcopenic obesity and dealing with the issue of muscle strength and capacity make comparative studies difficult. The sarcopenic obese patient needs as much attention as the cachectic one as their wasting is from within.
4. In sarcopenic obesity and cancer the presence of sarcopenia is likely to lead to which of the following?
A. Earlier death
B. Decreased capacity for therapy
C. Less treatment focus compared to nonsarcopenic patients
D. All of the above
Answer: D
The presence of sarcopenia correlates to all of the above particularly as the obese patient is thought to require less intensive attention than others.
Case
The patient is a 65-year-old white female who recently was discovered to have a 2-cm spiculated lung mass in the right upper lobe. She is undergoing an evaluation at present but her main complaint today is that of profound weakness and fatigue. Her appetite and energy level are noticeably less; her family ascribes this to anxiety and depression. Her other medical problems include diabetes, hypertension, osteoporosis, and obesity. The patient believes that she’s lost about 20-25 pounds recently, though her family is skeptical, adding that “she’s been heavy all her life.” Her body mass index is 40. What additional interventions would you add to her workup?
Background
Sarcopenic obesity occurs as a natural consequence of aging. As a general rule, as many as half the women and a quarter of the men over age 80 years are affected. A total of about 18 million people are involved.
One thought as to etiology is that as one ages, proteolysis outdoes protein synthesis. Fat then replaces the body’s muscle, permeates the viscera, and becomes the prominent body form. Chronic lipodeposition leads to chronic inflammation which, in turn, augments protein catabolism. The elderly become less energetic and less active, and the muscle mass decreases further. A vicious cycle develops. Concurrently with obesity, patients suffer with the onset of dyslipidemia, osteoarthritis, osteoporosis (due to vitamin D deficiency), insulin resistance, and an overall increase in frailty.
Sarcopenic obesity also plays a prognostic role in the management of cancer patients where the presence of sarcopenia correlates with earlier death and decreased capacity for therapy. Patients seen as obese are less likely to receive the intensive care (particularly nutritional support) that patients seen as a higher risk receive. The cancer cachexia is less pronounced. The obesity seen externally masks the wasting within.
Diagnosis and treatment
Sarcopenic obesity suffers from an inexact definition. According to the World Health Organization, obesity is defined, officially, as a body mass index of greater than 30 kg/m2. Muscle mass is an important part of this entity, too, but the inclusion of muscle function in this definition brings, seemingly, a point of conjecture. Is muscle function necessary? By what scale do you measure it? This imprecision makes comparative research in the field somewhat more difficult.
As clinical acumen remains the major diagnostic approach to this disease, confirmatory testing for sarcopenic obesity comprises MRIs/CTs and dual energy x-ray absorptiometry (DXA) scans. Presently DXA is used to assess bone density in the diagnosis of osteoporosis. It also reveals the decreased lean appendicular (extremity) muscle mass which, along with the increased BMI, forms the basic diagnosis of sarcopenic obesity. DXA scans are favored over CTs for the assessment of appendicular lean muscle mass. DXA scans provide a relatively inexpensive method of estimating fat, muscle, and additionally, bone density. CTs are less favored because of their radiation exposure as well as their high cost. Assessing muscle strength, using handgrip dynomometry, is available though not widely advocated.
Of the myriad modalities tried in sarcopenic obesity, many have shortcomings. No particular diet format can be advocated. Hypocaloric diets, with or without protein supplementation, offer little advantage to a good physical exercise program. The administration of vitamin D, with calcium, can be of benefit to those sarcopenically obese patients suffering with osteoporosis. Other medications, as exemplified by testosterone, vitamin K, myostatin inhibitors, or mesenchymal stem cells, are either anecdotal or dubious in nature. More research is definitely needed.
The key component for the treatment of sarcopenic obesity is exercise, both aerobic and resistant. Physical exercise recruits muscle satellite cells into the muscle fibers strengthening their composition. Growth factors are also released that stimulate the production of muscle satellite cells. Muscle mass becomes augmented and fortified. Aerobic exercise counteracts the negative metabolic effects of lipids. Resistance training is felt to improve strength when in combination with aerobic exercise, compared with aerobic exercise alone. Research has shown that high-speed resistance training, over a 12-week period, had shown a greater improvement in muscle power and capacity when compared to low-speed training. It was also recommended that patients exercise only until fatigued, not until “failure,” as a stopping point. Programs must be customized to fit the individual.
Sarcopenic obesity is a form of deconditioning that occurs naturally with age but is compounded by cancer. Research into this disease is confounded by a lack of accepted definitions. Radiographic workup and lifestyle changes are the mainstay of medical management. The foremost diagnostic tool remains, as always, clinical suspicion.
Dr. Killeen is a physician in Tampa, Fla. He practices internal medicine, hematology, and oncology, and has worked in hospice and hospital medicine.
Recommended reading
Gruber ES et al. Sarcopenia and Sarcopenic Obesity are independent adverse prognostic factors in resectable pancreatic ductal adenocarcinoma. PLoS One. 2019;14(5): e02115915.10.1371/journal.pone.0215915 [PMID 31059520].
Lombardo M et al. Sarcopenic Obesity: Etiology and lifestyle therapy. Eur Rev Med Pharmacol Sci. 2019; 23: 7152-62.
Petroni M et al. Prevention and treatment of Sarcopenic Obesity in women. Nutrients. 2019; Jun 8.10.3390/nu1161302 [PMID 31181771].
Barcos VE, Arribas L. Sarcopenic Obesity: Hidden muscle wasting and its impact for survival and complications of cancer therapy. Ann Oncol. 2018;29(suppl. 2):ii1-ii9.
Zhang X et al. Association of Sarcopenic Obesity with the risk of all-cause mortality among adults over a broad range of different settings: An update meta-analysis. BMC Geriatr. 2018;19:183-97.
Key points
- • In sarcopenic obesity a patient’s muscle loss in mass can be clouded, overshadowed by the obese body habitus. The major diagnostic tool initially is clinical suspicion.
- • The diagnostic tests for sarcopenic obesity are DXA and CT scans.
- • The best treatment for sarcopenic obesity is a good exercise plan.
Quiz
1. What is the best treatment for sarcopenic obesity?
A. Testosterone
B. Vitamin K
C. Myostatin inhibitors
D. None of the above
Answer: D
There is no particular pharmaceutical treatment, to date, for sarcopenic obesity. Only an exercise program has proved to be of benefit. Those for whom fatigue might be problematic could benefit perhaps by doing “energy banking” or taking programmed naps/rest periods prior to exercise.
2. DXA scans are favored over CT scans because of which of the following?
A. Less cost
B. Capacity to diagnose osteoporosis
C. Less radiation exposure
D. All of the above
Answer: D
DXA scans offer all of the above advantages over CT scans. Also, patients with sarcopenic obesity found to be osteoporotic could be started on vitamin D and calcium supplementation.
3. Which of the following hamper the diagnosis and treatment of sarcopenic obesity?
A. The issue of muscle function
B. Difficulties in comparative research studies
C. Remembering that muscle wasting can occur without external evidence of cachexia
D. All of the above
Answer: D
Obtaining a precise definition of sarcopenic obesity and dealing with the issue of muscle strength and capacity make comparative studies difficult. The sarcopenic obese patient needs as much attention as the cachectic one as their wasting is from within.
4. In sarcopenic obesity and cancer the presence of sarcopenia is likely to lead to which of the following?
A. Earlier death
B. Decreased capacity for therapy
C. Less treatment focus compared to nonsarcopenic patients
D. All of the above
Answer: D
The presence of sarcopenia correlates to all of the above particularly as the obese patient is thought to require less intensive attention than others.
Case
The patient is a 65-year-old white female who recently was discovered to have a 2-cm spiculated lung mass in the right upper lobe. She is undergoing an evaluation at present but her main complaint today is that of profound weakness and fatigue. Her appetite and energy level are noticeably less; her family ascribes this to anxiety and depression. Her other medical problems include diabetes, hypertension, osteoporosis, and obesity. The patient believes that she’s lost about 20-25 pounds recently, though her family is skeptical, adding that “she’s been heavy all her life.” Her body mass index is 40. What additional interventions would you add to her workup?
Background
Sarcopenic obesity occurs as a natural consequence of aging. As a general rule, as many as half the women and a quarter of the men over age 80 years are affected. A total of about 18 million people are involved.
One thought as to etiology is that as one ages, proteolysis outdoes protein synthesis. Fat then replaces the body’s muscle, permeates the viscera, and becomes the prominent body form. Chronic lipodeposition leads to chronic inflammation which, in turn, augments protein catabolism. The elderly become less energetic and less active, and the muscle mass decreases further. A vicious cycle develops. Concurrently with obesity, patients suffer with the onset of dyslipidemia, osteoarthritis, osteoporosis (due to vitamin D deficiency), insulin resistance, and an overall increase in frailty.
Sarcopenic obesity also plays a prognostic role in the management of cancer patients where the presence of sarcopenia correlates with earlier death and decreased capacity for therapy. Patients seen as obese are less likely to receive the intensive care (particularly nutritional support) that patients seen as a higher risk receive. The cancer cachexia is less pronounced. The obesity seen externally masks the wasting within.
Diagnosis and treatment
Sarcopenic obesity suffers from an inexact definition. According to the World Health Organization, obesity is defined, officially, as a body mass index of greater than 30 kg/m2. Muscle mass is an important part of this entity, too, but the inclusion of muscle function in this definition brings, seemingly, a point of conjecture. Is muscle function necessary? By what scale do you measure it? This imprecision makes comparative research in the field somewhat more difficult.
As clinical acumen remains the major diagnostic approach to this disease, confirmatory testing for sarcopenic obesity comprises MRIs/CTs and dual energy x-ray absorptiometry (DXA) scans. Presently DXA is used to assess bone density in the diagnosis of osteoporosis. It also reveals the decreased lean appendicular (extremity) muscle mass which, along with the increased BMI, forms the basic diagnosis of sarcopenic obesity. DXA scans are favored over CTs for the assessment of appendicular lean muscle mass. DXA scans provide a relatively inexpensive method of estimating fat, muscle, and additionally, bone density. CTs are less favored because of their radiation exposure as well as their high cost. Assessing muscle strength, using handgrip dynomometry, is available though not widely advocated.
Of the myriad modalities tried in sarcopenic obesity, many have shortcomings. No particular diet format can be advocated. Hypocaloric diets, with or without protein supplementation, offer little advantage to a good physical exercise program. The administration of vitamin D, with calcium, can be of benefit to those sarcopenically obese patients suffering with osteoporosis. Other medications, as exemplified by testosterone, vitamin K, myostatin inhibitors, or mesenchymal stem cells, are either anecdotal or dubious in nature. More research is definitely needed.
The key component for the treatment of sarcopenic obesity is exercise, both aerobic and resistant. Physical exercise recruits muscle satellite cells into the muscle fibers strengthening their composition. Growth factors are also released that stimulate the production of muscle satellite cells. Muscle mass becomes augmented and fortified. Aerobic exercise counteracts the negative metabolic effects of lipids. Resistance training is felt to improve strength when in combination with aerobic exercise, compared with aerobic exercise alone. Research has shown that high-speed resistance training, over a 12-week period, had shown a greater improvement in muscle power and capacity when compared to low-speed training. It was also recommended that patients exercise only until fatigued, not until “failure,” as a stopping point. Programs must be customized to fit the individual.
Sarcopenic obesity is a form of deconditioning that occurs naturally with age but is compounded by cancer. Research into this disease is confounded by a lack of accepted definitions. Radiographic workup and lifestyle changes are the mainstay of medical management. The foremost diagnostic tool remains, as always, clinical suspicion.
Dr. Killeen is a physician in Tampa, Fla. He practices internal medicine, hematology, and oncology, and has worked in hospice and hospital medicine.
Recommended reading
Gruber ES et al. Sarcopenia and Sarcopenic Obesity are independent adverse prognostic factors in resectable pancreatic ductal adenocarcinoma. PLoS One. 2019;14(5): e02115915.10.1371/journal.pone.0215915 [PMID 31059520].
Lombardo M et al. Sarcopenic Obesity: Etiology and lifestyle therapy. Eur Rev Med Pharmacol Sci. 2019; 23: 7152-62.
Petroni M et al. Prevention and treatment of Sarcopenic Obesity in women. Nutrients. 2019; Jun 8.10.3390/nu1161302 [PMID 31181771].
Barcos VE, Arribas L. Sarcopenic Obesity: Hidden muscle wasting and its impact for survival and complications of cancer therapy. Ann Oncol. 2018;29(suppl. 2):ii1-ii9.
Zhang X et al. Association of Sarcopenic Obesity with the risk of all-cause mortality among adults over a broad range of different settings: An update meta-analysis. BMC Geriatr. 2018;19:183-97.
Key points
- • In sarcopenic obesity a patient’s muscle loss in mass can be clouded, overshadowed by the obese body habitus. The major diagnostic tool initially is clinical suspicion.
- • The diagnostic tests for sarcopenic obesity are DXA and CT scans.
- • The best treatment for sarcopenic obesity is a good exercise plan.
Quiz
1. What is the best treatment for sarcopenic obesity?
A. Testosterone
B. Vitamin K
C. Myostatin inhibitors
D. None of the above
Answer: D
There is no particular pharmaceutical treatment, to date, for sarcopenic obesity. Only an exercise program has proved to be of benefit. Those for whom fatigue might be problematic could benefit perhaps by doing “energy banking” or taking programmed naps/rest periods prior to exercise.
2. DXA scans are favored over CT scans because of which of the following?
A. Less cost
B. Capacity to diagnose osteoporosis
C. Less radiation exposure
D. All of the above
Answer: D
DXA scans offer all of the above advantages over CT scans. Also, patients with sarcopenic obesity found to be osteoporotic could be started on vitamin D and calcium supplementation.
3. Which of the following hamper the diagnosis and treatment of sarcopenic obesity?
A. The issue of muscle function
B. Difficulties in comparative research studies
C. Remembering that muscle wasting can occur without external evidence of cachexia
D. All of the above
Answer: D
Obtaining a precise definition of sarcopenic obesity and dealing with the issue of muscle strength and capacity make comparative studies difficult. The sarcopenic obese patient needs as much attention as the cachectic one as their wasting is from within.
4. In sarcopenic obesity and cancer the presence of sarcopenia is likely to lead to which of the following?
A. Earlier death
B. Decreased capacity for therapy
C. Less treatment focus compared to nonsarcopenic patients
D. All of the above
Answer: D
The presence of sarcopenia correlates to all of the above particularly as the obese patient is thought to require less intensive attention than others.