Physical exam

What is the connection between anosmia, anasognosia and Alzheimer’s disease?

FA Manian MD, MPHLeave a comment

Both anosmia (loss of smell) and anosognosia (lack of awareness or insight of a deficit) appear to be strongly associated with higher risk of development of Alzheimer’s Disease (AD).1,2

In a study involving 90 patients with mild cognitive impairment (MCI) followed for up to 2 years, subjects with low olfaction scores were significantly more likely to develop AD than those with high scores (40% vs 0%, p<0.001).  In the same study, all patients with anosognosia (accounting for 84% of the low olfaction group) developed AD irrespective of higher baseline Mini Mental State Examination (MMSE) score. 1

A 2017 meta-analysis of olfactory dysfunction in MCI also found a significant association between olfactory deficits and MCI with tests of odor identification having larger effect sizes than those of odor detection threshold or memory.2

As for possible mechanisms, anosmia in AD is felt to be due to degeneration of neurons of the entorhinal- hippocampal-subicular complex associated with an observed increase in neurofibrillary tangles.3 Interestingly, the density of tau tangles in the entorhinal cortex have been shown to be inversely related to odor identification.4  There also seems to be a correlation between anosognosia and atrophy in the dorsal anterior cingulate cortex, reflected by the finding of hypometabolism on PET-FDG images6.

Bonus Pearl: Did you know that anosmia and ageusia (loss of sense of taste) are also common nonmotor feature of Parkinson’s Disease and can predate onset of motor symptoms by years? 5

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References

  1. Devanand DP, Michaels-Marston KD, Liu X, et al: Olfactory Deficits in Patients With Mild Cognitive Impairment Predict Alzheimer’s Disease at Follow-Up. Am J Psychiatry, 2000; 157:1399-405 https://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.157.9.1399                                   
  2. Roalf DR, Moberg MJ, Turetsky BI, et al: A quantitavie meta-analysis of olfactory dysfunction in mild cognitive impairment. J Neurology Neurosurg Psychiatry 2017;88:226-232. https://jnnp.bmj.com/content/88/3/226
  3. Talamo BR, Rudel R, Kosik KS, et al: Pathological changes in olfactory neurons in patients with Alzheimer’s disease. Nature 1989; 337:736–739. https://doi.org/10.1038/337736a0 
  4. Wilson RS, Arnold, SE, Schneider JA, et al: The relationship between cerebral Alzheimer’s disease pathology and odour identification in old age. J Neurol Neurosurg Psychiatry, 2007;78:30-5. https://doi.org/10.1136/jnnp.2006.099721
  5. Tarakad A, Jankovic J: Anosmia and Ageusia in Parkinson’s Disease. International Review of Neurobiology, 2017; 133:541-556https://doi.org/10.1016/bs.irn.2017.05.028
  6. Guerrier L, Le Men J, Gain, A, et al: Involvement of the Cingulate Cortex in Anosognosia: A Multimodal Neuroimaging Study in Alzheimer’s Disease Patients. Journal of Alzheimer’s Disease 2018; 65:443-453. https://content.iospress.com/articles/journal-of-alzheimers-disease/jad180324

Contributed by Jackie Fairchild MD, Mercy Hospital-St. Louis, St. Louis, Missouri

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy, its affiliate healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is the connection between anosmia, anasognosia and Alzheimer’s disease?

My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

Not likely! There is no evidence that TKA causes Baker’s cyst (also known as popliteal cyst). Instead, the finding of Baker’s cyst following TKA may be best explained by its well-known association with osteoarthritis, one of the main indications for TKA.1,6,7

In a study of 2025 patients who underwent primary TKA, 0.6% were diagnosed with Baker’s cysts within 6 weeks to 2 years postoperatively (75% symptomatic), but whether the cysts were present prior to TKA was unclear. There was no reported association between surgical technique or perioperative course and Baker’s cyst diagnosis.9

Actually, there might be a correlation between TKA and Baker’s cyst resolution.2,3 Among patients with known cysts preoperatively, 15% and 67% of patients may experience resolution of the cyst at 1 year and 4-6 years following surgery, respectively. 2,3

A Baker’s cyst is a fluid-filled pocket in the posterior aspect of the knee, typically seen in adults with degenerative changes in the patellofemoral joint, as may occur with meniscal tears and arthritis. When symptomatic, it can be treated non-operatively with ultrasound-guided aspiration and corticosteroid injection or operatively with surgical excision or attempted repair of the underlying defect. 4,8

 

Bonus Pearl: Did you know that the ‘crescent sign’ (bruising below the medial malleolus associated with fluid from ruptured cyst moving inferiorly toward the ankle) was first described in 1976 and may help distinguish calf pain due to Baker’s cyst from that of deep venous thrombophlebitis? 5

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 Contributed by Anamika Veeramani, Medical Student, Harvard Medical School

 

References

  1. Guermazi A., Hayashi D., Roemer F, et al. Cyst-like lesions of the knee joint and their relation to incident knee pain and development of radiographic osteoarthritis: The MOST study. Osteoarthritis and Cartilage 2010; 18:1386-1392. doi:10.1016/j.joca.2010.08.015. https://pubmed.ncbi.nlm.nih.gov/20816978/
  2. Hommel H., Becker R., Fennema P., et al. (2020). The fate of Baker’s cysts at mid-term follow-up after total knee arthroplasty. The Bone & Joint Journal, 2020;102-B(1):132-136. doi:10.1302/0301-620x.102b1.bjj-2019-0273.r2. https://pubmed.ncbi.nlm.nih.gov/31888367/
  3. Hommel, H., Perka, C., Kopf, S. The fate of Baker’s cyst after total knee arthroplasty. The Bone & Joint Journal 2016;98-B(9):1185-1188. doi:10.1302/0301-620x.98b9.37748. https://pubmed.ncbi.nlm.nih.gov/27587518/
  4. Leib AD, Roshan A, Foris LA, et al. Baker’s Cyst. [Updated 2020 Mar 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430774/
  5. Mizumoto, J. The crescent sign of ruptured baker’s cyst. Journal of General Family Medicine, 2019;20(5): 215-216. doi: 10.1002/jgf2.261. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6732489/
  6. Rupp, S., Seil, R., Jochum, P., & Kohn, D. Popliteal Cysts in Adults. The American Journal of Sports Medicine 2002; 30(1): 112-115. doi:10.1177/03635465020300010401. https://pubmed.ncbi.nlm.nih.gov/11799006/
  7. Sansone, V., Ponti, A. D., Paluello, G. M., & Maschio, A. D. Popliteal cysts and associated disorders of the knee. International Orthopaedics 1995;19(5): 275-279. doi:10.1007/bf00181107. https://pubmed.ncbi.nlm.nih.gov/8567131/
  8. Smith, M., Lesniak, B., Baraga, M., Kaplan, L., Jose, J. Treatment of Popliteal (Baker) Cysts with Ultrasound-Guided Aspiration, Fenestration and Injection: Long-term Follow-up. Sports Health 2015; 7(5): 409-414. doi: 10.1177/1941738115585520. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547114/
  9. Tofte, J. N., Holte, A. J., & Noiseaux, N. Popliteal (Baker’s) Cysts in the Setting of Primary Knee Arthroplasty. The Iowa Orthopedic Journal 2017;37:177-180. https://pubmed.ncbi.nlm.nih.gov/28852354/

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

Why is my diabetic patient complaining of arm pain and localized edema for couple of weeks without an obvious cause?

FA Manian MD, MPH, , , , , , , , , , , , , , Leave a comment

Aside from the usual suspects associated with a painful extremity (eg, trauma, deep venous thrombosis and soft tissue infections), think of spontaneous diabetic myonecrosis (DMN), also known as diabetic muscle infarction (1-3).

DMN is characterized by abrupt onset of painful swelling of the affected muscle, most often of the lower extremities, but also occasionally upper extremities. DMN occurs in patients with longstanding DM whose blood glucose control has deteriorated over time, often with nephropathy, retinopathy and/or neuropathy (1-3).

Couple of things to remember when considering DMN in your differential of a painful extremity. First, except for localized edema and tenderness over the involved muscle, the exam may be unremarkable. Specifically, there is no erythema or signs of compartment syndrome and fever is absent in the great majority of patients (~90%) (2). Even white blood cell count and creatine kinase (CK) are usually normal. The reason for normal CK at presentation is not clear but CK might have already peaked by the time of patient presentation (3). In contrast, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are usually elevated (>80%) (1).

MRI (without contrast in patients with renal insufficiency) is the imaging of choice with muscle enlargement and edema with hyperintense signal on T2-weighted images and other changes, including perifascial, perimuscular and or subcutaneous edema (1-3). Muscle biopsy is not currently recommended because of its adverse impact on time to symptomatic improvement. Non-surgical therapy, with rest, analgesia and glycemic control is usually recommended (1-3).

 
Though its exact cause is still unclear, atherosclerosis, diabetic microangiopathy, vasculitis with thrombosis and ischemia-reperfusion injury have been posited as potential precipitants for DMN. The role of anti-phospholipid syndrome, particularly in patients with type I DM, is unclear (1,2).

 
Bonus pearl: Did you know that symptoms of DMN may last for weeks with at least one-third of patients having a recurrence in the same muscle or elsewhere (1)?

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Reference
1. Horton WB, Taylor JS, Ragland TJ, et al. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Research and Care 2015;3:e000082.
2. Trujillo-Santos AJ. Diabetic muscle infarction. An underdiagnosed complication of long-standing diabetes. Diabetes Care 2003;26:211-15.
3. Diabetes muscle infarction in end-stage renal disease:A scoping review on epidemiology, diagnosis and treatment. World J Nephrol 2018;7:58-64.

Why is my diabetic patient complaining of arm pain and localized edema for couple of weeks without an obvious cause?

My patient with jaundice complains of abdominal fullness. How useful is the history or physical exam when assessing for ascites?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

Even in the age of ultrasound, history and physical exam can be useful in assessing for ascites.

History is a good place to start. Of all the questions we often ask when we suspect ascites (eg, increasing abdominal girth, weight gain and ankle swelling), lack of report of ankle swelling is probably the most helpful in excluding ascites (negative likelihood ratio [LR-], 0.1 in a study involving men), followed by no increase in abdominal girth (LR-, 0.17). Conversely, patient reported ankle swelling or increasing abdominal girth may be helpful in suspecting ascites (LR+ 4.12 and 2.8, respectively). 1

Of the various physical signs and maneuvers, absence of peripheral edema is highly associated with the lack of ascites, followed by lack of shifting dullness or fluid wave (LR-, 0.2, 0.3, 0.4, respectively). The presence of a fluid wave may be the most helpful in suspecting ascites, followed by peripheral edema, and shifting dullness (LR+ 6.0, 3.8, 2.7, respectively). 1  Relatively high sensitivities have been reported for shifting dullness (83-88%), while relatively high specificities have been reported for the fluid wave test (82-90%).2,3 An elevated INR may also improve the positive predictive value of shifting dullness and fluid waves.4

So if you don’t get a history of ankle edema and find no evidence of peripheral edema or shifting dullness on exam, the likelihood of ascites is pretty low. On the other hand, if you find a positive fluid wave, you can be pretty sure that the patient has ascites.

Of course, the actual likelihood of detecting ascites also depends on several other factors, including your pre-test probability and the volume of the ascites in the abdominal cavity, with at least ~500 ml of ascites necessary before it can be detected on exam (vs ~100 ml for ultrasound). 2,5

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References

  1. Williams JW, Simetl DL. Does this patient have ascites? How to divine fluid in the abdomen. JAMA 1992;267: 2645-48. https://jamanetwork.com/journals/jama/fullarticle/397285
  2. Cattau EL, Benjamin SB, Knuff TE, et al The accuracy of the physical examination in the diagnosis of suspected ascites. JAMA 1982;247:1164-66. https://www.ncbi.nlm.nih.gov/pubmed/7057606
  3. Cummings S, Papadakis M, Melnick J, et al. The predictive value of physical examinations for ascites. West J Med 1985;142:633-36. https://www.ncbi.nlm.nih.gov/pubmed/3892916
  4. Fitzgerald FT. Physical diagnosis versus modern technology. A review. West J Med 1990;152:377-82. https://www.ncbi.nlm.nih.gov/pubmed/2190412
  5. CDC. Assessment for ascites. https://www.cdc.gov/dengue/training/cme/ccm/Assess%20for%20Ascites_F.pdf. Accessed November 13, 2019.
My patient with jaundice complains of abdominal fullness. How useful is the history or physical exam when assessing for ascites?

My 70 year old male patient is admitted with 1 day of fever, dysuria, and urinary frequency and urgency, but has a negative urine dipstick test for nitrites and leukocyte esterase. Could he still have acute bacterial prostatitis?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

Short answer: Yes! In fact, no routine clinical imaging test can adequately rule out prostatic involvement in men with urinary tract infection (UTI) symptoms (1)! 

Although the presence of nitrites and leukocyte esterase (LE) may have a high positive predictive value for acute bacterial prostatitis (ABP) (~95%), their combined absence has a negative predictive value of only ~70%; ie, we may miss about one-third of patients with UTI symptoms if we relied solely on the results of nitrite and LE urine dipstick (2,3). Negative nitrites alone has a negative predictive value of only ~ 45%, while a negative LE has a negative predictive value of ~60% (3).

To evaluate for ABP, our patient should undergo rectal exam for prostatic tenderness, as should all men with UTI symptoms. The finding of a tender prostate in this setting is supportive of ABP, although its absence will still not rule out this diagnosis because the reported sensitivity of rectal exam may vary from 9% to 100% in ABP (1).

 
Although there may not be a general agreement on the definition of ABP, 2 studies utilizing indium-labeled leukocyte scintigraphy or a combination of PSA levels and transrectal ultrasound have provided evidence for frequent prostatic involvement in men with UTI symptoms (4,5).  In these studies, an inflammatory reaction within the prostate was seen in the majority of cases, even when the digital rectal examination was not painful or when clinicians diagnosed pyelonephritis without prostatitis.

Bonus pearl: Did you know that the lifetime probability of a man receiving a diagnosis of prostatitis is >25% (1)? 

Also see a related P4P pearl: Acute prostatitis and u/a

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References
1. Etienne M, Chavanet P, Sibert L, et al. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infect Dis 2008, 8:12 doi:10.1186/1471-2334-8-12. https://bmcinfectdis.biomedcentral.com/articles/10.1186/1471-2334-8-12
2. Lipsky BA, Byren I, Hoey CT. Treatment of bacterial prostatitis. Clin Infect Dis 2010;50:1641-1652. https://academic.oup.com/cid/article/50/12/1641/305217
3. Etienne M, Pestel-Caron M, Chavanet P, et al. Performance of the urine leukocyte esterase and nitrite dipstick test for the diagnosis of acute prostatitis. Clin Infect Dis 2008; 46:951-53. https://academic.oup.com/cid/article/46/6/951/351423
4. Velasco M, Mateos JJ, Martinez JA, et al. Accurate topographical diagnosis of urinary tract infection in male patients with (111)indium-labelled leukocyte scintigraphy. Eur J Intern Med 2004;15:157-61. https://www.ncbi.nlm.nih.gov/pubmed/15245717
5. Ulleryd P, Zackrisson B, Aus G, et al. Prostatic involvement in men with febrie urinary tract infection as measured by serum prostate-specific antigen and transrectal ultrasonography. BJU Int 1999;84:470-74. https://onlinelibrary.wiley.com/doi/full/10.1046/j.1464-410x.1999.00164.x

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My 70 year old male patient is admitted with 1 day of fever, dysuria, and urinary frequency and urgency, but has a negative urine dipstick test for nitrites and leukocyte esterase. Could he still have acute bacterial prostatitis?

My elderly patient with abdominal pain has a negative Murphy’s sign on physical exam. How accurate is Murphy’s sign in diagnosing cholecystitis?

FA Manian MD, MPH, , , , , , Leave a comment

Not as accurate as we might like! In fact, no single clinical finding has been found to carry sufficient weight in ruling in or excluding cholecystitis and Murphy’s sign (inability to take a deep breath due to pain upon palpation of the right upper quadrant) is no exception. 1

A meta-analysis of patients with Murphy’s sign reported a sensitivity of 65% and a specificity of 87% (positive LR 2.8, negative LR 0.4, with 95% C.I. including 1.0 in both). 1,2  However, among the elderly (mean age 79 y), the sensitivity may be as slow as 48% 2 and in patients with gangrenous cholecystitis as low as 33%.3  

In contrast, Murphy’ s sign elicited at the time of ultrasound of the gallbladder (ie,“sonographic Murphy’s) is generally thought to very sensitive  (>90%) for acute cholecystitis;3,4 1 study reported a sensitivity of 63%, however (specificity 94%).5  Remember that altered mental status may also mask sonographic Murphy’s sign. 

Indirect fist percussion of the liver has been suggested by some authors as a more sensitive alternative to Murphy’s sign (100% vs 80%) in a small series of patients with cholecystitis.2

Bonus pearl: Did you know that another technique originally described by the famed American surgeon, John Murphy, to diagnose acute cholecystitis consisted of the “hammer stroke maneuver” in which percussion of the right midsubcostal region with the bent middle finger of the left hand was performed using the right hand to strike the dorsum of the left hand with hammer-like blows? 6

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References

  1. Trowbridge RL, Rutkowski NK, Shojania KG. Does this patient have acute cholecystitis. JAMA 2003;289:80-86. https://jamanetwork.com/journals/jama/article-abstract/195707
  2. Ueda T, Ishida E. Indirect fist percussion of the liver is a more sensitive technique for detecting hepatobiliary infections than Murphy’s sign. Current Gerontol Geriat Res, Volume 2015, Article ID 431638. https://www.hindawi.com/journals/cggr/2015/431638/
  3. Simeone JF, Brink JA, Mueller PR, et al. The sonographic diagnosis of acute gangrenous cholecystitis. The importance of the Murphy sign. AJR 1989;152:289-90. https://www.ncbi.nlm.nih.gov/pubmed/2643262
  4. O’Connor OJ, Maher MM. Imaging of cholecystitis. AJR 2011;196:W36774. https://www.ajronline.org/doi/full/10.2214/AJR.10.4340
  5. Rallis PW, Lapin SA, Quinn MF, et al. Prospective evaluation of the sonographic Murphy sign in suspected acute cholecystitis. J Clin Ultrasound 1982;10:113-5. https://www.ncbi.nlm.nih.gov/pubmed/6804512
  6. Salati SA, al Kadi A. Murphy’s sign of cholecystitis-a brief revisit. Journal of Signs and Symptoms 2012;1:53-6. https://www.researchgate.net/publication/230820198_Murphy’s_sign_of_cholecystitis-_a_brief_revisit

 

 

My elderly patient with abdominal pain has a negative Murphy’s sign on physical exam. How accurate is Murphy’s sign in diagnosing cholecystitis?

My patient with angina symptoms also complains of neck pain with left arm numbness. Could they be related?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

Short answer, yes! Anterior chest pain associated with cervical intervertebral disk disease, ossified posterior longitudinal ligament or other spinal disorders is sometimes referred to as “cervical angina” (CA) or “pseudoangina” and is an often overlooked source of non-cardiac chest pain. 1-5

Although its exact prevalence is unknown, 1.4% to 16% of patients undergoing cervical disk surgery may have symptoms of CA. 1 Conversely, 1 study reported 5% of patients with angina pectoris having cervical nerve root pathology.5 Many patients describe their chest pain as “pressure” or crushing in quality mimicking typical cardiac ischemia chest pain, often resulting in extensive cardiac workup.  To add to the confusion, some patients even respond to nitroglycerin! One-half of patients also experience autonomic symptoms such as dyspnea, vertigo, nausea, diaphoresis, pallor, fatigue, and diploplia.1

Certain clues in the patient’s presentation should help us seriously consider the possibility of CA: 1-3

  • History of cervical radiculopathy eg, subjective upper extremity weakness or sensory changes, occipital headache or neck pain
  • Pain induced by cervical range of motion or movement of upper extremity
  • History of cervical injury or recent manual labor (eg, lifting, pulling or pushing)
  • Pain lasting greater than 30 min or less than 5 seconds and not relieved by rest
  • Positive Spurling maneuver ie, reproduction of symptoms by rotating the cervical spine toward the symptomatic side while providing a downward compression through the patient’s head

CA is often attributed to cervical nerve root compression, likely mediated by compression of C4-C8 nerve roots which also supply the sensory and motor innervation of the anterior chest wall.

Bonus Pearl: Did you know that experimental stimulation of spinothalamic tract cells in the upper thoracic and lower cervical segments have been shown to reproduce angina pain? 6

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 References

 

  1. Susman WI, Makovitch SA, Merchant SHI, et al. Cervical angina: an overlooked source of noncardiac chest pain. The Neurohospitalist 2015;5:22-27. https://www.ncbi.nlm.nih.gov/pubmed/25553225
  2. Jacobs B. Cervical angina. NY State J Med 1990;90:8-11. https://www.ncbi.nlm.nih.gov/pubmed/2296405
  3. Sheps DS, Creed F, Clouse RE. Chest pain in patients with cardiac and noncardiac disease. Psychosomatic Medicine 66:861-67. https://www.ncbi.nlm.nih.gov/pubmed/15564350
  4. Wells P. Cervical angina. Am Fam Physician 1997;55:2262-4. https://www.ncbi.nlm.nih.gov/pubmed/9149653
  5. Nakajima H, Uchida K, Kobayashi S, et al. Cervical angina: a seemingly still neglected symptom of cervical spine disorder. Spinal Cord 2006;44:509-513. https://www.ncbi.nlm.nih.gov/pubmed/16331305
  6.  Cheshire WP. Spinal cord infarction mimicking angina pectoris. Mayo Clin Proc 2000;75:1197-99. https://www.ncbi.nlm.nih.gov/pubmed/11075751

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

My patient with angina symptoms also complains of neck pain with left arm numbness. Could they be related?

How can I distinguish cardiac asthma from typical bronchial asthma?

FA Manian MD, MPH, , , , , , , , Leave a comment

Certain clinical features of cardiac asthma, defined as congestive heart failure (CHF) associated with wheezing, may be useful in distinguishing it from bronchial asthma, particularly in older patients with COPD (1-3).

• Paroxysmal nocturnal dyspnea associated with wheezing
• Presence of rales or crackles, ascites or other signs of CHF
• Poor response to bronchodilators and corticosteroids
• Formal pulmonary function test with bronchoprovocation demonstrating minimal methacholine response.

Cardiac asthma is not uncommon. In a prospective study of patients 65 yrs of age or older (mean age 82 yrs) presenting with dyspnea due to CHF, cardiac asthma was diagnosed in 35% of subjects. Even in non-elderly patients, cardiac asthma has been reported in 10-15% of patients with CHF (2).

The mechanism(s) underlying cardiac asthma is likely multifactorial. Pulmonary edema and pulmonary vascular congestion have traditionally been considered as key factors either through edema in the interstitial fluid of bronchi squeezing the bronchiolar lumen or by externally compressing the entire airway structure and the bronchiole wall. Reflex bronchoconstriction involving the vagus nerve, bronchial hyperreactivity, systemic inflammation, and airway remodeling may also play a role (1,3). 

Treatment of choice for cardiac asthma typically includes diuretics, nitrates and morphine, not bronchodilators or corticosteroids (1,3). 

Bonus Pearl: Did you know that the term “cardiac asthma” was first coined by the Scottish physician, James Hope, way back in 1832 to distinguish it from bronchial asthma!

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References
1. Litzinger MHJ, Aluen JKN, Cereceres R, et al. Cardiac asthma: not your typical asthma. US Pharm. 2013;38:HS-12-HS-18. https://www.uspharmacist.com/article/cardiac-asthma-not-your-typical-asthma
2. Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly patients: incidence, clinical presentation and outcome. BMC Cardiovascular Disorders 2007;7:16. https://www.ncbi.nlm.nih.gov/pubmed/17498318
3. Tanabe T, Rozycki HJ, Kanoh S, et al. Cardiac asthma: new insights into an old disease. Expert Rev Respir Med 2012;6(6), 00-00. https://www.ncbi.nlm.nih.gov/pubmed/23234454

How can I distinguish cardiac asthma from typical bronchial asthma?

What is the significance of Terry’s or Lindsay’s nails in my hospitalized patient?

FA Manian MD, MPH, , , , , , , , , , , , , Leave a comment

Terry’s nails were first described in 1954 in patients with hepatic cirrhosis (prevalence 82%, majority related to alcohol abuse) (1). Since then, they have been reported in a variety of other conditions, including adult-onset diabetes mellitus (AODM), chronic congestive heart failure, chronic renal failure, pulmonary tuberculosis, and Reiter’s syndrome (2).

A 1984 study found Terry’s nails in 25% of hospitalized patients (3).  In this study, cirrhosis, chronic congestive heart failure, and AODM were significantly associated with Terry’s nails, while pulmonary tuberculosis, rheumatoid arthritis and cancer were not. The presence of Terry’s nails may be particularly concerning in patients 50 y of age or younger as it increases the relative risk of cirrhosis, chronic congestive heart failure or AODM by 5-fold (18-fold for cirrhosis alone) in this age group (3).

Terry’s nails should be distinguished from Lindsay’s nails or “half and half” nails. Although both nail abnormalities are characterized by an opaque white proximal portion, Terry’s nails have a thinner distal pink to brown transverse band no more than 3 mm wide (3) (Fig 1), while the same anomaly is wider and occupies 20%-60% of the nail bed in Lindsay’s nails (Fig 2). Of interest, Lindsay’s nails have been reported in up to 40% of patients with chronic kidney disease (4,5).

References

1. Terry R. White nails in hepatic cirrhosis. Lancet 1954;266:757-59. https://www.ncbi.nlm.nih.gov/pubmed/13153107 
2. Nia AM, Ederer S, Dahlem K, et al. Terry’s nails: a window to systemic diseases. Am J Med 2011;124:603-604. https://www.ncbi.nlm.nih.gov/pubmed/21683827 
3. Holzberg M, Walker HK. Terry’s nails: revised definitions and new correlations. Lancet 1984;1(8382):896-99. https://www.ncbi.nlm.nih.gov/pubmed/6143196 
4. Pitukweerakul S, Pilla S. Terry’s nails and Lindsay’s nails: Two nail abnormalities in chronic systemic diseases. J Gen Intern Med 31;970.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4945547/ 
5. Gagnon AL, Desai T. Dermatological diseases in patients with chronic kidney disease 2013;2:104-109.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891143/

Figure 1. Terry’s nails in a patient with end-stage liver disease

Figure 2. Lindsay’s nails in a patient with chronic kidney disease

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What is the significance of Terry’s or Lindsay’s nails in my hospitalized patient?

How accurate are peripheral thermometers for estimating body temperature in my patient with chills?

FA Manian MD, MPH, , , , , , , , Leave a comment

Though convenient, oral, tympanic membrane, axillary, and temporal artery thermometers (AKA “peripheral thermometers”) may not be highly accurate in measuring body temperature.

A 2015 systematic review and meta-analysis of the performance of peripheral thermometers involving 75 studies (mostly in adults) found that compared to central thermometers (eg, pulmonary artery, urinary bladder, rectal), peripheral thermometers had a low sensitivity (64%, 95% CI 55%-72%), but much better specificity (96%, 95% CI 93%-97%) for fever (most commonly defined as 37.8° C [100° F] or greater).1

In the same study, for oral electronic thermometers, sensitivity was 74% with a specificity of 86%. For temporal artery thermometers, sensitivities ranged from 26% to 91%, while specificities ranged from 67% to 100%. For tympanic membrane thermometers, sensitivities ranged from 23% to 87%, with a specificity of 57% to 99%.

A 2016 study involving adult emergency department patients reported the sensitivity of peripheral thermometers (vs rectal temperature 38 C [100.4] or higher) as follows: oral (37%), tympanic membrane (68%), and temporal artery (71%). Specificity for fever was >90% for all peripheral thermometers. 2

So, it looks like while we may be pretty comfortable with a diagnosis of “fever” when our patient with chills has a high temperature recorded by a peripheral thermometer, lack of fever alone by these devices should not veer us away from the possibility of systemic infection. When in doubt and if possible, check a rectal temperature.

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References

  1. Niven DJ, Gaudet JE, Laupland KB. Accuracy of peripheral thermometers for estimating temperature: A systematic and meta-analysis. Ann Intern Med 2015;163:768-777. https://www.ncbi.nlm.nih.gov/pubmed/26571241
  2. Bijur PE, Shah PD, Esses D. Temperature measurement in the adult emergency department: oral tympanic membrane and temporal artery temperatures versus rectal temperature. Emerg Med J 2016;33:843-7. https://www.ncbi.nlm.nih.gov/pubmed/27334759

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

How accurate are peripheral thermometers for estimating body temperature in my patient with chills?