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?

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: https://pearls4peers.com/2017/07/27/should-male-patients-with-suspected-urinary-tract-infection-routinely-undergo-a-prostate-exam/

 

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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

 

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?

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 a 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?

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

 

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?

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?

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?

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.

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

 

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

My elderly nursing home patient is admitted with recent poor oral intake, falls and oral temperatures of 99.1°-99.3° F(37.3°-37.4°C). Is she considered febrile at these temperatures?

Yes! Even though we often think of temperatures of 100.4°F (38° C) or greater as fever, older people often fail to mount an appropriate febrile response despite having a serious infection. 1

Infectious Diseases Society of America (IDSA) guideline on evaluation of fever in older adult residents of long-term care facilities has defined fever in this population as:2

  • Single oral temperature >100° F (>37.8° C) OR
  • Repeated oral temperatures >99° F (>37.2° C) OR
  • Rectal temperatures >99.5° F (>37.5° C) OR
  • Increase in temperature of >2° F (>1.1° C) over the baseline temperature

Even at these lower than traditional thresholds for defining fever, remember that many infected elderly patients may still lack fever. In a study involving bacteremic patients, nearly 40% of those 80 years of age or older did not have fever (defined as maximum temperature over 24 hrs 100° F [37.8°C] or greater).3  

So our patient meets the criteria for fever as suggested by IDSA guidelines and, particularly in light of her recent poor intake and falls, may need evaluation for a systemic source of infection.

Now that’s interesting! Did you know that blunted febrile response of the aged to infections may be related to the inability of cytokines (eg, IL-1) to reach the central nervous system?1

References 

  1. Norman DC. Fever in the elderly. Clin Infect Dis 2000;31:148-51. https://academic.oup.com/cid/article/31/1/148/318030
  2. High KP, Bradley SF, Gravenstein S, et al. Clinical practice guidelines for the evaluation of fever and infection in older adult residents of long-term care facilities: 2008 update by the Infectious Disease Society of America. Clin Infect Dis 2009;48:149-71. http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/Fever%20and%20Long%20Term%20Care.pdf
  3. Manian FA. Fever, abnormal white blood cell count, neutrophilia, and elevated serum C-reactive protein in adult hospitalized patients with bacteremia. South Med J 2012;105;474-78. http://europepmc.org/abstract/med/22948327
My elderly nursing home patient is admitted with recent poor oral intake, falls and oral temperatures of 99.1°-99.3° F(37.3°-37.4°C). Is she considered febrile at these temperatures?

My patient with COPD has new clubbing of his finger tips. What is the mechanism of clubbing?

The mechanism behind digital clubbing has yet to be fully elucidated, with hypotheses ranging from a circulating vasodilator, tissue hypoxia, a neurocirculatory reflex, and genetic factors. 1 Although hypoxemia is often cited as a cause of clubbing, it is often absent in the presence of clubbing and many patients with hypoxemia do not have clubbing.

A potentially unifying pathophysiologic mechanism of clubbing revolves around platelet clustering and associated growth factor release. 2.3 Platelet clumps/megakaryocytes—either because of circumvention of the lung capillary network (eg, in intracardiac shunts or lung cancer) or increased production (eg, in left-sided endocarditis or chronic inflammatory conditions)—may wedge in the fine vasculature of distal fingertips or toes and cause release of platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF).

Together, PDGF and VEGF promote neovascularization, increase vessel dilation and permeability, and modify connective tissue to create the distinct club-like appearance. Local hypoxic condition from reduced capillary perfusion is thought to further stimulate the release of these growth factors.

Potential causes of clubbing in our patient include lung cancer, interstitial lung disease, bronchiectasis, core pulmonale and secondary polycythemia, among many others. 1

Fun Fact: Did you know that clubbing, also known as “Hippocratic finger”, was first described by Hippocrates in a patient with chronic empyema (don’t ask how chronic empyema was diagnosed in 400 BC!)?1

 

References

  1. McPhee SJ. Clubbing. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths;1990. Chapter 44. Available from https://www.ncbi.nlm.nih.gov/books/NBK366/
  2. Dickinson CJ, Martin JF. Megakaryocytes and platelet clumps as the cause of finger clubbing. Lancet 1987;2:1434-4. https://www.ncbi.nlm.nih.gov/pubmed/2891996/ 
  3. Atkinson S, Fox SB. Vascular endothelial growth factor (VEGF)-A and platelet-derived growth factor (PDGF) play a central role in the pathogenesis of digital clubbing. J Pathol 2004;203:721-8. https://www.ncbi.nlm.nih.gov/pubmed/15141388

 

Contributed by George Bugarinovic, Medical Student, Harvard Medical School

My patient with COPD has new clubbing of his finger tips. What is the mechanism of clubbing?

Can I rely on the physical exam to rule out symptomatic urinary tract infection (UTI) in my hospitalized patient?

Suprapubic tenderness, costovertebral angle tenderness (CVAT) and fever seem to be more helpful in ruling in than ruling out infection. And, before you hang your hat on the available data, remember that most of the studies involve women with uncomplicated UTI in primary care or emergency department settings, not our older hospitalized patients at risk of complicated infections.  With these caveats in mind….

Suprapubic tenderness has been reported in only about 15-20% of women with acute cystitis. 1

CVAT has been associated with symptomatic UTI but with only a weakly positive LR (1.7, 1.1-2.5), and an insignificant negative LR. 2  In a single center study involving hospitalized patients (mean age 53 y), CVAT was either absent or “obscure” in about 10% of patients with acute pyelonephritis on CT.3

Fever was associated with a positive likelihood ratio (1.6, 1.0-2.6) by 1 systematic study 2 but not another, 4 with insignificant negative LR in both. Fever was also absent in about 10% of hospitalized patients with pyelonephritis in the single center study above.3

So, when evaluating a patient with possible symptomatic UTI (particularly cystitis), the presence of physical exam findings  may be more helpful than their absence.

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References

  1. Kurowski K. The woman with dysuria. Am Fam Physician 1998, 57:2155-2164. https://www.aafp.org/afp/1998/0501/p2155.html
  2. Bent S, Nallamothu BK, Simel DL, et al. Does this woman have an acute uncomplicated urinary tract infection? JAMA 2002;287:2701-2710. https://www.ncbi.nlm.nih.gov/pubmed/12020306
  3. Lee Y-J, Cho S, Kim SR. Unilateral and bilateral acute pyelonephritis: differences in clinical presentation, progress and outcome. Postgrad Med 2014;90:80-85. https://www.ncbi.nlm.nih.gov/pubmed/24255118
  4. Median-Bombardo D, Jover-Palmer A. Does clinical examination aid in the diagnosis of urinary tract infections in women? A systematic review and meta-analysis. BMC Family Practice 2011;12:111. https://bmcfampract.biomedcentral.com/articles/10.1186/1471-2296-12-111

 

Can I rely on the physical exam to rule out symptomatic urinary tract infection (UTI) in my hospitalized patient?

What should I include in my hospital admission note to meet the criteria for “moderate” or “high-complexity encounter” as defined by the Centers for Medicare & Medicaid Services (CMS)?

Aside from clearly documenting the chief complaint or reason for the encounter to establish medical necessity for your service,  certain history, exam and medical decision making elements in the admission note are required to support your billing.

Level 2 (moderate complexity) and 3 (high complexity) initial hospital care have the same comprehensive history and exam requirements. If a required history or exam element is lacking, the documentation would support a level 1 (low complexity) service. If you are attesting to an admission note by housestaff, make sure these elements are covered in either of your notes. 

A. HISTORY

Comprehensive history requires:
• Chief complaint
• An extended history of present illness 
• Complete (10 or more elements) review of systems
• Past medical, family and social history
Note: Phrases such as ‘family history deferred/unknown’, ‘review of systems as per HPI’ or ‘ROS negative’ are not acceptable substitutes.

B. EXAM

Comprehensive physical exam requires a minimum 8 of 12 organ systems listed below:
o Constitutional
o Eyes
o Ears, nose, mouth and throat
o Cardiovascular
o Respiratory
o Gastrointestinal
o Genitourinary
o Musculoskeletal
o Skin
o Neurological
o Psychological
o Lymphatic/hematologic/immunologic
Note: Body areas such as head, neck or extremities do not qualify as an “organ system”.

C. MEDICAL DECISION MAKING

Requires assessment, clinical impression or diagnosis and the plan for each problem managed.

Reference
https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/Downloads/eval-mgmt-serv-guide-ICN006764.pdf 

 

Contributed by Jodie Medeiros CPC, COC, ICDCT-CM, Compliance Analyst & Educator, Mass General Hospital, Boston, MA

 

What should I include in my hospital admission note to meet the criteria for “moderate” or “high-complexity encounter” as defined by the Centers for Medicare & Medicaid Services (CMS)?