The biggest challenge in diagnosing septic arthritis is to think of it. Once you think of it, there is a diagnostic process that you activate. The second biggest challenge is that that diagnostic process we learn in training is flawed. We have no alternatives right now, so I will share with you my thoughts on how we should use our judgment as clinicians.


Triggers to consider septic arthritis essentially are the same triggers as infection anywhere. Celsus’ cardinal signs of inflammation are dolor (pain), calor (warmth), rubor (redness), tumor (swelling). Some authors have written that fluor (flow) should be the 5th cardinal sign and in this case the effusion is one of the most important clinical signs.


The detection of effusion at the bedside has been covered elsewhere but includes inspection, palpation, and milking. Smaller volumes of fluid are harder to detect. Ultrasound can be utilized to improve our accuracy.


The clinician generates hypotheses at the bedside and then circles back to revisit risk factors. This is an underappreciated process that deserves more attention. The following risk factors have high specificity:



-joint surgery (mainly recent)

-joint prosthesis (at any time)


There are others but those are the main ones. You might think of it as “compromised immune system” and “compromised joint.” If it helps you in remembering this, recall that the synovium is a vascular tissue. It lacks a basement membrane (which tends to filter out bacteria in other tissues, like the cornea). The joint relies on the immune system to protect us from bacterial translocation. Recall also that bacteria love to find crevices to hide in. A disrupted joint, or a compromised immune system creates the setting for septic arthritis.


They don’t all have to have those high risk features though. Often the clinician is left with enough suspicion to pursue a risk stratification process before considering a tap. In low risk patients that process can involve inflammatory markers (traditionally WBC, CRP, ESR, with emerging roles for procalcitonin and perhaps other markers) to lower your suspicion back below the threshold of further testing. I recommend you use as many of these as you need to reassure you in a low risk patient that there is no infection. All of them have limitations but if the results are normal, you are greatly reassured.


For patients where doubt continues to exist, the diagnostic pathway for septic arthritis ends in arthrocentesis, though its results may be less clear than we realize. Common practice is to use synovial blood counts (often 50K) as disease-defining, which does not actually work very well. Synovial WBC cutoffs at all levels will both miss and overcall septic arthritis. Even if you use the cutoff as 25K, it still misses as many as 1/4 of all cases, one prospective study said it would miss more than 1/3 of all cases (Margaretten JAMA2007). Meanwhile there will continue to be patients with WBC above 50K who have other causes (gout for example).


The gram stain sensitivity is as low as 40% (Ross Infect Dis Clin North Am2017). If you have strong suspicion based on risk factors, drain the joint and have them follow up in 24 hours, giving antibiotics while awaiting culture results.



-Septic arthritis is considered when the patient has an inflamed joint (effusion, warmth, pain).

-Inflammatory markers, if all normal, can lower your concern enough in a low risk patient to rule out disease.

-Risk factors (compromise of joint, compromise of immune system) may be more important than the other tests.

-Synovial WBC has significant limitations in sensitivity and specificity, and is not a disease-defining reference standard.


Selected References:


Septic Arthritis of Native Joints.

Ross JJ.

Infect Dis Clin North Am. 2017 Jun;31(2):203-218. doi: 10.1016/j.idc.2017.01.001. Epub 2017 Mar 30.


Does this adult patient have septic arthritis?

Margaretten ME, Kohlwes J, Moore D, Bent S.

JAMA. 2007 Apr 4;297(13):1478-88. Review.

PMID: 17405973



A patient presents with a rash and fever after recent travel to Bolivia. She was there for one week and returned 3 days ago. She took her antimalarial medication, so could this be dengue fever?

Fever in the returning traveler relies on Bayesian thinking. We start with probabilities based on endemic diseases and then the history and physical examination raises or lowers the probability of each. In this case malaria was prevented with doxycycline, so dengue fever is more likely.

Dengue fever is caused by a virus spread by mosquitos bites. The virus is brought to regional lymph nodes and then spreads throughout the body. It presents commonly with typical viral symptoms of fever, headache, nausea and vomiting, myalgia, maculopapular rash, etc. These findings are not diagnostically specific. Although it is called “breakbone fever,” in fact the finding of myalgia has no value in differentiating dengue from other febrile illnesses.(Low PLoS Neglected Tropical Diseases 2011) In a cohort study, half of patients were misdiagnosed as having upper respiratory infections.(Sirivichayakul, PLoS Neglected Tropical Diseases, 2012) To decide what is specific, consider the pathology.

The pathology at the cellular level is microvascular permeability. The vessels are not necessarily damaged, just leaking.(Nelson Pathology of Emerging Infections, 1998) Plasma leakage presents as edema and petechiae. The more severe the disease (such as dengue hemorrhagic fever or dengue shock syndrome) the more likely these specific features will be prominent. One might see pleural effusions, ascites, and widespread edema. The tourniquet test is a way of identifying microvascular permeability. Inflate a blood pressure cuff to a level between diastolic and systolic blood pressure and leave it there for five minutes. Now the capillaries are stressed. A positive result is the emergence of 10 petechiae per square inch (2.5 cm) on the forearm.(Gregory PLoS Neglected Tropical Diseases 2011) It is around 50% sensitive, with wide variation depending on the study. Its specificity ranges from the high 80s to mid 90s.

Other more specific findings might include hepatomegaly. Hematologic findings such as leukopenia and thrombocytopenia are characteristic of dengue fever and do raise the probability of this disease.

Take home points:

-The differential diagnosis for fever in the returning traveler depends on endemic diseases

-The pathology of dengue fever is vascular permeability, so look for petechiae or edema

-The capillary fragility test is a way of eliciting this vascular permeability



Cellulitis, when you think about it, is probably not the most helpful term. Literally, it means “infection of cells.” What cells? The anatomical area is actually the dermis, as well as the subcutaneous tissue.


A patient presenting with “dermitis” has a lesion that is clearly confined to the skin. A patient presenting with significant edema has involvement of subcutaneous tissues. These are the patients where we need to consider the surgical diseases: necrotizing fasciitis, pyomyositis, and abscess.


There is very little in the literature about palpation of the erythematous lesion. However, extensive induration might be the trigger that leads you to perform an ultrasound, and find an abscess.


The other traditional role for palpation is with erysipelas. This streptococcal infection is most commonly encountered in the lower extremities. Traditionally it was thought of as confined to the epidermis, palpable, with sharp borders. But now it is believed that erysipelas and cellulitis are the same disease, on a spectrum depending on how superficial the infection is.[Kilburn Cochrane Database Syst Rev. 2010]


Palpation in cellulitis probably does not receive enough attention in the medical literature. The next time you have a patient with cellulitis, pay particular attention to palpation. It may signal to you that there is something deeper to find on ultrasound.


Take home points:

Erythema of the skin sometimes hides something below

Use palpation to better understand where the inflammation is located


Most studies say that palpation of fever is inaccurate. I am not so sure. Many of the studies use oral temperature as a gold standard, which of course can be as low as 50% sensitive for true fever. These studies conclude that the mothers’ palpation over-called the diagnosis but I wonder whether rectal temperature assessment would not have proven many mothers to be correct.


I see people put their palm on the forehead to check for fever, and then pull it away 1 second later. I believe this is wrong on several levels. First, use the back of the hand, not the palm. The back of the hand is more sensitive to temperature. Second, don’t feel the forehead, try something less subject to the ambient environment. I often use the neck. Third, don’t pull it away, rather, leave it there. You are not feeling for whether it is warm. You are feeling for whether it is hot. I think we can tell the difference. Remember the sting of a hot tub? Hot tubs are never supposed to be above 104. Yet they really sting sometimes. Hold your hand there and if you feel that sting, it is probably a fever.


I found that once I used the above techniques I became a lot more accurate. I would ask skeptical nurses for rectal temperature assessment, and they would come back astonished at my predictive abilities. Palpate for the hot tub sting with the back of your hand in the axilla or neck and see if it works for you. My hope is that future studies would show better methodology.


Take home points:

Palpate for a fever using the back of the hand, not the palm

Palpate the neck or core body area, not the forehead

Palpate for at least 10-15 seconds


A patient presents with headache. The history and physical examination do not reveal the cause. You take a second look at the vital signs.  Oral temperature is 99.3.  You have the nurse check the rectal temperature. It is 101.9. What is the sensitivity and specificity of oral temperature for fever?


There are numerous studies on this topic, and unfortunately, the populations studied are far too heterogenous to truly give a range for sensitive and specificity. In some studies the sensitivity is as low as 47%.(Jensen J Adv Nurs 1994)


Correctly identifying a fever can change the workup in certain presentations. During residency I saw a patient with a 99 degree temperature elevation and back pain. The attending physician was sharp to perceive this and rectal temperature turned out to be 101.5.  We eventually diagnosed epidural abscess.


Another example might be delirium in the elderly. I recall a nursing home patient who presented in shock with an oral temperature of 98.1.  I asked the nurse to check rectal temperature. She was a bit skeptical. The reading was 102.1 and she was surprised and a little disappointed at how unreliable the oral temperature can be.


The lesson is this: oral temperature is not sufficiently sensitive.  It might work for screening, but slight abnormalities in high risk presentations may call for the gold standard: rectal temperature.


Take home points:

-Oral and even temporal temperature assessment can have low sensitivity

-Minor oral temperature elevation may call for rectal temperature assessment



In emergency medicine we occasionally encounter fever that won’t yield to a specific diagnosis. We speculate a viral cause and a self-limited course, but it is worth thinking through the next step. The term “fever of unknown origin” originates in internal medicine and refers to specific criteria that are appropriate for that setting. If the fever lasts three weeks, it is not necessarily consistent with a self-limited viral cause and this thought process is triggered.

Classic causes of fever of unknown origin are:

1. Infection

2. Connective Tissue Disease

3. Malignancy (often hematologic)

Additional noninfectious causes of elevated temperature in emergency medicine include environmental, toxicologic, and endocrine (hyperthyroidism).

Thinking about these possibilities may prompt the diagnostic process and establish the correct diagnosis early. Of course, even in the modern era, half of all cases of fever of unknown origin never have their cause discovered.(Bleeker-Rovers Medicine 2007)

Take Home Points:

-Fever of unknown origin classically is due to infection, connective tissue disease, or malignancy


A patient recently presented with a subcutaneous nodule that appeared to be an abscess.  It was raised, erythematous, tender, indurated, and had a central plug…wait, no, it had a central hole.  And he just got back from Belize.  We put a transparent membrane on it to see if there was a creature in there.  Sure enough, a snout pushed at the membrane, seeking air.  This established the diagnosis – myiasis, secondary to a bot fly bite.

Trying to remove that larvae was an ordeal.  These creatures don’t want to leave their cubby, and trying to pull them out is like trying to give a cat a bath.  We finally decided to leave the membrane in place.  The next morning the larva was dead, and my colleague removed it.

Other skin lesions that can be confused with an abscess include a brown recluse bite.  Reportedly a blue lesion, surrounded by concentric rings of pallor (ischemia) and then erythema (vasodilation) are classic for the brown recluse bite (Rogers 2011).


A patient presents with a chronic diabetic heel ulcer that has worsened over the past few weeks.  Could this be osteomyelitis?

It turns out that physical examination findings can significantly raise or lower the probability of this diagnosis. According to JAMA’s rational clinical examination series (Butalia 2008), 2 findings on physical examination have more powerful likelihood ratios than MRI:

-A crater breadth of 2 square cm or more has a positive LR of 7.2.

-Probing to bone has a positive LR of 6.4.

Take Home Points:

Osteomyelitis is more likely when the chronic wound is more deep and more broad