Intro:  According to CDC, the novel H1N1 influenza virus accounted for 98% of all influenza A viruses that were subtyped in the United States in the week of Jun 6-13. Only 0.2% of isolates were influenza B.  The CDC said overall flu activity declined but remained above normal for this time of year, with 11 states reporting widespread activity. The death of one child was linked to the novel virus.   

Link:   http://www.cidrap.umn.edu/cidrap/content/influenza/swineflu/news/jun2209funding.html

CIDRAP News, 6/22/09:  “Responding to lobbying by the Obama administration and public health advocates, Congress last week approved $7.65 billion for battling pandemic influenza, more than three times what the House and Senate had earlier proposed.

The money was included in a $106 billion supplemental appropriation bill dedicated mostly to funding the military campaigns in Iraq and Afghanistan. The Senate passed the bill Jun 18, following House passage 2 days earlier.

Most of the pandemic money is for activities by the Department of Health and Human Services (HHS) and the Centers for Disease Control and Prevention (CDC), but the bill includes $350 million to boost state and local capacity for responding to the novel H1N1 flu pandemic…..”

Incremental Value of Copeptin for Rapid Rule Out of Acute Myocardial Infarction

Reprint requests and correspondence: Prof. Dr. Christian Mueller, Department of Internal Medicine, University Hospital Basel, Petersgraben 4, Basel CH-4031, Switzerland (Email: chmueller@uhbs.ch ).

Objectives: The purpose of this study was to examine the incremental value of copeptin for rapid rule out of acute myocardial infarction (AMI).

Background: The rapid and reliable exclusion of AMI is a major unmet clinical need. Copeptin, the C-terminal part of the vasopressin prohormone, as a marker of acute endogenous stress may be useful in this setting.

Methods: In 487 consecutive patients presenting to the emergency department with symptoms suggestive of AMI, we measured levels of copeptin at presentation, using a novel sandwich immunoluminometric assay in a blinded fashion. The final diagnosis was adjudicated by 2 independent cardiologists using all available data.

Results: The adjudicated final diagnosis was AMI in 81 patients (17%). Copeptin levels were significantly higher in AMI patients compared with those in patients having other diagnoses (median 20.8 pmol/l vs. 6.0 pmol/l, p < 0.001). The combination of troponin T and copeptin at initial presentation resulted in an area under the receiver-operating characteristic curve of 0.97 (95% confidence interval: 0.95 to 0.98), which was significantly higher than the 0.86 (95% confidence interval: 0.80 to 0.92) for troponin T alone (p < 0.001). A copeptin level <14 pmol/l in combination with a troponin T  <0.01 µg/l correctly ruled out AMI with a sensitivity of 98.8% and a negative predictive value of 99.7%.

Conclusions: The additional use of copeptin seems to allow a rapid and reliable rule out of AMI already at presentation and may thereby obviate the need for prolonged monitoring and serial blood sampling in the majority of patients. (Advantageous Predictors of Acute Coronary Syndromes Evaluation [APACE]; NCT00470587 [ClinicalTrials.gov] )

Key Words: copeptin • rule out • acute myocardial infarction • troponin

Link:  http://www.cdc.gov/flu/weekly/usmap.htm?s_cid=ccu061909_SeasonalInfluenza2_e

Q: How do you stop a lawyer from drowning?
A: Shoot him before he hits the water.

But I digress….

This comes from NEJM and it presents a case of a woman with bug-eyes and a mass on the neck.  It would a grave situation if you don’t already know what it’s all about.
http://omniphysicians.com/2009/06/22/one-helluva-goiter/

Why rectals are important at any age.
http://omniphysicians.com/2009/06/22/colorectal-cancer-rates-are-rising-in-adults-under-age-50/

This study suggests that the initial management of Primary Spontaneous Pneumothorax with a small-bore catheter and Heimlich valve can easily be performed by emergency physicians in the community hospital setting and appears safe. About 22% were misplaced or dislodged though. http://omniphysicians.com/2009/06/22/primary-spontaneous-pneumothorax-small-bore-catheter-and-a-heimlich-valve/

A kid is out in the woods and comes back with a rash in the center of which is a black papule.  Hmmm……
http://omniphysicians.com/2009/06/22/a-black-papule/

Paul R.

LA Times, 6/22/09 (http://www.latimes.com/features/health/la-he-closer22-2009jun22,0,3729887.story)

Colorectal cancer rates are rising in adults under age 50 — people who are not typically screened for such cancers. The finding, gleaned from a cancer surveillance database and published in the June issue of Cancer Epidemiology Biomarkers & Prevention, reported a 17% increase in this age group over a decade.

Scientists aren’t sure why this is happening, but there are some things they know and suspect.

Source reference:
Oehler RL, et al “Bite-related and septic syndromes caused by cats and dogs” Lancet Infect Dis 2009; 9: 439-47.

Bite infections can contain a mix of anaerobes and aerobes from the patient’s skin and the animal’s oral cavity, including species of Pasteurella, Streptococcus, Fusobacterium, and Capnocytophaga. Domestic cat and dog bite wounds can produce substantial morbidity and often require specialised care techniques and specific antibiotic therapy. Bite wounds can be complicated by sepsis. Disseminated infections, particularly those caused by Capnocytophaga canimorsus and Pasteurella multocida, can lead to septic shock, meningitis, endocarditis, and other severe sequelae.

An emerging syndrome in veterinary and human medicine is meticillin-resistant Staphylococcus aureus (MRSA) infections shared between pets and human handlers, particularly community-acquired MRSA disease involving the USA300 clone. Skin, soft-tissue, and surgical infections are the most common. MRSA-associated infections in pets are typically acquired from their owners and can potentially cycle between pets and their human acquaintances.

Outpatient Management of Primary Spontaneous Pneumothorax in the Emergency Department of a Community Hospital Using a Small-bore Catheter and a Heimlich Valve (p 513-518)
Behzad Hassani, John Foote, Bjug Borgundvaag
Published Online: May 11 2009 11:05AM
DOI: 10.1111/j.1553-2712.2009.00402.x

 Acad Emerg Med

Objectives: The objective was to assess the effectiveness of a small-bore catheter (8F) connected to a one-way Heimlich valve in the emergency department (ED)-based outpatient management of primary spontaneous pneumothorax (PSP).

Methods: The authors conducted a structured chart audit in a retrospective case series of patients with PSP who were treated with a small-bore (8F) catheter and a Heimlich valve who were seen in the ED of a community hospital between April 2000 and March 2005. To be eligible, patients had to be available for a telephone interview. Main outcomes were success of treatment (sustained, complete lung reexpansion), admission, and surgical intervention rates. Secondary outcomes included number of chest x-rays (CXRs), number of visits to the ED, treatment duration, complications, and recurrence rates.

Results: The authors identified 62 discrete episodes of PSP in 50 patients, with a mean (±standard deviation [SD]) age of 25.5 ± 10.5 years (range = 14–53 years). In 50 of 62 episodes (81%, 95% confidence interval [CI] = 70.8% to 90.5%), patients were discharged directly from the ED. Patients were admitted to the hospital at some point for treatment in 27/62 episodes (43.5%, 95% CI = 31.2% to 55.9%). Surgery was performed for acute treatment failure in 17 episodes. Ultimately, 19 patients, who accounted for 21 of 62 episodes (33.9%, 95% CI = 22.1% to 45.6%), had surgery at some point in the study. Mean (±SD) time to admission for those patients initially discharged from the ED was 2.9 (±2.01) days (95% CI = 1.9 to 3.8 days). There were no serious complications from treatment; the minor complication rate (misplacement or dislodging of the chest tube) was 22.6% (95% CI = 12.2% to 33.0%). No association was found between the size of pneumothorax and treatment failure.

Conclusions: This study suggests that the initial management of PSP with a small-bore catheter and Heimlich valve can easily be performed by emergency physicians in the community hospital setting and appears safe. A larger study systematically comparing this approach with alternative therapies is needed.

Frequency of Acute Coronary Syndrome in Patients with Normal Electrocardiogram Performed during Presence or Absence of Chest Pain (p 495-499)
Samuel D. Turnipseed, William S. Trythall, Deborah B. Diercks, Erik G. Laurin, J. Douglas Kirk, David S. Smith, David N. Main, Ezra A. Amsterdam
Published Online: May 8 2009 10:39AM
DOI: 10.1111/j.1553-2712.2009.00420.x

 Acad Emerg Med

Objectives: The authors hypothesized that patients with active chest pain at the time of a normal electrocardiogram (ECG) have a lower frequency of acute coronary syndrome (ACS) than patients being evaluated for chest pain but with no active chest pain at the time of a normal ECG. The study objective was to describe the association between chest pain in patients with a normal ECG and the diagnosis of ACS.

Methods: This was a prospective observational study of emergency department (ED) patients with a chief complaint of chest pain and an initial normal ECG admitted to the hospital for chest pain evaluation over a 1-year period. Two groups were identified: patients with chest pain during the ECG and patients without chest pain during the ECG. Normal ECG criteria were as follow: 1) normal sinus rhythm with heart rate of 55–105 beats/min, 2) normal QRS interval and ST segment, and 3) normal T-wave morphology or T-wave flattening. “Normal” excludes pathologic Q waves, left ventricular hypertrophy, nonspecific ST-T wave abnormalities, any ST depression, and discrepancies in the axis between the T wave and the QRS. Patients’ initial ED ECGs were interpreted as normal or abnormal by two emergency physicians (EPs); differences in interpretation were resolved by a cardiologist. ACS was defined as follows: 1) elevation and characteristic evolution of troponin I level, 2) coronary angiography demonstrating >70% stenosis in a major coronary artery, or 3) positive noninvasive cardiac stress test. Chi-square analysis was performed and odds ratios (ORs) are presented.

Results: A total of 1,741 patients were admitted with cardiopulmonary symptoms; 387 met study criteria. The study group comprised 199 males (51%) and 188 females (49%), mean age was 56 years (range, 25–90 years), and 106 (27%) had known coronary artery disease (CAD). A total of 261 (67%) patients experienced chest pain during ECG; 126 (33%) patients experienced no chest pain during ECG. There was no difference between the two groups in age, sex, cardiac risk factors, or known CAD. The frequency of ACS for the total study group was 17% (67/387). There was no difference in prevalence of ACS based on the presence or absence of chest pain (16% or 42/261 vs. 20% or 25/126; OR = 0.77, 95% confidence interval = 0.45 to 1.33, p = 0.4).

Conclusions: Contrary to our hypothesis concerning patients who presented to the ED with a chief complaint of chest pain, our study demonstrated no difference in the frequency of acute coronary syndrome between patients with chest pain at the time of acquisition of a normal electrocardiogram and those without chest pain during acquisition of a normal electrocardiogram.

The Incremental Benefit of a Shortness-of-breath Biomarker Panel in Emergency Department Patients with Dyspnea (p 488-494)
Adam J. Singer, Henry C. Thode, Jr, Gary B. Green, Robert Birkhahn, Nathan I. Shapiro, Charles Cairns, Brigitte M. Baumann, Richard Aghababian, Douglas Char, Judd E. Hollander
Published Online: Apr 23 2009 12:33PM
DOI: 10.1111/j.1553-2712.2009.00415.x

 Acad Emerg Med

Objectives: The objective was to determine the incremental benefit of a shortness-of-breath (SOB) point-of-care biomarker panel on the diagnostic accuracy of emergency department (ED) patients presenting with dyspnea.

Methods: Adult ED patients at 10 U.S. EDs with SOB were included. The physician’s estimates of the pretest clinical probability of heart failure (HF), acute myocardial infarction (MI), and pulmonary embolism (PE) were recorded using deciles (0%–100%). Blood samples were analyzed using a SOB point-of-care biomarker panel (troponin I, myoglobin, creatinine kinase-myocardial band isoenzyme [CK-MB], D-dimer, and B-type natriuretic peptide [BNP]). Thirty-day follow-up for MI, HF, and PE was performed. Data were analyzed using logistic regression and receiver operating characteristics (ROC) curve analysis.

Results: Of 301 patients, the mean (±standard deviation [SD]) age was 61 (±18) years; 56% were female, 58% were white, and 38% were African American. Diagnoses included MI (n = 54), HF (n = 91), and PE (n = 16) in a total of 129 (43%) of the patients. High pretest clinical certainty (≥80%) identified 60 of these 129 (46.5%) cases. The SOB point-of-care biomarker panel identified 66 additional cases of MI (n = 24), HF (n = 31), and PE (n = 11). The overall adjusted sensitivity for any diagnosis was increased from 65% to 70% with the addition of the SOB point-of-care biomarker panel (difference = 5%, 95% CI = −1.1% to 11%) while specificity was increased from 82% to 83% (difference = 1%, 95% CI = −4% to 7%). The model containing pretest probability and the results of the SOB panel had an area under the curve (AUC) of 83.4% (95% CI = 78.4% to 88.5%), which was not significantly better than the AUC of 80.4% (95% CI = 75.1% to 85.7%) for clinical probability alone.

Conclusions: The addition of the SOB panel of markers did not improve the AUC for diagnosing the combined set of clinical conditions. Using the disease-specific SOB biomarkers increased the sensitivity on a disease-by-disease basis; however, specificity was reduced.

Outcomes After Intravenous Opioids in Emergency Patients: A Prospective Cohort Analysis (p 477-487)
Alec B. O’Connor, Frank L. Zwemer, Daniel P. Hays, Changyong Feng
Published Online: May 8 2009 10:38AM
DOI: 10.1111/j.1553-2712.2009.00405.x

 Acad Emerg Med

Objectives: Pain management continues to be suboptimal in emergency departments (EDs). Several studies have documented failures in the processes of care, such as whether opioid analgesics were given. The objectives of this study were to measure the outcomes following administration of intravenous (IV) opioids and to identify clinical factors that may predict poor analgesic outcomes in these patients.

Methods: In this prospective cohort study, emergency patients were enrolled if they were prescribed IV morphine or hydromorphone (the most commonly used IV opioids in the study hospital) as their initial analgesic. Patients were surveyed at the time of opioid administration and 1 to 2 hours after the initial opioid dosage. They scored their pain using a verbal 0–10 pain scale. The following binary analgesic variables were primarily used to identify patients with poor analgesic outcomes: 1) a pain score reduction of less than 50%, 2) a postanalgesic pain score of 7 or greater (using the 0–10 numeric rating scale), and 3) the development of opioid-related side effects. Logistic regression analyses were used to study the effects of demographic, clinical, and treatment covariates on the outcome variables.

Results: A total of 2,414 were approached for enrollment, of whom 1,312 were ineligible (658 were identified more than 2 hours after IV opioid was administered and 341 received another analgesic before or with the IV opioid) and 369 declined to consent. A total of 691 patients with a median baseline pain score of 9 were included in the final analyses. Following treatment, 57% of the cohort failed to achieve a 50% pain score reduction, 36% had a pain score of 7 or greater, 48% wanted additional analgesics, and 23% developed opioid-related side effects. In the logistic regression analyses, the factors associated with poor analgesia (both <50% pain score reduction and postanalgesic pain score of ≥7) were the use of long-acting opioids at home, administration of additional analgesics, provider concern for drug-seeking behavior, and older age. An initial pain score of 10 was also strongly associated with a postanalgesic pain score of ≥7. African American patients who were not taking opioids at home were less likely to achieve a 50% pain score reduction than other patients, despite receiving similar initial and total equianalgesic dosages. None of the variables we assessed were significantly associated with the development of opioid-related side effects.

Conclusions: Poor analgesic outcomes were common in this cohort of ED patients prescribed IV opioids. Patients taking long-acting opioids, those thought to be drug-seeking, older patients, those with an initial pain score of 10, and possibly African American patients are at especially high risk of poor analgesia following IV opioid administration.

Source reference:
The Association between Emergency Department Crowding and Analgesia Administration in Acute Abdominal Pain Patients

Acad Emerg Med

Objectives: The authors assessed the effect of emergency department (ED) crowding on the nontreatment and delay in treatment for analgesia in patients who had acute abdominal pain.

Methods: This was a secondary analysis of prospectively enrolled nonpregnant adult patients presenting to an urban teaching ED with abdominal pain during a 9-month period. Each patient had four validated crowding measures assigned at triage. Main outcomes were the administration of and delays in time to analgesia. A delay was defined as waiting more than 1 hour for analgesia. Relative risk (RR) regression was used to test the effects of crowding on outcomes.

Results: A total of 976 abdominal pain patients (mean [±standard deviation] age = 41 [±16.6] years; 65% female, 62% black) were enrolled, of whom 649 (67%) received any analgesia. Of those treated, 457 (70%) experienced a delay in analgesia from triage, and 320 (49%) experienced a delay in analgesia after room placement. After adjusting for possible confounders of the ED administration of analgesia (age, sex, race, triage class, severe pain, final diagnosis of either abdominal pain not otherwise specified or gastroenteritis), increasing delays in time to analgesia from triage were independently associated with all four crowding measures, comparing the lowest to the highest quartile of crowding (total patient-care hours RR = 1.54, 95% confidence interval [CI] = 1.32 to 1.80; occupancy rate RR = 1.64, 95% CI = 1.42 to 1.91; inpatient number RR = 1.57, 95% CI = 1.36 to 1.81; and waiting room number RR = 1.53, 95% CI = 1.31 to 1.77). Crowding measures were not associated with the failure to treat with analgesia.

Conclusions: Emergency department crowding is associated with delays in analgesic treatment from the time of triage in patients presenting with acute abdominal pain.

A 6-year-old boy with black spots

A 6-year-old boy was referred to rule out melanoma when he developed an asymptomatic “black dot” on the left tragus present for 2 days.

In addition, he reported subsequent development of mildly pruritic erythematous vesicles surrounding the black lesion and involving the anti-tragus. On exam, the tragus and anti-tragus revealed well-defined erythematous crusted vesicles and edematous papules coalescing into a plaque. At the periphery of the plaque is a well-defined 2 mm smooth shiny black papule. Further history revealed he was recently playing in the woods.

The diagnosis is black dot poison ivy.

Rhus dermatitis caused by poison ivy, oak or sumac is one of the most common causes of allergic contact dermatitis in the United States. These plants are part of the family Anacardiaceae and the genus Rhus, also known as Toxicodendron. Allergic contact dermatitis is a type IV, delayed type hypersensitivity reaction requiring prior sensitization before a reaction appears. It can develop throughout the year. The skin eruption is due to resins in the sap known as urushiol, a type of oleoresin, present throughout the plant.

Marissa L. Perman

Clinically, Rhus dermatitis typically presents as pruritic erythematous, edematous papules, plaques and vesicles often in a linear arrangement. The linear distribution is directly related to the areas of contact with the skin. The lesions can present as early as six hours after exposure, but are more commonly noted between 24 and 72 hours later. Black dot (or black lacquer) poison ivy characteristically presents with asymptomatic shiny black macules that cannot be removed with soap and water. Subsequently, there is development of typical pruritic urticarial and vesicular lesions.

The shiny black macules are due to oxidation of the yellowish- to-clear urushiol resin when exposed to air. The resin turns black after 24 hours either while still on the surface of the plant, on the skin or on clothing. It cannot be removed with washing. The black resin becomes lacquer-like by 72 hours. Referred to as “black spot” poison ivy, it is relatively rare in comparison to classic poison ivy but may be underrecognized. It is thought to occur when a highly concentrated amount of sap comes in contact with the skin such as when leaves or stems are crushed. When the oleoresin was diluted 1:50 in alcohol, application to skin in open air did not produce the black spots. A similar type of contact dermatitis can be acquired by contact with black lacquer-finished furniture because the lacquer is derived from a related plant.

On histopathologic examination of “black spot” poison ivy, an amorphous yellow material (the oleoresin) is found in the stratum corneum with areas of coagulation necrosis in the remaining epidermis. Neutrophils and nucleolar fragments may also be found at the site of necrosis. In the dermis, there is a superficial and deep lymphohistiocytic perivascular infiltrate. The yellow material and epidermal necrosis are absent on histopathology of classic poison ivy.

The lesions can be mistaken for a nevus or melanoma causing undue anxiety and prompting emergency room visits in some cases.

The treatment of “black spot” poison ivy remains the same as for classic poison ivy and includes washing the skin well with soap and water, application of medium – high potency topical steroids for symptomatic relief, and oral antihistamines for relief of pruritis. Topical antihistamines are not recommended because they can be sensitizing as well. In more severe cases, systemic steroids may be required for short periods. Resin adherent to fomites can remain for months, can repeatedly cause contact dermatitis and should be washed immediately. Clothing with black resin should be discarded. The black resin cannot be removed from the skin but eventually will peel off without scarring. Clinicians should be aware of this rare presentation of Rhus dermatitis.

For more information:

• Kurlan JG, Lucky AW. Black spot poison ivy: A report of 5 cases and a review of the literature. J Am Acad Dermatol. 2001;45(2):246-9.
• Schram SE, Willey A, Lee PK, Bohjanen KA, Warshaw EM. Black spot poison ivy. Dermatitis. 2008;19(1):48-51.

Link:  http://www.pediatricsupersite.com/view.aspx?rid=40516#diagnosis

An 11-month-old girl was admitted to our outpatient pediatrics clinic with the complaint of high fever, which appeared the night before admission. She has been followed up in our pediatrics clinic regularly for her well-child visits since she was 3 months old. Her medical history was insignificant, and she was fully immunized for age including Bacillus Calmette-Guérin (BCG) vaccination. She was well looking despite her high fever (39°C). On physical examination, no significant findings except for a mild hyperemia of the oropharynx were found. Complete blood count revealed a hemoglobin level of 12.2 g/dL and thrombocyte level of 468,000/mm³. ESR was 75 mm/h, and CRP was 3.15 mg/dL (normal: < 0.5 mg/dL). The urinalysis showed pyuria and after a urine culture was taken, she was given parenteral antibiotics (ceftriaxone 75 mg/kg) for the diagnosis of a urinary tract infection.

After the second dose of her antibiotic, she presented to our outpatient clinic for a follow-up visit. Her daily fever continued despite the antibiotic treatment. Her mother complained that there was redness on her arm around the localization of her BCG scar. Her physical examination revealed an erythema and induration of 3 × 3 cm in diameter involving the BCG scar (see Figure 1 and Figure 2). At this visit, she was irritable, and she had more marked erythema of the oropharynx with mildly erythematous lips and a mild conjunctival injection. Meanwhile, her urine culture and blood culture remained sterile.

DermatologyPublished in Pediatric Annals June 2009

An 11-month-old Girl with High Fever

Pediatr Ann. 2009 June;38(6):305-310.

 

by Tugba Erener Ercan, MD; Gokmen Ercan, MD; Muhsin Arpaozu, MD

 

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An 11-month-old girl was admitted to our outpatient pediatrics clinic with the complaint of high fever, which appeared the night before admission. She has been followed up in our pediatrics clinic regularly for her well-child visits since she was 3 months old. Her medical history was insignificant, and she was fully immunized for age including Bacillus Calmette-Guérin (BCG) vaccination. She was well looking despite her high fever (39°C). On physical examination, no significant findings except for a mild hyperemia of the oropharynx were found. Complete blood count revealed a hemoglobin level of 12.2 g/dL and thrombocyte level of 468,000/mm³. ESR was 75 mm/h, and CRP was 3.15 mg/dL (normal: < 0.5 mg/dL). The urinalysis showed pyuria and after a urine culture was taken, she was given parenteral antibiotics (ceftriaxone 75 mg/kg) for the diagnosis of a urinary tract infection.

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After the second dose of her antibiotic, she presented to our outpatient clinic for a follow-up visit. Her daily fever continued despite the antibiotic treatment. Her mother complained that there was redness on her arm around the localization of her BCG scar. Her physical examination revealed an erythema and induration of 3 × 3 cm in diameter involving the BCG scar (see Figure 1 and Figure 2). At this visit, she was irritable, and she had more marked erythema of the oropharynx with mildly erythematous lips and a mild conjunctival injection. Meanwhile, her urine culture and blood culture remained sterile.

Figure 1. Induration of 3 × 3 cm in diameter involving the BCG scar.

Figure 2. Erythema of 3 × 3 cm in diameter involving the BCG scar.

The inflammation of the BCG scar and the continuing daily fever with more marked erythema of the oropharynx led us to the presumptive diagnosis of incomplete Kawasaki disease on the third day of her fever. Her complete blood count showed a thrombocyte level of 519,000/mm³. ESR was 95 mm/h, and CRP was 3.09 mg/dL. Blood biochemistry was all normal except for hypoalbuminemia (2.9 g/dL). Cerebrospinal fluid examination was normal. Viral serology including Epstein-Barr virus and adenovirus was negative. Immunoglobulin levels were all normal. Abdominal ultrasonography revealed no pathology. Echocardiography showed no abnormalities involving coronary arteries.

On the fourth day of her fever, her erythematous lips became fissured, and conjunctival injection became more noticeable. A maculopapular rash appeared over the trunk and extremities. There were no changes on extremities and no lymphadenopathy was detected.

Diagnosis: Kawasaki Disease

Despite antibiotic treatment, her fever continued as did other findings (conjunctivitis, erythematous lips, and a maculopapular rash) suggestive of Kawasaki disease appeared, in addition to the inflammation of the BCG scar. Therefore, a diagnosis of incomplete Kawasaki disease was made. She was started on IV immune globulin therapy (IVIG, 2 gr/kg over 12 hours) and aspirin (80 mg/kg) on the sixth day of fever. The fever subsided dramatically after IVIG therapy, and erythema around the BCG scar disappeared. Subsequent complete blood count in the second week of illness demonstrated an increase in the thrombocyte level (808,000/mm³). Her repeat echocardiography 3 weeks after disease onset also revealed no abnormalities. Convalescent phase was unremarkable, and aspirin therapy was continued for 8 weeks.

DISCUSSION

Kawasaki disease is a multiorgan vasculitis that occurs predominantly in infants and young children.¹ Coronary artery aneurysms or ectasia develop in untreated patients. This is a case of an 11-month-old, fully immunized, girl whose BCG scar reactivation led us to an earlier diagnosis of incomplete Kawasaki disease. This rare but specific sign of Kawasaki disease can be used as a tool for an early diagnosis of Kawasaki/incomplete Kawasaki disease especially in countries where BCG vaccination is still a part of the immunization schedule, as in our country of Turkey.

Kawasaki disease was first described in Japan by Tomisaku Kawasaki in 1967. The etiology of Kawasaki disease remains unknown. Kawasaki disease is characterized by fever lasting 5 days or more (without other explanation), bilateral nonexudative conjunctivitis, erythema of the lips and oral mucosa, changes in the extremities, rash, and cervical adenopathy. Fever with at least four of the five principal clinical findings is needed for its diagnosis.² Coronary artery aneurysms or ectasia develop in 15% to 25% of untreated children.^1,3 Early diagnosis and prompt treatment of the acute syndrome is critical for preventing life threatening complications. However, diagnosis of the syndrome is based on signs and symptoms that also occur in other pediatric illnesses, which can result in diagnostic dilemmas, especially in atypical cases. In patients with fever and in fewer than four of the principal diagnostic features, detection of coronary artery abnormalities by two-dimensional echocardiography should lead to the diagnosis of atypical Kawasaki disease.^4-7 Although it is not included in the diagnostic criteria of Kawasaki disease, reactivation of a BCG scar that is characterized by erythema and induration of a previous BCG inoculation site is an important and specific sign of Kawasaki disease.^8-12

Kawasaki disease neither has a known etiology nor has a specific diagnostic test to confirm it. The diagnosis of Kawasaki disease has been based on the presence of fever for 5 or more days without other explanation and four of the five principal clinical features.² In 1987, Sonobe and Kawasaki¹³ stated that the presence of fewer than four of the principal clinical features accompanying fever and presence of coronary artery aneurysms allows the diagnosis of atypical Kawasaki disease. Atypical or incomplete cases of Kawasaki syndrome are being recognized with increasing frequency.⁴ Up to 10% to 45% of children are postulated to have an atypical or incomplete course.¹⁴ Early diagnosis of Kawasaki disease is extremely important since coronary artery aneurysms occur as a sequela of the vasculitis in 15% to 25% of untreated children.^1,3,7 In the literature, ages of the patients with atypical Kawasaki syndrome were reported to be between 2 months and 15 years.¹⁵ Atypical Kawasaki syndrome is mainly seen in children younger than 6 months, and cardiovascular complications are most common in young infants.

The American Heart Association recommends that echocardiography should be considered in any infant younger than 6 months with fever of 7 days or more in duration without any other explanation and laboratory evidence of systemic inflammation. Incomplete Kawasaki disease should be considered in any child with unexplained fever for ≥5 days with two or three of the principal clinical features of classic Kawasaki disease.⁷

Therefore, any finding that could lead to early diagnosis is worth taking into consideration. Erythema and induration of a previous BCG inoculation site is a specific and early manifestation of KD.^10-12,16 The local inflammatory reactivation of a BCG vaccination site was first highlighted in the Japanese literature as a specific and an early sign of Kawasaki disease.¹⁷

This inflammatory reactivation was hypothetically ascribed to the cross-reactivity between mycobacterial Heat Shock Protein (HSP) 65 and Human Homologue HSP63, which is a mitochondrial protein.^11,12,18 Studies have shown that T-cells obtained from the peripheral blood of KD patients recognize an epitope from HSP 65 and cross-reacted with the corresponding peptide sequence of human HSP 63.^12,19

There are few case reports emphasizing the usefulness of the inflammatory reactivation of BCG vaccination site in the diagnosis of Kawasaki disease, especially incomplete Kawasaki disease.

Our patient had a persistent fever despite antibiotic treatment. During the first few days of her fever, she had no typical physical findings suggestive of Kawasaki disease except for an erythema and induration of her BCG vaccination site, which led us to the suspicion of Kawasaki disease on the third day of illness. During follow up, she developed three of the five specific clinical findings suggestive of incomplete Kawasaki disease in addition to her persistent fever, increased acute phase reactants, and sterile pyuria, which is seen in 33 % of Kawasaki disease patients.⁷ With early diagnosis and treatment, prompt resolution of her symptoms occurred without any sequela involving coronary arteries.

CONCLUSION

Because Kawasaki/incomplete Kawasaki disease is a diagnostic dilemma, any sign that could help early diagnosis is useful. Inflammatory reactivation of a BCG vaccination site is an early and specific sign of Kawasaki disease. BCG vaccination is part of the national immunization schedule in Turkey. With this case report, we tried to emphasize the usefulness of BCG site reactivation in establishing a diagnosis of Kawasaki/incomplete Kawasaki syndrome so that clinicians should be aware of this clinical manifestation especially in countries where BCG vaccination is still a part of the immunization schedule.

REFERENCES

1. Dajani AS, Taubert KA, Gerber MA, et al. Diagnosis and therapy of Kawasaki disease in children. Circulation. 1993;87(5):1776-1780.
2. Rowley AH, Shulman ST. Kawasaki Disease. In: Nelson’s Text Book of Pediatrics. 17th ed. Behrman RE, Kliegman RM, Jenson HB, eds. Elsevier; 2004:823-826.
3. Kato H, Sugimura T, Akagi T, et al. Long-term consequences of Kawasaki disease. A 10- to 21-year follow-up study of 594 patients. Circulation. 1996;94(6):1379-1385.
4. Witt MT, Minich LL, Bohnsack JF, Young PC. Kawasaki disease: patients are being diagnosed who do not meet American Heart Association criteria. Pediatrics. 1999;104(1):10.
5. Pfafferott C, Wirtzfeld A, Permanetter B. Atypical Kawasaki syndrome: how many symptoms have to be present? Heart. 1997;78(6):619-621.
6. Boven K, De Graeff-Meeder ER, Spliet W, Kuis W. Atypical Kawasaki disease: an often missed diagnosis. Eur J Pediatr. 1992;151(8):577-580.
7. Newburger JW, Takahashi M, Gerber MA, et al; Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease; Council on Cardiovascular Disease in the Young; American Heart Association; American Academy of Pediatrics. Diagnosis, treatment, and long-term management of Kawasaki disease. Circulation. 2004;110(17):2747-2771.
8. Brogan PA, Bose A, Burgner O, et al. Kawasaki disease: an evidence based approach to diagnosis, treatment and proposals for future research. Arch Dis Child. 2002;86(4):288-290.
9. Hsu YH, Wang YH, Hsu WY, Lee YP. Kawasaki disease characterized by erythema and induration at the Bacillus Calmette-Guérin and purified protein derivative inoculation sites. Pediatr Infect Dis J. 1987;6(6):576-578.
10. Plantin P, Blayo M, Dupre D, et al. BCG reactivation: a rare but specific sign of Kawasaki disease. Presse Med. 1998;27(15):716.
11. Sinha R, Balakumar T. BCG reactivation: a useful diagnostic tool even for incomplete Kawasaki disease. Arch Dis Child. 2005;90(9):891.
12. Antony D, Jessy PL. Involvement of BCG scar in Kawasaki disease. Indian Pediatr. 2005;42(1):83-84.
13. Sonobe T, Kawasaki T. Atypical Kawasaki disease. Prog Clin Biol Res. 1987;250:367-378.
14. Kusinska B, Wróblewska-Kaluzewska M. What do we know about Kawasaki disease? Med Sci Monit. 2000;6(6):1227-1231.
15. Levi M, Koren G. Atypical Kawasaki disease: analysis of clinical presentation and diagnostic clues. Pediatr Infect Dis J. 1990;9(2):122-126.
16. Kuniyuki S, Asada M. An ulcerated lesion at the BCG vaccination site during the course of Kawasaki disease. J Am Acad Dermatol. 1997;37(2 Pt 2):303-304.
17. Takayama J, Yanase Y, Kawasaki T. Study of the changes of the site of the BCG inoculation in MCLS. Jpn J Pediatr. 1982;86:567-572.
18. Yokota S, Tsubaki K, Kuriyama T, et al. Presence in Kawasaki disease of antibodies to mycobacterial heatshock protein HSP65 and autoantibodies to epitopes of human HSP63 cognate antigen. Clin Immunol Immunopathol. 1993;67(2):163-170.
19. Sireci G, Diell F, Salerno A. T cells recognize an Immunodominant epitope of heat shock protein 65 in Kawasaki disease. Mol Med. 2000;6(7):581-590.

ABOUT THE AUTHORS

Tugba Erener Ercan, MD; Gokmen Ercan, MD; and Muhsin Arpaozu, MD, are with Maltepe University Medical Faculty, Department of Pediatrics, Istanbul, Turkey.

Address correspondence to: Tugba Erener Ercan, MD, Maltepe Universitesi Hastanesi, Ataturk Cad. Cam Sok. No. 3, 034843, Maltepe, Istanbul, Turkey; 90 216 370 97 19; e-mail address: tugbaerener@yahoo.com.

Dr. Tugba Erener Ercan; Dr. Gokmen Ercan; and Dr. Arpaozu have disclosed no relevant financial relationships.