A previously healthy, term, 5-week-old girl initially presented to her primary care physician with a solitary, enlarging scalp nodule. The infant was otherwise well without additional signs or symptoms of illness. Over the next several weeks, the nodule continued to grow, and additional lesions appeared on her scalp. An ultrasound of the primary nodule revealed a hypoechoic structure favored to represent a serosanguinous fluid collection. After evaluation by general surgery and dermatology, she underwent a scalp biopsy of the largest lesion. While biopsy specimen results were pending, her parents noted that she was developing increased irritability, difficulty closing her right eye, and facial weakness. She was referred to the emergency department where a right-sided facial droop involving the brow and forehead was noted. The skin biopsy specimen results, along with subsequent laboratory studies and imaging, led to the final diagnosis.

A 5-week-old infant born at 41 weeks’ gestation presented to her pediatrician for evaluation of a scalp rash. Per her parents, a “tiny bump” that was yellow-orange in color had appeared on her scalp and was gradually enlarging. The parents did not notice the bump at birth and thought it appeared when she was approximately “3 or 4” weeks old. The bump did not seem to bother the infant, and she did not cry when it was rubbed or touched. The parents denied fever, feeding intolerance, additional rashes, or any other symptoms of illness.

Regarding her birth history, the patient was the product of an uncomplicated, spontaneous vaginal delivery. Prenatal laboratories, including infectious and serological studies, were unremarkable apart from Coombs positivity. Serial bilirubin levels were managed after birth, and the infant was routinely discharged from the well-infant nursery without phototherapy or other interventions.

At her pediatrician’s office, the infant was well appearing. A solitary, yellow-orange nodule was noted on the central frontal aspect of her scalp. The nodule was nontender and nonfluctuant to palpation. There were no other rashes on her face, trunk, or extremities, and the remainder of the physical examination was unremarkable.

Dr Gans, if you saw an infant with a presentation similar to this in clinic, what would be on your differential diagnosis, and what would be your next steps in management?

My differential at this time includes juvenile xanthogranuloma,1,2  solitary mastocytoma,3,4  or nevus sebaceous.5,6  All of these lesions can appear on the head or face, are typically discrete, and could present with a yellow to orange appearance, similar to this patient’s presentation. Her skin findings do not seem to be consistent with an infectious process, especially because there are no other signs or symptoms of illness. Given the nodule’s gradual growth, one diagnosis to keep in mind is an early presentation of a “blueberry muffin” rash, which could represent extramedullary erythropoiesis or malignancy.79  This diagnosis, however, is less likely given the patient was the product of an unremarkable pregnancy and is otherwise well. Her nodule also did not have the characteristic purpuric appearance that lends to the rash’s unique name.

If a patient such as this presented to my clinic, I would plan to refer the patient to dermatology for further evaluation and possible biopsy given the lesion’s continued growth.

The patient’s pediatrician opted to refer the patient for an ultrasound of the lesion and then to pediatric general surgery clinic for further evaluation. The ultrasound was completed when the infant was 8 weeks of age and revealed an avascular, hypoechoic structure (2.0 × 0.3 × 2.1 cm) with superficial, subcutaneous soft tissue swelling, which was favored to represent a serosanguinous fluid collection. The infant was evaluated by a pediatric surgeon the same week of her ultrasound. By that time, the parents had noted several additional smaller nodules on her scalp in addition to continued growth of the primary nodule. In fact, the parents reported that the largest nodule had tripled in size over the previous 3 weeks. Apart from the skin findings, she exhibited no other clinical changes.

After her surgery appointment, she was referred to the pediatric dermatology clinic and was seen when she was 9 weeks old. Although initially asymptomatic, some of the nodules now appeared to bother the infant when touched. She remained otherwise well. On examination at that time, the patient was noted to have a large, indurated but nonfluctuant, yellow-orange nodule on the central frontal scalp; 2 similar, smaller nodules were noted on the lateral frontal scalp. Thin hair growth was noted within the lesions (Fig 1). The remainder of the skin examination was unremarkable, and there was no hepatosplenomegaly or regional lymphadenopathy.

FIGURE 1

Scalp photograph depicting 3 prominent nodules when the infant presented for dermatologic evaluation.

FIGURE 1

Scalp photograph depicting 3 prominent nodules when the infant presented for dermatologic evaluation.

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Dr Castelo-Soccio, what is on your differential diagnosis at this time? In this case, how did the ultrasound inform the differential diagnosis? Given the evolution of the patient’s skin findings, what would be the next steps in this patient's workup?

On examination, the nodule had almost no surface change and was firm, which suggests that the process was involving the dermis or deeper within the skin. The differential included dermal infiltrative processes including juvenile xanthogranuloma (because of the yellow color),2  Langerhans cell histiocytosis (because of the firm nature and location on the scalp),10,11  and malignant infiltrate (multiple nodules that were firm and did not fit perfectly into either of the other 2 categories).10,12 

The ultrasound suggested this was an avascular, infiltrative process and not a hematoma or vascular tumor. However, ultrasound is nonspecific for most solid tumors and cannot definitively identify the type of infiltration. Ultrasounds of solid lesions or tumors are helpful in identifying vascularity or characterizing general morphology.1316  This information can be helpful in biopsy planning, particularly for anticipating bleeding potential. For our patient, the ultrasound of her skin nodules was not a necessary part of her workup. Rather, biopsy and initial laboratory studies would be warranted.

The pediatric dermatologist obtained a 3-mm punch biopsy of the primary nodule and collected initial laboratory studies. A complete blood cell (CBC) count revealed a white blood cell (WBC) count of 10 200/μL (reference range: 6000–13 300/μL), hemoglobin of 10.5 g/dL (9.5–13.5 g/dL), and platelets of 341 000/μL (150 000–400 000/μL). The automated differential on the CBC count was unremarkable and lacked any leukemic blasts or other immature leukocytes. A complete metabolic panel was within the normal limits for her age. Her lactic acid dehydrogenase level was 773 U/L (reference range: 470–1200 U/L). A blood smear was deferred in the setting of normal initial laboratories.

Approximately 48 hours after the biopsy, the parents noted that the patient seemed more irritable than usual and intermittently could not close her right eye when she cried. They also noticed that her mouth was no longer completely symmetric when crying or eating. These symptoms prompted presentation to the emergency department (ED) for further evaluation. In the ED, she was afebrile and had vital signs within the normal limits for her age. The physical examination was notable for right facial weakness and difficulty closing her right eye (Fig 2). No other focal neurologic deficits were present, and the scalp lesions appeared consistent with her previous examination.

FIGURE 2

The infant’s parents took a photograph shortly before ED presentation revealing the patient’s inability to activate her right-sided facial muscles with associated right-sided facial droop.

FIGURE 2

The infant’s parents took a photograph shortly before ED presentation revealing the patient’s inability to activate her right-sided facial muscles with associated right-sided facial droop.

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Dr Scarfone, what are your concerns when evaluating an infant with new-onset facial droop? Does the infant’s ongoing workup of her scalp nodules affect your approach to this patient?

In the ED, the mother reported that when her daughter cried, her right eye would remain open and the right side of her mouth did not turn up. The patient was otherwise behaving and feeding normally, was afebrile, and had no eyelid swelling, conjunctival injection, or eye drainage. Her general physical examination revealed the scalp findings described earlier, and she did not have hepatosplenomegaly. A comprehensive neurologic examination was only notable for facial asymmetry with minimal activation of the right upper and lower face.

For a child presenting to the ED with facial droop, the most important initial step is to differentiate between central and peripheral motor neuron involvement. The innervation of the right lower face comes from the left side of the brain only.17  The innervation to the muscles of the right upper face originates from both sides of the brain. Thus, upper face function is preserved with a unilateral brain lesion.

The patient’s presentation, therefore, was most consistent with a peripheral facial nerve palsy with a lesion at or beyond the brainstem. Her history and examination were not consistent with etiologies such as stroke, intracranial tumor, or vasculitis. Similarly, the acute onset of this patient’s findings seemed to rule out congenital causes such as birth trauma or developmental defects.

The differential diagnosis for children presenting to the ED with a peripheral facial nerve palsy is lengthy, but the initial focus is centered on more common etiologies.18,19  The term Bell’s palsy should only be used to describe idiopathic cases and is therefore a diagnosis of exclusion. Lyme disease is a common infectious etiology, particularly in endemic areas. Facial nerve palsy is the most common neurologic manifestation of Lyme disease, occurring within the early disseminated phase of disease.1821  The absence of a known tick bite or an erythema migrans rash does not rule out this etiology. Other infectious diseases that have been associated with facial palsy include Epstein-Barr virus, cytomegalovirus, adenovirus, and influenza.18  Herpes simplex virus infection or activation is a common cause among adults; it is thought to account for fewer cases among children. A reactivation of varicella-zoster virus, as seen in Ramsay Hunt syndrome,22  is encountered less frequently among children, and this patient’s rash was not consistent with a vesicular eruption. The patient’s examination was not consistent with otitis media, cholesteatoma, or mastoiditis, which are also associated with facial nerve palsy.23 

What was unique about this child was her young age and the concerning scalp lesions already under evaluation. The patient’s new facial palsy in this setting was therefore highly concerning for a possible infiltrative or malignant process.

Immediately before the patient’s ED presentation, the pathology results from her biopsy returned and the specimen revealed atypical blue cells concerning for malignancy. In fact, the pediatric dermatology team had communicated these results to the oncology team just before the patient’s arrival in the ED and thus subsequently directed her workup there. The ED evaluation included a repeat CBC count, complete metabolic panel, and lactic acid dehydrogenase, which were notable only for a WBC count of 14 800/μL (reference range: 6000–13 300/μL). In addition, a uric acid level was performed and was 3.5 mg/dL (reference range: 1.4–5.5 mg/dL). Her chest radiograph revealed no mediastinal mass, and her electrocardiogram was within normal limits for age.

Drs Turn and Rheingold, on the basis of this infant’s clinical presentation and preliminary pathology results, what is on your oncologic differential at this time? Is it typical to see patients present as she did without clear systemic findings on examination or laboratories?

On physical examination, the main lesion could be arising from the bony skull or from the overlying dermis, making her oncologic differential diagnosis broad. High on the list for a child this age would be leukemia involving the skin (leukemia cutis), disseminated neuroblastoma or rhabdomyosarcoma, and Langerhans cell histiocytosis. The ultrasound report was more consistent with a subcutaneous or dermal lesion than an infiltrative bony lesion. The eruption of multiple lesions over the course of weeks would make other solid tumors like infantile fibrosarcoma less likely. Her preliminary biopsy results confirmed this was a homogeneous malignant infiltration that on further testing was consistent with a hematologic malignancy like leukemia. Her normal CBC count with no cytopenias is unusual, as most pediatric patients with skin lesions also have a bone marrow filled with leukemia cells causing cytopenias.24  Rarely, leukemic blasts can be seen on the peripheral smear of children with normal CBC counts. Leukemia cutis, or leukemia cell invasion of the skin, is seen in ∼25% to 30% of pediatric patients with acute myelogenous or acute lymphoblastic leukemia at presentation, but it is most common in infants.25  Infants still have active extramedullary hematopoiesis, which permits leukemia cells to cluster in nontypical locations like the skin or skull bones. In infants like this patient, we additionally would be concerned for a special genetic subtype of infant B-cell acute lymphoblastic leukemia, namely, KMT2A rearranged, which was previously known as mixed-lineage leukemia.26  Although the possibility of this rearrangement would not alter initial diagnostic workup or management, KMT2A rearrangement has a marked effect on prognosis and ultimate treatment. Any child with suspected leukemia, regardless of immunophenotypic or genetic subtype, is started on hyperhydration with non–potassium-containing fluids pending initiation of therapy. A uric acid reducer is initiated, regardless of initial uric acid level, to decrease the risk of acute kidney insufficiency and electrolyte disturbances due to tumor lysis syndrome.27 

As demonstrated in this case, many patients with newly diagnosed malignancies have an insidious presentation with only a few symptoms that mimic many other diseases. Malignancy is rare and appropriately should not always be on the top of the differential list. Observation is a common and appropriate first response to these lesions, with referral to a dermatologist or surgeon if growth continues. Every year, pediatric patients are diagnosed with leukemia on the basis of biopsies of unusual skin lesions that are growing or multiplying.28  We suspect that this patient presented early and that the scalp lesions served as a warning sign of her underlying systemic illness.

The acute development of the facial palsies and irritability required immediate evaluation but happened to occur just as the preliminary biopsy results were being communicated to oncology. If her family and medical team had not acted so swiftly, she likely would have eventually developed the classic systemic symptoms we typically associate with childhood leukemia, namely, persistent fevers, signs of cytopenias such as pallor or petechiae, poor weight gain, or growing abdominal girth due to organomegaly.24 

Given the facial palsies, the neurology service was consulted while the patient was in the ED. Dr Tencer, what is your suspicion of a malignant infiltrate leading to this patient's facial droop? Are there any other diagnoses under consideration? Where do you expect the patient’s lesion or lesions to localize, and what would be the best diagnostic test to further evaluate the patient?

We were definitely concerned about malignant infiltration as a cause of the facial weakness.

Upper and lower facial palsy always raises the possibility of involvement of the seventh cranial nerve (CN). The common teaching is to think of a peripheral seventh nerve palsy when there is upper face involvement. This is because of the bilateral innervation of the forehead leading to forehead sparing weakness when a unilateral cortical area is affected because the other hemisphere will provide appropriate innervation. One important anatomic detail, however, is that the seventh CN nucleus is located in the ipsilateral dorsal pons and then traverses the pons to exit ventrally.17,18  A lesion in that area can affect the origin of the nerve, leading to upper and lower facial weakness; thus, a typically “peripheral” clinical presentation can occur from an underlying central brainstem pathology.

Given the relatively small area of the pons, which contains multiple neuronal tracts and CN nuclei in a concentrated space, the seventh CN nucleus is in close proximity to other structures (especially the sixth CN). Thus, we would expect other neurologic deficits in our patient if the brainstem were in fact involved. The patient’s otherwise preserved neurologic examination, combined with the low likelihood of having such a small brainstem lesion to cause these isolated findings, made us favor a more peripheral process.

Infectious etiologies for a seventh CN palsy seemed unlikely for this infant. Other diagnostic considerations of facial nerve palsy include congenital causes (eg, Moebius syndrome), metabolic derangements (hyperthyroidism, vitamin A deficiency), inflammatory processes (nonspecific autoimmune inflammation, demyelinating lesions of the brainstem, sarcoidosis, Ramsay Hunt syndrome, Guillain-Barre syndrome), trauma to the nerve (traumatic forceps delivery), oncologic causes (nerve infiltration of surrounding tissue or brainstem mass), and vascular causes (infarct, anomalous sigmoid sinus, carotid artery aneurysm).1719,2123 

Facial weakness could also localize distal to the nerve in the neuromuscular junction with conditions such as myasthenia gravis or to the muscles themselves, either from an underlying myopathy or from inflammatory, infectious, or oncologic infiltration.19,29 

In terms of diagnostic testing, MRI of the head with and without contrast was recommended in this case. Contrast use can identify inflammatory, infectious, or oncologic destruction of blood vessels that would lead to contrast extravasation.30,31  When anyone presents with facial weakness, ischemic stroke is on the differential. However, given the patient’s upper facial weakness, age, and time course of symptoms outside of the window for any acute vascular intervention, we felt an MRI was appropriate rather than computed tomography of the head. Other testing considerations could include lumbar puncture, targeted infectious or metabolic serum studies, electromyogram or nerve conduction studies, or additional vascular imaging depending on the initial imaging results.

The patient was subsequently admitted to the oncology service for further evaluation with sedated head MRI and tentative plans for diagnostic lumbar puncture if imaging was reassuring against mass lesions.

One of the unique aspects of this case was the initial isolated skin findings in this patient. Of note, the skin nodules continued to evolve over the course of the week after initiation of chemotherapy while admitted to the oncology service (Fig 3). Dr Castelo-Soccio, what was the final diagnosis for the patient’s skin nodules? Were the patient’s nodules typical?

FIGURE 3

Evolution of scalp nodules revealed in a photograph taken ∼1 week after admission to the oncology service.

FIGURE 3

Evolution of scalp nodules revealed in a photograph taken ∼1 week after admission to the oncology service.

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The final diagnosis is leukemia cutis. The firmness of the nodules during examination and biopsy, the multiple nature, and color are consistent with leukemia cutis. More commonly, we see diffuse nodules with leukemia cutis rather than focal appearance in one location, which made this case more unique.25,32 

Drs Turn and Rheingold, can you comment on the patient’s course after admission, including the patient’s MRI findings and final oncologic diagnosis?

After admission, the patient underwent an MRI of the head with and without contrast, diagnostic lumbar puncture with intrathecal cytarabine, and bone marrow aspirate and biopsy. Her initial skin biopsy specimen and her bone marrow biopsy specimen both revealed a population of cells that were positive on flow cytometry and immunohistochemical staining for CD19, CD20, and CD22, consistent with a B-lymphoblastic neoplasm.33,34  These cells revealed round nuclei, immature chromatin, and conspicuous nucleoli consistent with lymphoblasts. Her bone marrow biopsy specimen revealed a similar population of cells, but this blast population comprised <25% of all cells in the marrow. In pediatric B-cell lymphoblastic neoplasms, those patients whose bone marrows have <25% blast involvement are classified as having B-cell lymphoblastic lymphoma rather than B-cell lymphoblastic leukemia.34  However, these 2 conditions are considered to exist on the same continuum and are treated identically with chemotherapy.34  In fact, as this patient presented early and with few systemic symptoms, she may have ultimately developed an increased population of lymphoblasts in the bone marrow if she had not been brought to medical attention so expeditiously.

Her cytogenetics revealed a KMT2A gene rearrangement with MLLT10, which is characteristic of infantile leukemia.35,36  Her initial lumbar puncture had a cerebrospinal fluid WBC count of 21/μL (reference range: 0–5/μL) and included 33% blasts, and her MRI revealed extensive enhancement of the meninges, calvarium (right greater than left), and muscles of mastication. These imaging findings were diagnostic of leukemic central nervous system (CNS) involvement, which mandates the use of increased intrathecal chemotherapy. Additionally, these finding suggested that our patient’s facial droop was likely due to both leukemic infiltration of her muscles and peripheral facial nerve. Emergent radiation can be used with severe CN or spinal cord involvement in older patients with leukemia, but every attempt is made to avoid its use in infants because of long-term toxicity. In general, only 3% to 5% of all pediatric patients with leukemia initially present with CNS positivity, and malignant disease in the cerebrospinal fluid or brain portends a worse prognosis and is suggestive of more advanced disease.37  In fact, KMT2A rearrangement is a risk factor for leukemic CNS involvement.36 

This patient was ultimately diagnosed with infantile, KMT2A-rearranged B-cell lymphoblastic lymphoma. Most pediatric cancers are treated on national clinical trials in an effort to cure more children, often adding experimental therapy to the best-known chemotherapy regimen. This patient was started on standard therapy, without investigational azacytidine, per a recently completed trial dedicated to infant KMT2A-rearranged leukemia (Children’s Oncology Group AALL15P1).38 

We describe a case of infantile, KMT2A-rearranged B-cell lymphoblastic lymphoma that initially presented with gradually proliferating scalp nodules followed by a unilateral facial droop. Multiple diagnoses could have been consistent with the patient’s initial skin findings. As part of the differential diagnosis of skin nodules, providers should be mindful to consider extramedullary hematopoiesis or malignant infiltrate despite its rarity in the pediatric population. Patients with suspicious or proliferating lesions or systemic symptoms warrant additional workup and subspecialty input. Ultrasounds for solid skin lesions can be useful for assessing vascularity and general morphology. For many infiltrative skin lesions, however, definitive diagnosis will require biopsy.

Our patient’s seventh nerve palsy was secondary to both leukemic infiltration of her muscles and peripheral facial nerve. Providers, however, should be mindful that the differential diagnosis for facial droop is broad. Evaluation of a patient with facial droop requires a sound understanding of neuroanatomy. Combined with a thorough neurologic examination, lesions can be localized to a central or peripheral origin. Clinicians should remember that pathology at the neuromuscular junction or skeletal muscle can also lead to facial droop. These initial steps help narrow the differential diagnosis to guide further workup and management.

Infantile, KMT2A-rearranged leukemia is aggressive, with a 4-year event-free survival rate of ∼40% to 50%.36  The addition of targeted therapies to chemotherapy is actively being investigated by the Children’s Oncology Group. Younger infants <3 months of age or those who present with a very elevated WBC count (>300 000/μL) at diagnosis have dismal outcomes (<20% survival) and are sometimes referred to transplant.36  Chimeric antigen receptor T-cell immunotherapy targeted against CD19 malignant B-cells is also being studied in this population as a less toxic and hopefully more efficacious regimen.

Our patient has thus far completed both induction and consolidation chemotherapy with few adverse effects. Her subcutaneous nodules have resolved aside from a small, flat area of discoloration at the site of the primary lesion. Additionally, her facial droop has almost completely resolved, and she is growing and developing normally.

Dr Gaw contributed to the conception and design of the case presentation, drafted the initial manuscript, and critically reviewed and revised the manuscript; Drs Turn, Rheingold, Castelo-Soccio, Tencer, and Gans contributed to the design of the case presentation and critically reviewed and revised the manuscript; Dr Scarfone contributed to the conception and design of the case presentation and critically reviewed and revised the manuscript; and all authors approved the final manuscript as submitted.

FUNDING: No external funding.

CBC

complete blood cell

CN

cranial nerve

CNS

central nervous system

ED

emergency department

WBC

white blood cell

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Competing Interests

POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.