NairalandDoctor:
By NairalandDoctor
A 16-year-old boy presents with 2 days of intense swelling over the scalp, forehead, and bilateral orbits. He also complains of severe pruritus and purulent scalp drainage. Two days ago, he received a haircut and washed his scalp with his mother’s shampoo. A few hours after washing his hair, he began to have intense worsening pruritus; facial swelling increased over the following days.
Two days after the development of symptoms, he presents to the pediatric emergency department. A culture of the scalp drainage is obtained and dermatology is consulted in the emergency department. He is discharged with clindamycin, griseofulvin, ibuprofen, and diphenhydramine. The swelling, pruritus, and purulent drainage worsen overnight.
He takes one dose of each medication and presents to the dermatology clinic. On physical examination, the adolescent has significant tenderness and pruritus over the vortex and anterior scalp. He denies difficulty breathing, vomiting, diarrhea, abdominal pain, hives, fevers, chills, nausea, or eye pain. He has not been able to open his eyes since the morning of ission but does feel that he can move them normally. In the clinic, a culture of the scalp drainage is again taken and the patient is referred to the emergency department for further evaluation.
The patient had been itted to the hospital 2 months ago with similar symptoms after washing his hair with selenium sulfide shampoo. During his previous ission, his scalp swelling was not as severe, but he did develop purulent drainage. He was treated with intravenous corticosteroids and clindamycin before being discharged with prescriptions for oral corticosteroids and clindamycin. His scalp culture grew methicillin-resistant Staphylococcus aureus, which showed good susceptibility to clindamycin.
The patient is an otherwise healthy adolescent boy with no history of food or drug allergies. He has a history of eczema but takes no medications on a regular basis. There is no personal or family history of asthma or allergies. The patient is itted to the hospital from the emergency department due to rapid progression of face and scalp swelling.
Vital signs on ission reveal a temperature of 36.7°C (98.1°F), heart rate of 85 beats/min, respiratory rate of 20 breaths/min, blood pressure of 121/66 mm Hg, and oxygen saturation of 96% in room air. On physical examination, the boy is well developed, alert, and oriented but uncomfortable. His head is notably misshapen due to extreme swelling and he is unable to open his eyes.
The right eyelid can be retracted, the pupil is reactive, and the eye has full extraocular movements. The left eyelid can only be retracted slightly without visibility of the pupil. Some yellow-tinged drainage is apparent on both eyelashes. The scalp, forehead, temples, and bilateral periorbital areas are grossly misshapen due to severe edema. The scalp is covered with patches of thin, grayish-yellow crusting, with areas of excoriation, erythema, and yellow-tinged drainage at the vortex (Fig 2) and anterior aspect of the scalp. The scalp is also diffusely tender to palpation, with guarding by the patient. Microvesicles and pustules are noted over the scalp and helices of the ear. The mouth and cheeks are not edematous. The remainder of the physical examination findings are unremarkable.
A complete blood cell count reveals:
White blood cell count: 12,200/μL (12.2 × 109/L) (72.9% neutrophils)
Hemoglobin: 17.0 g/dL (170 g/L)
Platelet count: 222 × 103/μL (222 × 109/L)
C-reactive protein: 4.74 mg/L (47.4 nmol/L)
Gram stain of the scalp drainage shows 3+ granulocytes and no organisms.
Diagnosis
The patient was diagnosed with severe allergic dermatitis with bacterial superinfection. He was treated with intravenous methylprednisolone 1 mg/kg per day and intravenous clindamycin 40 mg/kg per day divided every 8 hours. Dermatology was consulted and recommended fluocinolone acetonide scalp oil 0.01% twice daily and oral diphenhydramine and ibuprofen as needed for pain and pruritus. Both cultures from the scalp drainage grew mixed skin flora. As his physical examination findings and symptoms improved (Fig 3), the methylprednisolone and clindamycin were converted to oral istration on day 3 of ission, and he was discharged on a prednisone tapering regimen, fluocinolone acetonide scalp oil, and a 10-day total course of clindamycin. He was referred for outpatient patch testing to determine the allergen triggering the reaction.
At his dermatology appointment, further history was obtained that the patient was using a “Bigen” hair dye intermittently without problems until his two inpatient issions for itching, weeping, and swelling of his scalp and face, which occurred 10 days after applying the dye. “Bigen” hair dye is a permanent powder manufactured in Japan. The timing and severity of the patient’s symptoms were most suggestive of allergy to hair dye rather than to a shampoo. Patch testing revealed 3+ reactions to paraphenylenediamine, aminophenols and para-toluene diamine, all of which are contained in the hair dye.
The Condition
Allergic dermatitis is a T-cell-mediated type IV hypersensitivity reaction from with an exogenous substance. Type IV hypersensitivity, also known as delayed type, is a reaction characterized by CD4+ helper T cells recognizing a macrophage in a Class 2 major histocompatibility complex. Macrophages stimulate proliferation of more CD4+ T helper cells, which secrete interleukin-2 and interferon-gamma, mediating an immune response. This reaction can take up to 2 to 3 days to develop. Some examples of type IV hypersensitivity reactions include type 1 diabetes mellitus, Mantoux (tuberculosis) test, multiple sclerosis, and rheumatoid arthritis.
Among the common allergens are plants, metals, preservatives, medications, adhesives, and personal care products. Substances applied to the scalp, including shampoo, coloring agents, relaxers, or other hair care products, can result in dermatitis to the scalp and adjacent areas such as the neck and eyelids. Sensitization can develop after multiple uses of a product. Patch testing is very useful for patients with eruptions after allergen exposure to determine sensitivity to specific allergens.
The primary symptom of allergic dermatitis is a pruritic rash, but pain, burning, and a stinging sensation also may occur. Lesions seen on physical examination include scaly erythematous papules and plaques. The papules are caused by collections of fluid in the epidermis that can be associated with weeping. In severe cases, bullae and vesicles can be seen. Edema can also involve the eyelids, neck, and periauricular areas with scalp dermatitis. Acute allergic dermatitis can evolve into subacute and chronic dermatitis if untreated. The dermatitis has a significant potential for infection due to intense pruritus. Folliculitis is common in patients with allergic dermatitis due to bacterial invasion of the hair follicle from scratching, which causes inflammation and disruption of the epidermis.
Differential Diagnosis
The differential diagnosis for a child with a scalp eruption is broad. History and physical examination play key roles in diagnosis. In school-age children, tinea capitis and head lice are two very common causes of scalp dermatitis and pruritus.
Tinea capitis, caused by dermatophytes, is one of the most common causes of scalp eruptions in children and is spread from other children and also animals, particularly cats. Symptoms of tinea vary from inflammatory scaly patches or plaques to nodules with exudates such as a kerion. In addition, there often are circular areas of alopecia and posterior cervical lymphadenopathy. The most common fungus in the United States causing tinea capitis is Trichophyton tonsurans, and the condition frequently occurs in Nigerian patients. T tonsurans does not fluoresce under a Woods lamp, but cases caused by Microsporum canis do. A potassium hydroxide (KOH) or fungal culture from the hair shaft can confirm the diagnosis.
Pediculosis capitis (head lice) presents as pruritus of the scalp, most commonly in the posterior scalp, postauricular area, and neck, often without a scalp eruption. Nits can be found near the base of the hair shaft if the infection is active. The nit is not easily removed from the hair shaft, which can help to distinguish this condition from seborrheic dermatitis.
Sarcoptes scabiei subspecies hominis (scabies) does not often involve the scalp, although this is possible in young children and immunocompromised patients. Involvement of the palms, soles, interdigital web spaces, axillae, and umbilicus is typical. Dermoscopy or scraping the skin can reveal the mite.
Other causes of scalp eruptions more likely in adolescents and adults are dermatomyositis, dermatitis herpetiformis, psoriasis, dissecting scalp cellulitis (a rare condition causing pustules and scarring with permanent hair loss of unknown cause), herpes zoster, discoid lupus erythematosus, lichen planopilaris (a rare scalp disorder causing follicular erythema with permanent hair loss), and bullous diseases such as pemphigus vulgaris.
Management and Prognosis
The treatment for allergic dermatitis depends on the severity and extent of involvement. The mainstay of allergic dermatitis management involves avoidance of the allergen. In addition, alleviating symptoms of pruritus, hydrating the skin with emollients, and using topical anti-inflammatory medications are pertinent for control.
Topical corticosteroids are the most common treatment for localized allergic dermatitis. For cases involving the face or flexural areas, low- or medium-potency topical corticosteroids applied once or twice daily for 1 to 2 weeks have been proven effective. High-dose topical corticosteroids are used when the hands, feet, or nonflexural areas are involved and are applied once or twice daily for 2 to 4 weeks.
Topical calcineurin inhibitors (Table) are effective in cases of chronic localized allergic dermatitis, when the face or flexural areas are involved, or if the condition is resistant to topical corticosteroids. Tacrolimus 0.1% ointment or pimecrolimus 1% cream is applied twice daily until symptoms have resolved. Topical calcineurin inhibitors have a slower onset of action than topical corticosteroids and have more adverse effects (including localized stinging or burning sensation when applied to site).
However, because calcineurin inhibitors are a relatively new class of medication, not much is known about the long-term adverse effects. Rare cases of malignancy have been reported. Accordingly, calcineurin inhibitors should be used for short-term treatment only and not in children younger than 2 years of age or in immunosuppressed patients. Calamine lotions, aluminum acetate compresses, and oatmeal baths may help to reduce pruritus and sooth patient discomfort.
Systemic corticosteroids are important when allergic dermatitis is more extensive and when the face, hands, Instruments, or feet are involved. Studies show that systemic corticosteroids are useful if the dermatitis involves more than 10% to 20% of the body surface area. Oral prednisone can be used at a dose of 0.5 to 1.0 mg/kg per day for 7 days, followed by a taper over the subsequent 1 to 2 weeks.
Antihistamines are beneficial for patients with significant symptoms of pruritus and more extensive disease. Also, systemic antibiotics are useful if there is a concern for secondary bacterial infection. Antimicrobials should address common skin bacteria such as Staphylococcus and Streptococcus. Phototherapy and systemic immunosuppressive agents have been used in cases of corticosteroid-resistant chronic allergic dermatitis.
Management of allergic dermatitis is complex and involves avoidance of the allergen, use of topical anti-inflammatory agents, restoration of the skin barrier, and skin protection. Patch testing may be necessary to determine the offending allergen.
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Herpes Virus is often terminal to newborns l as it leaves them with Herpes Encephalitis and other dire brain issues.
You Can read this article as it explains broadly about the topic. https://www.herpescurecare.com/the-insiders-guide-to-neonatal-herpes-simplex/
ceaser:
Not just viral meningitis but also oral herpes (kissing virus), the latter more common as many visitors would want to innocently carry the baby and give it a peck. You can't blame them for wanting to do so though, Yorùbás have an adage which says that "no sensible person hates a newly born, they are usually a joyful sight to behold"
And you may update the list with the novel Corona "birus" covid-19.
Modified: I eventually read thru the report to see that Herpes simplex virus-1 (HSV-1) has been mentioned.
For those who kpansh indiscriminately, know that there is genital herpes caused by HSV-2, it is an STI and used to be strictly so until recently when you now have the anomaly of HSV-1 (that used to be sole cause of oral herpes) now causing genital herpes, and vice versa with HSV-2
The cause of this anomaly: Oral s3x
And on the flip side, to those cursing people because they are happy to see and touch a newborn, well I've got news for you. Getting a newborn exposed to some environmental microbes may be beneficial in the long term, some findings have suggested.
It was discovered that there has been increased rate of diseases such as Peptic Ulcer Disease, obesity, allergies and a couple of others I can't really recall now amongst children of the 21st century. Reason was adduced to the fact that Ceaserean section has become the common means of child delivery and children born via CS tend to have these problems in higher proportion.
The logic behind this: the human immune system has two types namely the innate immunity and the adaptive immunity. The innate are your skin, integuments and mucous membranes, digestive juice of the mouth, acid of the stomach and these are just basic while the adaptive are principally cellular and humoral with a large chunk of it in the blood, and of course are more versatile. The "adaptive" as the name suggests is designed to adapt, change and morph as needed and according to the prevailing situation. Think of it as a photosensory cells of the skin of the chameleon that changes according to the incident colour it gets exposed to.
But unlike the innate (inborn) immunity which has just a basic degree/qualification/B.Sc, the "adaptation" of the adaptive immunity needs to be trained to attain a professional/specialized status/P.hD. This training involves exposure to various stimuli in form of all kinds of microbes. Think of this as the way your antigen based vaccine works. With prior exposure to a microbe comes the ability for faster response, attack and eventual defeat of such microbe on subsequent exposure.
The mother's birth canal is filled with various good microbes and bad microbes. The good ones are constantly present to keep in check the bad ones from overgrowth/overpopulation which may lead to things such as bacterial vaginosis and some other like that. These microbes especially the good ones are also there for the baby. In utero, the amniotic sac (birth sac/bag) ensures that the milieu of the baby is completely sterile (free from germs). At birth, this birth bag will first need to be broken and that is when you see that water comes out of the mother's "vaga-ina" (in the dicktator's voice - the dictator is a comedy movie you should see). With this breakage, the baby is no longer protected from the environment filled with good and bad bugs and especially exposure to the good bugs which is desirable. If he is not quickly delivered within minutes to hours, the bad bugs can also get access and that's the problem that isn't desirable.
During delivery per vaga-ina, the movement of the baby thru the birth canal ensures that it carries with it the whole gamut of microbes that is in the mother's vaga-ina, a recipé to provide for the child some level of adaptive immunity being the first ever, naturally designed microbe it is exposed to. This exposure helps it to formulate some body mechanisms and processes that guide against some issues like PUDx, obesity etc amongst other things.
Cesarean section byes all these natural selective processes so babies born via CS might not have the opportunity of getting the whole recipé or "microbe soup" during birth.
Aside the issue of CS, another issue that has contributed to increased PUDx amongst twentieth century dudes is the increased use of antibiotics. Some bugs are meant to be in the gastrointestinal system as protectors but indiscriminate use of antibiotics kill these good bugs giving way for the only bug able to stay cool in the acidic environment of the stomach (bad guy Helicobacter pylori) and the only implicated microbe in gastritis, PUDx and gastric cancer to flourish and well, have its way.
I hope someone has been educated this morning.
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Thecompleteheal(m): 3:48am On Aug 04, 2022 