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1.
Neoreviews ; 24(4): e229-e242, 2023 04 01.
Article in English | MEDLINE | ID: mdl-37002398

ABSTRACT

Extremely low-birthweight (ELBW) infants are at increased risk for infection because the innate immune function of their skin is underdeveloped as they lack a competent epidermal barrier. Thus, neonatal clinicians need to pay careful attention to skin care practices, particularly for periviable infants. In this review, we describe the challenges of skin care in ELBW infants and summarize strategies to prevent skin injury, minimize damage when it occurs, and enhance cutaneous innate immunity.


Subject(s)
Infant, Extremely Low Birth Weight , Skin Care , Infant, Newborn , Humans , Infant , Birth Weight
2.
Adv Neonatal Care ; 22(4): 325-332, 2022 Aug 01.
Article in English | MEDLINE | ID: mdl-35901469

ABSTRACT

INTRODUCTION: Methicillin-susceptible Staphylococcus aureus (MSSA) infections cause diseases ranging from localized skin infections to serious invasive infections. Neonates are immunosuppressed, placing them at increased risk for MSSA infections, including staphylococcal scalded skin syndrome (SSSS), a rare severe skin presentation of MSSA. CLINICAL FINDINGS: We present a case series of 3 preterm infants with SSSS receiving care at a level 3 neonatal intensive care unit. PRIMARY DIAGNOSIS: The infants presented with symptoms of sepsis, including temperature instability, apnea, and bradycardia episodes. The infants had peeling skin at sites of external pressure, including peripheral intravenous (IV) sites, under dressings, or where devices had been in contact with skin. INTERVENTIONS: The infants were soaked in a tub with gel baby wash and water to remove leads without traumatizing the skin. Laboratory values were drawn, and cultures were obtained. Wound care was provided using mupirocin, soft silicone mesh wound contact layer, and soft cotton bandage gauze. Supportive respiratory care was provided, and IV antibiotics were administered. OUTCOMES: The infants were discharged to their homes with intact skin. One infant experienced a loss of pigment that persisted several weeks. All patients were without scarring by early childhood. PRACTICE RECOMMENDATIONS: Thorough assessment and careful hygiene of neonates' skin is crucial. MSSA is an infection that can appear on the skin. It is important to quickly diagnose and treat this type of infection, especially when it presents as a localized pustule, boil, tear, peeling, or crust before it becomes systemic.


Subject(s)
Staphylococcal Infections , Staphylococcal Scalded Skin Syndrome , Anti-Bacterial Agents/therapeutic use , Child, Preschool , Humans , Infant , Infant, Newborn , Infant, Premature , Intensive Care Units, Neonatal , Staphylococcal Infections/diagnosis , Staphylococcal Infections/drug therapy , Staphylococcal Scalded Skin Syndrome/diagnosis , Staphylococcal Scalded Skin Syndrome/drug therapy , Staphylococcus aureus
3.
Am J Physiol Heart Circ Physiol ; 294(3): H1326-34, 2008 Mar.
Article in English | MEDLINE | ID: mdl-18203849

ABSTRACT

Lymphangiogenesis is considered a promising approach for increasing fluid drainage during secondary lymphedema. However, organization of lymphatics into functional capillaries may be dependent upon interstitial flow (IF). The present study was undertaken to determine the importance of lymphangiogenesis for lymphedema resolution. We created a lymphatic obstruction that produces lymphedema in mouse tail skin. The relatively scar-free skin regeneration that occurred across the obstruction allowed the progression of lymphangiogenesis to be observed and compared with the evolution of lymphedema. The role of vascular endothelial growth factor-C (VEGF-C)/VEGF receptor (VEGFR)-3 signaling in lymphedema resolution was investigated by exogenous administration of VEGF-C or neutralizing antibodies against VEGFR-3. VEGF-C protein improved lymphedema at 15 days [reducing dermal thickness from 742 +/- 105 to 559 +/- 141 microm with 95% confidence intervals (CIs), P < 0.05] without increasing lymphatic capillary coverage (11.6 +/- 6.4% following VEGF-C treatment relative to 9.6 +/- 6.2% with 95% CIs, P > 0.50). Blocking VEGFR-3 signaling did not inhibit lymphedema resolution at 25 days (dermal thickness of 462 +/- 127 microm following VEGFR-3 inhibition relative to 502 +/- 87 microm with 95% CIs) or inhibit IF, although VEGFR-3 blocking prevented lymphangiogenesis (reducing lymphatic coverage to 0.2 +/- 0.7% relative to 8.7 +/- 7.3% with 95% CIs, P < 0.005). A second mouse tail lymphedema model was employed to investigate the ability of VEGF-C to increase fluid drainage across a scar. We found that neither neutralization of VEGFR-3 nor administration of VEGF-C affected the course of skin swelling over 25 days. These findings suggest that resolution of lymphedema in the mouse tail skin may be more dependent upon IF and regeneration of the extracellular matrix across the obstruction than lymphatic capillary regeneration.


Subject(s)
Extracellular Fluid/physiology , Lymphedema/physiopathology , Skin/physiopathology , Animals , Antibodies, Blocking/pharmacology , Female , Fluorescent Antibody Technique , Immunohistochemistry , Lymphangiogenesis/physiology , Lymphedema/pathology , Mice , Mice, Inbred BALB C , Receptors, Vascular Endothelial Growth Factor/antagonists & inhibitors , Receptors, Vascular Endothelial Growth Factor/metabolism , Regeneration , Skin/pathology , Tail , Vascular Endothelial Growth Factor A/metabolism , Vascular Endothelial Growth Factor A/pharmacology
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