7. Impetigo
• Staphylococcus aureus, B-Hemolytic
streptococci
• Nonbullous (70%)
• insect bites, abrasions, lacerations,
chickenpox, scabies pediculosis,and burns.
• Vesicle or oustule -> honey-colored crusted
plaque <2mm
• Bullous
• Flaccid, transparent bullae develop most
commonly on skin of the face,buttocks, trunk,
perineum, and extremities.
• localized staphylococcal scalded skin
syndrome anddevelop on intact skin.
8. Impetigo – Differential Diagnosis
• Non-Bullous: viruses (herpes simplex, varicella-zoster),
fungi (tinea corporis, kerion), arthropod bites, and
parasitic infestations (scabies, pediculosis capitis
• Bullous: epidermolysis bullosa, bullous mastocytosis,
herpetic infection, and early scalded skin syndrome. In
older children, allergic contact dermatitis burns, erythema
multiforme, linear immunoglobulin
9. Impetigo - Complications
• Rare - osteomyelitis, septic arthritis, pneumonia, and septicemia.
• Infection with nephritogenic strains of GABHS may result in acute
poststreptococcal glomerulonephritis
• 3-7 yr of age.
• The latent period from onset of impetigo to glomerulonephritis is 18-21 days
10. Impetigo : Treatment
• Topical therapy with mupirocin 2%, and retapamulin 1% 2-3 times a day for 10-14
days -localized disease caused by S. aureus.
• Systemic theraphy with oral antibiotics – widespread involvent
• Cephalexin, 25-50 mg/kg/day in 3-4 divided doses for 7-10 days
• if a satisfactory clinical response is not achieved within 7 days, -> CULTURE
and SENSITIVITY, - additional 7 days
11. Subcutaneous Tissue Infection
• Non-necrotizing
• responds to antibiotic therapy alone
• Necrotizing
• prompt surgical removal of all devitalized tissue in addition to antimicrobial
therapy.
• rapidly advancing local tissue destruction and systemic toxicity
• (+) necrosis
• Cellulitis
• inflammatory infectious process (-) necrosis or tissue destruction
12. Cellulitis
• infection and inflammation of loose connective tissue limited to the
dermis , relative sparing of the epidermis.
• Predisposed by
• break in the skin from previous trauma, surgery, or an underlying skin lesion
• Common seen – patients with lymphatic stasis, diabetes mellitus, or
immunosuppression
• Streptococcus pyogenes (group A streptococcus) and S. aureus –
common etiologic agent
• Pseudomonas aeruginosa – in immunocompromised or diabetic
patients
• Eschericia coli - children with relapsed nephrotic syndrome
13. Cellulitis
• area of edema, warmth, erythema, and tenderness.
• lateral margins tend to be indistinct because the process is deep in the
skin, primarily involving the subcutaneous tissues in addition to the
dermis. Application of pressure may produce pitting.
• Staphylococcus aureus
• localized with suppuration
• S. pyogenes (group A streptococci)
• spread more rapidly
• lymphangitis.
14. Cellulitis – Complications
• subcutaneous abscess, bacteremia, osteomyelitis, septic arthritis,
thrombophlebitis, endocarditis, and necrotizing fasciitis.
• Lymphangitis or glomerulonephritis can also follow infection with S.
pyogenes
15. Cellulitis - Treatment
• Penicillinase resistant penicillin such as dicloxacillin or cloxacillin or a
firstgeneration cephalosporin (cephalexin)
• MRSA – Clindaymycin
• improvement is not noted or the disease progresses significantly in the
1st 24-48 hr of therapy, parenteral therapy is necessary
• If fever, lymphadenopathy, or constitutional signs are present,
parenteral therapy should be initiated.
16.
17. Necrotizing Faciitis
• subcutaneous tissue infection that involves the deep layer of
superficial fascia but may spare adjacent epidermis, deep fascia, and
muscle
• Polymicrobial - S. aureus, streptococcal species (S. pyogenes - group
A streptococcus), Klebsiella species, E. coli, and anaerobic bacteria.
18. Necrotizing Faciitis
• highest in hosts with systemic or local tissue
immunocompromise, such as those with
diabetes mellitus, neoplasia, or peripheral
vascular disease, post operative, intravenous
drugs users,undergoing immunosuppressive
treatment
• acute onset
• edema, erythema, tenderness, and heat.
• Fever, pain, tenderness, and constitutional
signs are disproportionate to cutaneous sign
• Lymphangitis and lymphadenitis may or may
not be present.
19. Necrotizing Faciitis
• Diagnosis – Surgical exploration
• Necrotic fascia and subcutaneous tissue are gray and offer little
resistance to blunt probing.
• CT and MRI - delineating the extent and tissue planes of involvement
• Gram staining of tissue - Gram-positive cocci - S. pyogenes,
20. Necrotizing Faciitis - Treatment
• Early supportive care, surgical debridement, and parenteral antibiotic
• Wound debridement within 24-36 hr
• Parenteral antibiotic therapy.
• Initial empirical therapy should be instituted with vancomycin,
linezolid, daptomycin, or quinupristin to cover Gram-positive and
piperacillin-tazobactam to cover Gram-negative organisms.
• Addition of ceftriaxone with metronidazole- mixed aerobic–anaerobic
organisms.
• Penicillin with clindamycin is indicated for documented group A
streptococcal necrotizing fasciitis.
VIRAL ENCEPHALITUS, DENGUE, DM TYPE 2 0 DE LEON, DEVHERLENE
PAROTITIS, SECONDARY TO ODONTOGENIC INFECTION – MENDOZA MARIA DAENERY 4/F
ATP EXUDATIVE - ESLOFOR, RAYM FERNANDO 4/M
ATP NON-EXUDATIVE – LOZANO GREYSON CARL ARCENO 1/M
DE LEON, Devherlene 14/F
CC: drowsiness
HPI
Three months prior to consult, patient experienced polydipsia, polyphagia, and generalized body weakness. No hematuria, oliguria, nocturia, weight loss nor appetite changes. Patient sought consult with you po for the 1st time and advised lab workups which revealed the ff:
(01/08/23) outpatient
FBS 211.49mg/dL
Cholesterol 6.34 H
Trigly 4.29 H
HDL 0.82 L
LDL 3.58 H
VLDL 1.95 H
SGOT 79.36 H
SGPT 94.04 H
Patient was managed as a case of DM 2 and was started on Metformin 500mg/tab, 1 tab TID and Atorvastatin + Ezetimibe 10mg/10mg/tab. 1 tab OD. Patient took Metformin for only 2 months and stopped due to side effects of nausea, headache, and vomiting.
3 weeks PTC, patient had 1day history of fever (Tmax 38.9C) with no associated cough, colds, dysuria nor loose stools. Patient was brought to a different private physician and lab workups revealed:
CBCPC outpatient (3/14)
Hgb 12.2
Hct 37.1
WBC 11.7
Seg 60
Lym 30
Eos 3
Mon 6
Bas 1
Plt 290
Urinalysis outpatient (3/14)
Light yellow, hazy
pH 5
spgr 1.015
Gluc neg
Prot neg
Pus 3-4
RBC 10-12
Epith few
Mucus none
Bact few
Amorp. urates rare
She was given Cefuroxime 500mg/tab, 1 tab BID for 5 days and later on given Co-amoxiclav 625mg/tab, 1 tab BID for 7 days, both completed with no recurrence of fever.
On the day of consult, patient went for ffup consult with you po with the ff lab results:
Thyroid function test outpatient (3/23(
FT4 18.72
TSH 1.89
FT3 3.89
KUB UTZ outpatient (3/23)
Fatty infiltration of liver
U/R UTZ of gallbladder
However, patient experienced sudden onset of drowsiness and chills, hence, was advised consult at the ER.
Last meal: 4/3 7:30am today
Last UO: 4/3 8am
PMH: Dengue Fever (2019, admitted for 4 days, no blood transfusions)
FMH: DM 2 (maternal),
NutHx: prefers vegetables, but sometimes drink soda; not fond of sweets, chocolates, milktea nor fruit smoothies
Immunization Hx: completed primary vaccines c/o local health center with COVID19 vaccine
Environmental Hx: Patient lives with both parents and grandmother who are all COVID19 vaccinated with boosters, without symptoms nor exposure.
MensHx:
M - 13 years, I - Irregular, D - 4 days, A - 10 panty liners, S - none
Months w/ period: (2022) January, April, June, July, Novermber, December; (2023) March
Months off-period: (2022) March, May, August, September, October 2022; (2023) January, February
Anthropometrics:
Weight: 49 kg
BP 120/80, HR: 125, RR: 22, T: 37.2, SpO2: 100%
Patient came is ambulatory, not in distress, drowsy but answers to question, no pallor, cyanosis nor jaundice, slightly sunken eyeballs, pink palpebral conjunctiva, no CLADS, normal heart rate & regular rhythm, no murmur, soft nondistended abdomen, direct tenderness on epigastric area, full & equal pulses, no edema, CRT <2seconds, GCS 15
A: DM 2; rule out DKA
At the ER, CBG stat is 314 and serum ketone is 0.1.
Patient is initially hooked to PNSS 2FM + Mild and O2 at 1-2lpm via nasal cannula. Lab workups done: Na, K, VBG, ABG, Crea, CBG Q1
Dr. Feliciano updated via phonecall
- Facilitate ABG
- Defer Na, K, Crea
- Continue CBG Q1
- Revise IVF to PNSS 1L Mild in 8hrs
- Observe patient at ER for now
—————
CBG:
12nn 273
12:30nn: 267
Dr. Feliciano updated:
- Revise IVF to PNSS 1L Mild in 6hrs
- Defer VBG, facilitate ABG
—————
Rounds with Dr. Feliciano
- Start Metformin 500mg/tab, 1 tab now then BID
- Start Cholecalciferol 25,000 IU/amp, 1 amp PO 1x/week for 3 months
- Continue IVF hydration PNSS Mild in 6hrs
- Facilitate CBCPC now, Urinalysis
- Continue CBG Q3
- May have DM diet once fully awake
————
Good afternoon po Ma’am. Respectfully updating you po of your private patient here in ER Main non-COVID area:
Pedia Bed #1
DE LEON, Devherlene 14/F
Wt 49kg
DM 2; rule out UTI
Patient does not complain of recurrence of epigastric pain, however with 1st onset of fever 3pm 37.8C, resolved with TSB, however, fever recurred at 4pm 39C on left axilla, 38.2C on right axilla; no nausea, vomiting, no dysuria, with urge to urinate but uncomfortable at the ER. Patient also does not want to eat po Ma’am with decreased appetite
BP 120/80, HR 82, RR 21, T 38.2C, SpO2 100%
Patient is asleep but easily arousable, answers to questions when asked but is irritable to HCW, not in distress, slightly sunken eyeballs, but pink & moist lips & oral mucosa, no pallor, clear breath sounds, normal heart rate & regular rhythm, soft nondistended abdomen, nontender upon palpation, no CVA tenderness, good peripheral pulses & skin turgor, no edema, GCS 15
CBG Q3
2pm: 225
5pm: 220
CBCPC (4/3)
Hgb 113 L
Hct 0.36 L
WBC 12.5 H
RBC 3.9
Neu 0.69
Lymp 0.25 L
Eos 0.01 L
Mono 0.04
Baso 0.01
MCV 91.6
MCH 29.1
MCHC 317 L
RDW 12.1
Plt 197
Also Ma’am, upon rehistory, patient took Cefuroxime 500mg/tab, 1 tab BID for 5 days and Co-amoxiclav 625mg/tab, 1 tab BID for 7 days, both completed
Relatives highly advised admission for observation and consented po Ma’am
Suggested Admitting Plans
⁃ Will continue IVF Hydration PNSS 1L Mild in 6hrs then reassess thereafter
⁃ Will continue meds:
1. Metformin 500mg/tab, 1 tab BID
2. Cholecalciferol 25,000IU/amp, 1 amp 1x/week
⁃ Will start Ceftriaxone 2g IV OD (adult dose)
⁃ Will give Paracetamol 300mg IV now then Q4 PRN for fever
⁃ Will facilitate urinalysis once with specimen, to include Urine CS prior starting Ceftriaxone
⁃ Will continue strict I&O monitoring
⁃ Will continue CBG Q3
⁃ Will continue DM diet once fully awake
Will facilitate plans if okay with you po Ma’am?
Thank you po.
Lyn Abad/DLSUMC ER
———-
Dr. Feliciano updated
Ok with plans Lyn. Thanks
Just give oral paracetamol 500 mg now then q 4 for fever
———-
Noted po Ma’am, also, will not refer to IDS for clearance since patient has no other COVID symptoms (only fever) and will facilitate RAgT for patient only (relative - mother is fully COVID19 vaccinated with booster and no COVID symptoms nor exposure po Ma’am)
Dr. Feliciano: Ok
- Continue CBG monitoring q 3 hours (revise time to 9-12-3-6-9-12).
- if CBG>=200, inject regular insulin 5 units.
————
Also Ma'am, patient still has no UO (last UO at 8am po Ma'am), but with urge to void.
Alternate warm and cold compress done po Ma'am, but patient still has no UO and now complains of dysuria
Upon reassessment, patient has improved nonsunken eyeballs but with slightly distended bladder
Respectfully suggesting po Ma'am if we may do straight catheterization to collect specimen for urinalysis and urine CS and observe for spontaneous urination after removal of straight catheter?
Dr. Feliciano agreed.
Cellulitis Secondary to Infected Wound. -- NOLLAS, Rhiana Rein Cereno 4/F
TC UTI ARAFEL, Athena Evangelista 7 mos old/F
DISSEMINATED TUBERCILOSIS – BANICO
ATP NE - LOZANO, Greyson Carl Arceno 1/M ABSCESS, LEFT AXILLA< ATOPIC DERMATITIS, BASILIO, IZZIAH 7 MOS/M
PREAURICULAR SINUS, ASD, -MANRIQUEZ, JUAN NICCOLO
ADD NANO
NANO
Room 2309
NANO, Rain Henry 12/M
Wt: 48.7 kg Ht: 145 cm BSA: 1.4
CC: ear pain
Patient is a known case of Constitutional Mismatch Repair Deficiency Syndrome since 2022.
2 week PTC, during holiday, patient went home to their province at pangasigan, and went on swimming at a beach.
In the interim, the patient had no subjective complaints. No fever, cough, colds, ear pain, abdominal pain, dysuria, nor changes in BM.
Until 4 days prior to consultation, patient had colds with watery nasal discharge, and non productive cough. No fever episode.
Patient was given Salbutamol neb which gave slight relief of symptoms.
In the interim, there was progression of symptoms. Patient had progression of colds with yellowish discharge, and had productive cough. No fever episode, no chest pain, nor difficulty of breathing, still with good appetite, and activity. No medications was given, nor consult done.
1 day PTC, patient now complained of left ear pain, associated with ear fullness. Still with persistence of other symptoms. Patient also developed chest pain when coughing.
On the day of consult, due to persistence or symptoms, patient was brought in for consult po with you, and was advised for admission.
RTPCR (4/22(sad) negative
Past Medical Hx: Known case of Constitutional Mismatch Repair Deficiency Syndrome: Glioblastoma multiforme, recurrence, S/P XRT and Chemotherapy;
Rectal Carcinoma, S/P Colonoscopy with biopsy (December 2022); B-cell, Acute lymphoblastic leukemia, average risk, in remission; S/P Chemotherapy (2020); Constitutional Mismatch Repair Deficiency
Maintenance medications:
1. Levetiracetam 100mg/ml 2ml BID
2. Dexamethasone 4mg 1/2 tab OD
Family Medical Hx: (+) Colon cancer, paternal grandfather; (+) Hypertension both sides
Immunization Hx: complete primary immunization with no booster doses. Fully vaccinated against COVID 19
O: 120/80mmHg, 82bpm, 17cpm, 36.4C, 98%
Multiple striae on abdomen, axilla and thigh, cushingoid facies, no tragal tenderness AU, oral leukoplakia on soft palate and uvula, clear and equal breath sounds, flabby, soft-nontender abdomen, good pulses
Otoscopy:
AS: Erythematous, bulging tympanic membrane
AD: Unremarkable
A: Otitis Media, Otomycosis AS; URTI, Costochondritis in an immunocompromised; Constitutional Mismatch Repair Deficiency Syndrome
Plans:
Will facilitate admitting orders
IVF: D5NM FM rate
Diagnostics: CBCPC, Chest Xray, ALT, AST, TBDBIB, Crea, Na, K, Mg, Phos, LDH, Uric acid, CEA
Therapeutics:
1. Cefuroxime IV Q8 (92mkD)
2. Fluconazole 150mg/tab 1 tab OD (3mkD)
3. Paracetamol 1g IV drip Q8 PRN
4. PNSS NEB Q4-6 PRN
5. Dexamethasone 4mg/tab 1/2 tab OD
Diet: DAT
Will relay labs once available
Thank you po, Maam
Good afternoon, everyone. Today we're going to talk about a subject that's close to every parent's heart: their child's health. Specifically, we'll be discussing pediatric skin and soft tissue infections, which can be a real cause for concern for many families.
While these types of infections are generally not life-threatening, they can be uncomfortable, painful, and even lead to scarring if left untreated. Plus, they're highly contagious and can spread quickly in schools and other communal settings. That's why it's so important to understand what causes these infections and how they can be prevented.
-Most common skin infection in children throughout the world
-Staphylococci generally spread from the nose to normal skin then infect the skin
-In contrast to GABHS an average of 10 days
before development of impetigo.
Lesions are associated
with little to no pain or surrounding erythema, and constitutional
symptoms are generally absent. Pruritus occurs occasionally, regional
adenopathy is found in up to 90% of cases, and leukocytosis is present
in approximately 50%.
Bullous impetigo is always caused by S. aureus strains that produce
exfoliative toxins, (ETA, ETB,
ETD) blister the superficial epidermis by hydrolyzing human desmoglein
1, resulting in a subcorneal vesicle.
The latent period from onset of impetigo to development of poststreptococcal glomerulonephritis averages 18-21 days
longer than the 10-day latency period
after pharyngitis.
Systemic therapy with oral antibiotics should be prescribed for
patients with streptococcal or widespread involvement of staphylococcal
infections; when lesions are near the mouth, where topical medication
may be licked off; or in cases with evidence of deep involvement,
including cellulitis, furunculosis, abscess formation, or suppurative
lymphadenitis. Cephalexin, 25-50 mg/kg/day in 3-4 divided doses for
7-10 days, is an excellent choice for initial therapy.
No evidence suggests
that a 10-day course of therapy is superior to a 7-day course.
The
emergence of methicillin-resistant S. aureus (MRSA) dictates that if a
satisfactory clinical response is not achieved within 7 days, a culture
should be performed and an appropriate antibiotic based on drug
sensitivity should be given for an additional 7 days. If MRSA is suspected,
clindamycin, doxycycline or sulfamethoxazole-trimethoprim
is indicated.
Bibliography is available
Regional adenopathy and constitutional signs and
symptoms such as fever, chills, and malaise are common.
Aspirates from the site of inflammation, skin biopsy, and blood cultures
allow identification of the causal organism in approximately 25%
of cases of cellulitis. Blood cultures are usually negative in immunocompetent
patients with mild to moderate infection. Yield of the causative
organism is approximately 30% when the site of origin of the
cellulitis is apparent, such as an abrasion or ulcer. An aspirate taken
from the point of maximum inflammation yields the causal organism
more often than a leading-edge aspirate. Lack of success in isolating an
organism stems primarily from the low number of organisms present
within the lesion. Ultrasonography is used if an associated subcutaneous
abscess is suspected.
The differential diagnosis should include an exuberant immuneallergic
reaction to insect bites particularly mosquito bites (Skeeter
syndromes) (see Chapter 146). The skeeter syndrome is characterized
by swelling disproportionate to erythremia; there is pruritus but
usually no tenderness.
Figure 665-2 Purulent skin and soft-tissue infections (SSTIs)—Mild infection: For purulent SSTI, incision and drainage is indicated. Moderate
infection: Patients with purulent infection with systemic signs of infection. Severe infection: Patients who have failed incision and drainage plus
oral antibiotics or those with systemic signs of infection such as temperature >38°C (100.4°F), tachycardia (heart rate >90 beats/min), tachypnea
(respiratory rate >24 breaths/min) or abnormal white blood cell count (<12,000 or <400 cells/μL), or immunocompromised patients. Nonpurulent
SSTIs—Mild infection: Typical cellulitis/erysipelas with no focus of purulence. Moderate infection: Typical cellulitis/erysipelas with systemic signs
of infection. Severe infection: Patients who have failed oral antibiotic treatment or those with systemic signs of infection (as defined above under
purulent infection), or those who are immunocompromised, or those with clinical signs of deeper infection such as bullae, skin sloughing, hypotension,
or evidence of organ dysfunction. Three newer agents, oritavancin, tedizolid, and dalbavancin, are also effective agents in SSTIs, including
those caused by methicillin-resistant Staphylococcus aureus. C & S, culture and sensitivity; I & D, incision and drainage; MRSA, methicillin-resistant
Staphylococcus aureus; MSSA, methicillin-susceptible Staphylococcus aureus; Rx, treatment; TMP/SMX, trimethoprim-sulfamethoxazole. (Modified
from Stevens DL, Bisno AL, Chambers HF, et al: Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014
update by the Infectious Diseases Society of America. Clin Infect Dis 59:147–159, 2014, Fig. 1.)
The
infection can also occur in healthy individuals after minor puncture
wounds, abrasions, or lacerations; blunt trauma; surgical procedures,
particularly of the abdomen, gastrointestinal or genitourinary tracts,
or the perineum; or hypodermic needle injection.
Skin changes may
appear over 24-48 hr as nutrient vessels are thrombosed and cutaneous
ischemia develops. Early clinical findings include ill-defined cutaneous
erythema and edema that extends beyond the area of erythema. Additional
signs include formation of bullae filled initially with strawcolored
and later bluish to hemorrhagic fluid, and darkening of affected
tissues from red to purple to blue. Skin anesthesia and, finally, frank
tissue gangrene and slough develop owing to the ischemia and necrosis.
Vesiculation or bulla formation, ecchymoses, crepitus, anesthesia,
and necrosis are ominous signs indicative of advanced disease. Children
with varicella lesions may initially show no cutaneous signs of
superinfection with invasive S. pyogenes, such as erythema or swelling.
Significant systemic toxicity may accompany necrotizing fasciitis,
including shock, organ failure, and death. Advance of the infection in
this setting can be rapid, progressing to death within hours. Patients
with involvement of the superficial or deep fascia and muscle tend to
be more acutely and systemically ill and have more rapidly advancing
disease than those with infection confined solely to subcutaneous
tissues above the fascia. In an extremity, a compartment syndrome
Parenteral antibiotic therapy should be initiated as soon as possible
with broad-spectrum agents against all potential pathogens
