1000-2000 5 ьшò

cellulitis (1)[C]

No evidence for steroid use

First Line

Uncomplicated posttraumatic periorbital cellulitis

–Usually due to skin flora, including Staphylococcus and Streptococcus

–Cephalexin 500 mg PO q6h or dicloxacillin 500 mg PO q6h

–Clindamycin 300 mg PO TID, doxycycline 100 mg PO BID, or trimethoprim-sulfamethoxazole (TMP-SMX) 1 to 2 DS tablets PO q12h if

MRSAis suspected

Extension from sinusitis

–Amoxicillin-clavulanate 875 mg PO BID

–3rd-generation cephalosporin (e.g., cefdinir 300 mg PO BID)

Dental abscess

– Amoxicillin-clavulanate 875 mg PO BID or clindamycin 300 mg PO TID Bacteremic cellulitis

–May be associated with meningitis

–Ceftriaxone 1 g IV q24h plus vancomycin 15 mg/kg/dose IV q8–12h or clindamycin 600 to 900 mg IV q8h to cover MRSA

–Duration of therapy: A10to 14-day course is usually sufficient. Follow patients treated with oral antibiotics for presumed periorbital cellulitis closely (daily follow-up until improvement occurs) for response to antibiotics and possible progression to orbital cellulitis. If symptoms do not improve within 24 hours, reevaluate for IV antibiotic therapy.

ISSUES FOR REFERRAL

Consult ENT and ophthalmology if there is concern for orbital cellulitis or if first-line treatment fails (3).

SURGERY/OTHER PROCEDURES

Usually not indicated in uncomplicated cases

If there is an abscess or potential compromise of critical structures, orbital surgery is indicated.

Diplopia is the strongest clinical predictor for surgery.

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

If the patient is stable and there are no systemic signs of toxicity, mild cases in

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adults and children >1 year of age can be safely managed on an outpatient basis.

Consider hospitalization and IV antibiotics:

–If patient appears systemically ill

–Children <1 year of age (3,4)[C]

–Patients not immunized against S. pneumoniae or H. influenzae

–If patients do not improve or deteriorate within 24 hours of oral antibiotics

–High suspicion for orbital cellulitis (eyelid swelling with reduced vision, diplopia, abnormal light reflexes, or proptosis)

No strict guidelines indicate when to switch from parenteral to PO therapy. In general, a switch from IV to oral antibiotics is reasonable once eyelid edema and erythema have significantly improved. A10to 14-day course of antibiotics is indicated.

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Patient Monitoring

Follow for signs of orbital involvement, including decreased visual acuity or painful/limited ocular motility.

PATIENT EDUCATION

Maintain good skin hygiene.

Avoid skin trauma.

Report early skin changes (swelling, redness, and pain) if recurrent after a course of therapy.

PROGNOSIS

With timely treatment, patients do well.

Recurrent periorbital cellulitis occurs with ≥3 periorbital infections in 1 year with at least 1 month of in between episodes; must be differentiated from treatment failure due to antibiotic resistance (1)[C]

COMPLICATIONS

Orbital cellulitis; orbital abscess formation Scarring

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Vision loss

Cavernous sinus thrombosis

Osteomyelitis

REFERENCES

1.Hauser A, Fogarasi S. Periorbital and orbital cellulitis. Pediatr Rev. 2010;31(6):242–249.

2.Baring DE, Hilmi OJ. An evidence based review of periorbital cellulitis. Clin Otolaryngol. 2011;36(1):57–64.

3.Upile NS, Munir N, Leong SC, et al. Who should manage acute periorbital cellulitis in children? Int J Pediatr Otorhinolaryngol. 2012;76(8):1073–1077.

4.Georgakopoulos CD, Eliopoulou MI, Stasinos S, et al. Periorbital and orbital cellulitis: a 10-year review of hospitalized children. Eur J Ophthalmol. 2010;20(6):1066–1072.

ADDITIONALREADING

Mahalingam-Dhingra A, Lander L, Preciado DA, et al. Orbital and periorbital infections: a national perspective. Arch Otolaryngol Head Neck Surg. 2011;137(8):769–773.

Yeilding RH, O’Day DM, Li C, et al. Periorbital infections after Dermabond closure of traumatic lacerations in three children. J AAPOS. 2012;16(2):168– 172.

CODES

ICD10

L03.211 Cellulitis of face

CLINICALPEARLS

Periorbital (preseptal) and orbital (postseptal) cellulitis occur most commonly in children.

Orbital cellulitis typically has fever, pain with eye movement, diplopia, and/or proptosis. Prompt imaging is necessary if there is a concern for orbital cellulitis.

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CT scan of sinuses and orbits can differentiate periorbital cellulitis from orbital cellulitis.

The two most important predisposing factors for periorbital cellulitis are upper respiratory infections and eyelid trauma; sinusitis is more typically associated with orbital cellulitis.

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CEREBRALPALSY

Christina Mezzone, DO, MS Maria Lombardi, DO

BASICS

DESCRIPTION

Cerebral palsy (CP) is a group of clinical syndromes characterized by motor and postural dysfunction due to permanent and nonprogressive disruptions in the developing brain. Motor impairment resulting in activity limitation is necessary for this diagnosis. CPis classified by the nature of the movement disorder and its functional severity. Individuals with this disorder are affected with secondary musculoskeletal and neurologic problems (intellectual, sensory, speech and language impairment, and seizures).

EPIDEMIOLOGY

Incidence

Overall, 1.5 to 2.5/1,000 live births

Incidence increases as gestational age (GA) at birth decreases:

–146/1,000 for GAof 22 to 27 weeks

–62/1,000 for GAof 28 to 31 weeks

–7/1,000 for GAof 32 to 36 weeks

–1/1,000 for GAof 37+ weeks

Prevalence

3 to 4/1,000 of the population

ETIOLOGYAND PATHOPHYSIOLOGY

Multifactorial; CPresults from static injury or lesions in the developing brain, occurring prenatally, perinatally, or postnatally.

Neuropathology linked to GAat time of brain insult

Cytokines, free radicals, and inflammatory response are likely contributing factors.

Etiology is most likely multifactorial and depends on timing of brain insult: prenatally, perinatally, or postnatally (see “Risk Factors”).

Spastic CPis most common, usually related to premature birth, with either periventricular leukomalacia or germinal matrix hemorrhage.

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Dystonic or athetotic CP, often resulting from kernicterus, is now rare due to improved management of hyperbilirubinemia.

Genetics

There are reports of associations between CPand polymorphisms of certain genes: thrombophilic, cytokines, and apolipoprotein E.

RISK FACTORS

Prenatal: congenital anomalies, multiple gestation, in utero stroke, intrauterine infection (cytomegalovirus [CMV], varicella), intrauterine growth retardation (IUGR), clinical and histologic chorioamnionitis, antepartum bleeding, maternal factors (cognitive impairment, seizure disorders, hyperthyroidism), abnormal fetal position (e.g., breech)

Perinatal: preterm birth, low-birth weight, periventricular leukomalacia, perinatal hypoxia/asphyxia, intracranial hemorrhage/intraventricular hemorrhage, neonatal seizure or stroke, hyperbilirubinemia

Postnatal: traumatic brain injury or stroke, sepsis, meningitis, encephalitis, asphyxia, and progressive hydrocephalus

GENERALPREVENTION

Treating mothers with magnesium sulfate during preterm delivery is neuroprotective for fetus and may reduce the risk of CP. Effect on term fetus is unknown.

Improved management of hyperbilirubinemia with decrease in kernicterus has greatly reduced dyskinetic CP.

Prevention or reduction of chorioamnionitis and premature births

COMMONLYASSOCIATED CONDITIONS

Seizure disorder (22–40%)

Intellectual impairment (23–44%)

Behavioral problems

Speech and language impairment (42–81%)

–May have an impact on expressive and/or receptive language

–May be nonverbal

Sensory impairments

–Hearing deficits

–Visual (62–71%): poor visual acuity, strabismus (50%), or hemianopsia

Feeding impairment, swallowing dysfunction, and aspiration: when severe,

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may require gastrostomy feedings

Poor dentition, excessive drooling

GI conditions: constipation (59%), vomiting (22%), gastroesophageal reflux

Decreased linear growth and weight abnormalities (underand overweight)

Osteopenia

Bowel and bladder incontinence

Orthopedic: contractures, hip subluxation/dislocation, scoliosis (60%)

DIAGNOSIS

Aclinical diagnosis including

–Delayed motor milestones

–Abnormal tone

–Abnormal neurologic exam suggesting a cerebral etiology for motor dysfunction

–Absence of regression (not losing function)

–Absence of underlying syndromes or alternative explanation for etiology

Although the pathologic lesion is static, clinical presentation may change as the infant grows and develops.

Accurate early diagnosis remains difficult. Neurologic abnormalities observed in the first 1 to 2 years of life may resolve; be cautious of diagnosing CP before age 2 years.

Serial exams are often required for a definitive diagnosis.

HISTORY

Presentation: concerns over movements or delayed motor development Ask about

–Prenatal, perinatal, and postnatal risk factors

–Neurobehavioral signs

Poor feeding/frequent vomiting

Irritability

–Timing of motor milestones: Delay in milestones is not sensitive or specific until after 6 months of age.

–Abnormal spontaneous general movements

–Asymmetry of movements such as early hand preference

Regression of motor skills does not occur with CP.

PHYSICALEXAM

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Assess for more than one type of neurologic impairment:

–Spasticity: increased tone/reflexes/clonus

–Dyskinesia: abnormal movements

–Hypotonia: decreased tone

–Ataxia: abnormal balance/coordination

Areas of exam

–Tone: may be increased or decreased

–Trunk and head control: often poor but may be advanced due to high tone

–Reduced strength and motor control

–Persistence of primitive reflexes

–Asymmetry of movement or reflexes

–Decreased joint range of motion and contractures

–Brisk deep tendon reflexes

–Clonus

–Delayed motor milestones: serial exams most effective

–Gait abnormalities: scissoring, toe-walking

CPis classified by the following:

–Muscle tone or movement disorder Spasticity

■Unilateral: hemiplegic

■Bilateral: diplegic (lower extremity [LE] > upper extremity [UE]

involvement) or quadriplegic (UE ≥ LE involvement) Dystonia: hypertonia and reduced movement

Choreoathetosis: irregular spasmodic involuntary movements of the limbs or facial muscles

Ataxia: loss of orderly muscular coordination

–Motor function severity

The Gross Motor Function Classification System (GMFCS) scores I to V are the following:

■Score of I: ambulates without limitation

■Score of II: ambulates without assistive devices but some limitation

■Score of III: ambulates with assistive mobility devices

■Score of IV: self-mobility limited, but technology can help

■Score of V: self-mobility severely limited, even with technology

The Manual Ability Classification System (MACS) can be used to assess UE and fine motor function.

DIFFERENTIALDIAGNOSIS

Benign congenital hypotonia, brachial plexus injury, familial spastic paraplegia,

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dopa-responsive dystonia, transient toe-walking, muscular dystrophy, metabolic disorders (e.g., glutaric aciduria type 1), mitochondrial disorders, genetic disorders (e.g., Rett syndrome)

DIAGNOSTIC TESTS & INTERPRETATION

CPis a clinical diagnosis based on history, physical, and risk factors. Laboratory testing is not needed to make diagnosis but can help exclude other etiologies.

Testing for metabolic and genetic syndromes (1)[C]

–Not routinely obtained in the evaluation for CP

–Considered if no specific etiology is identified by neuroimaging or there are atypical features in clinical presentation

–Detection of certain brain malformations may warrant genetic or metabolic testing to identify syndromes.

Screening for coagulopathies: Diagnostic testing for coagulopathies should be considered in children with hemiplegic CPwith cerebral infarction identified on neuroimaging (1)[C].

Initial Tests (lab, imaging)

Neuroimaging is not essential, but it is recommended in children with CPfor whom the etiology has not been established (1)[C].

MRI is preferred to CT if need to determine etiology and timing of a brain insult (1)[C].

Abnormalities found in 80–90% of patients: brain malformation, cerebral infarction, intraventricular or other intracranial hemorrhage, periventricular leukomalacia, ventricular enlargement, or other CSF space abnormalities

Diagnostic Procedures/Other

The Communication Function Classification System has recently been developed as another means of assessing verbal performance.

International Classification of Functioning, Disability and Health for CPhave been newly developed to standardize functional assessments.

Screening for comorbid conditions: developmental delay/intellectual impairment, vision/hearing impairments, speech and language disorders, feeding/swallowing dysfunction, or seizures

Electroencephalograms (EEGs) should only be obtained if there is a history of suspected seizures.

Test Interpretation

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Perinatal brain injury may include the following:

White matter damage

–Most common in premature infants

–Periventricular leukomalacia: gliosis with or without focal necrosis with resulting cysts and scarring; may be multiple lesions of various ages. Necrosis can lead to cysts/scarring.

–Germinal matrix hemorrhage: may lead to intraventricular hemorrhage

Gray matter damage: more common in term infants; cortical infarcts, focal neuronal damage, myelination abnormalities

TREATMENT

Focuses on control of symptoms; treatments reduce spasticity to prevent painful contractures, manage comorbid conditions, and optimize functionality and quality of life.

GENERALMEASURES

Early intervention programs for preterm infants influences motor and cognitive outcomes (2)[A].

Referral to early intervention for children ages 0 to 3 years is essential. Various therapy modalities enhance functioning:

–Physical therapy to improve posture stability and gait, motor strength and control, and prevent contractures

–Occupational therapy to increase functional activities of daily living and other fine motor skills

–Speech therapy for verbal and nonverbal speech and to aid in feeding

Equipment optimizes participation in activities:

–Orthotic splinting (ankle–foot orthosis) maintains functional positioning and prevents contractures.

–Spinal bracing (body jacket) may slow down scoliosis.

–Augmentative communication with pictures, switches, or computer systems for nonverbal individuals

–Therapeutic and functional electrical stimulation decreases activity limitation in gait.

–Use of adaptive equipment such as crutches, walkers, gait trainers, and wheelchairs for mobility and standers for weight bearing

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