Sandbox:Eman

### 1.Normal variants of growth
Familial short stature=None needed. Reassurance; monitor growth
Constitutional delay of growth and puberty=None needed. Reassurance; monitor growth; +/ treatment with sex steroids during puberty.
SGA infant, with catch-up growth=Monitor growth to distinguish from the 10% of SGA infants who do not have catch-up growth.
Systemic disorders or processes with secondary effects on growth=
Undernutrition=Reverse nutritional deficit.
Glucocorticoid therapy=Minimize glucocorticoid dose or give on alternate days if feasible; consider alternate drugs.
GI disease (especially Crohn disease and celiac disease)=Diagnose and treat underlying disease, improve nutrition, avoid glucocorticoids.
Rheumatologic disease (especially systemic onset juvenile idiopathic arthritis)=Diagnose and treat underlying disease, improve nutrition, avoid glucocorticoids
Renal disease (CKD, renal tubular acidosis)=Diagnose and treat underlying disease, maximize nutrition; GH if needed.
Cancer=Ensure adequate nutrition; treat any secondary pituitary hormone deficiencies (eg, GH deficiency)
Pulmonary disease (eg, cystic fibrosis, immune deficiencies with recurrent pulmonary infections, or severe asthma)=Diagnose and treat underlying disease, ensure adequate nutrition, avoid glucocorticoids
Immunologic disease=Diagnose and treat underlying disease
Endocrine causes of growth failure
Hypothyroidism=Thyroid hormone replacement
Cushing syndrome=Diagnose and treat underlying disease
GH deficiency=rGH
Precocious puberty=Treatment depends on type of precocious puberty
Genetic diseases with primary effects on growth
Turner syndrome=Estrogen, GH
SHOX mutations=Consider GH.
Noonan syndrome=Consider GH.
Silver-Russell syndrome=Consider GH
Skeletal dysplasias
Achondroplasia=Management of complications, which may include craniocervical junction compression, sleep apnea, spinal stenosis.
Hypochondroplasia=Surveillance for spinal stenosis, with surgery as needed.
Spondyloepiphyseal dysplasia=Surveillance for spinal disorders and osteoarthritis, with surgery as needed
Osteogenesis imperfecta=Bisphosphonates, fracture management

## Characteristics of the rash: Macules, papules, nodules, or plaques=

## Noninfectious
Erythema multiforme
Systemic lupus erythematosus
Dermatomyositis
Drug hypersensitivities
Gianotti-Crosti syndrome
Inflammatory bowel disease
Pityriasis rosea (fever rare)
Sarcoidosis
"Serum sickness"
Sweet syndrome (acute febrile neutrophilic dermatosis)
Still's disease (juvenile idiopathic arthritis)

## Bacterial
Arcanobacterium haemolyticum
Bacillus anthracis
Bartonella bacilliformis
Bartonella henselae (cat scratch disease)
Bartonella quintana (trench fever)
Borrelia burgdorferi (Lyme disease)*
Borrelia spp (relapsing fever)
Brucella spp (brucellosis)*
Calymmatobacterium granulomatis (donovanosis)*
Chlamydia psittaci (psittacosis)
Ehrlichiosis*
Ehrlichia chafeensis (HME)
Human granulocytic erlichiosis
Erysipelothrix rhusiopathiae (erysipeloid)
Francisella tularensis (tularemia)
Listeria monocytogenes
Leptospira spp (leptospirosis)*
Mycobacterium leprae*
Mycobacterium marinum*
Mycobacterium tuberculosis
Mycoplasma pneumoniae
Neisseria gonorrhoeae (gonorrhea)*
Neisseria meningitidis (meningococcemia)*
Pseudomonas aeruginosa
Rickettsia akari (rickettsialpox)
Rickettsia prowazekii (epidemic/louse-borne typhus)
Rickettsia rickettsii (RMSF-early lesions)*
Rickettsia orientalis/tsutsugamushi (scrub typhus)
Rickettsia typhi (endemic/murine typhus)
Salmonella typhi (typhoid fever)*
Spirillum minor (rat-bite fever)

## Fungal
Blastomyces dermatitidis*
Candida spp
Coccidioides immitis
Cryptococcus neoformans
Histoplasma capsulatum
Other disseminated deep fungal infections in immunocompromised patients

## Viral
Adenovirus
Arbovirus
Atypical measles*
Chikungunya virus
Colorado tick fever
Coxsackieviruses A and B
Cytomegalovirus, primary infection
Dengue virus
Epstein-Barr virus, primary infection
Echoviruses
Hepatitis B (urticaria)*
Human herpesvirus 6 (exanthem subitum)*
Human immunodeficiency virus (HIV-1)*
Kawasaki syndrome (presumed viral)
Molluscum contagiosum
Orf
Parvovirus B19 (erythema infectiosum )
Rubella (German measles)*
Rubeola (measles)*
Varicella (chickenpox)*
Varicella-zoster (disseminated)
Viral hemorrhagic fevers (many)
West Nile virus
Zika virus

## Vesicles, bullae, or pustules

## Noninfectious
Erythema multiforme bullosum
Toxic epidermal necrolysis
Dermatitis from plants
Drug hypersensitivities

## Bacterial
Bacillus anthracis
Ehrlichia canis
Listeria monocytogenes
Mycoplasma pneumoniae
Neisseria gonorrhoeae*
Neisseria meningitidis*
Pseudomonas aeruginosa
Rickettsia akari
Rickettsia rickettsii*
Staphylococcus aureus (TSS, SSSS)
Streptococcus group A
Treponema pallidum (secondary syphilis)
Vibrio vulnificus

## Fungal
Histoplasma capsulatum

## Viral
Colorado tick fever
Coxsackie A5, 9, 10, 16, B2, 7
Echoviruses
Eczema herpeticum
Herpes simplex (disseminated)
Varicella (chickenpox)
Varicella-zoster (disseminated)

## Purpuric macules, purpuric papules, or purpuric vesicles

## Noninfectious
"Allergic" vasculitis
Erythroderma
Cholesterol embolization
Disseminated intravascular coagulation (purpura fulminans)
Drug hypersensitivities
Fat embolism
Henoch-Schonlein purpura
Immune thrombocytopenic purpura
Granulomatosis with polyangiitis (Wegener's)

## Bacterial
Bacteremia
Borrelia spp
Clostridium spp
Infective endocarditis (many species)
Haemophilus influenzae type B
Neisseria gonorrhoeae (disseminated gonococcal infection)*
Neisseria meningitidis (acute or chronic meningococcemia)*
Pseudomonas aeruginosa
Rickettsia prowazekii
Rickettsia rickettsii
Spirillum minor
Staphylococcus aureus (bacteremia)
Streptobacillus moniliformis
Streptococcus group A (streptococcal toxic shock syndrome, scarlet fever)
Streptococcus pneumoniae (asplenic patient)
Vibrio vulnificus
Yersinia pestis

## Viral
Adenovirus (rare)
Atypical measles*
Chikungunya virus
Colorado tick fever
Congenital cytomegalovirus
Coxsackie A and B (rare, types A-9, B2-5)
Dengue fever
Epstein-Barr virus (rare)
Echoviruses (rare, types 3, 4, 9)
Rubella*
Varicella-zoster virus
West Nile virus
Yellow fever

## Widespread erythema with or without edema followed by desquamation

## Noninfectious
Erythroderma
Drug hypersensitivities
Graft-versus-host reaction
Stevens-Johnson syndrome
Toxic epidermal necrolysis
von Zumbusch pustular psoriasis

## Bacterial
Streptococcus group A (scarlet fever, streptococcal toxic shock syndrome)
Stapylococcus aureus (TSS, SSSS)

## Viral
Kawasaki syndrome (presumed viral)
1.Burn injuries are amongst one of the most devastating of all injuries, having a great impact on the patients physically, physiologically and psychologically. Burns are still one of the top causes of death and disability in the world. Physicians have searched for and formulated a myriad of treatments for burns over the centuries but these treatments mostly were of little benefit to the victims mainly because the fundamental understanding of the patho-physiological impact of burns was not known yet. There was an exponential increase in biomedical research and knowledge from the 18th to early 20thcentury in burn care, such as the recognition of the importance of burn surface area and skin grafting by Reverdin. However, this was not reflected in improving survival and many patients still died of shock and infection. It was not until the past 50 years that the mortality of burns has been dramatically improved, thanks to the better understanding of the patho-physiology of burn injury.  The treatment of burns is a major undertaking and involves many components from the initial first aid, assessment of the burn size and depth, fluid resuscitation, wound excision, grafting and coverage, infection control and nutritional support. Progress in each of these areas has contributed significantly to the overall enhanced survival of burn victims and this article aims to explore the history of burns to identify milestones and step-changes in each of these areas in the patients care. As in the case of the advancement in the treatment of trauma, these step-changes were mainly related to wars. Napoleons surgeons contributions to wound management that are still applicable today is an example. In burns, fire disasters as the Rialto fire in 1921 and Coconut Grove nightclubs fire in 1942 led to research that provided the first glimpse of the modern understanding of the patho-physiology of burns.
1.overvew;Syringomyelia is a generic term referring to a disorder in which a cyst or tubular cavity forms within the spinal cord. This cyst, called a syrinx, can expand and elongate over time, destroying the spinal cord. Since the spinal cord connects the brain to nerves in the extremities, this damage may result in pain, weakness, and stiffness in the back, shoulders, arms, or legs. Other symptoms may include headaches and a loss of the ability to feel extremes of hot or cold, especially in the hands {wikipedia}= Syringomyelia is a spinal cord cavitation, which is a central dilation due to cystic degradation expands and destroyed the spinal cord. Caused by an injury, tumors or congenital malformation like hernia. The damage can Effect the brain and nerves, that leade to Bilateral loss of pain and temperature sensation in upper extremities. weakness, stiffness, hyperReflexives in lower extremities with hyposcoliosis.
2.Risk factors for the development of syringomyelia depend on the underlying etiology: =  The main risk factors associated with the development of syringomyelia are based on the underlying causes.
3.The natural course of disease in syringomyelia is unpredictable(history)=  The essential Course of disease in Syringomyelia is temperamental.
4.80% of patients respond to surgical treatment in terms of hault to progression of symptoms and mild relief.{prognosis)= The symptoms of 80% of patients usually end due to their response to surgical treatment, as well a mild cure.
5{.Physical examination} findings of syringomyelia may include the=  The following includes how syringomyelia might be revealed
6.Spinal MRI may help to diagnose and follow up syringomyelia. It is characterized by the following findings{MRI}?
Syringomyelia may be diagnosed as an incidental finding on CT scan. However, delayed CT scan may have a diagnostic importance in early cases of syringomyelia without clinical manifestaions.(CT)?
7.It uses a contrast material combined with x ray or CT to image spinal cord in case of syringomyelia. However, CT metrimised myelography is more sensitive to diagnose syringomyelia as compared to conventional myelography.{mylogram}?
management??
reference:25,37,38,39,65
RED EYE RESIDENT SURVIVAL GUIDE (PDIATRICS)
TREATMENT:
1.Emergency--- urgent ophthalmic surgery.
2.Acute ----#SEVERA.Viral conjunctivitis=Good hygiene, such as meticulous hand washing ---decreasing the spread of acute viral conjunctivitis/ ----B.bacterial conjunctivitis=Any ophthalmic antibiotic
- .Mild allergic conjunctivitis=over-the-counter antihistamine/vasoconstrictor agent, or with a more effective second-generation topical histamine H1 receptor antagonist
- .moderate dry eye= Anti-inflammatory agents (e.g., topical cyclosporine ), topical corticosteroids, and systemic omega-3 fatty acids
3.chronic blepharitis=  1-eyelid hygiene and topical antibiotics if not benefit-----  oral tetracycline or doxycycline.

## Inhalation injury in burns
The interest in pulmonary function in burns patients probably started in the 1970s when physicans started to note that pulmonary complications were common in burn patients. With improvements in the treatment of burn shock and sepsis, inhalational injury has now replaced these two causes as the main cause of mortality in burn patients. Inhalational injury by itself has been shown to be associated with pulmonary dysfunction for at least 6 months after the injury.
Pulmonary complications in burn patients can arise from direct injury to the respiratory tract via the inhalation of heated air and chemicals released by combustion, and also iatrogenic factors such as fluid-overloading during resuscitation and lung damage by mechanical ventilation.
Airway and pulmonary inflammation can also result from smoke inhalation alone. An autopsy study by Zikria et al., in 1972 showed that 70% of all burn victims who died within 12 hours of injury had inhalational injury which could be linked to the toxic products of combustion. A study by Herndon et al., in 1985 using an experimental sheep model of smoke inhalation injury showed that the pulmonary edema that occurred after smoke inhalation was the result of an increase in microvascular permeability and hypothesized that this may be secondary to neutrophil degradation. The global immunosuppression that accompanies burn injuries increases the risk of developing respiratory tract infections.
The treatment of burns itself can contribute to the development of lung injury. Moore et al., noted that although fluid resuscitation and blood transfusions prevented acute renal failure in trauma patients, these patients went on to develop pulmonary complications. Pruitt et al., hypothesized that pulmonary insufficiency in burns patients was due to a complex mechanism of interstitial edema leading to alveolar epithelial cell (type 2) damage and pulmonary circulation constriction secondary to vasoactive substances. Achauer et al., proposed a number of measures to prevent pulmonary edema including the use of pulmonary artery wedge and central venous pressure monitoring and also the supplementation of crystalloids with albumin to reduce the amount of fluid required. This was supported by animal studies by Holleman et al., which found that animals that were given only crystalloids post-scald injury had a higher water content in their lungs and recommended the addition of colloids to resuscitation fluid. The view on using colloids however, has changed in the last 40 years. Moncrief, from the U.S. Army of Surgical Research, hypothesized that the use of colloid was of no benefit in the first 24 hours due to the disturbed capillary permeability.
In addition to overhydration, Moore et al., also recognized that inhalational lung injury could be exacerbated by tracheostomy and mechanical ventilation at high oxygen tension. Traditionally, mechanical ventilation is acheived using tidal volumes of 1015 ml per kilogram of body weight which is larger than in normal subjects at rest (78 ml per kilogram), which can lead to an excessive distension of the lung leading to disruption of the pulmonary epithelium and endothelium, and the release of inflammatory mediators. The use of lower tidal volumes (TV) during ventilation of patients with acute lung injury and acute respiratory distress syndrome has been shown by a landmark study by the Acute Respiratory Distress Syndrome Network in 2000 to reduce mortality by 22% and increase the number of ventilator-free days. There is evidence as well that low TV ventilation protects against pulmonary complications in patients without acute respiratory distress syndrome. Most burn centers now adopt this low TV approach to reduce ventilator-induced injury.

# Lifestyle and home remedies
To treat minor burns, follow these steps:
- Cool the burn. apply a cool water  (not cold) , wet compress until the pain eases. Don't use ice. Putting ice directly on a burn can cause further damage to the tissue.
- Remove rings or other tight items. Try to do this quickly and gently, before the burned area swells.
- Don't break blisters. Fluid-filled blisters protect against infection. If a blister breaks, clean the area with water (mild soap is optional). Apply an antibiotic ointment. But if a rash appears, stop using the ointment.
- Apply lotion. Once a burn is completely cooled, apply a lotion, such as one that contains aloe vera or a moisturizer. This helps prevent drying and provides relief.
- Bandage the burn. Cover the burn with a sterile gauze bandage (not fluffy cotton). Wrap it loosely to avoid putting pressure on burned skin. Bandaging keeps air off the area, reduces pain and protects blistered skin.
- Take a pain reliever. Over-the-counter medications, such as ibuprofen (Advil, Motrin IB, others), naproxen sodium (Aleve) or acetaminophen (Tylenol, others), can help relieve pain.
- Consider a tetanus shot. Make sure that your tetanus booster is up to date. Doctors recommend that people get a tetanus shot at least every 10 years.
Whether your burn was minor or serious, use sunscreen and moisturizer regularly once the wound is healed.

## Surgical and other procedures
You may need one or more of the following procedures:
- Breathing assistance. If you've been burned on the face or neck, your throat may swell shut. If that appears likely, your doctor may insert a tube down your windpipe (trachea) to keep oxygen supplied to your lungs.
- Feeding tube. People with extensive burns or who are undernourished may need nutritional support. Your doctor may thread a feeding tube through your nose to your stomach.
- Easing blood flow around the wound. If a burn scab (eschar) goes completely around a limb, it can tighten and cut off the blood circulation. An eschar that goes completely around the chest can make it difficult to breathe. Your doctor may cut the eschar to relieve this pressure.
- Skin grafts. A skin graft is a surgical procedure in which sections of your own healthy skin are used to replace the scar tissue caused by deep burns. Donor skin from deceased donors or pigs can be used as a temporary solution.
- Plastic surgery. Plastic surgery (reconstruction) can improve the appearance of burn scars and increase the flexibility of joints affected by scarring.
Red eye
Lids/lashes
Conjunctiva
Cornea
Anterior chamber/iris
Iris/lens