Sandbox:Eman

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.[24][25]

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

1. .Mild allergic conjunctivitis=over-the-counter antihistamine/vasoconstrictor agent, or with a more effective second-generation topical histamine H1 receptor antagonist

1. .moderate dry eye= Anti-inflammatory agents (e.g., topical cyclosporine [Restasis]), 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.[109] Inhalational injury by itself has been shown to be associated with pulmonary dysfunction for at least 6 months after the injury.[109]

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.[110] 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.[111] The global immunosuppression that accompanies burn injuries increases the risk of developing respiratory tract infections.[112]

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.[113] 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.[114] 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.[115] 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.[116] 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.[117]

In addition to overhydration, Moore et al.,[113] 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 10–15 ml per kilogram of body weight which is larger than in normal subjects at rest (7–8 ml per kilogram)[118], 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.[119,120] 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.[121] Most burn centers now adopt this low TV approach to reduce ventilator-induced injury.[122]