flavus and A. fumigatus are the most common types of Aspergillus to cause fungal keratitis. F. Solani is the most common type of Fusarium and others include Curvularia and Acremonium. C. albicans, C. guilliermondii and C. parapsilosis are the main types of Candida to cause fungal keratitis. Pathophysiology
The precipitating event for fungal keratitis is trauma with a vegetable / organic matter. A thorn injury, or in agriculture workers, trauma with a wheat plant while cutting the harvest is typical. This implants the fungus directly in the cornea. The fungus grows slowly in the cornea and proliferates to involve the anterior and posterior stromal layers. The fungus can break through the descemets membrane and pass into the anterior chamber. The patient presents a few days or weeks later with fungal keratitis. Diagnosis
The diagnosis is made by an ophthalmologist/optometrist correlating typical history, symptoms and signs. Many times it may be missed and misdiagnosed as bacterial ulcer. A definitive diagnosis is established only after a positive culture report (lactophenol cotton blue, calcoflour medium), typically taking a week, from the corneal scraping. Recent advances have been made in PCR ref 3./immunologic tests which can give a much quicker result. Classification
Infectious keratitis can be bacterial, fungal, viral, or protozoal. Remarkable differences in presentation of the patient allows presumptive diagnosis by the eye care professional, helping in institution of appropriate anti-infective therapy. Prevention
Prevention of trauma with vegetable / organic matter, particularly in agricultural workers while harvesting can reduce the incidence of fungal keratitis.
Peripheral vasoconstriction accounts for the cold extremities (hands and feet), increased heart rate, increased cardiac output (and associated chest pain). Eventually, there will be less perfusion to the kidneys, resulting in decreased urine output. Diagnosis
Hypovolemia can be recognized by a fast heart rate, low blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.In children, compensation can result in an artificially high blood pressure despite hypovolemia (a decrease in blood volume). Children typically are able to compensate (maintain blood pressure despite hypovolemia) for a longer period than adults, but deteriorate rapidly and severely once they are unable to compensate (decompensate). Consequently, any possibility of internal bleeding in children should be treated aggressively.Signs of external bleeding should be assessed, noting that individuals can bleed internally without external blood loss or otherwise apparent signs.There should be considered possible mechanisms of injury that may have caused internal bleeding, such as ruptured or bruised internal organs. If trained to do so and if the situation permits, there should be conducted a secondary survey and checked the chest and abdomen for pain, deformity, guarding, discoloration or swelling. Bleeding into the abdominal cavity can cause the classical bruising patterns of Grey Turners sign (bruising along the sides) or Cullens sign (around the navel).