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Definition
Sabaceous cyst which is also known as an epidermoid cyst is derived from hair follicles and it is a closed sac under the skin that is filled with a cheese like or oily material. It may be felt as small lumps or bumps under the skin.

Incidence
Sabaceous cyst represent one of the commonest skin lesions, occurring at any age after childhood. They are often multiple and occur in any hair bearing site on the body most commonly on the trunk, face and neck and particularly on the scalp and scrotum. They do not occur on the palms and soles.

Clinical Features
The main symptom is usually a small, non-painful lump beneath the skin.

If the lump becomes infected or inflamed, other symptoms may include:

Skin redness
Tender or sore skin
Warm skin in the affected area

Grayish-white, cheesy, foul-smelling material may drain from the cyst.

The lesions are well defined and hemi spherical, growing slowly from 1-2 cm across. they lie in the subcutaneous tissue but are tethered to the skin by blocked duct, there being a pit on the surface at the site of hair follicle. gentle squeezing of the skin over the cyst demonstrates this point of tethering though the punctum is sometimes difficult to demonstrate, particularly over the scalp; when present it is diagnostic.

Important things to remember in relation to sabaceous cysts
Sabaceous cysts are associated with osteomas and intestinal polyps in Gardner’s syndrome.
Sabaceous cysts may occasionally ulcerate and in these cases can look very much like a malignant skin lesion.

Etiology
Sebaceous cysts most often arise from swollen hair follicles. Skin trauma can also induce a cyst to form. Excessive testosterone production will also cause such cysts.

Management
Surgical excision of a sebaceous cyst is a simple procedure to completely remove the sac and its contents. There are three general approaches used: traditional wide excision, minimal excision, and punch biopsy excision.

Another method of treatment involves placement of a heating pad directly on the cyst for about fifteen minutes, twice daily, for about 10 days (depending on size and location of the cyst) to promote drainage

The skin functions as a barrier against potentially harmful physical and chemical agents as well as against different microorganisms. Sometimes different features may be seen that help to differentiate different systemic diseases.

A brief list of the skin manifestations of non malignant systemic diseases is given here:

1. Erythema

Collagen disease
Carcinoid
Mitral valve disease
Polycythemia
Superior vena caval obstruction
Liver disease
Hyperviscosity syndrome

Facies in Primary Polycythemia vera.

2. Erythema Multiforme

Fever
Inflammatory bowel disease
Rheumatoid arthritis
Thyrotoxicosis
Viral Infections

Erythema Multiforme (target skin lesions)

3. Urtricaria

Collagen disorders
Xanthomatoses
Hereditary angioneurotic edema
Urtricaria pigmentosa
Henoch-Schonlein purpura
Cold aglutinins

4. Scaling

Vitamin deficiencies
Hypothyroidism
Acromegaly
Malabsorption
Refsum’s and Reiter’s diseases
Infections

5. Papules and Nodules

Bechet’s disease
Erythema nodosum
Erythema induratum
Garner’s syndrome
Necrobiosis lipoidica
Neurofibromatosis
Polyarteritis nodosum
Pseudoxanthoma elasticum
Sarcoid
Tuberous sclerosis
Xanthoma

6. Blisters

Dermatitis herpetiformis
Drugs
Gulcagonoma
Pemphigus
Porphyria
Vascular diseases

7. Angiomas

Multiple vascular malformations.

Although most of the conditions are rarely seen in common clinic practice but should be kept i mind to understand the skin manifestations of non malignant systemic diseases.

Introduction: Episcleritis is a common and benign inflammation of the episclera, typically affecting young and middle-aged adults. Seventy percent of cases occur in females.

The episclera lies just beneath the bulbar conjunctiva. Its vessels are large, run in a radial direction,
and can be seen beneath the overlying conjunctiva. Episcleral and conjunctival vessels blanch with the use of topical 5% phenylephrine drops, unlike deep episcleral vessels.

Clinical Features:

Patients may complain of foreign body sensation, mild tenderness, irritation, mild photophobia, and excessive lacrimation.
Pain is unusual but can occur, particularly in chroniccases.
One-half of cases are bilateral.
Eye findings are notable for a localized pink or bright red conjunctival injection, with involvement of the vessels in the superficial episcleral vascular plexus.
Visual acuity is normal.

Associated Conditions: Episcleritis is usually an isolated condition, though it may be associated with a number of systemic diseases, including rheumatoid arthritis, inflammatory bowel disease, lupus, and vasculitis.

Important Points To Remember:
1. It is important to differentiate episcleritis from sight threatening scleritis. Episcleritis presents with only mild pain and bright red episcleral vessels, which will blanch with topical phenylephrine.
2. Conjunctivitis is a more common cause of red eye, and symptoms usually include morning crusting. Injection that is localized rather than diffuse is more likely to be episcleritis

Management: For many patients, the condition is self-limited and will resolve within 3 weeks, with or without treatment. For mild cases, use over-the-counter artificial tears. For those with recurrent or recalcitrant lesions, referral to the ophthalmologist is indicated.

Herpes Simplex virus infection may be caused by type I or type II virus and the infection may be primary or recurrent.

Primary Infection
The manifestations of primary Infection includes:

1. Systemic infection: e.g fever, sore throat and lymphadenopathy that may pass unnoticed. If the patient is immunocompromised, then the disease may become life threatening with fever, lymphadenopathy, pneumonitis and hepatitis.

2. Gingivostomatitis: Ulcers filled with yellow slough appear in the mouth.

3. Herpetic Whitlow: A breach in the skin that may be due to any minor trauma allows the virus to enter the finger, causing a vesicle to form. Often this condition is seen in children nurses.

4. Traumatic Herpes: Also known as Herpes gladiatorum. In this condition vesicles develop at any site where herpes simplex virus have been inoculated on the skin by brute force.

5. Eczema Herpeticum: HSV infection superimposed on eczematous skin. Usually seen in children.

6. Herpes Simplex Meningitis: This is uncommon and if occurs it is usually self limiting.

7. Genital Herpes: It is usually caused by HSV type II. In males it presents as grouped vesicles and papules that develop around anus and penis associated with fever, pain and dysuria. In females the symptoms are more severe and there are blisters and vesicles appearing on the on the external genitalia, labia majora, labia minora, vaginal vestibule, and introitus. In moist areas, the vesicles rupture, leaving exquisitely tender ulcers. The vaginal mucosa is inflamed and edematous. There is severe burning and pain on micturition and there is associated flu like symptoms including fever, headache and lymphadenopathy.

8. HSV Keratitis: It presents as corneal dendritic ulcers.

9. Herpes Simplex Encephalitis: Usually caused by HSV type I. Spreads cenripetally, e.g from cranial nerve ganglia to frontal and temporal lobes. Suspect if patient presents with fever, fits, headache, odd behaviour, hemiparesis or coma. Diagnosis is made by urgent PCR on CSF sample and CT scan or MRI and EEG may show temporal lobe changes but these are non-specific and unreliable.

Recurrent HSV Infections
They commonly occur at the lips and adjoining skin the condition is known as Herpes Labialis. HSV lying dormant in ganglion cells may be reactivated by illness, immunosuppression, mensturation or even sunlight. Genitial herpes lesions also commonly recur.

InvestigationsHerpes simplex virus infection is usually diagnosed clinically and by rising antibody titres in primary infection. Culture may be done as well as PCR is available for fast diagnosis.

Treatment

For mild infection no specific treatment is needed other then symptomatic management.
For severe infections Acyclovir is available in oral, topical cream and IV preparations. Also eye drops are available.
In genital herpes give proper analgesia for pain relief along with famciclovir 250 mg/8 hrly (500 mg if patient is immunocompromised) per oral for 5 days. Advise condoms and if disease is frequent or recurrent then give continous Acyclovir 400 mg per oral 12 hrly.
If Herpetic keratitis is suspected avoid steroids and give acyclovir eye drops.
In Herpes encephalitis patients needs ICU care and immediately start Acyclovir 10 mg/kg/8hrly IV for 10 days

Different types of tumor may occur in the salivary gland and may be benign or malignant. A brief discription of the common tumors occuring in the salivary gland is given here:

1. Pleomorphic Adenoma
The pleomorphic adenoma- mixed salivary gland tumor- is a benign tumor, and the commonest salivary gland tumor. It is most commonly seen in the parotid gland and typically forms a mass in the lateral lobe, which slowly enlarges over many years, women in their forties are most often being affected.

Clinical Features
On palpation the tumor is firm, non tender and smooth or lobulated in texture. initially spherical and encapsulated, it may eventually spread more deeply, with the result that recurrence after resection is common. On oral examination the deep part of the gland may have pushed the tonsil and pillar of the fauces towards the midline.

Histology:

Histologically, it is highly variable in appearance, even within individual tumors. Classically it is biphasic and is characterized by an admixture of polygonal epithelial and spindle-shaped myoepithelial elements in a variable background stroma that may be mucoid, myxoid, cartilaginous or hyaline. Epithelial elements may be arranged in duct-like structures, sheets, clumps and/or interlacing strands and consist of polygonal, spindle or stellate-shaped cells (hence pleiomorphism). Areas of squamous metaplasia and epithelial pearls may be present. The tumor is not enveloped, but it is surrounded by a fibrous pseudocapsule of varying thickness. The tumor extends through normal glandular parenchyma in the form of finger-like pseudopodia, but this is not a sign of malignant transformation.

Pleomorphic adenoma consists of mixed epithelial (left) and mesenchymal cell components (right). The latter often exhibits myxofibrous appearance and in some instances shows chondromatous differentiation.
2. Adenolymphoma (Warthin’s Tumor)
It is a bening tumor and the second most common salivary tumor and is found exclusively in the parotid gland. It usually affects males in their fifties, forming a slow growing, painless swelling over the angle of the jaw, there is a high incidence of bilateral disease.

Clinical features
The tumor is smooth, soft and often fluctuant, its superficial nature and slight mobility sometimes giving the appearance that it is separate from the gland.

Histology:

The appearance of this tumor under the microscope is unique. There are cystic spaces surrounded by two uniform rows of epithelial cells with centrally placed pyknotic nuclei. The cystic spaces have epithelium referred to as papillary infoldings that protrude into them. Additionally, the epithelium has lymphoid stroma with germinal center formation.

3. Less Common Benign Tumors
The other less common benign tumors occurring in the salivary glands include

Monomorphic Adenoma and
Oncocytoma.

4. Malignant Tumors
Adenocystic Carcinoma is the commonest malignant salivary tumor and occurs in the sub mandibular, sub lingual and minor glands. In contrast Mucoepidermoid carcinoma predominantlyoccurs in the parotid. other malignant tumor types are adenocarcinoma, squamous carcinoma and malignant mixed tumors.

Clinical Features
Typically malignant tumors produce indistinct, rapidly growing masses and malignant cervical lymphadenopathy. For the sub mandibular gland, numbness of the anterior two-thirds of the tongue from lingual nerve infiltration is diagnostic, whereas sublingual tumors may cause deviation of the tongue from invasion and fixation.

Malignant parotid tumors tend to occur in older age groups and most take the form of solitary hard nodules with deep fixation. there may be local pain exacerbated by opening the mouth.

Squamous cell carcinoma should be considered metastatic, until proven otherwisw, and a primary tumor sought.

X ray chest of a 48 year old woman who presented with generalized weakness is shown below:

Description: Chest X-ray shows an oval soft tissue density which overlays over most of the minor fissure. It is well-defined, no calcification seen and the surrounding lung is clear.

Diagnosed as Pseudotumor.

Comments And Explanation: Loculation within the fissure gives appearance of a tumor and is referred as pseudotumor. The pulmonary pseudotumor is sharply marginated collection of pleural fluid contained either within an interlobar pulmonary fissure or in a subpleural location adjacent to a fissure. Pseudotumors are identified on chest X-rays on their lenticular pattern.
CT chest confirms a loculated effusion within the fissure with Hounsfield value that of a transudate. The pseudotumor resolves with conservative management.
Most occur in the minor (horizontal) fissure and are seen on both the frontal and lateral radiograph; those that occur in the oblique or major fissure may only be seen on the lateral view. Pseudotumors may be erroneously diagnosed as parenchymal lung nodules or masses.

Clinical Discussion: Pseudotumor or vanishing tumor of the lung is an appropriate designation for a
localized transudative interlobar pleural fluid collection. It derives its name from its frequent resemblance to a tumor on X-ray chest and from its tendency to vanish following appropriate management.

Encapsulation is due to adhesions between contiguous pleural surfaces. Therefore, it is often seen after episodes of pleuritis. The pleural encapsulation can be mistaken for pulmonary consolidation, collapse, or a mediastinal tumor. The borders of a loculated effusion are convex unlike pulmonary collapse or consolidation. There may be pleural thickening elsewhere in the thorax. It is most commonly seen in the minor fissure.
The possibility of a vanishing lung tumor should be considered and excluded in any patient presenting with congestive heart failure or apparent lung mass on a chest X-ray.

Acute angle-closure glaucoma (ACG) is secondary to narrowing or closure of the anterior chamber angle, resulting in increased intraocular pressure (IOP), with subsequent damage to the optic nerve.

Pathophysiology: Normally, aqueous humor drains out of the anterior chamber via Schlemm canal in the anterior chamber angle. In ACG, this flow is impeded, and the IOP rises from a normal range of 10 to 21 mm Hg to 50 mm Hg or higher.

Clinical Presentation: ACG presents as an acutely inflamed eye. Nausea and vomiting are common and may be the presenting complaints. Eye pain and headache vary in severity. As the IOP reaches
the 50 to 60 mm Hg range, fluid is forced into the cornea, resulting in corneal edema. Patients report blurred vision and rainbow-colored halos around lights.

Acute Angle-Closure Glaucoma. The cornea is edematous, manifest by the indistinctness of the iris markings and the irregular corneal light reflex. Conjunctival hyperemia is also present.

Clinical findings include:

tearing,
perilimbal injection (“ciliary flush”),
a cloudy (“steamy”) cornea,
a nonreactive mid-dilated pupil,
anterior chamber inflammation, and
an increased IOP.
Using a penlight or slit-lamp microscopy, the anterior chamber may appear shallow.

Management:

ACG is an emergency that requires ophthalmology consultation, and treatment is directed at reducing the IOP. Aqueous outflow is increased by topical myotics (pilocarpine) that pull the peripheral iris taut away from the anterior chamber angle.

Decreased production of aqueous is accomplished with topical β-blockers (timolol), an α-adrenergic agonist (apraclonidine), or a carbonic anhydrase inhibitor (acetazolamide or methazolamide systemically, dorzolamide topically).

Osmotic agents reduce the aqueous volume within the eye and include glycerol, oral isosorbide, and IV mannitol.

Latanoprost, a prostaglandin derivative, increases aqueous outflow through nontrabecular meshwork pathways.

The definitive treatment of ACG is laser peripheral iridectomy, done usually after the IOP normalizes.

Points To Remember:

1. Vision loss and blindness can occur during the course of the attack (hours to days). ACG is a true ophthalmologic emergency.

2. Medicines with anticholinergic effects are capable of inducing pupillary dilation which might provoke an angle closure attack. These include over-the-counter decongestants, motion sickness medications, antipsychotics, and antidepressants.

3. ACG often occurs in the evening, when lower light levels cause mydriasis.

4. ACG patients may easily be misdiagnosed initially as having a migraine headache or a CNS catastrophe because they may present with severe headache and vomiting.

5. The elevated IOP in acute ACG can be reduced pharmacologically by three mechanisms: first, by opening the closed angle with myotics; second, by reducing aqueous formation with β-blockers, α-agonists, or carbonic anhydrase inhibitors; and third, by reducing the aqueous volume within the eye by osmotic agents.

Foot infections are the most common problems in persons with diabetes. These individuals are predisposed to foot infections because of a compromised vascular supply secondary to diabetes.

A diabetic foot is a foot that exhibits any pathology that results directly from diabetes mellitus or any long-term (or “chronic”) complications of diabetes mellitus. Presence of several characteristic diabetic foot pathologies is called diabetic foot syndrome.

Infections in patients with diabetes are difficult to treat because these individuals have impaired microvascular circulation, which limits the access of phagocytic cells to the infected area and results in a poor concentration of antibiotics in the infected tissues.

Etiology
Diabetes mellitus is a disorder that primarily affects the microvascular circulation. In the extremities, microvascular disease due to “sugar-coated capillaries” limits the blood supply to the superficial and deep structures. Pressure due to ill-fitting shoes or trauma further compromises the local blood supply at the microvascular level, predisposing the patient to infection, which may involve the skin, soft tissues, bone, or all of these combined.

Diabetes also accelerates macrovascular disease, which is evident clinically as accelerating atherosclerosis and/or peripheral vascular disease. Most diabetic foot infections occur in the setting of good dorsalis pedis pulses; this finding indicates that the primary problem in diabetic foot infections is microvascular compromise.

Risk factors
Two main risk factors that cause diabetic foot ulcer are Diabetic Neuropathy and micro as well as macro ischemia. Diabetic patients often suffer from diabetic neuropathy due to several metabolic and neurovascular factors. Type of neuropathy called peripheral neuropathy causes loss of pain or feeling in the toes, feet, legs and arms due to distal nerve damage and low blood flow. Blisters and sores appear on numb areas of the feet and legs such as metatarso-phalangeal joints, heel region and as a result pressure or injury goes unnoticed and eventually become portal of entry for bacteria and infection.

Microbial Organisms involved in Infection
The microbiologic features of diabetic foot infections vary according to the tissue infected. In patients with diabetes, superficial skin infections, such as cellulitis, are caused by the same organisms as those in healthy hosts, namely group A streptococci and Staphylococcus aureus.

Deep soft-tissue infections in diabetic persons can be associated with gas-producing, gram-negative bacilli.

Acute osteomyelitis usually occurs as a result of foot trauma in an individual with diabetes. The distribution of organisms is the same as that in an individual without diabetes who has acute osteomyelitis. In chronic osteomyelitis, however, the pathogens include group A and group B streptococci, aerobic gram-negative bacilli, and Bacteroides fragilis.

Other pathogens implicated in chronic osteomyelitis in patients with diabetes include B fragilis, Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae.

Pseudomonas aeruginosa is generally not a pathogen in chronic osteomyelitis in these individuals. Although P aeruginosa is frequently cultured from samples obtained from a draining sinus tract or deep penetrating ulcers in patients with diabetes, these organisms are superficial colonizers and are generally not the cause of the bone infection.

Patient education
Patients with diabetes must be careful to avoid foot trauma and to properly care for their feet to minimize the possibility of infection. In addition, they must understand that chronic osteomyelitis cannot be cured with antibiotics alone and that adequate surgical debridement is necessary.

Clinical Presentation
Local trauma and/or pressure (often in association with lack of sensation because of neuropathy), in addition to microvascular disease, may lead to a diabetic foot infection. However, patients may not necessarily have a history of trauma or have suffered a previous infection.

Cellulitis
Cellulitis may involve tender, erythematous, nonraised skin lesions on the lower extremity that may or may not be accompanied by lymphangitis.

Deep-skin and soft-tissue infections
Patients with deep-skin and soft-tissue infections may be acutely ill, with painful induration of the soft tissues in the extremity. These infections are particularly common in the thigh area, but they may be seen anywhere on the leg or foot. Wound discharge is usually not present.

In mixed infections that may involve anaerobes, crepitation may be noted over the afflicted area. Extreme pain and tenderness indicate the possibility of a compartment syndrome.

Acute osteomyelitis
Unless peripheral neuropathy is present, the patient has pain at the site of the involved bone. Usually, fever and regional adenopathy are absent.

Chronic osteomyelitisIn chronic osteomyelitis, the patient’s temperature is usually less than 102°F. Discharge is commonly foul. No lymphangitis is observed, and pain may or may not be present, depending on the degree of peripheral neuropathy.

The deep, penetrating ulcers and deep sinus tracts (which are diagnostic of chronic osteomyelitis) are usually located between the toes or on the plantar surface of the foot. In patients with diabetes, chronic osteomyelitis usually does not occur on the medial malleoli, shins, or heels.

Treatment and Management
Cellulitis is the easiest diabetic foot infection to cure, because it does not pose the same circulatory limitations that the more serious infections do, making it easier for medications to reach the infection site. In contrast, chronic osteomyelitis, which is the most difficult diabetic foot infection to cure, requires surgical debridement before antibiotic therapy can be effective. The patient may participate in activities as tolerated. However, weight bearing may be contraindicated.

Infections in patients with diabetes are difficult to treat because they have impaired microvascular circulation, which limits the access of phagocytic cells to the infected area and results in a poor concentration of antibiotics in the infected tissues.

Adequate surgical debridement, in addition to antimicrobial therapy, is necessary to cure chronic osteomyelitis. Immobilization is important in acute or chronic osteomyelitis.

Dry gangrene is usually managed with expectant care, and gross infection is usually not present. Wet gangrene usually has an infectious component and requires surgical debridement and/or antimicrobial therapy to control the infection.

Introduction: The uvea is the middle layer of the eye. Its anterior portion includes the iris and ciliary body; the posterior portion includes the choroid. Inflammation of the anterior portion is called anterior uveitis or iritis.

Etiology: It is often idiopathic, but approximately half of cases are associated with systemic
disease. These include :

Inflammatory disorders (rheumatoid arthritis, Behçet disease, sarcoid),
HLA-B27-associated conditions (ankylosing spondylitis, inflammatory bowel disease, Reiter syndrome), and
Infectious causes (zoster, tuberculosis, toxoplasmosis, AIDS).

Clinical features include conjunctival hyperemia, hyperemic perilimbal vessels (“ciliary flush”), miosis, decreased visual acuity, photophobia, tearing, and pain.

Anterior Uveitis. Marked conjunctival injection and perilimbal hyperemia (“ciliary flush”) are seen in this patient with recurrent iritis

The slit-lamp may demonstrate a hypopyon, cells, flare, and keratic precipitates.
Keratic precipitates are agglutinated inflammatory cells adherent to the posterior corneal endothelium. These precipitates appear either as fine gray-white deposits or as a large, flat, greasy-looking area (“mutton fat”).
The IOP may be decreased due to decreased aqueous production by the inflamed ciliary body, or increased secondary to inflammatory debris within the trabeculae of the anterior chamber angle obstructing outflow.

Learning Points:
1. Iritis is usually associated with a miotic pupil, pain, and redness primarily at the limbus (“ciliary flush”).
2. When uveitis is associated with a systemic disorder, the associated condition is usually evident. Common exceptions include sarcoidosis and syphilis.
3. In patients with uveitis of unknown etiology, a chest x-ray looking for sarcoidosis and serologic testing for syphilis are reasonable.
4. Visual loss may occur with uveitis.
5. Topical analgesics do not significantly ameliorate the pain of anterior uveitis.
6. Consider sympathetic ophthalmia with unexplained uveitis and a history of eye trauma.

Management:

The patient’s history forms the basis for the evaluation and laboratory testing. The history should focus on rheumatic illness, dermatologic problems, bowel disease, infectious exposures, and sexual history.
Treatment of the uveitis is nonspecific.
Topical cycloplegics and corticosteroids may be prescribed in conjunction with the ophthalmologist. Antibiotics are not usually prescribed.

A 45 years old male came to radiology department for X-ray chest with history of cough, mild fever and weight loss. The x ray is shown below:

X-ray chest shows fibro infiltrative lesions in right upper zone with areas of early calcification and moderate pleural effusion on left sidewith minimal tracheal pull to right side.

Comments And Explanation: Pleural effusion is the accumulation of fluid in the pleural space, i.e.
between the visceral and parietal layers of pleura. The fluid may be transude, exudate, blood, chyle or rarely bile.
Pleural fluid casts a shadow of the density of water on the chest radiograph. The most dependent recess of the pleura is the posterior costophrenic angle. A small effusion will, therefore, tend to collect posteriorly, however, a lateral decubitus view is the most sensitive film to detect small quantity of free pleural effusion (as small as 50 ml). 100–200 ml of pleural fluid is required to be seen above the dome of the diaphragm on frontal chest radiograph. As more fluid is accumulated, a
homogeneous opacity spreads upwards, obscuring the lung base.
Typically this opacity has a fairly well-defined, concave upper edge (as seen in picture above), which
is higher laterally and obscures the diaphragmatic shadow. Frequently the fluid will track into the pleural fissures.
A massive effusion may cause complete radiopacity of a hemithorax. The underlying lung will retract
towards its hilum, and the space occupying effect of the effusion will push the mediastinum towards the opposite side.
USG chest confirms the presence or absence of the pleural fluid; it also shows the septations within the pleural fluid with or without solid component within the lesion. USG helps in guiding aspiration of pleural fluid.
CT scan is the most sensitive modality for detection of presence of minimal fluid. It allows distinction between free and loculated fluid showing its extent and localization.

Diagnosis: Pleuropulmonary tuberculosis.

Clinical Discussion:
Pleural effusion is either transudate or exudate. In transudate, the protein level is 1.5–2.5 g/dL and is seen in congestive heart failure, constrictive pericarditis, cirrhosis, nephrotic syndrome and hypothyroidism.
Exudate results from increased permeability of abnormal pleural capillaries with release of high-protein fluid into pleural space, protein level > 3 g/dL seen in empyema, tuberculosis and actinomycosis.

Tuberculous pleural effusions occur in up to 30% of patients with tuberculosis.
The current hypothesis for the pathogenesis of tuberculous pleural effusion is that a subpleural caseous focus in the lung ruptures into the pleural space 6–12 weeks after a primary infection. Mycobacterial antigens enter the pleural space and interact with T-cells previously sensitized to
mycobacteria, resulting in a delayed hypersensitivity reaction and the accumulation of fluid. It seems that this reaction of the pleura augments the entry of fluid into the pleural space by increasing the permeability of pleural capillaries to serum proteins, and thereby increasing the oncotic
pressure in the pleural fluid.
It appears that tuberculous pleurisy is due to a delayed hypersensitivity reaction rather than to a tuberculous infection.
Involvement of the lymphatic system probably also contributes to the accumulation of pleural fluid. An impaired clearance of protein from the pleural space has been reported in human tuberculous effusions. It is known that the clearance of proteins and fluid from the pleural space is carried out by lymphatics in the parietal pleura. Fluid gains access to the lymphatics through openings in the parietal pleura.

Definition: The most common cause of conductive deafness, otosclerosis is the slow formation of spongy bone in the otic capsule, particularly at the oval window.

Incidence: It occurs in at least 10% of the population in the United States. It commonly affects both ears and is seen in many females between the ages of 15 and 30.

Causes
Otosclerosis appears to result from a genetic factor transmitted as an autosomal dominant trait; many patients report family histories of hearing loss (excluding presbycusis). Pregnancy may trigger the onset of this condition.

Signs and symptoms
Spongy bone in the otic capsule immobilizes the footplate of the normally mobile stapes, disrupting the conduction of vibrations from the tympanic membrane to the cochlea. This causes progressive unilateral hearing loss, which may advance to bilateral deafness. Other symptoms include tinnitus and paracusis of Willis (hearing conversation better in a noisy environment than in a quiet one).

Diagnosis

Early diagnosis is based on a Rinne test that shows bone conduction lasting longer than air conduction (normally, the reverse is true). As otosclerosis progresses, bone conduction also deteriorates.
Audiometric testing reveals hearing loss ranging from 60 db, in early stages, to total loss.
Weber’s test detects sound lateralizing to the more affected ear.
Physical examination reveals a normal tympanic membrane.

Treatment
Oral fluoride, calcium, or vitamin D may help stabilize hearing loss. A hearing aid also may be used. Effective treatment consists of stapedectomy (removal of the stapes) and insertion of a prosthesis to restore partial or total hearing. This procedure is performed on only one ear at a time, beginning with the ear that has suffered greater damage. Alternative surgery includes stapedotomy (laser creation of a small hole in the stapes’ footplate, through which a wire and piston are inserted).
Postoperatively, treatment includes hospitalization for 2 to 3 days and an antibiotic to prevent infection. If surgery isn’t possible, a hearing aid (air conduction aid with molded ear insert receiver) enables the patient to hear conversation in normal surroundings, although this therapy isn’t as effective as stapedectomy.

A 50 year old woman was seen in emergency after ingesting a chemical substance . Esophagogastrodudenoscopy was performed and the picture is shown below.

Initial esophagoscopy. (A) Middle esophagus shows whitish discoloration. (B) Distal esophagus shows exudates with easy touch bleeding.

The case was diagnosed as Corrosive Esophagitis

Corrosive Esophagitis Case Discussion

Introduction

Inflammation and damage to the esophagus after ingestion of a caustic chemical is called corrosive or caustic esophagitis. Similar to a burn, this injury may be temporary or lead to permanent stricture (narrowing or stenosis) of the esophagus that requires corrective surgery.
Severe injury can quickly lead to esophageal perforation, mediastinitis, and death from infection, shock, and massive hemorrhage (due to aortic perforation).

Causes
The most common chemical injury to the esophagus follows the ingestion of lye or other strong alkalies; less commonly, injury follows the ingestion of strong acids. The type and amount of chemical ingested determine the severity and location of the damage.
In children, household chemical ingestion is accidental; in adults, it’s usually a suicide attempt or gesture. The chemical may damage only the mucosa or submucosa, or it may damage all layers of the esophagus.

Pathology

Esophageal tissue damage occurs in three phases:

in the acute phase, edema and inflammation;
in the latent phase, ulceration, exudation, and tissue sloughing; and
in the chronic phase, diffuse scarring.

Signs and symptoms
Effects vary from none to intense pain in the mouth and anterior chest, marked salivation, inability to swallow, and tachypnea. Bloody vomitus that contains pieces of esophageal tissue signals severe damage. Signs of esophageal perforation and mediastinitis, especially crepitation, indicate destruction of the entire esophagus. Inability to speak suggests laryngeal damage.
The acute phase subsides in 3 to 4 days, enabling the patient to eat again. Fever suggests secondary infection. Symptoms of dysphagia return if stricture develops, usually within weeks.

Diagnosis
A history of chemical ingestion and physical examination that reveals oropharyngeal burns (including white membranes and edema of the soft palate and uvula) usually confirm the diagnosis. The type and amount of the chemical ingested must be identified; sometimes this can be done by examining empty containers of the ingested material or by calling the poison control center.
Endoscopy (in the first 24 hours after ingestion) delineates the extent and location of the esophageal injury and assesses the depth of the burn. This procedure may also be performed a week after ingestion to assess stricture development.

Treatment
The patient may be treated conservatively through monitoring his condition, or he may require bougienage or surgery.
Bougienage
This procedure involves passing a slender, flexible, cylindrical instrument called a bougie into the esophagus to dilate it and minimize stricture.
Surgery
Immediate surgery may be necessary for esophageal perforation; it may also be performed later to correct stricture that isn’t treatable with bougienage. Corrective surgery may involve transplanting a piece of the colon to the damaged esophagus. Even after surgery, stricture may recur at the site of the anastomosis.
Supportive treatment
Other treatment includes I.V. therapy, to replace fluids, and total parenteral nutrition while the patient can’t swallow, gradually progressing to clear liquids and a soft diet.

ECG Findings
• ST segment elevation in the precordial leads (V2-V6) and high lateral leads (I, aVL).
• Reciprocal ST segment depressions in the inferior leads (II, III, aVF).
• ST segment elevation in AVR coupled with reciprocal ST depressions may indicate AMI from left main disease.

Significant ST elevation is present in the precordial leads (V2-V6) and high lateral leads (I and aVL) (arrows). In this example, significant Q waves have appeared, signaling infarction (arrowhead).

Clinical Pearls
1. The left main coronary artery branches into the left anterior descending artery and the circumflex artery.It supplies blood to the ventricular septum and the anterior and lateral aspects of the left ventricle, usually sparing the posterior and inferior portion, which is most often served by the right coronary artery.

2. Normal R-wave progression (increasing R-wave amplitude across the precordial leads) may be interrupted.
3. Risk of cardiogenic shock is high since so much of the left ventricle is served by the left main coronary artery.
4. A left main coronary thrombosis is also known as the “widowmaker lesion.”
5. Isolated ST segment elevation in lead aVR may also indicate acute myocardial ischemia from left main coronary artery disease.

Anisocoria is a disparity of pupil size.
To determine the abnormal pupil, compare pupil sizes in light and dark. It is accentuated in the paretic muscle. If the iris sphincter (or its innervation) is involved, the anisocoria will be increased in bright light. If the iris dilator muscle (or its innervation) is affected, it will be more
pronounced in darkness.

Up to 20% of normal individuals have physiologic anisocoria of 1 to 2 mm.

Other causes of anisocoria with an abnormally large pupil include
- mydriatic drops,
- contamination from a scopolamine patch,
- an Adie pupil, and
- ocular trauma with iris sphincter damage.

Post traumatic Anisocoria. Marked chronic anisocoria secondary to prior trauma as a child

A dilated pupil due to anticholinergic agents (eg, atropine) does not react to light, although a dilated pupil due to sympathomimetics still has some response.

An abnormally small pupil may be secondary to Horner syndrome, chronic Adie pupil (8 weeks or more after the event), iritis, and eye drops (pilocarpine).
Miosis secondary to pupillary sphincter muscle spasm may be transiently observed after ocular trauma, followed by mydriasis.

Important Learning Points:
1. A patient with a dilated pupil, ptosis, and abnormal extraocular movements should be evaluated emergently for an aneurysm or expanding supratentorial mass with tentorial herniation.
2. With physiologic anisocoria, the pupil size disparity is the same in light and dark, and there are no other ocular findings.
3. A driver’s license or ID badge may be helpful to document a preexisting anisocoria.
4. Some brands of eye make-up contain belladonna alkaloids which can cause mydriasis.
5. An Adie pupil initially is dilated, but may become miotic over time. It is a benign condition that affects young adults, women more often than men, and is associated with decreased reflexes.

Management and Disposition
Evaluation is dependent on clinical presentation. A patient with the acute onset of third-nerve palsy with associated headache or trauma should be evaluated as a neurosurgical emergency.
Pilocarpine may be helpful to differentiate the etiology of pupil dilation. With low concentrations (0.125%), an Adie pupil will constrict more than the unaffected eye secondary to denervation supersensitivity. With higher concentrations (1%), a pupil that fails to constrict is most likely secondary to topical anticholinergic mydriatics (scopolamine, atropine, or cyclopentolate). Unlike the mydriasis seen with intracranial pathology, pharmacologic mydriasis is not associated with pain, ptosis, or diplopia. Other pathology within the iris sphincter muscle that prevents constriction to 1% pilocarpine includes iris muscle trauma and synechiae.

Introduction

Also called tinea or ringworm, dermatophytosis is a disease that can affect the scalp (tinea capitis), body (tinea corporis), nails (tinea unguium), feet (tinea pedis), groin (tinea cruris), and bearded skin (tinea barbae).
Tinea infections are quite prevalent in the United States and are usually more common in males than in females. With effective treatment, the cure rate is very high, although about 20% of persons with infected feet or nails develop chronic conditions.

Causes
Tinea infections (except for tinea versicolor) result from dermatophytes (noncandidal fungi) of the genera Trichophyton, Microsporum, and Epidermophyton that involve the stratum corneum, nails or hair.
Transmission can occur directly (through contact with infected lesions) or indirectly (through contact with contaminated articles, such as shoes, towels, or shower stalls). Some cases come from animals or soil.

Signs and symptoms
Lesions vary in appearance and duration with the type of infection:

Tinea capitis, which mainly affects children, is characterized by round erythematous patches on the scalp, causing hair loss with scaling. In some children, a hypersensitivity reaction develops, leading to boggy, inflamed, commonly pus-filled lesions (kerions).

Tinea corporis produces flat lesions on the skin at any site except the scalp, bearded skin, groin, palms, or soles. These lesions may be dry and scaly or moist and crusty; as they enlarge, their centers heal, causing the classic ring-shaped appearance.

Tinea unguium (onychomycosis) infection typically starts at the tip of one or more toenails (fingernail infection is less common) and produces gradual thickening, discoloration, and crumbling of the nail, with accumulation of subungual debris. Eventually, the nail may be destroyed completely.

Tinea pedis causes scaling and blisters between the toes. Severe infection may result in inflammation, with severe itching and pain on walking. A dry, squamous inflammation may affect the entire sole.

Tinea cruris (jock itch) produces red, raised, sharply defined, itchy lesions in the groin that may extend to the buttocks, inner thighs, and the external genitalia. Warm weather and tight clothing encourage fungus growth.

Tinea barbae is an uncommon infection that affects the bearded facial area of men.

Diagnosis
Microscopic examination of lesion scrapings prepared in 10% to 20% potassium hydroxide solution usually confirms tinea infection. Other diagnostic procedures include Wood’s light examination (which is useful in only about 5% of cases of tinea capitis) and culture of the infecting organism.

Treatment

Tinea infections usually respond to topical agents such as imidazole cream or to oral griseofulvin, which is especially effective in tinea infections of the skin and hair.
Oral terbinafine or itraconazole is helpful in nail infections.
However, topical therapy is ineffective for tinea capitis; oral griseofulvin for 1 to 3 months is the treatment of choice.
In addition to imidazole, other antifungals include naftifine, ciclopirox, terbinafine, haloprogin, and tolnaftate. Topical treatments should continue for 2 weeks after lesions resolve.
Supportive measures include open wet dressings, removal of scabs and scales, and application of keratolytics such as salicylic acid to soften and remove hyperkeratotic lesions of the heels or soles.

A 45 years male patient came to radiology department for X-ray chest with history of cough and expectoration of several months duration.

The X ray is shown below:

Chest X-ray (in the above picture) shows a large plaque of calcification covering the lateral and anterior part of left lung. There is crowding of overlying ribs.
Calcified pleural plaques have a characteristic rolled edge along its margin
Left upper lobe shows fibrotic lesions with bronchiectatic change and calcific spots are also seen.

Explanation:
Magnified view (shown below) shows that pleural calcification plaques have a characteristic rolled edge along its margin. (marked by arrows)

In general, pleural calcification is sequelae of hemothorax, empyema, tuberculosis or asbestos exposure.

Hemothorax is usually confirmed by a history of significant chest trauma.
There may be associated healed rib fractures. Although pulmonary contusion may have accompanied the acute episodes, contusion usually resolves without significant residual effect. Associated parenchymal scarring thus favors a diagnosis other than previous hemothorax.

Clinical Discussion:
Chronic empyema is a more common cause of pleural calcification. Recent CT studies indicate that chronic empyemas may calcify around their periphery while retaining collections of fluid for years. Occasionally, calcified pleural thickening from empyema does assume unusual or bizarre configurations and may be very extensive. It must be remembered that the interlobar fissures are part of the pleural space and may, therefore, be involved by an empyema.

In tuberculosis, pleural reaction is most commonly apical and asymmetric. Associated apical parenchymal scarring, cavities, or even multiple calcified granulomas are virtually diagnostic of tuberculosis.

Asbestos exposure is a common cause of pleural calcifications measuring less than 3–4 cm. The pleural calcifications resulting from asbestos exposure most commonly affect the domes of the diaphragmatic pleura. They may be extensive and bilateral but are often asymmetric.

High Resolution CT has shown to be the most sensitive means for detecting minimal pleural changes from asbestos exposure. Pleural calcification is not seen in all cases of asbestos exposure, but can lead to one of the most specific appearances in chest radiology.

Calcified pleural plaques seen en face has a characteristic rolled edge along their margins, denser than in the central portion of the plaque.

A middle aged lady presented with a vesicular rash on her face that was seen to be involving the ophthalmic division of the trigeminal nerve.

The case was diagnosed as Herpes Zoster Opthalmicus

Case Discussion:
Reactivation of endogenous latent varicella-zoster virus within the trigeminal ganglion with neuronal spread through the ophthalmic branch results in crops of grouped vesicles on the forehead and periocularly.

Clinical features; Patients typically present with periocular rash and an injected eye, along with a watery discharge. The most common corneal lesion is punctate epithelial keratitis, in which
the cornea has a ground-glass appearance because of stromal edema. Pseudodendrites, also very common, form from mucous deposition, are usually peripheral, and stain moderate to poorly with fluorescein. These may be differentiated from the dendrites of herpes simplex in that the pseudodendrites lack the rounded terminal bulbs at the end of the branches, and are broader and more plaquelike. Anterior stromal infiltrates may be seen in the second or third week after the acute
infection. Follicles (hyperplastic lymphoid tissue that appears as gray or white lobular elevations, particularly in the inferior cul-de-sac) and regional adenopathy may or may not be present. Iritis is seen in approximately 40% of patients.

Herpes Zoster Ophthalmicus. A large circular dendrite is seen in this patient with ocular involvement from HZV

Management:

Treat patients with epithelial defects with topical broad-spectrum antibiotics to prevent secondary infection. Initiate oral antivirals within 72 hours of onset, and treat for 7 to 10 days.
Use cycloplegics if an iritis is present.
Artificial tears or ointment may be helpful and narcotic analgesics may be required.
Ophthalmologic consultation is indicated.

Clinical Pearls
1. Ocular complications may follow the rash by many months to years. These complications have a highly variable presentation that can mimic almost any ophthalmic condition.
2. Recurrence is more common in the immunocompromised host.
3. Perform a careful eye exam with corneal staining. Nearly two-thirds of patients will develop ocular lesions.
4. Corneal hypesthesia and the appearance of dendrites with fluorescein staining are seen in both herpes zoster ophthalmicus and herpes simplex keratitis.
5. Patients with skin lesions on the tip of the nose (Hutchinson sign) are at high risk for ocular involvement. However, the eye may be involved without a nasal lesion.

Also known as infectious or epidemic parotitis, mumps is an acute viral disease caused by a paramyxovirus. It’s most prevalent in unvaccinated children between ages 2 and 12, but it can occur in other age-groups. Infants younger than age 1 seldom get this disease because of passive immunity from maternal antibodies. Peak incidence occurs during late winter and early spring.

The prognosis for complete recovery is good, although mumps sometimes causes complications.

Etiology

The mumps paramyxovirus is found in the saliva of an infected person and is transmitted by droplets or by direct contact. The virus is present in the saliva 6 days before to 9 days after onset of parotid gland swelling; the 48-hour period immediately preceding onset of swelling is probably the time of highest communicability.

The incubation period ranges from 14 to 25 days (the average is 18 days). One attack of mumps (even if unilateral) almost always confers lifelong immunity.

Signs and symptoms
Signs and symptoms of mumps vary widely. An estimated 30% of susceptible people have subclinical illness. Mumps usually begins with prodromal signs and symptoms that last for 24 hours; these include myalgia, anorexia, malaise, headache, and low-grade fever, followed by an earache that’s aggravated by chewing, parotid gland tenderness and swelling, a temperature of 101° to 104° F (38.3° to 40° C), and pain when chewing or when drinking sour or acidic liquids. Simultaneously with the swelling of the parotid gland or several days later, one or more of the other salivary glands may become swollen.

Complications
Epididymo-orchitis and mumps meningitis are complications of mumps.

Epididymo-orchitis, which occurs in about 25% of postpubertal males who contract mumps, produces abrupt onset of testicular swelling and tenderness, scrotal erythema, lower abdominal pain, nausea, vomiting, fever, and chills. Swelling and tenderness related to mumps may last for several weeks.

Mumps meningitis complicates mumps in 10% of patients and affects three to five times more males than females. Signs and symptoms include fever, meningeal irritation (nuchal rigidity, headache, and irritability), vomiting, drowsiness, and a lymphocyte count in cerebrospinal fluid ranging from 500 to 2,000/µl.
Recovery is usually complete. Less-common effects are pancreatitis, deafness, arthritis, myocarditis, encephalitis, pericarditis, oophoritis, and nephritis.

Diagnosis
In mumps, a diagnosis is usually made after the characteristic signs and symptoms develop, especially parotid gland enlargement with a history of exposure to mumps. Serologic antibody testing can verify the diagnosis when parotid or other salivary gland enlargement is absent. If comparison between a blood sample obtained during the acute phase of illness and another sample obtained 3 weeks later shows a fourfold rise in antibody titer, the patient most likely had mumps.

Treatment
Effective treatment includes an analgesic for pain, an antipyretic for fever, and adequate fluid intake to prevent dehydration from fever and anorexia. If the patient can’t swallow, I.V. fluid replacement may be necessary.

Introduction:

Incidence of malignant melanoma, a neoplasm that arises from melanocytes, has increased by 50% in the past 20 years. In particular, an increase in incidence of melanoma in situ suggests earlier detection. The disorder varies in different populations but is about 10 times more common in white than in nonwhite populations.

The four types of melanomas are

superficial spreading melanoma,
nodular malignant melanoma,
lentigo maligna melanoma, and
acral-lentiginous melanoma.

Melanoma spreads through the lymphatic and vascular systems and metastasizes to the regional lymph nodes, skin, liver, lungs, and central nervous system (CNS). Its course is unpredictable, however, and recurrence and metastasis may occur more than 5 years after resection of the primary lesion. If it spreads to regional lymph nodes, the patient has a 50% chance of survival.
The prognosis varies with tumor thickness. Generally, superficial lesions are curable, whereas deeper lesions tend to metastasize. The Breslow Level Method measures tumor depth from the granular level of the epidermis to the deepest melanoma cell. Melanoma lesions less than 0.76 mm deep have an excellent prognosis, whereas deeper lesions (more than 0.76 mm deep) are at risk for metastasis. The prognosis is better for a tumor on an extremity (which is drained by one lymphatic network) than for one on the head, neck, or trunk (which is drained by several networks).

Causes & Risk Factors
Several factors may influence the development of melanoma:

Excessive exposure to ultraviolet light. Melanoma is most common in sunny, warm areas and commonly develops on parts of the body that are exposed to the sun. A person who has a blistering sunburn before age 20 has twice the risk of developing melanoma.
Skin type. Most persons who develop melanoma have blond or red hair, fair skin, and blue eyes; are prone to sunburn; and are of Celtic or Scandinavian descent. Melanoma is rare among blacks; when it does develop, it usually arises in lightly pigmented areas (the palms, plantar surface of the feet, or mucous membranes).
Autoimmune factors. Genetic and autoimmune effects may be causes.
Hormonal factors. Pregnancy may increase risk and exacerbate growth.
Family history. A person with a family history of melanoma has eight times the risk of developing the disorder.
History of melanoma. A person who has had one melanoma has 10 times the risk of developing a second.

Clinical Manifestations
Common sites for melanoma are on the head and neck in men, on the legs in women, and on the backs of people exposed to excessive sunlight. Up to 70% arise from a preexisting nevus. They rarely appear in the conjunctiva, choroid, pharynx, mouth, vagina, or anus.

Suspect melanoma by using the ABCD Rule of Melanoma:

Asymmetry of borders
Bleeding or crusting
Color blue/black or variegated
Diameter greater than 2¼? (5.7 cm).

Each type of melanoma has special characteristics:

Superficial spreading melanoma arises on chronically sun-exposed areas, such as the legs and upper back. Characteristically, it has a red, white, and blue color over a brown or black background and an irregular, notched margin. Its surface is irregular, with small, elevated tumor nodules that may ulcerate and bleed. Horizontal growth may continue for many years; when vertical growth begins, the prognosis worsens.

Nodular malignant melanoma occurs more commonly in men and can be located anywhere on the body. It’s the most frequently misdiagnosed melanoma because it resembles a blood blister or polyp.

Lentigo maligna melanoma commonly develops under the fingernails, on the face, and on the backs of the hands. This lesion looks like a large (1? to 2? [2.5- to 5-cm]), flat freckle of tan, brown, black, whitish, or slate color, and has irregularly scattered black nodules on the surface. It develops slowly, usually over many years, and eventually may ulcerate.

Acral-lentiginous melanoma is more common in Asian and Black individuals.

Diagnosis
A skin biopsy with histologic examination can distinguish malignant melanoma from a benign nevus, seborrheic keratosis, and pigmented basal cell epithelioma; it can also determine tumor thickness. Physical examination, paying particular attention to lymph nodes, can point to metastatic involvement.
Baseline laboratory studies include a complete blood count with differential, erythrocyte sedimentation rate, platelet count, liver function studies, and urinalysis. Depending on the depth of tumor invasion and metastasis, baseline diagnostic studies may also include a chest X-ray and computed tomography (CT) scan of the chest and abdomen. Signs of bone metastasis may call for a bone scan; CNS metastasis, a CT scan of the brain.

Treatment
A patient with malignant melanoma requires surgical resection to remove the tumor. The extent of resection depends on the size and location of the primary lesion. Closure of a wide resection may require a skin graft. Surgical treatment may also include regional lymphadenectomy. Cutaneous melanoma is nearly 100% curable by excision if diagnosed when malignant cells are confined to the epidermis.
Deep primary lesions may merit adjuvant chemotherapy and biotherapy or immunotherapy to eliminate or reduce the number of tumor cells. Radiation therapy is usually reserved for metastatic disease; gene therapy may also be a treatment option.
Regardless of the treatment method, melanomas require close, long-term follow-up to detect metastasis and recurrences.

Ocular herpetic disease may be neonatal, primary, or recurrent.

Neonatal disease occurs secondary to passage through an infected birth canal, and is usually HSV type 2.

Primary ocular herpes may present as a blepharitis (grouped eyelid vesicles on an erythematous base), conjunctivitis, or keratoconjunctivitis.
Patients with keratoconjunctivitis commonly note pain, irritation, foreign body sensation, redness, photophobia, tearing, and occasionally decreased visual acuity. Follicles and preauricular adenopathy may be present. Initially, the keratitis is diffuse and punctate, but after 24 hours, fluorescein demonstrates either serpiginous ulcers or multiple diffuse epithelial defects. True dendritic ulcers are rarely seen in primary disease.

Ocular Herpes Simplex. This patient has a history of ocular herpes simplex since childhood. Grouped vesicles on an erythematous base with periorbital erythema are seen. Honey-colored crusts suggest secondary impetigo

Recurrent: Most ocular herpetic infections are manifestations of recurrent disease rather than a primary ocular infection.
These may be triggered by ultraviolet laser treatment, topical ocular medications (β-blockers, prostaglandins), and immunosuppression (especially ophthalmic topical glucocorticoids).
Recurrent disease most commonly presents as keratoconjunctivitis with a watery discharge, conjunctival injection, irritation, blurred vision, and preauricular lymph node involvement. Corneal involvement initially is punctate, but evolves into a dendritic keratitis. The linear branches classically end in bead-like extensions called terminal bulbs. Fluorescein dye demonstrates primarily the corneal defect; the terminal bulbs are best seen with rose stain. In addition to the dendritic pattern, fluorescein stain may instead take on a geographic or ameboid shape, secondary to widening of the
dendrite.

Most patients (80%) with herpes simplex keratitis have decreased or absent corneal sensation in the area of the dendrite or geographic ulceration. Deeper corneal stromal inflammation may also occur (disciform keratitis). Recurrent disease can also present with iritis or with blepharitis, with vesicles grouped in focal clusters.

Management
There is a high association in neonatal ocular herpes infections between ocular HSV disease and serious systemic or neurologic infection, and an emergency pediatric or infectious disease consult is necessary. IV acyclovir is indicated, and the ocular disease itself may be treated with topical antivirals (idoxuridine, vidarabine, trifluorothymidine). Other sexually transmitted diseases such as chlamydia or gonorrhea should be explored.

Treatment of those with primary ocular herpes (beyond the neonatal period) presenting as blepharitis or periocular dermatitis consists of good local hygiene and a prophylactic topical antiviral such as trifluorothymidine or idoxuridine ointment. Patients with corneal involvement should additionally
receive topical antibiotics to prevent secondary bacterial infection.

In those with recurrent disease, topical antivirals (trifluridine, ganciclovir, acyclovir, vidarabine) are effective, as is oral acyclovir. If the cornea is involved, trifluorothymidine and topical antibiotics are added. Ophthalmology consultation is required in patients with ocular HSV disease. Episodes of recurrent stromal disease may be limited by the long-term use of low-dose oral antivirals.

Important Learning Points
1. Most ocular HSV infections are manifestations of recurrent disease.
2. Corneal disease is the most prevalent form of ocular HSV disease.
3. Oral antivirals are now frequently used for keratitis because of their convenience, although topical optical antivirals are equally effective.
4. HSV dendrites, when stained with fluorescein, appear as branching lesions with terminal bulbs.
5. Corneal hypesthesia may be easily overlooked in the initial evaluation of a red eye. If a topical anesthetic has been given, a reexamination 1 hour later is helpful for evaluating hypesthesia.

A Brief Introduction To Sabaceous Cyst

Skin Manifestations Of Non Malignant Systemic Diseases

Episcleritis - A Brief Introduction

Infections Causes By Herpes Simplex Virus

Salivary Gland Tumors

Pseudotumor Of The Lung On Chest X ray

Acute Angle-Closure Glaucoma

Introduction to Diabetic Foot

Anterior Uveitis (Iritis)

Pleuropulmonary Tuberculosis - Chest X-Ray

Brief Summary of Otosclerosis

Corrosive Esophagitis

Left Main Coronary Artery Lesion - ECG

Anisocoria

Introduction to Dermatophytosis

Pleural Calcification On Chest X ray

Herpes Zoster Opthalmicus

Introduction to Mumps

Malignant Melanoma

Ocular Herpes Simplex.