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External Ear Injuries - Brief Description With Pictures.

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Injuries to the external ear may be open or closed.

  • Blunt external ear trauma may cause a hematoma (otohematoma) of the pinna, which, if untreated, may result in cartilage necrosis and chronic scarring or further cartilage formation and permanent deformity (“cauliflower ear”). 
  • Open injuries include lacerations (with and without cartilage exposure) and avulsions

Pinna Hematoma. A hematoma has developed, characterized by swelling, discoloration, ecchymosis, and flocculence.  Immediate incision and drainage or aspiration is indicated, followed by an ear compression dressing.

Management: Pinna hematomas must undergo incision and drainage or large needle aspiration using sterile technique, followed by a pressure dressing to prevent reaccumulation of the hematoma.
This procedure may need to be repeated several times; hence, after Emergency department drainage, the patient is treated with antistaphylococcal antibiotics and referred to ENT or plastic surgery for follow- up in 24 hours. Lacerations must be carefully examined for cartilage involvement; if this is present, copious irrigation, closure, and postrepair oral antibiotics covering skin flora are indicated.

Pinna Contusion. Contusion without hematoma is present. Reevaluation in 24 hours is recommended to ensure a drainable hematoma has not formed.

Simple skin lacerations may be repaired primarily with nonabsorbable 6-0 sutures. The dressing after laceration repair is just as important as the primary repair. If a compression dressing is not placed, hematoma formation can occur.
Complex lacerations or avulsions normally require ENT or plastic surgery consultation.

Important Points: 
1. Pinna hematomas may take hours to develop, so give patients with blunt ear trauma careful discharge instructions, with a follow-up in 12 to 24 hours to check for hematoma development.
2. Failure to adequately drain a hematoma, reaccumulation of the hematoma owing to a faulty pressure dressing, or inadequate follow-up increases the risk of infection of the pinna (perichondritis) or of a disfiguring cauliflower ear.

Cauliflower Ear. Repeated trauma to the pinna or undrained hematomas can result in cartilage necrosis and subsequent deforming scar formation.

3. Copiously irrigate injuries with lacerated cartilage, which can usually be managed by primary closure of the overlying skin.
Direct closure of the cartilage is rarely necessary and is indicated only for proper alignment, which helps lessen later distortion. Use a minimal number of absorbable 5-0 or 6-0 sutures through the perichondrium.
4. Lacerations to the lateral aspect of the pinna should be minimally debrided because of the lack of tissue at this site to cover the exposed cartilage.
5. In the case of an avulsion injury, the avulsed part should be cleansed, wrapped in saline-moistened gauze, placed in a sterile container, and then placed on ice to await reimplantation by ENT.

Pleural effusion On Chest X ray

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A 28 years old male came to radiology department for X-ray chest with history of breathlessness on exertion since 10 days.
X-ray chest  shows a large pleural effusion on left side, the trachea and mediastinum are pushed to the right, right lung field is clear.

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 , 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.

Clinical Discussion: Large pleural effusion often presents with shortness of breath, dyspnea, sharp chest pain worsening with a deep inspiration, cough and symptoms of underlying cause.
Small effusions go unnoticed many times. In large effusion there are clinical signs such as decreased movement of chest on affected side, stony dullness on percussion over the fluid, diminished
breath sounds, decreased resonance and fremitus and pleural friction rub.
Pleural effusion is either transudate or exudates.

  • Transudative effusion is formed when fluid leaks from blood vessels into the pleural cavity such as in congestive cardiac failure, nephritic syndrome and hepatic cirrhosis.
  • Exudative effusion is caused by the inflammation of pleura itself and is often due to lung pathology such as pneumonia, tuberculosis, lung malignancy. 

Whenever pleural effusion is diagnosed underlying cause should be explored to reduce further morbidity.

Treatment: Therapeutic aspiration is sufficient in small effusion. Large effusions require insertion of intercostal drainage tube. In any case the underlying cause should be treated to prevent recurrence. Thoracocentesis may be needed in malignant effusion.

Chondrodermatitis nodularis helicis

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Chondrodermatitis nodularis helicis (CNH) is a common and benign condition characterised by the development of a painful nodule on the ear.



Causes: It is thought to be caused by factors such as persistent pressure on the ear (e.g. secondary to sleep, headsets), trauma or cold. CNH is more common in men and with increasing age.

Clinical Presentation: The classic presentation of chondrodermatitis nodularis chronica helicis (CNH) is a middle-aged to elderly man with a spontaneously appearing painful nodule on the helix or antihelix. The nodule usually enlarges rapidly to its maximum size and remains stable. Onset may be precipitated by pressure, trauma, or cold. When asked, the patient usually admits to sleeping on the affected side.

On Examination: Nodules are firm, tender, well demarcated, and round to oval with a raised, rolled edge and central ulcer or crust. Removal of the crust often reveals a small channel. Color is similar to that of the surrounding skin, although a thin rim of erythema may be noted.
Size may range from 3-20 mm. The right ear is affected more commonly than the left, and occasionally bilateral distribution is reported.  Lesions develop on the most prominent projection of the ear. The most common location is the apex of the helix. Distribution on the antihelix is more common in women.

Prognosis: The prognosis for patients with chondrodermatitis nodularis chronica helicis (CNH) is excellent, although long-term morbidity is common. Spontaneous resolution is the exception; remissions may occur, but chondrodermatitis nodularis chronica helicis usually continues unless adequately treated.

Management

  • reducing pressure on the ear: foam 'ear protectors' may be used during sleep
  • other treatment options include cryotherapy, steroid injection, collagen injection
  • surgical treatment may be used but there is a high recurrence rate

A 55-year-old woman complains of generalized fatigue, weakness and a rash.....

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A 55-year-old woman complains of generalized fatigue, weakness, inability to climb stairs, arthralgias, and dysphagia.
Physical examination reveals definite proximal muscle weakness, a periorbital heliotrope rash, and skin findings associated with the hands (shown here).

The most likely diagnosis is
A) Lupus erythematosus
B) Sarcoidosis
C) Sjögren’s disease
D) Dermatomyositis
E) Polymyalgia rheumatica

Answer:
The answer is D. (Dermatomyositis)

Discussion: Dermatomyositis presents with a heliotrope rash and the presence of Gottron’s papules. The rash is violaceous in color and involves the periorbital areas. Gottron’s papules are erythematous or violaceous papules or plaques that form over the bony prominences, particularly the metacarpophalangeal joints, the proximal and distal interphalangeal joints. The condition is also associated with a myopathy that involves the proximal muscles. The shoulders and pelvic
girdle are mainly affected in a symmetric pattern.

 Symptoms include fatigue, weakness, inability to climb stairs, or weakness in rising from a
squatting or sitting position. Dysphagia is also seen. Approximately 20% of patients have an associated malignancy.

Laboratory tests include elevated serum creatine kinase or aldolase, or both. Electromyographic studies and a muscle biopsy can also provide additional diagnostic information.

The mainstays of treatment are systemic steroids. Other options include immunosuppressant agents and hydroxychloroquine. Those who are older and have severe myositis, dysphagia, associated malignancy, and a poor response to corticosteroids have a poorer prognosis.

Acute Right Ventricular Myocardial Infarction - ECG

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Right Ventricular Myocardial Infarction. This ECG was obtained with right-sided lead placement.

ECG Findings
• ST elevation in right-sided V leads (V4R, V5R).
• ST elevation greater in lead III than lead II suggests RV MI.
• ST elevation in the normally obtained V1 also strongly suggests RV MI.

• Often associated with inferior MI and/or posterior MI.

ST elevation in V4R and V5R (arrows), with the V4 and V5 leads placed in their mirror-image locations on the right side of the chest. Any ST elevation seen in the right-sided precordial leads is significant.

Important Points: 
1. The smaller muscle mass of the right ventricle produces a less intense injury pattern that is
overwhelmed by the left ventricle in the normally obtained ECG. Placement of right-sided V leads, with V1-V6 in mirror-image locations on the right side of the chest, is important in detecting
right ventricular injury.
2. The heart with an injured right ventricle is very preload dependent. Beware of lowering preload with nitrates in any patient with suspected RV MI as severe hypotension may occur. Treat hypotension with volume.
3. Obtain a right-sided ECG in any patient with inferior or posterior MI, and in any patient with a significant hypotensive response to nitrates

A 19 Year Old Woman With Fever And Sore Throat

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A 19-yr-old woman presents with a severe sore throat, fever and malaise. She has marked cervical lymphadenopathy, gross splenomegaly and scattered petechiae on the soft palate, with enlarged tonsils covered by a confluent white exudate.


Her White cell count is mildly elevated, her serum ALT and AST concentrations are twice normal and her ALP is slightly elevated.
Which one of the following investigations is most likely to help guide your management?
A. FNA of a LN
B. HBsAg
C. CMV IgM
D. Heterophilic antibodies
E. HIV test

Answer:
D. Heterophilic antibodies

Discussion: The Hx is strongly suggestive of infectious mononucleosis, which can be confirmed by a
heterophilic antibody test (Monospot). Around 80% of pts at this stage of the illness will have a
positive test. However, if the Monospot test is negative, it should be repeated a few days later.
Specific serological tests to detect the presence of Epstein–Barr virus should be requested if it
is still negative and there is a high clinical suspicion of glandular fever. If the EBV tests are
negative then other causes for heterophilic negative acute mononucleosis – including HIV, CMV
and toxoplasmosis – should be considered. The LFTs are not sufficiently elevated in this Pt for
acute viral hepatitis. Other features of a systemic viral infection are present and therefore there
is no indication for requesting Lymph node aspiration. Clearly, management of this Pt depends on a correct diagnosis. The most frequent misdiagnosis is of bacterial tonsillitis and antibiotic Rx given to someone with glandular fever might result in a severe drug reaction. Confirmation of glandular fever would suggest the need for corticosteroid management of this Pt who is toxic and has profound
thrombocytopenia. It would be unusual for the acute HIV retroviral syndrome to present with
marked exudative tonsillitis and splenomegaly, although a reported sexual Hx negative for risk factors does not exclude HIV infection.

Uncal Herniation Syndrome After Severe Head Injuries

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Severe head injury can result in extra-axial hematoma, cerebral contusion, or diffuse cerebral edema which, in turn, may cause one of five brain herniation syndromes:

  1. uncal, 
  2. central
  3. transtentorial, 
  4. cerebellotonsillar, 
  5. subfalcine, and external.

Uncal herniation occurs when the uncus of the temporal lobe is displaced inferiorly through the medial edge of the tentorium.
Compression of cranial nerve III can cause an ipsilateral dilated pupil. Typically, patients with uncal herniation are unconscious and require intubation. A contusion to the eye may also result in a dilated, non responsive pupil and arouse suspicion for severe head injury and uncal herniation
but typically these patients will be alert.

                                         Ipsilateral Dilated Pupil due to Uncal Herniation.
      ( CT revealed an epidural hematoma and unilateral effacement of the quadrigeminal cistern. )

Management: Intubate unconscious head trauma patients with a unilateral dilated pupil and transfer them immediately to a facility capable of caring for traumatic brain injury. A noncontrasted head CT scan can identify a subdural or epidural hematoma, diffuse edema, or temporal lobe contusion. These conditions often cause midline shift of cerebral structures and compression of the quadrigeminal cistern. Unilateral effacement of the quadrigeminal cistern confirms uncal herniation.


Initial management focuses on maintaining cerebral perfusion pressure and normal tissue oxygenation as hypotension and hypoxia significantly contribute to secondary brain injury. Mannitol,
hypertonic saline, burr holes, and hyperventilation should be considered in ED patients with uncal herniation. Definitive care requires neurosurgical consultation.

Important Points: 
1. Uncal herniation is the most common of the five herniation syndromes.
2. If a patient has a unilateral dilated pupil after head and face trauma but is awake and talking, be suspicious for isolated traumatic anisocoria.
3. Steroids have no role in the ED management of traumatic brain injury.
4. A temporal lobe contusion in an initially neurologically intact patient may continue to expand and cause uncal herniation.
5. Excessive hyperventilation (PaCO2 < 25 mm Hg) in patients with severe traumatic brain injury is associated with cerebral ischemia.
6. Effacement of the quadrigeminal cistern is the hallmark CT finding of uncal herniation.

Contact Dermatitis - Brief Introduction

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Definition: Contact dermatitis can be defined as a red, itchy rash caused by any substance that comes in contact with the skin.

It could be caused by an allergy, or because the protective layer of the skin gets damaged.

There are two main types of contact dermatitis
1. Irritant contact dermatitis: common nonallergic reaction due to weak acids or alkalis (e.g. detergents). Often seen on the hands. Erythema is typical, crusting and vesicles are rare

2.Allergic contact dermatitis: type IV hypersensitivity reaction. Uncommon often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself. Topical treatment with a potent steroid is indicated.

Clinical Signs And Symptoms: 
  • Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue is present in the epidermis (the outermost layer of skin) and the outer dermis (the layer beneath the epidermis)
  • Contact dermatitis results in large, burning, and itchy rashes. These can take anywhere from several days to weeks to heal. This differentiates it from contact urticaria (hives), in which a rash appears within minutes of exposure and then fades away within minutes to hours. Even after days, contact dermatitis fades only if the skin no longer comes in contact with the allergen or irritant.
  • Red rash or bumps
  • Itching, which may be severe
  • Dry, cracked, scaly skin, if your condition is chronic
  • Blisters, draining fluid and crusting, if your reaction is severe.
Diagnosis:  To diagnose a case of contact dermatitis the genera; physician may need to  refer the patient to an allergy specialist or dermatologist to pinpoint the cause of contact dermatitis. The specialist can perform allergy testing (called a ‘patch test’), which involves exposing a small patch of the skin to an allergen. If the skin reacts, the allergy specialist can determine the likely cause of the contact dermatitis

Management:
1. If the substance that caused the rash is identified completely avoid it later and never touch it.
2. Wash the skin with mild soap and cool water right away, if possible. This helps get rid of all or most of the problem substance. and could help cut back on symptoms.
3. Applying prescription steroid creams can help if initial home remedies fail.
4. In severe cases, the doctor may prescribe oral corticosteroids to reduce inflammation, antihistamines to relieve itching or antibiotics to fight a bacterial infection.

A Case Of Encysted Pleural Effusion

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A 26 years male came to radiology department for X-ray chest with history of cough and fever.
The X -Ray is shown below:


Radiological Findings On X-Ray Examination:
X-ray chest (in the picture above) shows encysted pleural effusion (arrow) along left lateral chest wall, i.e. costoparietal in position, and on right side there is free pleural effusion (twin arrow).

Comments And Explanation: 
The chest radiographic appearance depends on the site of the loculus, the amount of fluid and the radiographic projection. When seen en face it usually appears as an oval opacity, its margin partially well-defined and partially ill defined. When viewed tangentially, it is sharply defined on its convex pulmonary aspect. In moderate and massive effusion there is significant shift of the trachea and the apex of the heart to the opposite side. In the case of encysted effusions the inner margins may be more convex and the mediastinal shift minimal. If the encystment occurs in the interlobar regions there may be formation of rounded or oval opacities which may resemble a tumor.
This may disappear with treatment and hence these are termed pseudo-tumors or phantom tumors. Chest
ultrasound and CT is helpful to differentiate pleural fluid and other pleural and chest wall lesions.

Diagnosis In The Above Case: Encysted pleural effusion

Clinical Discussion: 
Patient may present with dyspnea, chest pain, cough and symptoms of underlying cause. In encysted pleural effusion fluid accumulates between the two layers of visceral pleura within the fissure or between partially fused parietal and visceral pleura adjacent to chest wall, diaphragm or mediastinum.

Encysted effusion can either be:

  • costoparietal, 
  • interlobar,
  • subpulmonic or 
  • mediastinal. 

Costoparietal effusion is the commonest and most often results from infections. Interlobar encystment comes next in frequency and most often results from congestive cardiac failure.

Causes: Tuberculosis is the commonest cause of encysted pleural effusions, followed by pyogenic infection and congestive cardiac failure.

Management: Aspiration of fluid is the treatment of choice. Ultrasound guided needle aspiration
is helpful for costoparietal effusion

Acute Posterior Myocardial Infarction - ECG

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                                 Acute Posterior Myocardial Infarction (Click on the image to enlarge)

ECG Findings
• With acute injury pattern—ST segment depression in lead V1 and/or V2 with acute injury pattern
• With infarction pattern—Small S wave and large R wave greater than 4 ms duration in lead V1 or V2 with infarction
• With infarction pattern—R-wave/S-wave ratio greater than 1 in lead V1 or V2 with infarction.

Important Learning Points:
1. The posterior portion of the left ventricle has no EKG electrodes directly overlying it and is the last portion of ventricle to depolarize. It receives its blood supply from either the right coronary artery (in 85% of individuals) or the circumflex artery (in 15% of individuals).
2. V1 and V2 are primarily affected as the most anterior leads and indirectly assess the posterior left ventricle, though in an “inverted” orientation. Instead of observing downgoing Q waves and ST elevation, one expects to see large upgoing R waves and ST depression. By holding the EKG
up to a backlight upside down and horizontally flipped, the more classic injury pattern can be observed by looking through the EKG paper (see picture below).


By inverting and rotating the EKG, the characteristic ST-elevation injury pattern is easily seen (arrow). This can be done in practice by flipping the EKG upside down and looking through the printed EKG with a backlight

3. Posterior involvement may be confirmed with posterior leads. V8 is located at inferior tip of left scapula; V9 is positioned between V8 and the spine at the same level.
4. Frequently, an inferior MI is also present with a posterior MI, since the right coronary artery serves both areas. In the above example, there is subtle ST elevation in the lateral leads, indicating posterior-lateral injury.

The ST depression is subtle and down sloping. However, the R-wave amplitude approximates that of the S wave, and the R-wave duration is significant (>4 ms). This is actually an “inverted Q wave” from a posterior infarction that has evolved since the initial tracing.

A Brief Discussion On Viral Conjunctivitis

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Viral Conjunctivitis. Note the characteristic asymmetric conjunctival injection. Symptoms first developed in the left eye, with symptoms spreading to the other eye a few days later. A thin watery discharge is also seen.

Viral conjunctivitis is a common presentation of the red eye.
Findings are mild and include :

  • a thin watery discharge, 
  • crusting in the morning, 
  • burning or irritation, 
  • conjunctival injection (typically diffuse), and 
  • lid edema. 

The tarsal conjunctiva may appear bumpy secondary to hyperplastic lymphoid tissue (follicles). Preauricular adenopathy may be present. The visual acuity is normal. The infection usually begins in one eye, but both eyes usually become involved due to autoinoculation.
There are few to no systemic complaints.

 Adenovirus is the most common virus. A point of care test now available may aid clinicians to avoid empiric antibiotic therapy.

Epidemic keratoconjunctivitis (EKC) is a severe and highly contagious adenovirus infection that also involves the cornea. Additional features may include:


  • foreign body sensation,
  • photophobia, and 
  • pseudomembranes overlying the palpebral conjunctiva. 
  • By the eighth day, a painful punctate keratitis that stains with fluorescein may develop; 
  • by the end of the second week, these are replaced by white macular subepithelial infiltrates located in the central cornea (that no longer stain). 
  • These may cause a decrease in visual acuity, but eventually resolve spontaneously.

Pharyngoconjunctival fever, usually caused by adenovirus type 3, is highly contagious and should be considered if there is associated upper respiratory tract infection and fever.

Management: 
1. Viral conjunctivitis is self-limited and usually mild.
2. Warm or cool compresses may be helpful.
3. Careful hand washing by patient and staff is important.
4. Over-the-counter topical antihistamines may provide symptomatic relief.
5. The eye irritation and discharge should improve after 5 to 7 days, but may take 2 to 3 weeks for complete resolution of all symptoms.
6. Antivirals and antibiotics are ineffective.
7. Patients with keratitis should follow up with an ophthalmologist.

Points To Remember: 
1. A nonspecific adenovirus conjunctivitis will improve after 5 to 7 days and resolve in 10 to 14 days, but a virulent adenovirus causing EKC will peak in 5 to 7 days and may last 3 to 4 weeks.
2. Consider and rule out serious causes of red eye (acute ACG, iritis).
3. Frequent hand washing and the use of separate linens are advised for patients and family members.
4. Fastidious hand and equipment hygiene is necessary to prevent nosocomial transmission, as adenovirus can be recovered for extended periods of time from these surfaces.

Dermatitis herpetiformis - A Brief Discussion

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Dermatitis herpetiformis is an autoimmune blistering skin disorder associated with coeliac disease. It is caused by deposition of IgA in the dermis.
 Despite its name, DH is neither related to nor caused by herpes virus: the name means that it is a skin inflammation having an appearance similar to herpes.

Clinical Features: 
The age of onset is usually about 15-40, but Dermatitis herpetiformis can also affect children and the elderly. Men and women are equally affected.
 Symptoms include:
  • Extremely itchy bumps or blisters, most often on the elbows, knees, back, and buttocks
  • The rash is usually the same size and shape on both sides
  • The rash can look like eczema
  • Some people may have scratch marks and skin erosions instead of blisters
  • Most people with dermatitis herpetiformis have damage to their intestines from eating gluten. But only some have intestinal symptoms.
                                          Classic vesicles of dermatitis herpetiformis.

Diagnosis: Dermatitis herpetiformis is often misdiagnosed, being confused with drug eruptions, contact dermatitis, eczema , and even scabies.
The diagnosis can be confirmed by a skin biopsy: direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis.

Management: 
1. An antibiotic called dapsone is very effective.
2. A strict gluten-free diet will also be recommended to help control the disease. Sticking to this diet may eliminate the need for medicines and prevent later complications.
3. Drugs that supress the immune system may be used, but are less effective.

Prognosis: The disease may be well-controlled with treatment. Without treatment, there may be a significant risk of intestinal cancer.

Central venous Line/ Catheter Related Infections In ICU Setting.

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Introduction:

Majority of patients in ICU have central venous lines placed in order to provide fluids and medicines. They may be life saving but at the same time these can result in serious blood stream infections. These catheter related blood infections are reported to occur in about 3 to 8% of inserted catheters and are the number one cause of nosocomial infections in ICU settings.

A few Definitions:
1. A central venous catheter or a central venous line is a catheter whose tip resides in a central vein.


                                                      An Adult Central venous catheter 
2. Catheter related blood stream infections refer to an infection that is attributed to an intravenous catheter by quantitative culture of the catheter tip or by difference in growth between catheter and peripheral venipuncture blood culture specimens.

3. Central line associated blood infections is defined as an infection that appears in the presence of a central venous catheter or within 48 hours of removal of a central venous line and which cannot be attributed to an infection unrelated to the catheter.

Risk factors:
The risk factors for these central venous line related blood infections include :
  • Patient’s severity of illness
  • Compromised immune system
  • Presence of a distant skin infection
  • Site of the catheter with greatest chances of infection with groin insertions.
  • If aseptic techniques are not proper;y used while insertion of the catheter.
Background Information:
Addressing the issue of central venous line associated blood infections is challenging. Different countries and organizations have setup different guidelines to prevent these infections. These include:
  • Hand hygiene and decontamination with antiseptic soaps or alcohol based gels before catheter insertion.
  • Antiseptic care during insertion, maintenance and replacement of these intravascular central catheters.
  • Use of maximum sterile barrier precautions like cap, mask, sterile gloves and gown while inserting central venous catheters.
  • Proper education and training for the staff involved in taking care of patients with central venous lines in ICU.
  • Catheter material is also very important to take into consideration for prevention of these infections. The material should be biostable and biocompatible. Also the catheter should be flexible, resistant, not altered by drugs, as radio opaque as possible and thin walled with a high internal to external diameter ratio.
  • The subclavian vein should be the insertion point of choice.
  • It is important to remove the central venous catheters as soon as they are no longer needed. The longer they are in place there are increased chances for infection.
  • Although routine antibiotic prophylaxis is not recommended it can be used for high risk patients with central venous lines.
The microorganisms that are most commonly involved in these infections include:
  • Staphylococci ( Both Staphylococcus aureus and the coagulase negative staphylococci)
  • Enterococci
  • Aerobic gram negative bacilli
  • Yeasts.
Diagnosis: The diagnosis of catheter related blood stream infection is made if a patient with an intravascular central line develops the clinical or the laboratory criteria of the systemic inflammatory response syndrome . these include:
  • A temperature < 36 C or > 38 C
  • Heart rate >90/minute
  • Respiratory rate >20/ minute
  • Peripheral white blood cell count <4000/microliter or > 12,000/microliter.

Catheter-related bloodstream infection remains the most serious complication of central venous access and a leading cause of nosocomial infection in the ICU. It is important to take appropriate measure to prevent it.

ECG Findings In Different Types Of Heart Block.

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Heart Block is an abnormality in the electrical rhythm of the heart and it occurs when the electrical signals that moves through the heart are slowed or disrupted. There are different types of heart blocks that are mostly diagnosed by the finding on the ECG.

Normal Electrical Activity Of the Heart:A normal heartbeat is initiated when the heart’s natural pacemaker in the sino-atrial node located at the top of the right atrium creates the electrical signal which then travel through the atrium and reaches the atrio-ventricular node. After crossing the AV node these signals pass through the bundle of His. This bundle then divides into thin structures called as bundle branches which then extend into the right and the left ventricles. Through these bundle branches the signals finally reach within the muscle cells of the ventricles causing them to contract. In this way the ventricular muscles contracts as a whole and pumps the blood to the body. If this normal electrical passage is interrupted anywhere it leads to a condition known as heart block.

1. First Degree Heart Block:
In the first degree heart block the electrical impulses are slowed as they move from the atria to the ventricles, but they all reach successfully to the ventricles. This condition rarely causes any symptoms and usually do not require any treatment. On ECG patients with a first degree heart block will have a longer , flatter line between the P and the R wave. In other words the PR interval is prolonged.



2. Second Degree Mobitz type I:
In this type of heart block the electrical impulses are gradually delayed more and more with each heart beat until an impulse fails to reach the ventricles entirely resulting in a skipped beat. This condition sometimes may cause dizziness and usually does not require treatment. On ECG patients with Second degree Mobitz type I heart block shows a characteristic gradual prolongation of the PR interval until a dropped beat with an absent QRS complex.



3. Second Degree Mobitz type II:
In this type of heart block some of the electrical impulses don’t reach the ventricles but the pattern is less regular as compared to Mobitz type I. This condition is less common but more serious than Mobitz type I and may need a pace maker as it may progress into a third degree complete block. On ECG patients with this condition shows QRS wave follows the P wave at a normal speed but some of the QRS waves are missing that indicates a block. 




4. Third Degree Heart Block:
Also known as complete heart block in which none of the electrical impulses reach the ventricles. When the ventricles do not receive the impulse they start generating their own electrical activity but this backup is much slow than the normal heart rate and so the patient will feel light headed or may feel dizzy as the blood is not pumped to the body appropriately. The symptoms may be life threatening leading to medical emergency and conditions like cardiac arrest. Treatment is done with an artificial pacemaker. On ECG the normal patteren is disrupted and the P waves are at a faster rate and are not coordinated with the QRS complex.


Allergic Conjunctivitis

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Allergic conjunctivitis is a condition whereby airborne allergens precipitate type 1 IgE-mediated hypersensitivity reactions in the conjunctiva. 

Allergic Conjunctivitis. Conjunctival injection, chemosis, and a follicular response in the inferior palpebral conjunctiva are seen in this patient

Allergens include:

  • pollens, 
  • animal dander, 
  • mites, 
  • mold, and 
  • dust. 

Approximately 50% of patients have a personal or family history of allergic conditions such as
atopy, eczema, asthma, and allergic rhinitis.

Clinical Features: Itching is the hallmark symptom. Associated clinical features include:

  • conjunctival injection and edema, 
  • burning, 
  • discharge (clear, white, or mucopurulent), 
  • chemosis, and 
  • eyelid redness and swelling. 
  • Small papillae may be seen on the tarsal conjunctiva.

Vernal conjunctivitis is a rare but serious form of allergic conjunctivitis. The highest incidence is seen in the arid areas of the Middle East and North Africa secondary to wind and dust storms. Symptoms are similar to allergic conjunctivitis, but are more intense. Itching is severe and a vigorous knuckle rubbing is a typical observation. Giant, raised, pleomorphic papillae (“cobblestones”)
seen over the upper tarsal plate are pathognomonic.


Vernal Conjunctivitis. The tarsal conjunctiva demonstrates giant papillae and a cobblestone appearance pathognomonic for vernal conjunctivitis

Management:

  1. The initial approach is to eliminate the allergen. Avoiding animal dander, using air conditioners with appropriate filters, and limiting time outdoors will improve the condition.
  2. Topical tear substitutes are effective to dilute or wash away the allergen. 
  3. H1 antihistamine-vasoconstrictor combinations such as over-the-counter Naphcon A are recommended to relieve mild itching and redness. 
  4. For more severe or frequent attacks, olopatadine, an antihistamine with mast cell stabilizing properties, is more effective. 
  5. Mild topical steroids are an option only after consultation with an ophthalmologist.
  6. Options for vernal conjunctivitis include cromolyn, aspirin, and cold compresses. 
  7. Topical cyclosporin may be useful in resistant cases.
Important Points To Remember: 

1. Itching is the hallmark symptom of allergic conjunctivitis.
2. Itching is not common in nonallergic conjunctivitis.
3. Symptoms are usually bilateral.
4. Naphcon A and olopatadine are effective in treating allergic conjunctivitis.
5. Complications of topical corticosteroid use include glaucoma, cataract formation, secondary infection, and corneal perforation.

Insulinoma- A Pancreatic Islet Cell tumor

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Introduction:
Insulinoma is a benign pancreatic islet cell tumor that produces excessive insulin and is derived from beta cells of the pancreas. The constant secretion of insulin from the tumor leads to hypoglycemia ( low blood sugar levels).

Incidence:
Insulinomas are rare tumors and mostly occur as a single small non cancerous growth is adults. People with genetic disorder known as multiple endocrine neoplasia type I are more prone to have this type of tumor. Its incidence is only 3-4 per million people making it one of the very rare tumors.

Clinical features:
  • Patients usually present with:
  • Recurrent headache
  • Lethargy
  • Anxiety
  • Behavioral changes
  • Blurred vision
  • Seizures
  • Coma if severe hypoglycemia occurs.
  • Confusion
  • Hunger
  • Sweating
  • Tremors
Diagnosis:
The diagnosis of a patient having an insulinoma is made after some blood work and imaging studies. Blood glucose levels as well as insulin and C peptide are measured. A low blood glucose along with high insulin leads to the diagnoses of insulinoma. the C peptide is measured to differentiate the insulin synthesized in the body from the injected insulin. If insulin is injected there will be no C peptide. Later a CT scan or MRI of the abdomen may be done to look for the tumor in the pancreas.

Treatment:
The definitive treatment is the surgical removal of the tumor. Medications like diazoxide or somatostatin may be used to block the release of insulin in patients who are not good candidates for surgery.

Prognosis:
In most cases the tumor is benign and surgery cures the disease. But sometimes a severe hypoglycemia may lead to life threatening condition unless treated immediately to bring blood glucose levels back to normal.

Dacryocystitis - Clinical Features And Management.

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Definition: Dacryocystitis is an inflammation of the lacrimal sac, positioned immediately distal to the canaliculi and proximal to the nasolacrimal duct.

Etiology: Inflammation is usually secondary to obstruction of the nasolacrimal duct.

Clinical findings include:

  • swelling over the lacrimal sac, 
  • redness, 
  • tearing, 
  • eyelash matting and crusting, 
  • conjunctival redness. 

During examination tears and mucopurulence may be expressed from the punctum when pressure is applied over the lacrimal sac.

Dacryocystitis. Swelling and erythema over the medial lower lid and lacrimal sac developed in this 10-year-old patient with streptococcal pharyngitis.

Complications include:

  • conjunctivitis and 
  • orbital or preseptal cellulitis.

Up to 20% of normal newborns have a closed nasolacrimal passage, and 90% spontaneously open within the first 6 months.


Management: 

  • Ophthalmologic consultation is recommended. 
  • The most common organisms isolated in children are S aureus, Staphylococcus epidermidis, and α-hemolytic Streptococci. 
  • Oral clindamycin for 7 to 10 days is recommended for outpatient management.
  • Febrile and acutely ill patients require IV vancomycin in combination with a third-generation cephalosporin.
  • Treatment of nasolacrimal duct obstruction is managed initially with downward lacrimal sac massage (“Crigler” massage) 2 to 3 times a day. 
  • Unresolved nasolacrimal duct obstruction requires lacrimal duct probing by the ophthalmologist.
Important Points To Remember:
1. Nasolacrimal duct obstruction is the most common cause of persistent tearing and ocular discharge in children.
2. Swelling is localized to the extreme nasal aspect of the lower lid and may be confused with a hordeolum. Occasionally, conjunctival redness may be present.
3. Dacryocystitis may be confirmed by pressure on the lacrimal sac and the reflux of tears and purulent material from the punctum. The lacrimal sac and lacrimal fossa lie in the inferior medial aspect of the orbit, not on the side of the nose.
4. Urgent referral should be made for any signs of orbital cellulitis. These include proptosis, limitation of extraocular movements, and loss of vision.

Dacryoadenitis - Case Discussion

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This young patient is referred to the ophthalmologist with the presenting complains of unilateral upper eyelid swelling and tenderness.

The case of diagnosed as Dacryoadenitis.

Case Discussion :
Dacryoadenitis is the inflammation of the lacrimal glands

Acute dacryoadenitis typically involves children and young adults with associated systemic infections such as gonorrhea, mumps, Epstein-Barr virus, and Staphlyococcus species.

Clinical Findings are localized to the outer one-third of the upper eyelid and include fullness or swelling, erythema, and tenderness.
A characteristic “S”-shaped deformity with ptosis of the lid may be seen.
In more advanced cases proptosis, inferonasal globe displacement, ophthalmoparesis, and diplopia may be present.

Chronic dacryoadenitis is more common, is seen in older patients, and is usually due to tumor or associated inflammatory disorders such as sarcoidosis, Sjögren syndrome, or IgG4-related diseases.


Important Learning Points: 
1. Swelling is localized over the lateral one-third of the upper lid and imparts an “S”-shaped curve to the lid margin.
2. Acute dacryoadenitis is usually seen as a complication of mumps, with (bilateral) parotid swelling.
3. Chronic dacryoadenitis is more common, and is seen in older patients. Malignancy should be considered.
4. IgG4-related disease should be considered in patients (particularly middle-aged and older men) with bilateral disease and either salivary gland enlargement or pancreatitis
of unknown origin.
5. Urgent referral is recommended for patients with diplopia, limitation of the extraocular muscles, or reduction of vision.

Management: 

  • For acute dacryoadenitis, amoxicillin-clavulanate or IV ampicillin-sulbactam are used, depending on the severity and patient’s toxicity. 
  • In cases of dacryoadenitis due to mumps or Epstein-Barr virus, warm compresses are recommended.
  • Resolution occurs spontaneously. 
  • Patients should return to the ED for symptoms suggestive of orbital cellulitis such as decreased ocular motility or proptosis.
  • Treatment of chronic dacryoadenitis involves treatment of the underlying disorder.
  • Nonemergent ophthalmology follow-up is appropriate.


Introduction To Bradycardia

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Bradycardia is defined as heart rate of less than 60 beats per minute.

Clinical Presentation
  • Often patients do not have any symptoms and it is detected as an incidental finding on routine physical examination.
  • Some patients may present with faints or blackouts, drop attacks, dizziness, breathlessness or lack of energy.
  • Findings on examination are slow pulse rate; normal or low BP with or without an evedence of secondary heart failure.
  • Sometimes there may be symptoms and signs of any associated disease that may help in diagnosing the cause of bradycardia.
InvestigationsA patient presenting with bradycardia with or without any associated symptoms should have following basic investigations done:

ECG: Ambulatory ECG may help with diagnosis of intermittent bradycardia as in sick sinus syndrome.
Blood tests: Thyroid function tests, Complete blood count, ESR, Urea, creatinine, LFTs, and digoxin levels (if pt taking digoxin).

Types Of Bradycardia

1. Sinus Bradycardia
There is a constant bradycardia and ECG shows normal P waves and P-R interval is <0.2 sec. 

Causes of sinus bradycardia are:
  • Physiological e.g atheletes
  • Vasovagal attack
  • Drugs e.g b -blockers, digoxin
  • Inferior wall MI
  • Sick sinus syndrome
  • Hypothyroidism
  • Hypothermia
  • Increased intracranial pressure
  • Jaundice
If patient is symptomatic management is hospital admission and cardiology referral.

2. AV node block (Heart block)Causes are
  • Ischemic heart disease
  • Drugs e.g digoxin, verapamil
  • Myocarditis
  • Cardiomyopathy
  • Fibrosis
  • Lyme’s disease
Types of heart block
  1. 1st degree heart block: Fixed P-R interval >200ms on ECG.
  2. 2nd degree block: It has two types :
  3. Mobitz type I: There is progressive lengthening of P-R interval followed by a dropped beat.
  4. Mobitz type II: constant P-R interval with regular dropped beats.
  5. 3rd degree block: it is a complete block in which P-P intervals are constant and R-R intervals are constant but not related to each other.
Patients with heart block should be referred to a cardiologist even if asymptomatic.

3. Stokes-Adams attack
It is defined as cardiac arrest due to AV block. Patients present with sudden loss of consciousness due to cerebral anoxia. The patient becomes pale and pulseless but respiration continues. attacks usually lasts apprx. 30 sec though occasionally are fatal. On recovery the patient becomes flushed. patients should be referred to cardiologist if suspected.

4. Sick sinus syndromeDue to sinus node dysfunction causing bradycardia with or without asystole, sino-atrial block, atrial fibrillation or supraventricular tachycardia. It is common among elderly patients. If symptomatic patients will need a pace maker.

Scleritis

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Definition: Scleritis is defined as inflammation of the sclera ( which is the white outer coating of the eye).Scleritis is painful, destructive, and potentially blinding condition of the eye.

Clinical features: The pain is constant and boring and may radiate to the face and periorbital
region. Associated features include tearing, photophobia, globe tenderness to palpation, and painful ocular movement.
The conjunctival vessels are injected. The eye itself may be intensely red with a violaceous or purple hue secondary to engorgement of the deep vessels of the episclera and scleral thinning. These deep vessels do not move when the overlying conjunctiva is moved with a cotton-tipped applicator, nor do
they blanch with topical phenylephrine.

On slit-lamp microscopy, the episcleral vessels are displaced outward by scleral edema.

Corneal involvement, iritis (with cells and flare in the anterior chamber), and decreased visual acuity may accompany scleritis.

Scleritis. A 55-year-old female with scleritis of the left eye associated with rheumatoid arthritis. Note dilation of the deep conjunctival and episcleral vessels and blue hue suggesting thinning of the sclera temporally

Etiology: An associated scleritis may occur with severe infectious keratitis. Primary infectious
scleritis is rare. In either instance, topical and systemic antibiotics are indicated after appropriate cultures are obtained.
In up to 50% of cases, scleritis is associated with underlying autoimmune or infectious systemic disease, rheumatoid arthritis the most common. It occurs more frequently in women and in the fourth to sixth decades of life.

Management: Ophthalmology consultation is required. Treatment varies according to underlying disease (if present), and can involve NSAID therapy, glucocorticoids, and immunosuppressive
medications.
Rheumatology consultation by the ophthalmologist is often required for optimal management in patients with underlying autoimmune disorders.

Points To Remember: 
1. Scleritis is associated with a systemic disease in approximately 50% of cases, most commonly rheumatoid arthritis.
2. Most cases of scleritis involve the anterior portion (anterior to the insertion of the medial and lateral rectus muscles).
3. Pain is exacerbated with ocular movements because the extraocular muscles insert into the sclera itself.
4. Anterior uveitis can occur in up to 40% of patients because the uvea is immediately adjacent to the sclera.
5. Check intraocular pressure (IOP) to rule out acute Acute Closed angle Glaucoma as another cause of painful red eye.
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