Ramsay Hunt Syndrome(clinical)

CAUSES:
Classic Ramsay Hunt syndrome is ascribed to infection of the geniculate ganglion by herpesvirus 3 (varicella-zoster virus [VZV]).



HISTORY:
*Patients usually present with paroxysmal pain deep within the ear. The pain often radiates outward into the pinna of the ear and may be associated with a more constant, diffuse, and dull background pain.

*The onset of pain usually precedes the rash by several hours and even days.

*Classic Ramsay Hunt syndrome can be associated with the following:
-Vesicular rash of the ear or mouth (as many as 83% of cases),The rash might precede the onset of facial paresis/palsy.
-Ipsilateral lower motor neuron facial paresis/palsy (CN VII)
-Vertigo and ipsilateral hearing loss (CN VII)
-Tinnitus,Otalgia,Headaches,DysarthriaGait,ataxia.
-Fever,Cervical adenopathy.

*Facial weakness usually reaches maximum severity by one week after the onset of symptoms.

*Other cranial neuropathies might be present and may involve cranial nerves (CNs) VIII, IX, X, V, and VI.

*Ipsilateral hearing loss has been reported in as many as 50% of cases.

*Blisters of the skin of the ear canal, auricle, or both may become secondarily infected, causing cellulitis.


EXAMINATION:

.The primary physical findings in classic Ramsay Hunt syndrome include peripheral facial nerve paresis with associated rash or herpetic blisters in the distribution of the nervus intermedius.
.The location of the accompanying rash varies from patient to patient, as does the area innervated by the nervus intermedius. It may include the following:
1.Anterior two thirds of the tongue
2.Soft palate
3.External auditory canal
4.Pinna
.The patient may have associated ipsilateral hearing loss and balance problems.
.A thorough physical examination must be performed, including neuro-otologic and audiometric assessment.

Toxoplasmosis in Immune-Suppressed Patients

Toxoplasma encephalitis (inflammation of the brain) and Toxoplasma myocarditis (inflammation of the heart) are well recognised opportunistic infections in patients who are immune suppressed, particularly in relation to AIDS and chemotherapy for cancer. The Toxoplasma encephalitis has the usual appearance of an encephalitis from any cause, that is, focal areas of death of cerebral tissue associated with a mononuclear inflammatory cell infiltrate. But in addition, Toxoplasma cysts are found in the affected brain tissue.

This figures are from the heart of a middle aged male who died from AIDS. The Toxoplasma cyst is expanding the myocardial muscle fibre. In this case there is no inflammatory reaction associated with the cyst. The presence of an inflammatory reaction is variable.

Infectious Diseases in Critical Care

Infections and their complications are a very important clinical area in the intensive care unit setting. Community-acquired infections and nosocomial infections both contribute to the high level of disease acquisition common among critically ill patients. The accurate diagnosis of nosocomial infections and the provision of appropriate therapies, including antimicrobial therapy effective against the identified agents of infection, have been shown to be important determinants of patient outcome.

Critical care practitioners are in a unique position in dealing with infectious diseases. They are often the initial providers of care to seriously ill patients with infections. Additionally, they have a responsibility to ensure that nosocomial infections are prevented and that antimicrobial resistance is minimized by prudently employing antibiotic agents. It is the editors’ hope that this book will provide clinicians practicing in the intensive care unit with a reference to help guide their care of infected patients. To that end they have brought together a group of international authors to address important topics related to infectious diseases for the critical care practitioner.

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Diplopia in a Patient with HIV Infection

A 25-year-old man with human immunodeficiency virus (HIV) infection who was receiving highly active antiretroviral therapy presented with a 1-week history of diplopia and headache. The CD4 count was 218 cells per cubic millimeter, and the viral load was 50,000 copies per milliliter.
The neurologic examination revealed an inability to abduct the right eye with horizontal gaze, a finding that was consistent with an isolated right abducens nerve palsy (rightward gaze, Panel A; leftward gaze, Panel B). The examination of other cranial nerves was normal. The remainder of the motor and sensory examination was within normal limits.
The patient reported having had low back pain and constipation for the previous week. There was no history of bowel or bladder incontinence. A gadolinium-enhanced magnetic resonance image of the brain showed a minimally enhancing mass filling and expanding the right cavernous sinus (Panel C, arrow). Lumbar-spine imaging showed a mass with similar radiographic characteristics involving the ventral epidural compartment.
Biopsy of the spinal lesion revealed diffuse large-B-cell lymphoma. A chemotherapeutic regimen of cyclophosphamide, doxorubicin, vincristine, and prednisolone, along with the monoclonal antibody rituximab (R-CHOP), was started. Progressive leg weakness from spinal involvement developed, and the patient had a poor response to corticosteroids and radiation therapy and died 3 months later.

Fournier's Gangrene Reconstructed By Pedicle Thigh Flap(step by step photo images)

Fournier's gangrene is a rare condition and delayed treatment results in fatal outcome. We managed a case of Fournier's gangrene by initial radical debridement followed by scrotal reconstruction using pedicle thigh flap to cover the bare testes with excellent results.

35-year-old male presented in the emergency department with the swelling over scrotum and watery discharge ......

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TB and STAFF

BCG vaccination will be offered to healthcare workers, irrespective of age, who fulfil all the following criteria:

1. previously unvaccinated (that is, without adequate documentation or a characteristic scar)
2. will have contact with patients or clinical materials.
3. are Mantoux (or interferon-gamma test for latent tuberculosis) negative.

All staff in contact with patients with smear positive pulmonary tuberculosis should be aware of the following principles.
-The importance of BCG immunisation as a basic protection
-The need to report to Occupational Health or senior ward staff if they are unusually susceptible e.g. transplant recipient taking immunosuppressive therapy, HIV positive.
-The extremely low risk of occupationally acquired tuberculosis where appropriate precautions are taken.
-The need to report any symptoms suggestive of tuberculosis to the Occupational
Health Department.

Staff in contact with open pulmonary tuberculosis do not normally need follow up. A decision on this will be made by the Occupational Health Department in conjunction with a Consultant Microbiologist or Consultant Respiratory Physician.

Mucormycosis

A 44-year-old woman with a 20-year history of poorly controlled diabetes mellitus presents with headache and unilateral proptosis. The patient is febrile and appears toxic. Her serum glucose level is 640 mg/dL. An urgent CT scan of the head reveals a retroorbital abscess and severe opacification of the frontal and ethmoid sinuses.
Which of the following organisms is most likely responsible for this infection?

• a. Cryptococcus neoformans
• b. Mucormycosis
• c. Mycobacterium tuberculosis
• d. Toxoplasma gondii
• e. Listeria monocytogenes
• f. Staphylococcus epidermis

The answer is (b).
Mucormycosis is a rare fungal disease (Rhizopus species are the most common causative organisms ) limited to persons with preexisting illness and may be seen in poorly controlled diabetic patients. Severe infection of the facial sinuses, which may extend into the brain, is the most common presentation. Patients present with fever, nasalcongestion, sinus pain, diplopia, and coma.
Physical examination may reveal a necrotic nasal turbinate, reduced ocular motion, proptosis, and blindness. CT scan or MRI will reveal the extent of sinus involvement prior to surgery.

Postmortem photograph of a woman with diabetes and left rhinocerebral mucormycosis complicating ketoacidosis. Rhizopus oryzae was the causative organism. Note the orbital and facial cellulitis and the black nasal discharge. (Courtesy of A. Allworth, MD, Brisbane, Australia)

Ramsay Hunt Syndrome

What is it? Ramsay Hunt syndrome is defined as an acute peripheral facial neuropathy associated with erythematous vesicular rash of the skin of the ear canal, auricle (also termed herpes zoster oticus,Hunt's Syndrome ), and/or mucous membrane of the oropharynx.
This syndrome is also known as geniculate neuralgia or nervus intermedius neuralgia. Ramsay Hunt syndrome can also occur in the absence of a skin rash, condition known as zoster sine herpete.

Pathophysiology:

Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves might be also involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy.

VZV infection causes 2 distinct clinical syndromes. Primary infection, also known as varicella or chickenpox, is a common pediatric erythematous disease characterized by a highly contagious generalized vesicular rash. The annual incidence of varicella infection has significantly declined after the introduction of mass vaccination programs in most countries of the world. After chickenpox, VZV remain latent in neurons of cranial nerve and dorsal root ganglia. Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome.

Mortality/Morbidity:

Ramsay Hunt syndrome is not usually associated with mortality. It is a self-limiting disease; the primary morbidity results from facial weakness. Unlike Bell palsy, this syndrome has a complete recovery rate of less than 50%.

SYMPTOMS OF MALARIA

Sometimes symptoms of malaria infection are not always dramatic, and can easily be dismissed as unimportant.


Plasmodium falciparum normally take 7 to 14 days to show symptoms while Plasmodium vivax and ovale normally take 8 to 14 days (but in some cases can survive for some months in the human horst) and Plasmodium malariae 7 to 30 days.

Symptoms may appear and disappear in phases and may come and go at various time frames. These cyclic symptoms of malaria are caused by the life cycle of the parasites - as they develop, mature, reproduce and are once again released into the blood stream to infect even more blood and liver cells.

Infection: Microbiology and Management

Infection: Microbiology and Management provides a core resource for the understanding of medical microbiology and infectious diseases. Content covers microbiological and clinical diagnosis, through to clinical management, epidemiology and the control of infectious conditions as they occur both in the hospital and community setting.

With a concise, systems-based approach, the third edition has been revised and restructured and now covers wider epidemiological and public concerns. Key feature boxes, self assessment and case studies assist learning in each chapter.

Designed to be used either as a basic learning text, or as a practical textbook in the clinical setting, Infection: Microbiology and Management, previously titled Infectious Disease, will continue to appeal to students at all stages of their career, candidates for higher examinations, the general physician and surgeon, epidemiologists and experts in public health.

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Recommendations for post-sexual exposure HIV prophylaxis

Post exposure HIV prophylaxis is recommended if there is:-

* unprotected receptive anal intercourse
* unprotected receptive vaginal intercourse
* unprotected insertive vaginal intercourse
* unprotected insertive anal intercourse
* unprotected receptive fellatio with ejaculation

with a HIV positive person or if the person is a HIV risk group (gay or bisexual men, injection drug users or sex workers), and if the exposure is isolated and the patient is commited to safer sex in the future and the exposure occurred within 72 hours of presentation for care.

Exposure to persons known to be HIV infected

• if medication regimen of source patient is unknown => prescribe Zivudine (AZT/ZDV) 300mg bid + Lamivudine (Epivir) 150mg bid + Indinavir (Crixivan) 800mh q8h or nelfinavir (Virasept) 1250mg bid or 750mg tid
• Combivir 1 tablet bid may be substituted for zidovudine and lamivudine
• if medication regimen of source patient is known => prescribe 2 NRTIs and 1 protease inhibitor that are different from the source patient's regimen
• possible substitues for zidovudine and lamivudine:- stavudine (d4T/Zerit) 40mg bid for > 60kg and 30mg bid <> 60kg and 125mg for <>

Exposure to person or persons of unknown HIV status but who probably have high HIV risk factors :

• significant exposures => treat as if an exposure to a known HIV-infected person with an unknown medication regimen, as above
• exposures that might result in HIV infection => treat with zidovudine and lamivudine without a protease inhibitor

Exposure to person or persons of unknown HIV status but who probably have low HIV risk factors

• significant exposures => treat with zidovudine and lamivudine. A protease inhibitor could be added if the patient requests it, if the provider believes that the exposure history is unclear, other exposures also occurred, or if other factors relating to exposure history or HIV status are compelling
• exposures that might result in HIV infection => treat with zidovudine and lamivudine without a protease inhibitor

Additional caveats

* PEP should not be provided to patients whose exposure history has no known possibility for HIV transmission
* PEP should not be given to persons already infected with HIV
* providers may consider PEP for any patient who appears to be at risk after an HIV exposure but whose circumstances are not delineated in the above categories

Providers are reminded that PEP should only be prescribed as part of a comprehensive program to reduce future HIV risk-related behaviours. Multiple prescription requests for PEP should be strongly discouraged and must be averted through risk reduction counselling.

Definitions:
High HIV risk factors: trading sex for drugs or money, IV drug use, unprotected anal or vaginal intercourse with persons with HIV risk factors
Significant exposures include the following: anal or vaginal intercourse without a condom or with condom breakage; exposure to semen or blood onto mucosal or nonintact surfaces, and intravenous needle sharing
Examples of exposures that might result in HIV infection are as follows: cunnilingus, fellatio, semen or blood on healing skin wounds

TREATMENT OF Ramsay Hunt syndrome

*Medical:

.Corticosteroids and oral acyclovir are commonly used
.Recently,combined therapy using corticosteroids plus intravenous acyclovir did not show benefit over corticosteroids alone in promoting facial nerve recovery after 6 months. However, randomized clinical trials evaluating both therapies are required.
.Vestibular suppressants may be helpful if vestibular symptoms are severe.
.As with Bell palsy, care must be taken to prevent corneal irritation and injury.
.Temporary relief of otalgia may be achieved by applying a local anesthetic or cocaine to the trigger point, if in the external auditory canal.
.Carbamazepine may be helpful, especially in cases of idiopathic geniculate neuralgia.

*Surgical:

Surgical decompression of the facial nerve has no role in this syndrome.

INVESTIGATION OF Ramsay Hunt Syndrome

Laboratory Studies:

1.The diagnosis of Ramsay Hunt syndrome is usually made without difficulty when the clinical characteristics are present. If necessary, varicella zoster virus (VZV) may be isolated from vesicle fluid and inoculated into susceptible human or monkey cells for identification by serologic means.

2.WBC count, erythrocyte sedimentation rate (ESR), and serum electrolytes are helpful in distinguishing the infectious and inflammatory nature of this syndrome.

3.As CNS complications are suspected (eg, meningitis, meningoencephalitis, myelitis, arteritis [large and small vessel], and ventriculitis), spinal fluid analysis and CNS imaging studies are recommended.

4.Viral studies ,
.VZV isolation in conventional cell culture is considered the definite diagnostic test. However, growing VZV in cell culture can be difficult and is usually too slow to be clinically helpful.
The sensitivity of conventional cell culture is 30-40%, with a specificity of 100%.
.Other tests, including Tzanck test, electron microscopy, and polymerase chain reaction (PCR) are generally more rapid and sensitive. The sensitivity of conventional PCR technique is estimated to be 60%.
.VZV has been detected by PCR in the tear fluid of patients with Bell palsy (prevalence, 25-35%).
.VZV antigen detection by direct immunofluorescence assay (DFA) is also possible, with sensitivity of 90% and specificity close to 99%.5
.Antibody determinations on paired sera may be helpful in establishing the diagnosis by comparing titers at time of presentation and a few weeks later.

Imaging studies:

-Structural lesions can be ruled out by CT scan, MRI, or magnetic resonance (MR) angiography.
-Gadolinium enhancement of the vestibular and facial nerves on MRI has been described in Ramsay Hunt syndrome.
-Recent advances in clinical MRI images (eg, 3-Tesla MRI, multichannel phased array coil, 3-dimensional fluid-attenuated inversion recovery [FLAIR]) allow the evaluation of subtle alterations at the level of the blood-labyrinthine barrier.

Tests:
-Audiometry usually reveals sensorineural hearing loss.
-Unilateral caloric weakness may be present on electronystagmography (ENG).
-Electrodiagnostic methods, such as facial motor nerve conductions studies (electroneurography), electromyography of facial innervated muscles, the blink reflex, and nerve excitability testing, could add information regarding the extent of seventh cranial nerve (CN VII) involvement, as well as prognostic factors.

Procedures:

-In the setting of a peripheral facial palsy, cerebrospinal fluid (CSF) rarely is analyzed. Although lumbar puncture is not recommended in the diagnosis of this disease, CSF findings can be helpful in confirming the diagnosis. In one study, CSF findings were abnormal in 11% of 239 patients with idiopathic peripheral facial palsy, in 60% of 17 patients with Ramsay Hunt syndrome (abnormal finding was pleocytosis), in 25% of 8 patients with Lyme disease, and in all 8 patients with HIV infection. Thus, if the CSF is abnormal, a specific cause should be sought.
-Temporary relief of otalgia in geniculate neuralgia may be achieved by applying a local anesthetic or cocaine to the trigger point, if in the external auditory canal.

Histologic Findings:

-The affected ganglia of the cranial nerve roots are swollen and inflamed.
-The inflammatory reaction is chiefly of a lymphocytic nature, but a few polymorphonuclear leukocytes or plasma cells may also be present.
-Some of the cells of the ganglia are swollen and others degenerated.