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NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

Friday, April 17, 2015

Prenatal Vitamin Overdose

Case presentation:
A 16 - year - old female intentionally overdosed on an unknown quantity of “ vitamins. ” She
arrives at the emergency department 4 hours after the overdose complaining of nausea, vomiting, and epigastric abdominal pain. Her initial vital signs reveal pulse 123 beats per minute, blood pressure 85/34 mmHg, respiration 24 breaths per minute, and temperature 37.2 ° C. Her examination is signifi cant only for epigastric tenderness on palpation of her abdomen.

Her laboratory studies are signifi cant for the following: iron 567 mg/dL, serum bicarbonate 15 mEq/L, glucose 256 mg/dL, and white blood count 13.2 × 10 9 /L. A radiograph of her abdomen is pictured here.


Question: Which of the following is the next most appropriate management step for this patient?


A. Begin an intravenous infusion of deferoxamine
B. Administer dimercaprol (BAL) intramuscular
C. Infuse calcium disodium ethylenediaminetetraacetate (EDTA)
D. Administer succimer (DMSA) orally
E. Administer d-penicillamine orally

Answer: A
Diagnosis: Iron toxicity
Discussion: Acute iron toxicity occurs from the ingestion of iron supplements. The total elemental iron ingested is dependent upon the type of preparation. Common formulations include ferrous gluconate (containing 12% of elemental iron), ferrous sulfate (20%), and ferrous fumarate
(33%). Studies have shown that most iron poisonings are unintentional due to accidental ingestion of prenatal vitamins, which have a high content of iron about 60 – 65 mg elemental iron (multivitamins usually containing about 15 – 18 mg). Intentional ingestions are most commonly seen in females in their teens and twenties. Mortality from intentional ingestions has been reported to be as high as 10%.
Iron toxicity is dose - dependent. Toxic effects (gastrointestinal symptoms) generally occur at greater than 20 mg/ kg elemental iron. Severe toxicity (shock) generally occurs at doses higher than 60 mg/kg. The primary mechanism of injury is free radical production and lipid peroxidation.


Five classic clinical phases have been described: 
• Phase 1 (30 minutes – 6 hours): Gastrointestinal distress predominates initially due to the direct corrosive effects of the iron. Symptoms include abdominal pain, diarrhea, and emesis. In severe cases, hypovolemic shock may occur, resulting in death. In most individuals with mild - to - moderate toxicity, gastrointestinal  symptoms will resolve within a few hours and will not progress from this phase.

• Phase 2 (6 – 24 hours): A “ latent ” phase may be seen, where gastrointestinal symptoms subside but end - organ toxicity continues. This phase might be absent in patients with severe toxicity. Care should be taken to continuously re - evaluate the patient to determine whether he or she is progressing to the next phase or whether the toxicity has truly resolved.

• Phase 3 (6 – 72 hours): Multisystem organ failure ensues.  Symptoms include hypotension, cardiotoxicity, oliguria,  anuria, coagulopathy, lethargy, seizures, shock, coma, and possibly death.
• Phase 4 (1 – 4 days): Fulminant liver failure may develop. Liver failure is the second most common cause of death.
• Phase 5 (2 – 8 weeks): Initial gastrointestinal corrosive injury obstruction occurs at different levels from luminal scarring.

Evaluation includes a thorough history and physical examination. An iron level should be obtained and a repeat level drawn to assure that iron levels are not increasing. Peak iron concentrations usually occurs 4 – 6 hours after overdose. Serum iron levels over 500 ì g/dL are commonly associated with systemic toxicity. Total iron - binding capacity is unreliable and should not be used to estimate free iron levels. Patient can have an anion gap metabolic acidosis. The iron tablets may be seen on
abdominal X - rays (Figure ).
radioopacity arrow dissolved iron tab in stomach


 A negative X - ray is does not rule out iron ingestion (children ’ s chewable multivitamin products are not radio - opaque). There is limited utility of gastrointestinal decontamination following iron overdose. Ipecac and gastric lavage are generally not recommended. Activated charcoal does not adsorb iron and should not be administered. Whole - bowel irrigation may be useful, especially if tablets are visible on X - ray or levels are rising. Adequate fluid resuscitation and supportive care are the primary initial interventions.



Deferoxamine is the antidote of choice as it chelates free iron and increases its excretion. Indications include signifi cant clinical signs of toxicity (e.g., protracted vomiting or diarrhea), metabolic acidosis, shock, serum iron levels greater than 500 ì g/dL and/or an X - ray positive for multiple pills.

 Deferoxamine infusions are given intravenously at a starting rate of 15 mg/kg per hour and continued for 6 hours. The patient should then be re - evaluated. Deferoxamine - induced hypotension may occur at fast rates due to histamine release, and adequate hydration should be assured before initiation of the infusion.

As iron is chelated and excreted, the urine will develop a characteristic rusty - red ( “ vin rose ” ) appearance (Figure ).
“vin rose” urine Chelated with deferoxamine

Wednesday, April 15, 2015

2-day history of dysuria

A 20-year-old female patient presents with a 2-day history of dysuria, lower abdominal pain and low-grade fever. Her urine is cloudy with pyuria and abundant grampositive bacteria.

She is a college student who is sexually active with no previous history of sexually transmitted diseases.


lower abdominal pain 
Which organism is most likely responsible for this
woman’s symptoms?
a. Enterococcus faecalis
b. Escherichia coli
c. Neisseria gonorrhoeae

d. Staphylococcus saprophyticus

e. Candida albicans

The answer is d. T he patient’s urinary tract infection (UT I) is caused by gram-positive bacteria. T his excludes E coli and N gonorrhoeae, both of which are gram-negative, and C albicans, which is a yeast. Enterococcus faecalis and S saprophyticus are gram-positive bacteria that can cause UT I, but the second agent is a more likely cause of UT I in young women. Staphylococcus saprophyticus colonizes the rectum or the urogenital tract of approximately 5% to 10% of women and is second only to E coli as the causative agent of uncomplicated urinary tract infections in young sexually active women. Such infections are successfully treated with fluoroquinolones or trimethoprim-sulfamethoxazole.

Tuesday, April 14, 2015

Intense Pain Following High-pressure Injection Injury

Intense Pain Following High-pressure Injection Injury


Case presentation: A 30-year-old automobile technician presents to the emergency department with a complaint  of pain and swelling in the dorsum of his left hand near the metacarpophalangeal (MCP) joint of his index finger after injury with a grease injector. 

On examination, there is slight swelling of the dorsum of the hand and a small pinpoint puncture wound just proximal to the MCP joint of the index finger as noted in the picture. There is pain with passive movement and good capillary refill of
the index finger and thumb, and no neurologic deficits distal to the injury are appreciated.
Question: 

What is the most appropriate management?
A. Check tetanus status, prescribe analgesics, and discharge home
B. Prescribe antibiotics and analgesics, check tetanus status, and discharge home
C. Obtain an X-ray, check tetanus status, immobilize with a splint, and discharge home with a prescription for antibiotics and analgesics and instructions to follow-up with an orthopedist in 3–5 days
D. Provide parenteral analgesia, obtain an X-ray, check tetanus status, arrange an immediate surgical
consultation for exploration and decompression debridement, and provide prophylactic antibiotics
E. Insert a 14-gauge angiocatheter and aspirate the injected material


Answer: D
Diagnosis: High - pressure injection injury
Discussion: Injection injuries that involve the hand or upper extremity are uncommon but are very high - risk. Most are job - related. The usual mechanism is the injection of fuel oil, grease, cement, paints, or solvents into the body through high - pressure industrial equipment. 

Surgical exploration of the case described in the text.Note the marked tissue edema and damage induced.

The lower the viscosity of the injected substance, the higher  the potential for spread through soft tissue. A pressure of 100 pounds per square inch (psi) can  break the skin. It is not uncommon for airless spray - guns or fuel injectors to generate up to 3,000 – 5,000 psi. The patient who presents with this type of injury is typically a young male with an injury to the nondominant hand. The injured site commonly appears as a small puncture with some surrounding soft tissue swelling. 


Clinicians can sometimes be misled by this benign presentation, which can delay defi nitive care. Care delays can increase the chance of signifi cant functional morbidity and/or loss of limb. Emergent management should include tetanus prophylaxis, analgesia, and broad - spectrum antibiotics. A digital block should not be utilized as this may worsen vascular compromise. Radiographs of the involved areas can help determine the extent of the soft tissue spread of the injected material. Some, but not all, of the injectable materials are radio - opaque. Also, subcutaneous emphysema caused by the high - pressure injection may be appreciated on X - ray. Immediate consultation for surgical decompression (Figure ), exploration, and debridement is required to maximize recovery and functional outcome.

--DrSudeepKC

Thursday, April 9, 2015

Painless Penile Ulcer

Painless Penile Ulcer:

Case presentation: 

A 35-year-old male presents to the emergency department complaining of a “sore” that he
recently noticed on his penis. He describes the “sore” as painless and he denies any associated penile discharge.  He has never had this problem before. He is currently in a “stable” relationship with a man and recently had an HIV test that was negative. 

painless penile ulcer due to syphilis
On examination, there is a single ulcer on the distal end of the penis. The ulcer is 2 cm in diameter and has a slightly raised indurated margin with a clean base. His inguinal lymph nodes are mildly enlarged bilaterally. They feel slightly rubbery, but are discrete and nontender.
Question: What is the next most appropriate management strategy at this time?

A. Discharge the patient to home without treatment
B. Treat the patient empirically for herpes
C. Be reassured by the patient’s reported negative HIV test result and suggest no further testing for HIV in
the future
D. Treat empirically for syphilis based on the history, physical examination, and knowledge of the
 epidemiology of genital ulcers in your geographic area
E. Perform urinalysis and treat based on the results




Answer: D
Diagnosis: Chancre of primary syphilis Discussion: Genital ulcers occur in sexually active individuals
throughout the world. Physicians encountering patients with ulcers tend to rely heavily on history and
physical examinations in order to make a diagnosis, but this approach may be inappropriate. There is considerable variation and overlap in presentation, and generally additional diagnostic tests need to be performed. Also, concomitant infection with HIV can subtly alter the clinical presentation and compound the diffi culty in diagnosing  the cause of genital ulcers. Physicians need to use the  opportunity of having the patient physically present to administer appropriate therapy under the assumption
that follow-up of patients, although ideal, may not occur.

The Centers for Disease Control and Prevention (CDC) currently recommend an approach to the diagnosis and
treatment of genital ulcers that relies heavily on clinical presentation and a knowledge of local epidemiologic data on the prevalence of causes of genital ulcers in a specific geographic area.

The typical clinical presentation of syphilis is a single painless, indurated ulcer with firm, nontender
inguinal adenopathy. HSV tends to present with   multiple vesicles or a cluster of painful ulcers preceded by vesiculopustular lesions. Tender inguinal lymph nodes are commonly associated.

 Chancroid ulcers tend to be multiple, painful, and purulent, and are often associated with inguinal lymphadenopathy with fluctuance or overlying erythema. The lymphadenopathy is often unilateral and is often painful. Lymphogranuloma venereum and granuloma inguinale rarely cause genital ulcers in the United States.

Diagnostic tests should be performed whenever possible and should be directed towards ascertaining the cause of the genital ulcer, as well as screening for commonly occurring co-infections with other sexually transmitted diseases (such as Chlamydia trachomatis, Neisseria gonorrhoeae, HIV, hepatitis B, and hepatitis C).

For syphilis, options to assist in making a correct diagnosis include: serologic tests (i.e., VDRL and RPR),
dark-field microscopy, and tissue biopsy. For HSV, one can do Tzanck smears, direct fluorescence antibody tests, viral cultures, or polymerase chain reaction. In the case of Haemophilus ducreyi (chancroid), Gram stain and culture on selective media is suggested.


Treatment should ideally be directed towards the identified cause. Since diagnostic tests are often not available at the time of presentation and may not always yield a specific cause, or if patient compliance is in question, empiric therapy should be based on the clinical presentation and the epidemiology of the etiologic agents in a given area. If necessary, patients may require treatment for HSV, syphilis, and chancroid (in areas of high incidence) on the day of their initial visit. Also, all patients should be offered HIV counseling and testing on the day of presentation, and they should be counseled about safesex
practices.

Follow-up should be encouraged to discuss laboratory results, ensure treatment was appropriate, and
ascertain if healing of the ulcer has occurred. Finally, patients should be advised to encourage their partners to seek care for potential coexistent sexually transmitted disease.

Wednesday, April 8, 2015

IC

Ichthyosiform dermatoses: 

The ichthyosiform dermatoses are a heterogeneous group of disorders presenting with excessive scaling of the skin. The intherited forms of the icthyoses are most common , although the condition can occur secondary to other disease.   

The term ichthyosis is derived from the Greek root ichthy, meaning fish, indicative of the scales on the skin of affected  individuals.

How common are the congenital ichthyoses? How are they inherited?

• Ichthyosis vulgaris: Incidence of 1:250; autosomal dominant
• X-linked ichthyosis: Incidence of 1:6000; X-linked recessive
• Epidermolytic hyperkeratosis: Incidence of 1:300,000; autosomal dominant
• Congenital ichthyosiform erythroderma (CIE): Incidence of 1:100,000; autosomal recessive
• Lamellar ichthyosis: Incidence of 1:300,000; autosomal recessive
• Harlequin fetus: Rare; autosomal recessive
figure:A, Grandfather and granddaughter
with ichthyosis vulgaris. 

B, Palmar hyperkeratosis, a finding often associated with ichthyosis vulgaris. 

C, X-linked ichthyosis, showing characteristic coarse, brown scales. 


D, Young child with congenital ichthyosiform erythroderma demonstrating diffuse erythema and scale.








Ichthyosis vulgaris (Fig. A,B) usually develops around school age, and is characterized by generalized xerosis
and scale, with characteristic sparing of the flexural skin. Additional findings include follicular accentuation (keratosis pilaris), hyperlinearity of palms and soles, and a personal or family history of atopy. Rare patients may have an associated palmar-plantar keratoderma. Skin biopsy demonstrates a decreased granular cell layer associated with moderate hyperkeratosis.

X-linked ichthyosis, in contrast, is usually present by one year of age, affects the posterior neck with “dirty”- appearing scales, and spares the palms and soles (Fig.C). The skin changes—gradually worsening with age— with the neck, face, and trunk ultimately developing thick, brown scales. The disease is caused by a defect in steroid sulfatase, an enzyme important in cholesterol synthesis and vital for normal development and function of the stratum corneum. Accumulation of cholesterol sulfate and a lack of tissue cholesterol ensue, leading to a disturbance in steroid hormone metabolism. Skin biopsy of X-linked ichthyosis is rarely diagnostic, and demonstrates a normal granular layer
with hyperkeratosis.


A collodion baby is a newborn infant whose skin looks like a “baked apple,” with a shiny, tough, membrane-like covering. This term describes a phenotype that occurs in several types of ichthyosis. Although congenital ichthyosiform erythroderma is the most common underlying condition (Fig. 1D), lamellar ichthyosis, Netherton’s syndrome, Conradi’s syndrome and others may also present as a collodion baby. Collodion babies may also go on to have normal skin. These infants are at increased risk for infections and fluid and electrolyte imbalances due to cutaneous fissures and impaired barrier function of the skin. Treatment in a high-humidity environment with frequent application of
petrolatum allows gradual sloughing of the collodion membrane. Manual debridement and keratolytics are not recommended.

--DrSudeepKC

Tuesday, April 7, 2015

MC

Molluscum Contagiosum

molluscum contagiosum

DEFINITION AND CLINICAL FEATURES 
Benign papules caused by a poxvirus that present
as shiny, umbilicated, slightly translucent, pink or
skin-coloured papules. They grow slowly, usually
being less than 1 cm in diameter 
Lesions can occur at any site, usually on the head,
neck, and flexures; they are more widespread and
larger in immunosuppressed patients and those
with HIV infection. Rarely, grouped lesions can
form large plaques. The infection mainly occurs
in childhood, but may be sexually transmitted
in adults.
DIFFERENTIAL DIAGNOSIS
Solitary giant lesions can be confused with a wide
variety of lesions including keratoacanthoma,
basal cell carcinoma, and viral warts.
INVESTIGATIONS
None routinely necessary. Histology of lesions
shows diagnostic changes. Consider HIV testing
in adults with widespread infection.
TREATMENT
Treatment is usually not necessary as the infection
is usually self limiting. Troublesome lesions can
be treated by curettage, cryotherapy, or by gently
expressing or disrupting the contents.

molluscum contagiosum

Saturday, April 4, 2015

lightning strike

case :21 - year - old man was lying naked in a sleeping bag in his tent on the Lumbini  when a massive thunderstorm entered the region. He was ‘ ‘ jolted ’ ’ following a nearby lightning strike and had immediate pain in his shoulder. 


He presented to the emergency department with the skin findings noted in the photo here.


Punctate burns on the patient ’ side.


Question: What is the name of this skin finding that is pathognomonic for a lightning strike?

A. Kissing
B. Jellyfish
C. Feathering
D. Satellite
E. Treeing

Answer: C

Diagnosis: Feathering

Discussion: The case figure demonstrates a depressed, gray, punctuate wound on his shoulder corresponding with an entrance wound with surrounding feathering. Figure shows multiple discrete punctuate burns along the side of his body where he was in contact with the sleeping bag ’ s metal zipper. Figure reveals two depressed punctuate lesions on the lateral aspect of his foot and on the end of his great toe, corresponding with exit wounds (known as the “ tiptoe ” sign).
Cloud - to - ground lightning strikes occur approximately 30 million times each year.

These lightning strikes are associated with approximately 24 deaths and 98 injuries annually. The electrical current generated by a nearby lightning strike will preferentially flow through a person ’ s body rather than the ground. This is called “ step voltage. ” Two skin findings associated with lightning are present in this case. Feathering burns arepathognomonic of lightning and are not true burns but rather transient skin marks. Punctate burns are multiple, discrete circular burns that range in diameter from a few millimeters to a centimeter.

--DrSudeepKC

Thursday, April 2, 2015

image

CAPUT MEDUSAE


Fig : Caput medusae due to cirrhosis of liver

DESCRIPTION:
Dilated veins of the abdominal wall, named after the snakes that made up the hair of the goddess Medusa in Greek mythology.

CONDITION/S ASSOCIATED WITH:
Any condition causing portal hypertension, e.g.:
• Cirrhosis of the liver
• Severe heart failure
• Inferior vena cava obstruction

MECHANISM:
Portal hypertension causes backflow from the portal vein to the para-umbilical veins. The increased pressure and blood volume distend the veins.

SIGN VALUE:
Caput medusae is a sign of advanced liver disease and portal hypertension and is rare. 

Normally, only a few prominent veins may be present. To distinguish between inferior vena cava obstruction and portal hypertension with caput medusa, occlusion of the vein is required.