Exploding head syndrome is a condition that causes the sufferer occasionally to experience a tremendously loud noise as originating from within his or her own head, usually described as the sound of an explosion, roar, waves crashing against rocks, loud voices or screams, a ringing noise, or the sound of electrical arcing (buzzing).
This noise usually occurs within an hour or two of falling asleep, but is not necessarily the result of a dream and can happen while awake as well.While the sound is perceived as extremely loud, it is usually not accompanied by pain. Attacks appear to change in number over time, with several attacks occurring in a space of days or weeks followed by months of remission. Sufferers often feel a sense of fear and anxiety after an attack, accompanied by elevated heart rate. Attacks are also often accompanied by perceived flashes of light (when perceived on their own, known as a "visual sleep start") or difficulty in breathing. The condition is also known as "auditory sleep starts". It is not thought to be dangerous, although it is sometimes distressing to experience. Sufferers may experience an inability to vocalize any sound, or mild forms of sleep paralysis during an attack.
Reference to the condition was made in an episode of the ITV drama Doc Martin, which was instrumental in many sufferers becoming aware that the problem was in fact a known medical condition, and not one to be concerned about.
Causes
The cause of the exploding head syndrome (EHS) is not known, though some physicians have reported a correlation with stress or extreme fatigue. The condition may develop at any time during life and women suffer from it slightly more often than men.[citation needed] Attacks can be one-time events, or can recur.
The mechanism is also not known, though possibilities have been suggested; one is that it may be the result of a sudden movement of a middle ear component or of the eustachian tube, another is that it may be the result of a form of minor seizure in the temporal lobe where the nerve cells for hearing are located.[citation needed] Electroencephalograms recorded during actual attacks show unusual activity only in some sufferers, and have ruled out epileptic seizures as a cause.[2] But an attack must happen during an episode. If results are normal during the test, only then can epilepsy be completely ruled out.
SSRI withdrawals have also been known to cause similar phenomena (i.e. brain zaps).
People that believe in the "Out of the Body experience"(O.O.B.E.), have stated that this is a result of returning back to the body too quickly while in an O.O.B.E. state. Supposedly, you can be in this state without an awareness of it, believing it only to be a dream.
Symptoms
Exploding head syndrome is a condition that causes the sufferer to occasionally experience a tremendously loud noise as originating from within his or her own head, usually described as the sound of an explosion, gunshot, door slamming, roar, waves crashing against rocks, loud voices, a ringing noise, or the sound of an electrical short circuit (buzzing). In some cases an instant flash of what is perceived as video "static" is reported.
This syndrome can also cause the sufferer to feel an extreme rush or adrenaline kick going through his or her head, sometimes multiple times. In most cases, it occurs when they are in a state between asleep and awake. Some sufferers report familiarization with the subsequent fear or panic element such that they no longer consciously experience it.
In some cases repeated attacks lead to the sufferer gaining a fear of sleeping or resting, as this is the most common time for attacks to take place, and this can lead to the development of sleeping disorders such as insomnia.
Treatment
Symptoms may be resolved spontaneously over time. It may be helpful to reassure the patient that this symptom is harmless. Clomipramine has been used in three patients, who experienced immediate relief from this condition
Friday, June 25, 2010
Foreign Accent Syndrome
Foreign Accent Syndrome
Foreign accent syndrome (FAS) is a speech disorder that causes sudden changes in speech pattern, intonation and pronunciation so that the victim is perceived to speak with a "foreign" accent. FAS usually results from severe trauma to the brain, such as a stroke or head injury, and typically develops within one or two years of the injury
Foreign accent syndrome is a rare medical condition involving speech production that usually occurs as a side effect of severe brain injury, such as a stroke or head trauma. Two cases have been reported of individuals with the condition as a development problem [1] and one associated with severe migraine. [2] Between 1941 and 2009 there have been sixty recorded cases.[1] Its symptoms result from distorted articulatory planning and coordination processes. It must be emphasized that the speaker does not suddenly gain a foreign language (vocabulary, syntax, grammar, etc); they merely pronounce their native language with a foreign or dialectical accent. Despite a recent unconfirmed news report that a Croatian speaker has gained the ability to speak fluent German after emergence from a coma[3], there has been no verified case where a patient's foreign language skills have improved after a brain injury.
Description
To the untrained ear, those with the syndrome sound as though they speak their native languages with a foreign accent; for example, an American native speaker of English might sound as though they speak with a south-eastern English accent, or a native British speaker might speak with a New York American accent. However, researchers at Oxford University have found that certain, specific parts of the brain were injured in some foreign-accent syndrome cases, indicating that certain parts of the brain control various linguistic functions, and damage could result in altered pitch or mispronounced syllables, causing speech patterns to be distorted in a non-specific manner. More recently, there is mounting evidence that the cerebellum, which controls motor function, may be crucially involved in some cases of foreign accent syndrome, reinforcing the notion that speech pattern alteration is mechanical, and thus non-specific.[4][5] Thus, the perception of a foreign accent is likely a case of pareidolia on the part of the listener.
For example, damage to the brain might result in difficulty pronouncing the letter 'r' at the end of words, forcing a rhotic speaker to use a non-rhotic accent, even if they have never spoken with one. In the U.S., non-rhoticity is a particularly notable feature of a Boston accent, thus the person might seem to speak with a Boston accent to the casual listener. However, many of the other features of a Boston accent may be wholly missing.
Some have suggested that in order to maintain a sense of normality and flow, someone with the syndrome then augments the accent effect by imitating the rest of the accent. Depending on how important a certain phoneme is to a person's original accent, they might find speaking in a different accent to be much easier and their usual accent very difficult to consistently pronounce after some motor skills have been lost.
Foreign accent syndrome (FAS) is a speech disorder that causes sudden changes in speech pattern, intonation and pronunciation so that the victim is perceived to speak with a "foreign" accent. FAS usually results from severe trauma to the brain, such as a stroke or head injury, and typically develops within one or two years of the injury
Foreign accent syndrome is a rare medical condition involving speech production that usually occurs as a side effect of severe brain injury, such as a stroke or head trauma. Two cases have been reported of individuals with the condition as a development problem [1] and one associated with severe migraine. [2] Between 1941 and 2009 there have been sixty recorded cases.[1] Its symptoms result from distorted articulatory planning and coordination processes. It must be emphasized that the speaker does not suddenly gain a foreign language (vocabulary, syntax, grammar, etc); they merely pronounce their native language with a foreign or dialectical accent. Despite a recent unconfirmed news report that a Croatian speaker has gained the ability to speak fluent German after emergence from a coma[3], there has been no verified case where a patient's foreign language skills have improved after a brain injury.
Description
To the untrained ear, those with the syndrome sound as though they speak their native languages with a foreign accent; for example, an American native speaker of English might sound as though they speak with a south-eastern English accent, or a native British speaker might speak with a New York American accent. However, researchers at Oxford University have found that certain, specific parts of the brain were injured in some foreign-accent syndrome cases, indicating that certain parts of the brain control various linguistic functions, and damage could result in altered pitch or mispronounced syllables, causing speech patterns to be distorted in a non-specific manner. More recently, there is mounting evidence that the cerebellum, which controls motor function, may be crucially involved in some cases of foreign accent syndrome, reinforcing the notion that speech pattern alteration is mechanical, and thus non-specific.[4][5] Thus, the perception of a foreign accent is likely a case of pareidolia on the part of the listener.
For example, damage to the brain might result in difficulty pronouncing the letter 'r' at the end of words, forcing a rhotic speaker to use a non-rhotic accent, even if they have never spoken with one. In the U.S., non-rhoticity is a particularly notable feature of a Boston accent, thus the person might seem to speak with a Boston accent to the casual listener. However, many of the other features of a Boston accent may be wholly missing.
Some have suggested that in order to maintain a sense of normality and flow, someone with the syndrome then augments the accent effect by imitating the rest of the accent. Depending on how important a certain phoneme is to a person's original accent, they might find speaking in a different accent to be much easier and their usual accent very difficult to consistently pronounce after some motor skills have been lost.
Thursday, June 17, 2010
Radiological features of acquired valvular diseases
Mitral Stenosis
Stenosis of the mitral valve causes resistance to the flow of blood from the LA to LV. The LA dilates. Blood will then accumulate in the lungs causing pulmonary congestion. The pulmonary vessel will then respond to long standing congestion by arteriolar vasoconstriction. This will cause rise in pulmonary artery pressure (pulmonary hypertension) and will partly relieve pulmonary congestion. Pulmonary hypertension may – if severe – cause severe right ventricular, hypertrophy, dilatation and failure, and right atrial dilatation and may end in congestive heart failure
X-ray Picture
Mild stenosis of the mitral valve causes dilatation of the left atrial appendage and straightening and mitralization of the left border of the heart.
As the stenosis becomes more severe pulmonary congestion will start to appear and left atrial dilatation will progress until the right border of the left atrium extends beyond the right border of the heart. However, extreme left atrial enlargement is rarely seen except if there is associated mitral regurgitation. Severe cases will show Kerley A lines in the lungs which are straight, dense lines up to 4 cm in length running toward the hilum. Kerley’s B lines are also seen as dense short horizontal lines most commonly present in the costophrenic angles and are caused by edema and thickening of interlobular septa
The pulmonary hypertension will then set in causing severe dilatation of the main pulmonary artery and its branches. The left border of the heart will show small aortic knob due to reduced cardiac output followed by a convexity representing the enlarged pulmonary artery then another convexity due to the dilatation of left atrial appendage followed by the cardiac apex which may be displaced outwards by right ventricular enlargement
Mild mitral stenosis
Moderately severe mitral stenosis causing left atrial enlargement
Stenosis of the mitral valve causes resistance to the flow of blood from the LA to LV. The LA dilates. Blood will then accumulate in the lungs causing pulmonary congestion. The pulmonary vessel will then respond to long standing congestion by arteriolar vasoconstriction. This will cause rise in pulmonary artery pressure (pulmonary hypertension) and will partly relieve pulmonary congestion. Pulmonary hypertension may – if severe – cause severe right ventricular, hypertrophy, dilatation and failure, and right atrial dilatation and may end in congestive heart failure
X-ray Picture
Mild stenosis of the mitral valve causes dilatation of the left atrial appendage and straightening and mitralization of the left border of the heart.
As the stenosis becomes more severe pulmonary congestion will start to appear and left atrial dilatation will progress until the right border of the left atrium extends beyond the right border of the heart. However, extreme left atrial enlargement is rarely seen except if there is associated mitral regurgitation. Severe cases will show Kerley A lines in the lungs which are straight, dense lines up to 4 cm in length running toward the hilum. Kerley’s B lines are also seen as dense short horizontal lines most commonly present in the costophrenic angles and are caused by edema and thickening of interlobular septa
The pulmonary hypertension will then set in causing severe dilatation of the main pulmonary artery and its branches. The left border of the heart will show small aortic knob due to reduced cardiac output followed by a convexity representing the enlarged pulmonary artery then another convexity due to the dilatation of left atrial appendage followed by the cardiac apex which may be displaced outwards by right ventricular enlargement
Mild mitral stenosis
Moderately severe mitral stenosis causing left atrial enlargement
Tuesday, June 15, 2010
Rett Syndrome (It’s Not Just for Girl’s Anymore)
Rett Syndrome
Clinical Characteristics
Developmental regression
Progressive microcephaly
Stereotyped hand movements
Seizures
Characteristics
Disordered breathing
Ataxia
Scoliosis
Time course progression
Stage I
Age 6-18 months
Minor delays
Postural reflexes delayed
‘Bottom shuffling’ common
Often normal
Stage II
Age 1-2yr
Regression
Personality phenotype
Difficult to control
Screaming fits
Occasional self injurious behavior
Hand movements
Wringing
Flapping
Automatisms
Disordered breathing
Hyperventilation
Apnea
Air swallowing
Stage III
Usually begins age 3-4
Regaining and improving communication
Improved behavior
Stable to slowly declining motor function
Seizures
Generalized or partial
Late stage II to early III
Sleep disturbance
Night laughter Early stage III (83%)
Night screaming fits later stage III
Bruxism
Scoliosis
Stage IV
Adult life
Progressive lower motor deterioration
Progressive severe neurogenic scoliosis
Preserved communication
Improved control of seizures
Improved behavioral phenotype
Epidemiology
1:10,000-15,000 females
Rare but present in males
Unknown atypical prevalence
Genetics
MECP2 Gene
X-Chromosome inactivation
Mosaicism
Prognosis/Life expectancy
Classic Rett Syndrome
7% survive beyond age 40
Unexplained sudden death common
Atypical Rett Syndrome
Mosaics
Clinical Implications
Genetic testing
Females (incl atypical presentations)
Males (mosaics)
Genetic couselling
Recognition of carrier state
Prenatal testing
New medication options
Buspirone for breathing abnormalities
Melatonin for sleep disturbances
L-carnitine in preserving neurologic function.
Targeting learning modalities
Music
Non-speech communication
Future
Expanded genetic testing
Recognition of more atypical presentations
Mouse model testing of therapeutics
Further understanding of gene’s regulatory role
Clinical Characteristics
Developmental regression
Progressive microcephaly
Stereotyped hand movements
Seizures
Characteristics
Disordered breathing
Ataxia
Scoliosis
Time course progression
Stage I
Age 6-18 months
Minor delays
Postural reflexes delayed
‘Bottom shuffling’ common
Often normal
Stage II
Age 1-2yr
Regression
Personality phenotype
Difficult to control
Screaming fits
Occasional self injurious behavior
Hand movements
Wringing
Flapping
Automatisms
Disordered breathing
Hyperventilation
Apnea
Air swallowing
Stage III
Usually begins age 3-4
Regaining and improving communication
Improved behavior
Stable to slowly declining motor function
Seizures
Generalized or partial
Late stage II to early III
Sleep disturbance
Night laughter Early stage III (83%)
Night screaming fits later stage III
Bruxism
Scoliosis
Stage IV
Adult life
Progressive lower motor deterioration
Progressive severe neurogenic scoliosis
Preserved communication
Improved control of seizures
Improved behavioral phenotype
Epidemiology
1:10,000-15,000 females
Rare but present in males
Unknown atypical prevalence
Genetics
MECP2 Gene
X-Chromosome inactivation
Mosaicism
Prognosis/Life expectancy
Classic Rett Syndrome
7% survive beyond age 40
Unexplained sudden death common
Atypical Rett Syndrome
Mosaics
Clinical Implications
Genetic testing
Females (incl atypical presentations)
Males (mosaics)
Genetic couselling
Recognition of carrier state
Prenatal testing
New medication options
Buspirone for breathing abnormalities
Melatonin for sleep disturbances
L-carnitine in preserving neurologic function.
Targeting learning modalities
Music
Non-speech communication
Future
Expanded genetic testing
Recognition of more atypical presentations
Mouse model testing of therapeutics
Further understanding of gene’s regulatory role
Angelman Syndrome
Angelman Syndrome
Features
Seizures
Developmental delay/MR DQ20-35
Strabismus
Sleep disturbance
Hypermotoric behavior/tremulousness
Ataxia
Excessive happiness
Constipation
Microcephaly
CAUSE
Overall cause is loss of maternally imprinted copy of genes on Chr15.
Prader-Willi is parental lost.
Causes of lost maternal imprint
Deletion on maternal chromosome 15. (70%)
Uniparenteral disomy of Chromosome 15 (2-3%)
Two copies of father’s Chr 15.
Mutation of maternal UBE3A gene. (5-7%)
Imprinting defect (3-5%)
Unknown (15%)
Management:
Seizure Management
Partial motor, often minor movements
Difficult to distinguish from tremulousness.
Often difficult to control.
Valproate and clonazepam often work best
Developmental delay
Minimum of spoken words, ~20
Begin non-verbal communication early.
Sign, difficult with ataxia
Picture boards
Ataxia
Supportive sitting
Gait training
Sleep disturbance
Create “safe sleeping” area
High rails
Cushioning
Low to floor
Medications:
Chloral
Benedryl
Melatonin 0.3mg 1hr prior to sleep
Orthopedic problems
90% of AS children learn to walk.
However, commonly have subluxed or pronated ankles or tight gastrocs.
May require bracing and alignment surgeries.
Scoliosis is common
Prognosis/Outcome
Adulthood
Improvement of hyperactivity/Sleep patterns.
Daytime continence usually achieved.
Reduced seizure activity.
May transition to group home, but not independent.
Worsening scoliosis
Improve in receptive speech and sign language.
Limited expressive speech (~20 words).
Most walk, but may need assistive devices.
Normal life span
Features
Seizures
Developmental delay/MR DQ20-35
Strabismus
Sleep disturbance
Hypermotoric behavior/tremulousness
Ataxia
Excessive happiness
Constipation
Microcephaly
CAUSE
Overall cause is loss of maternally imprinted copy of genes on Chr15.
Prader-Willi is parental lost.
Causes of lost maternal imprint
Deletion on maternal chromosome 15. (70%)
Uniparenteral disomy of Chromosome 15 (2-3%)
Two copies of father’s Chr 15.
Mutation of maternal UBE3A gene. (5-7%)
Imprinting defect (3-5%)
Unknown (15%)
Management:
Seizure Management
Partial motor, often minor movements
Difficult to distinguish from tremulousness.
Often difficult to control.
Valproate and clonazepam often work best
Developmental delay
Minimum of spoken words, ~20
Begin non-verbal communication early.
Sign, difficult with ataxia
Picture boards
Ataxia
Supportive sitting
Gait training
Sleep disturbance
Create “safe sleeping” area
High rails
Cushioning
Low to floor
Medications:
Chloral
Benedryl
Melatonin 0.3mg 1hr prior to sleep
Orthopedic problems
90% of AS children learn to walk.
However, commonly have subluxed or pronated ankles or tight gastrocs.
May require bracing and alignment surgeries.
Scoliosis is common
Prognosis/Outcome
Adulthood
Improvement of hyperactivity/Sleep patterns.
Daytime continence usually achieved.
Reduced seizure activity.
May transition to group home, but not independent.
Worsening scoliosis
Improve in receptive speech and sign language.
Limited expressive speech (~20 words).
Most walk, but may need assistive devices.
Normal life span
Monday, June 14, 2010
Pathergy Test:
Pathergy Test
The pathergy test is helpful in diagnosing Behcet's Disease although not 100% specific. It is a simple test in which the forearm is pricked with a small, sterile needle. Occurrence of a small red bump or pustule at the site of needle insertion, 1 to 2 days after the test, constitutes a positive test. Although a positive pathergy test is helpful in the diagnosis of Behçet's disease, only a minority of Behçet's patients demonstrate the pathergy phenomenon (i.e., have positive tests).
The pathergy test is helpful in diagnosing Behcet's Disease although not 100% specific. It is a simple test in which the forearm is pricked with a small, sterile needle. Occurrence of a small red bump or pustule at the site of needle insertion, 1 to 2 days after the test, constitutes a positive test. Although a positive pathergy test is helpful in the diagnosis of Behçet's disease, only a minority of Behçet's patients demonstrate the pathergy phenomenon (i.e., have positive tests).
ANTI PSEUDOMONAL DRUGS
Pseudomonal infections are treated with a combination of an antipseudomonal beta-lactam (eg, penicillin or cephalosporin) and an aminoglycoside. Carbapenems (eg, imipenem, meropenem) with antipseudomonal quinolones may be used in conjunction with an aminoglycoside. With the exception of cases involving febrile patients with neutropenia, in whom monotherapy with ceftazidime or a carbapenem (eg, imipenem, meropenem) is used, a 2-drug regimen is recommended.
Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Gentamicin
Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.
Not the DOC. Consider if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.
Dosing regimens are numerous. Adjust dose based on CrCl and changes in volume of distribution. May be administered IV/IM.
• Dosing
Adult
Serious infections and normal renal function: 3 mg/kg/d IV q8h
Loading dose: 1-2.5 mg/kg IV q8h
Maintenance dose: 1-1.5 mg/kg IV q8h
Extended-dosing regimen for life-threatening infections: 5 mg/kg/d IV/IM q6-8h
Follow each regimen by at least a trough level drawn on the third or fourth dose (0.5 h before dosing); may draw a peak level 0.5 h after 30-min infusion
Pediatric
<5 years: 2.5 mg/kg/dose IV/IM q8h
>5 years: 1.5-2.5 mg/kg/dose IV/IM q8h or 6-7.5 mg/kg/d divided q8h; not to exceed 300 mg/d; monitor as in adults
•
Ticarcillin and clavulanate
Inhibits biosynthesis of cell wall and is effective during stage of active growth. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes.
• Dosing
Adult
3.1 g IV q4-6h
Pediatric
75 mg/kg IV q6h
•
Piperacillin and tazobactam
Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall and is effective during stage of active multiplication.
• Dosing
Adult
3.375 g IV q6h
Pediatric
75 mg/kg IV q6h
•
Imipenem and cilastatin
Extremely potent broad-spectrum beta-lactam antibiotic. Rapidly hydrolyzed by enzyme dehydropeptidase I located on brush border of renal tubular cells, hence its combination with cilastatin (a reversible inhibitor of dehydropeptidase I). For treatment of multiple-organism infections in which other agents do not have wide-spectrum coverage or are contraindicated due to potential for toxicity.
• Dosing
Adult
Base initial dose on severity of infection and administer in equally divided doses
250-500 mg IV q6h; not to exceed 3-4 g/d
500-750 mg IM or intra-abdominally q12h
Pediatric
<12 years: Not established; 15-25 mg/kg/dose IV q6h suggested for > 3 mo
Fully susceptible organisms: Not to exceed 2 g/d
Moderately susceptible organisms: Not to exceed 4 g/d
•
Aztreonam
Monobactam that inhibits cell wall synthesis during bacterial growth. Active against gram-negative bacilli but very limited gram-positive activity and not useful for anaerobes. Lacks cross-sensitivity with beta-lactam antibiotics. May be used in patients allergic to penicillins or cephalosporins.
• Dosing
Adult
500-2000 mg IV/IM q8-12h
Pediatric
90-120 mg/kg/d IV/IM divided q6-8h
•
Ciprofloxacin
Exerts bactericidal effect against both actively dividing and dormant bacteria. Fluoroquinolone effective against pseudomonads, streptococci, some MRSA, Staphylococcus epidermidis, and most gram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth. Trovafloxacin (Trovan) overcomes many of these limitations but has been removed from general use. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms disappear.
• Dosing
Adult
250-750 mg PO q12h
400 mg IV q8h
Pediatric
<18 years: Not recommended
>18 years: Administer as in adults
•
Cefepime
For the treatment of Pseudomonas infections. Fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage. Cefepime is a zwitterion that rapidly penetrates gram-negative cells. Best beta-lactam for IM administration. Poor capacity to cross blood-brain barrier precludes use for treatment of meningitis.
• Dosing
Adult
1-2 g IV q12h; pseudomonal infections require higher or more frequent doses
Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: 0.5-2 g IV q12-24h
CrCl 50-10: 0.5-2 g/d IV
CrCl <10: 0.25-0.5 g/d IV
HD: as for CrCl <10, with an extra 0.25 g after HD
During peritoneal dialysis: 1-2 g IV q48h
Pediatric
50 mg/kg IV q8h; not to exceed 2 g/dose
•
Ceftazidime
Third-generation cephalosporin with high activity against Pseudomonas. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
• Dosing
Adult
1-2 g IV/IM q8-12h; not to exceed 6 g/d
Pediatric
Neonates: 30 mg/kg IV q12h
Infants and children: 30-50 mg/kg/dose IV q8h; not to exceed 6 g/d
Adolescents: Administer as in adults
•
Tobramycin
Obtained from Streptomyces tenebrarius. Two to 4 times more active against pseudomonal organisms as compared to gentamicin.
• Dosing
Adult
Endocarditis: 8 mg/kg/d IV divided q8h; alternatively, 1 mg/kg IV q8h
Pediatric
6-7.5 mg/kg/d IV divided tid/qid (2-2.5 mg/kg q8h or 1.5-1.9 mg/kg q6h)
•
Meropenem
Semisynthetic carbapenem antibiotic that inhibits bacterial cell wall synthesis.
• Dosing
Adult
1 g IV q8h
Pediatric
<10 years: Not established
>10 years: Administer as in adults
Pseudomonal infections are treated with a combination of an antipseudomonal beta-lactam (eg, penicillin or cephalosporin) and an aminoglycoside. Carbapenems (eg, imipenem, meropenem) with antipseudomonal quinolones may be used in conjunction with an aminoglycoside. With the exception of cases involving febrile patients with neutropenia, in whom monotherapy with ceftazidime or a carbapenem (eg, imipenem, meropenem) is used, a 2-drug regimen is recommended.
Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Gentamicin
Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.
Not the DOC. Consider if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.
Dosing regimens are numerous. Adjust dose based on CrCl and changes in volume of distribution. May be administered IV/IM.
• Dosing
Adult
Serious infections and normal renal function: 3 mg/kg/d IV q8h
Loading dose: 1-2.5 mg/kg IV q8h
Maintenance dose: 1-1.5 mg/kg IV q8h
Extended-dosing regimen for life-threatening infections: 5 mg/kg/d IV/IM q6-8h
Follow each regimen by at least a trough level drawn on the third or fourth dose (0.5 h before dosing); may draw a peak level 0.5 h after 30-min infusion
Pediatric
<5 years: 2.5 mg/kg/dose IV/IM q8h
>5 years: 1.5-2.5 mg/kg/dose IV/IM q8h or 6-7.5 mg/kg/d divided q8h; not to exceed 300 mg/d; monitor as in adults
•
Ticarcillin and clavulanate
Inhibits biosynthesis of cell wall and is effective during stage of active growth. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes.
• Dosing
Adult
3.1 g IV q4-6h
Pediatric
75 mg/kg IV q6h
•
Piperacillin and tazobactam
Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall and is effective during stage of active multiplication.
• Dosing
Adult
3.375 g IV q6h
Pediatric
75 mg/kg IV q6h
•
Imipenem and cilastatin
Extremely potent broad-spectrum beta-lactam antibiotic. Rapidly hydrolyzed by enzyme dehydropeptidase I located on brush border of renal tubular cells, hence its combination with cilastatin (a reversible inhibitor of dehydropeptidase I). For treatment of multiple-organism infections in which other agents do not have wide-spectrum coverage or are contraindicated due to potential for toxicity.
• Dosing
Adult
Base initial dose on severity of infection and administer in equally divided doses
250-500 mg IV q6h; not to exceed 3-4 g/d
500-750 mg IM or intra-abdominally q12h
Pediatric
<12 years: Not established; 15-25 mg/kg/dose IV q6h suggested for > 3 mo
Fully susceptible organisms: Not to exceed 2 g/d
Moderately susceptible organisms: Not to exceed 4 g/d
•
Aztreonam
Monobactam that inhibits cell wall synthesis during bacterial growth. Active against gram-negative bacilli but very limited gram-positive activity and not useful for anaerobes. Lacks cross-sensitivity with beta-lactam antibiotics. May be used in patients allergic to penicillins or cephalosporins.
• Dosing
Adult
500-2000 mg IV/IM q8-12h
Pediatric
90-120 mg/kg/d IV/IM divided q6-8h
•
Ciprofloxacin
Exerts bactericidal effect against both actively dividing and dormant bacteria. Fluoroquinolone effective against pseudomonads, streptococci, some MRSA, Staphylococcus epidermidis, and most gram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth. Trovafloxacin (Trovan) overcomes many of these limitations but has been removed from general use. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms disappear.
• Dosing
Adult
250-750 mg PO q12h
400 mg IV q8h
Pediatric
<18 years: Not recommended
>18 years: Administer as in adults
•
Cefepime
For the treatment of Pseudomonas infections. Fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage. Cefepime is a zwitterion that rapidly penetrates gram-negative cells. Best beta-lactam for IM administration. Poor capacity to cross blood-brain barrier precludes use for treatment of meningitis.
• Dosing
Adult
1-2 g IV q12h; pseudomonal infections require higher or more frequent doses
Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: 0.5-2 g IV q12-24h
CrCl 50-10: 0.5-2 g/d IV
CrCl <10: 0.25-0.5 g/d IV
HD: as for CrCl <10, with an extra 0.25 g after HD
During peritoneal dialysis: 1-2 g IV q48h
Pediatric
50 mg/kg IV q8h; not to exceed 2 g/dose
•
Ceftazidime
Third-generation cephalosporin with high activity against Pseudomonas. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
• Dosing
Adult
1-2 g IV/IM q8-12h; not to exceed 6 g/d
Pediatric
Neonates: 30 mg/kg IV q12h
Infants and children: 30-50 mg/kg/dose IV q8h; not to exceed 6 g/d
Adolescents: Administer as in adults
•
Tobramycin
Obtained from Streptomyces tenebrarius. Two to 4 times more active against pseudomonal organisms as compared to gentamicin.
• Dosing
Adult
Endocarditis: 8 mg/kg/d IV divided q8h; alternatively, 1 mg/kg IV q8h
Pediatric
6-7.5 mg/kg/d IV divided tid/qid (2-2.5 mg/kg q8h or 1.5-1.9 mg/kg q6h)
•
Meropenem
Semisynthetic carbapenem antibiotic that inhibits bacterial cell wall synthesis.
• Dosing
Adult
1 g IV q8h
Pediatric
<10 years: Not established
>10 years: Administer as in adults
Criteria's for fat embolism
Gurd’s criteria
Major criteria
Axillary or subconjunctival petechiae
Hypoxaemia PaO2 <60 mm Hg, FIO2 = 0.4
Central nervous system depression disproportionate to
hypoxaemia
Pulmonary oedema
Minor criteria
Tachycardia <110 bpm
Pyrexia <38.5°C
Emboli present in the retina on fundoscopy
Fat globules present in urine
A sudden inexplicable drop in haematocrit or platelet values
Increasing ESR
Fat globules present in the sputum
Lindeque’s criteria
Sustained Pao2 <8 kPa
Sustained PCO2 of >7.3 kPa or a pH <7.3
Sustained respiratory rate >35 breaths min-1, despite sedation
Increased work of breathing: dyspnoea, accessory muscle use,
tachycardia, and anxiety
Schonfeld’s criteria
Petechiae 5
Chest X-ray changes (diffuse alveolar infiltrates) 4
Hypoxaemia (Pao2 < 9.3 kPa) 3
Fever (>38°C) 1
Tachycardia (>120 beats min–1) 1
Tachypnoea (>30 bpm) 1
Cumulative score >5 required for diagnosis
Major criteria
Axillary or subconjunctival petechiae
Hypoxaemia PaO2 <60 mm Hg, FIO2 = 0.4
Central nervous system depression disproportionate to
hypoxaemia
Pulmonary oedema
Minor criteria
Tachycardia <110 bpm
Pyrexia <38.5°C
Emboli present in the retina on fundoscopy
Fat globules present in urine
A sudden inexplicable drop in haematocrit or platelet values
Increasing ESR
Fat globules present in the sputum
Lindeque’s criteria
Sustained Pao2 <8 kPa
Sustained PCO2 of >7.3 kPa or a pH <7.3
Sustained respiratory rate >35 breaths min-1, despite sedation
Increased work of breathing: dyspnoea, accessory muscle use,
tachycardia, and anxiety
Schonfeld’s criteria
Petechiae 5
Chest X-ray changes (diffuse alveolar infiltrates) 4
Hypoxaemia (Pao2 < 9.3 kPa) 3
Fever (>38°C) 1
Tachycardia (>120 beats min–1) 1
Tachypnoea (>30 bpm) 1
Cumulative score >5 required for diagnosis
Saturday, June 12, 2010
Retzius' space
Also known as:
Cave of Retzius
Space of Retzius
Retzius cavity
Synonyms:
Cavum retzii, spatium retropubicum, retropubic space.
The pre-vesical space or retro-pubic space. The prevesical space between the symphysis, the bladder, and the anterior abdominal. It contains loose connective tissue and fat and affords the surgeon access to the bladder without opening the peritoneal cavity.
ANGLE OF GISSANE PRESENT IN FRACTURE OF
A.Femur
B.Tibia
C.Fibula
D.Talus
ANS:TALUS
Critical angle of Gissane
*In 1947, Gissane described his critical angle or crucial angle.
*He noted a distinct angular cortical platform that parallels the lateral process of the talus on lateral radiographic projection.
*This cortical density represents the dense subchondral bone lying beneath the posterior, anterior and middle facets.
*The angular measurements vary from 130 to 145 degrees, with an average of 130 degrees.
*During an axial impaction load, the lateral process of the talus is driven through the posterior facet in a wedge like manner that facilitates the primary fracture. This extends from the lateral cortical vertex of the crucial angle and exits plantarly through the neutral triangle.
*The initial fracture, as described by Essex Lopresti, is located on the anterior distal lip of the posterior facet and connects to the primary fracture line. This fracture extends through the facet, splits it into one or multiple fragments, and impacts the lateral portions into the body.
*The crucial angle reveals the angular relationship of the calcaneal facets and should appear identical when taken bilaterally.
*Unlike Bohler’s angle, which may be aberrant with displaced extraarticular and intraarticular fractures, the crucial angle is more specific for intraarticular distortion
A.Femur
B.Tibia
C.Fibula
D.Talus
ANS:TALUS
Critical angle of Gissane
*In 1947, Gissane described his critical angle or crucial angle.
*He noted a distinct angular cortical platform that parallels the lateral process of the talus on lateral radiographic projection.
*This cortical density represents the dense subchondral bone lying beneath the posterior, anterior and middle facets.
*The angular measurements vary from 130 to 145 degrees, with an average of 130 degrees.
*During an axial impaction load, the lateral process of the talus is driven through the posterior facet in a wedge like manner that facilitates the primary fracture. This extends from the lateral cortical vertex of the crucial angle and exits plantarly through the neutral triangle.
*The initial fracture, as described by Essex Lopresti, is located on the anterior distal lip of the posterior facet and connects to the primary fracture line. This fracture extends through the facet, splits it into one or multiple fragments, and impacts the lateral portions into the body.
*The crucial angle reveals the angular relationship of the calcaneal facets and should appear identical when taken bilaterally.
*Unlike Bohler’s angle, which may be aberrant with displaced extraarticular and intraarticular fractures, the crucial angle is more specific for intraarticular distortion
March fracture usually occurs in the :
a) 1st metatarsal
b) 2nd metatarsal
c) 4th metatarsal
d) Head of talus
ANS:2ND METATARSAL
Stress fracture can occur at many sites in the body, but in particular a stress fracture occurring at metatarsal bones is called a march fracture. March fracture usually occurs in the shaft of the second or less often in the third metatarsal bone; stress fracture of the fifth metatarsal is a distinct fracture (the Jones fracture). In runners, march fracture occurs most often in the metatarsal neck, while in dancers it occurs in the proximal shaft. In ballet dancers, fracture mostly occurs at the base of the second metatarsal and at Lisfranc joints. This fracture always occurs following a prolonged stress or weight bearing, and the history of direct trauma is very rare. Consideration should always be given to osteoporosis and osteomalacia. Cavus feet are a risk factor for march fracture
a) 1st metatarsal
b) 2nd metatarsal
c) 4th metatarsal
d) Head of talus
ANS:2ND METATARSAL
Stress fracture can occur at many sites in the body, but in particular a stress fracture occurring at metatarsal bones is called a march fracture. March fracture usually occurs in the shaft of the second or less often in the third metatarsal bone; stress fracture of the fifth metatarsal is a distinct fracture (the Jones fracture). In runners, march fracture occurs most often in the metatarsal neck, while in dancers it occurs in the proximal shaft. In ballet dancers, fracture mostly occurs at the base of the second metatarsal and at Lisfranc joints. This fracture always occurs following a prolonged stress or weight bearing, and the history of direct trauma is very rare. Consideration should always be given to osteoporosis and osteomalacia. Cavus feet are a risk factor for march fracture
Friday, June 11, 2010
Intro
Hi ,i am a new one to blogging,
a doctor by profession
like to lead a peaceful life
want to spread happiness wherever i am
at least want to be good human....
i will be posting all related to life,sports,medical,current topics
pls do post ur views replies
willing to make up this blog helpful to somebody sooner then later
a doctor by profession
like to lead a peaceful life
want to spread happiness wherever i am
at least want to be good human....
i will be posting all related to life,sports,medical,current topics
pls do post ur views replies
willing to make up this blog helpful to somebody sooner then later
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