Classification Criteria for Adult Still Disease

●Yamaguchi criteria – The Yamaguchi criteria require the presence of five features, with at least two being major diagnostic criteria . In addition, the presence of any infection, malignancy, or other rheumatic disorder known to mimic ASD in its clinical features precludes the diagnosis of ASD, at least for the purpose of research.

The four major Yamaguchi criteria are:

•Fever of at least 39ºC (102.2ºF) lasting at least one week

•Arthralgias or arthritis lasting two weeks or longer

•A nonpruritic macular or maculopapular skin rash that is salmon-colored in appearance and usually found over the trunk or extremities during febrile episodes

•Leukocytosis (10,000/microL or greater), with at least 80 percent granulocytes

The minor Yamaguchi criteria include:

•Sore throat

•Lymphadenopathy

•Hepatomegaly or splenomegaly

•Abnormal liver function studies, particularly elevations in aspartate and alanine aminotransferase and lactate dehydrogenase concentrations

•Negative tests for antinuclear antibody (ANA) and rheumatoid factor (RF)

Bhopalwala. H

Useful Pediatrics mobile apps

Technology is a crucial part of our life nowadays. Below are some apps that can make a pediatric student/resident/specialist life easier :D

1- Uptodate

The famous app for the well-known website “ Uptodate” where you can get peer-reviewed data for nearly any subject you may think of. It also has a section for adult and pediatric medication dosing which can be helpful. Another nice section is the patient education section that is really helpful to explain complex medical things to parents in layman terms.

  

Keep in mind that you ll need an account which may be provided to your through your residency program, a friend or you yourself paying for Uptodate.

2- Medscape

The app for the amazing peer-reviewed website Medscape. Just create an account and search for any disease you like (epidemiology, incidence, clinical presentation, treatment, prognosis..etc).

3- Medstudy and Medstudy audio apps

The apps for the Medstudy book series. Listen to a medstudy chapter on your way somewhere or revise some pages through your app. These apps require an active Medstudy subscription

4- PCO / Pediatric Care Online 

A nice app by the American Academy of Pediatrics (AAP). Through this app, you get access to “Red Book”, one of the most famous books/sources for Infectious diseases and their treatments, “Bright futures” which is helpful to hone your skills in your continuity clinic among many other things.

  

To get access completely, you need an AAP account which will be provided by your residency program. 

5- Heartpedia

A great app from Cincinnati Children’s Hospital. Through this app, you can have a 3D visual construction of the most common congenital heart anomalies (ASD, VSD, PDA, COA..etc). Choose the angle you like, zoom in or out. The app also has links to youtube videos explaining the defect. This app is particularly very helpful if you are trying to explain a congenital heart defect for a parent and for further clarification to a student.   

6- CDC Vaccine Schedules (Vaccinations, catchup, contraindication)

Vaccines are a vital part of any Well Child Check visit. This app from the CDC has all the tables for Pediatrics and Adult vaccines including the catch-up schedule as well as the contraindications for these vaccines.

An amazing website to help with this is : https://www.vacscheduler.org/

Just enter the age of the patient, the vaccines that he/she got and the website will tell you what the patient needs

7- Bilicalc

For nursery folks, you should have Bilicalc on your smart-phones, it is the best app to know the lightable levels (LL) for babies. Just enter the baby’s hours of life as well as the bili result and wait for the app to tell you the LL for low, medium and high risk curves.

It does the same job that www.bilitool.org does.

 8- eBooks by inkling

This app acts like a “template” through which you can read different books. A must-to-have book is Harriet-Lane (every Pediatrician should have this book :D). To access it, use the code that is located on the first page of the book’s hardcopy. It is given by most residency programs to the residents. If not, you should consider buying it for sure.

  

9- MDcalc

Scoring systems in medicine are endless. This is the best app that can be your savior. Are you looking for: Westley’s croup scoring? Pediatric Asthma scoring? Calculating maintenance fluids for a child? Well, you just hit the jackpot.

 
10- GoodRx

Help your patients find coupons so they can buy the medications they need at a lower price.

  

11- Google keep

Although not medical but this app is wonderful to take notes and to create lists. Write all your lists in one place and use different colors. Synchronize all your notes/lists with any other device: tablet, laptop..etc. Organize your life, a much 

  

12- Anki

Another non medical app, Anki is a wonderful flashcards app. It acts like a template that you can create flashcards with or use already pre-made shared cards. Add your notes to any deck you like, synchronize between your devices and have your info with you everywhere. 

 Comment below if you have any apps or websites that may be helpful for pediatricians or anyone who is interested in Pediatrics :)

-Murad

HAP and VAP

Pneumonia types — The 2016 Infectious Diseases Society of America (IDSA)/American Thoracic Society (ATS) guidelines distinguish the following types of pneumonia :

●Hospital-acquired (or nosocomial) pneumonia (HAP) is pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admission.

●Ventilator-associated pneumonia (VAP) is a type of HAP that develops more than 48 hours after endotracheal intubation.

Bhopalwala. H

qSOFA Score for Sepsis

The qSOFA (quick Sequential Organ Failure Assessment) score is easy to calculate since it only has three components, each of which are readily identifiable at the bedside and are allocated one point:

●Respiratory rate ≥22/minute

●Altered mentation

●Systolic blood pressure ≤100 mmHg

Bhopalwala. H

Cogan's Syndrome

●Cogan's syndrome (CS) is a chronic inflammatory disorder that most commonly affects young adults. Clinical hallmarks are interstitial keratitis (IK) and vestibuloauditory dysfunction, and associations between CS and systemic vasculitis, as well as aortitis, also exist. There are a range of pathologic findings, most of which reflect immune-mediated injury of the affected tissues; however, despite an association with systemic vasculitis, eye and inner ear specimens of those with CS do not reveal any evidence of vasculitis. The underlying mechanisms responsible for the eye and inner ear disease in CS are unknown.

●The predominant ocular feature of CS is IK, which typically causes eye redness, pain, photophobia, and blurred vision. Slit-lamp examination commonly demonstrates a patchy, deep, granular corneal infiltrate. IK is not essential for the diagnosis; ocular inflammation may involve other parts of the eye and may lead to iridocyclitis, conjunctivitis, episcleritis, anterior or posterior scleritis, or retinal vasculitis.

●The inner ear manifestations of CS are Ménière-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, and caloric testing often reveals absent vestibular function. Recurrent episodes of inner ear disease frequently result in profound sensorineural hearing loss. Noninflammatory down-fluctuations in hearing may be difficult to distinguish from those of inflammatory origin. If hearing loss is associated with eye inflammation or other features of active CS or does not resolve within three to five days, an inflammatory origin is more likely.

●When present, the systemic vasculitis associated with CS is a large- or medium- to small-sized vessel vasculitis or an aortitis. The pattern of vessel involvement may be overlapping. Other systemic manifestations of CS include fever, fatigue, weight loss, lymphadenopathy, hepatomegaly, hepatitis, splenomegaly, pulmonary nodules, pericarditis, abdominal pain, arthralgia, arthritis, myalgia, and urticaria. An association with inflammatory bowel disease has also been observed.

●Evaluation of the patient with possible CS requires ophthalmologic examination to establish the presence of IK, scleritis, or episcleritis and to exclude other diseases and ocular pathology; neurologic and otologic examination to establish the presence of vestibuloauditory abnormalities; and rheumatologic examination to seek evidence of systemic vasculitis. We diagnose CS based upon the presence of characteristic inflammatory eye disease and vestibuloauditory dysfunction. The eye and inner ear are nearly equally likely to be the cause of presenting symptoms, while less than 5 percent of patients initially present with systemic manifestations

Bhopalwala. H

GPA vs MPA Flares

The distinction between GPA ( Granulomatosis with Polyangiitis) and MPA (Microscopic Polyangiitis) is important chiefly because of differential tendencies to flare. Although both diseases may flare after the achievement of remission, GPA is substantially more likely to relapse.

That's all.

Bhopalwala. H

ANCA titers and Disease flare.

Does a rise in ANCA titers predict a disease flare? — This has been a controversial area in the literature almost since ANCA were first identified in the 1980s. However, several rigorous studies have demonstrated that elevations in the titers of ANCA do not predict disease flares in a timely manner . The largest of these studies was performed on a clinical trial cohort of 180 patients (Wegener's Granulomatosis Etanercept Trial [WGET] Research Group, 2005), with serum samples drawn at three-month intervals and ANCA assays performed at the Mayo Clinic . The following findings were observed:
●Among patients who were PR3-ANCA positive compared with negative at baseline, there were no differences in the median time to relapse, disease activity score , or organ involved at relapse. Decreases in PR3-ANCA levels were not associated with a shorter time to remission, and increases were not associated with relapse.
●Relapses occurred among 46 of 101 patients (46 percent) who were mature-PR3-ANCA positive at baseline and achieved remissions of at least six months' duration. However, the proportion of patients who experienced a disease flare within one year of an elevation in ANCA titer was only 40 percent.
Other studies have come to slightly different conclusions, indicating that persistently high or rising titers of ANCA are associated with an increased risk of disease relapse . However, even in those studies, the temporal relationship between a rise in ANCA titer and the occurrence of a disease flare was poor. As an example, in a prospective study of 100 ANCA-positive patients observed over a two-year period, relapse did not occur in 43 and 29 percent of those with a rise in ANCA titers by immunofluorescence and in PR3-ANCA titers by ELISA, respectively .
In addition, a meta-analysis of 18 studies found that neither a rise in ANCA titer nor a persistently elevated ANCA titer were strong predictors of a subsequent disease flare . Therapies for relapsed ANCA-associated vasculitis (often, high doses of glucocorticoids and cytotoxic agents) carry substantial risk, including severe infections, cystitis, bladder cancer, lung fibrosis (rarely), and death. Treating all patients with increases in ANCA titers would result in unnecessary risks of toxicity in a substantial percentage of patients, nearly 30 percent in the study mentioned above. Because of these concerns, using a rise in ANCA titer as the sole parameter to justify altering immunosuppressive therapy cannot be endorsed.
A reasonable recommendation is to closely follow patients with rising ANCA titers but not to alter their therapy unless there are clear clinical signs of active disease.

Bhopalwala. H

POTS Syndrome

●The postural tachycardia syndrome (POTS) is defined as a form of orthostatic intolerance characterized by an excessive increase in heart rate that occurs on standing without arterial hypotension.

●The etiology of POTS is not clear, but the disorder may be heterogeneous. Abnormalities in autonomic regulation that may either be genetic or acquired are described. Proposed mechanisms include partial sympathetic denervation leading to discordant cardiac and vascular sympathetic control, hypovolemia and impairment of the renin-angiotensin-aldosterone system, venous abnormalities and baroreflex dysfunction.

●The clinical symptoms of POTS are varied and nonspecific, and include dizziness, lightheadedness, weakness, blurred vision, and fatigue upon standing. The orthostatic nature of the symptoms is the primary clue to the diagnosis.

●The diagnosis of POTS is established from the history and head-up tilt testing which demonstrates a heart rate increase of >30 bpm over baseline or to >120 bpm. Dehydration, prolonged bedrest, medications, and other dysautonomias should be excluded as etiologies.

●The optimal therapy of POTS is not established. Patients should avoid precipitating factors, and physical activity should be encouraged. We suggest volume repletion and fludrocortisone (0.05 to 0.2 mg per day) as the first line of therapy . Some patients may benefit from midodrine or beta blocking agents. Other therapies remain under investigation, and further confirmation of benefit is needed before they can be recommended.

Bhopalwala. H

Classification of Cryoglobulinemia

●The Brouet classification criteria is the most commonly used system that classifies cryoglobulinemia into three different subgroups based on their Ig composition. These classification criteria are also useful in that the subgroups partly correlate with pathogenicity and clinical manifestations.

•In type I cryoglobulinemia, the cryoglobulins are monoclonal Ig, typically IgG or IgM, and less commonly IgA or free Ig light chains. Type I cryoglobulinemia develops in the setting of protein-secreting monoclonal gammopathies such as a monoclonal gammopathy of undetermined significance (MGUS) or a B-cell lineage malignancy (eg, multiple myeloma, Waldenström macroglobulinemia, or chronic lymphocytic leukemia).

•In type II cryoglobulinemia, the cryoglobulins are composed of a mixture of a monoclonal IgM (or IgG or IgA) with rheumatoid factor (RF) activity and polyclonal Ig. Type II cryoglobulins are often associated with persistent viral infections, particularly hepatitis C virus (HCV) infection, and are associated with the mixed cryoglobulinemia syndrome. Other clinical associations with type II cryoglobulinemia include other infections such as hepatitis B virus (HBV), HIV, autoimmune diseases (mainly systemic lupus erythematosus [SLE] and Sjögren's syndrome), and lymphoproliferative disorders.

•In type III cryoglobulinemia, the cryoglobulins are composed of a mixture of polyclonal IgG (all isotypes) and polyclonal IgM. These cases are often secondary to autoimmune disorders, but can also be associated with infections (mainly HCV).

Bhopalwala. H

Eye Findings in GCA

●Anterior ischemic optic neuropathy – At least 80 percent of cases of vision loss in patients with GCA are caused by AION . The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve.

Only about five percent of the total occurrences of AION are due to GCA, the majority being nonarteritic and secondary to atherosclerotic disease . About 40 percent of patients who suffer nonarteritic AION regain some amount of visual acuity, in contrast to visual loss due to GCA, which is more often massive and irreversible .

●Central retinal artery occlusion – CRAO is responsible for approximately 10 percent of the cases of visual loss in GCA . On the other hand, approximately two percent of older patients with CRAO have underlying GCA . Bilateral CRAOs in an older adult should prompt evaluation for GCA.

●Posterior ischemic optic neuropathy – PION occurs in less than five percent of patients with GCA . It results from the interruption of blood flow to the retrobulbar portion of the optic nerve. Histopathologic examination typically reveals inflammatory occlusion of the short nutrient posterior ciliary arteries .

●Branch retinal artery occlusion – BRAO is distinctly uncommon in GCA, though it has been described.

●Cerebral ischemia — Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. The most common cause in GCA is an occipital lobe infarction resulting from a lesion in the vertebrobasilar circulation. In rare cases, bilateral occipital lobe involvement leads to bilateral homonymous field defects and to the development of cortical blindness.

Bhopalwala. H

Imaging Findings in PMR

Imaging —

As discussed above, there are characteristic features of periarticular structures (eg, bursitis and tenosynovitis) that can be seen on ultrasonography, magnetic resonance imaging (MRI), and positron emission tomography (PET) . Routine radiographs do not show abnormalities in patients with PMR.

Ultrasound (US) and MRI can demonstrate synovitis of the glenohumeral and hip joints and frequent involvement of extraarticular structures, especially the subacromial/subdeltoid bursa, long head of the biceps, and trochanteric bursa. While subdeltoid/subacromial bursitis is a characteristic imaging feature of PMR, it is not specific and is seen in patients with rheumatoid arthritis (RA) and other shoulder pathology .

Bhopalwala. H

How to Diagnose Polymyalgia Rheumatica?

General approach — There is no pathognomonic test or established diagnostic criteria for polymyalgia rheumatica (PMR). We use the presence of all of the following empirically formulated criteria for the clinical diagnosis of PMR in whom another disease to explain the findings is not present :

●Age 50 years or older at disease onset.

●Proximally and bilaterally distributed aching and morning stiffness (lasting at least 30 minutes or more) persisting for at least two weeks. The stiffness should involve at least two of the following three areas: neck or torso, shoulders or proximal regions of the arms, and hips or proximal aspects of the thighs.

●Erythrocyte sedimentation rate (ESR) ≥40 mm/hour.

●Rapid resolution of symptoms with low-dose glucocorticoids. Symptoms are generally 50 to 70 percent better within three days in patients with PMR started on prednisone at a dose of 10 to 20 mg/day, and almost all patients respond completely within three weeks of beginning treatment. The lack of response to initial therapy strongly suggests an alternative diagnosis. Symptomatic improvement with low-dose glucocorticoid treatment can also be seen in patients with rheumatoid disease, psoriatic arthritis, and other inflammatory arthritides.

Bhopalwala. H

Adalimumab (Humira)

Use

Ankylosing spondylitis: Treatment (to reduce signs/symptoms) of active ankylosing spondylitis in adults

Crohn disease: Treatment (to reduce signs/symptoms and to induce and maintain clinical remission) of active Crohn disease (moderate to severe) in adults and pediatric patients ≥6 years of age (Humira only) with an inadequate response to conventional therapy or who have lost response to or are intolerant to infliximab.

Hidradenitis suppurativa (Humira only): Treatment of moderate to severe hidradenitis suppurativa in adults and children ≥12 years of age

Juvenile idiopathic arthritis: Treatment (to reduce signs/symptoms) of active polyarticular juvenile idiopathic arthritis (moderate to severe) in pediatric patients ≥2 years of age (Humira) or ≥4 years of age (Amjevita; Cyltezo); may be used alone or in combination with methotrexate

Plaque psoriasis: Treatment of chronic plaque psoriasis (moderate to severe) in adults who are candidates for systemic therapy or phototherapy, and when other systemic therapies are less appropriate (with close monitoring and regular follow-up)

Psoriatic arthritis: Treatment (to reduce signs/symptoms, inhibit progression of structural damage, and improve physical function) of active psoriatic arthritis in adults; may be used alone or in combination with nonbiologic disease-modifying antirheumatic drugs (DMARDs)

Rheumatoid arthritis: Treatment (to reduce signs/symptoms, induce major clinical response, inhibit progression of structural damage, and improve physical function) of active rheumatoid arthritis (moderate to severe) in adults; may be used alone or in combination with methotrexate or other nonbiologic DMARDs

Ulcerative colitis: Treatment (to induce and sustain clinical remission) of active ulcerative colitis (moderate to severe) in adults who have had an inadequate response to immunosuppressants such as corticosteroids, azathioprine, or 6-mercaptopurine. (Note: Efficacy in patients that are intolerant to or no longer responsive to other TNF blockers has not been established.)

Uveitis (Humira only): Treatment of non-infectious intermediate, posterior, and panuveitis in adults and children ≥2 years of age

Mechanism of Action

Adalimumab is a recombinant monoclonal antibody that binds to human tumor necrosis factor alpha (TNF-alpha), thereby interfering with binding to TNFα receptor sites and subsequent cytokine-driven inflammatory processes. Elevated TNF levels in the synovial fluid are involved in the pathologic pain and joint destruction in immune-mediated arthritis. Adalimumab decreases signs and symptoms of psoriatic arthritis, rheumatoid arthritis, and ankylosing spondylitis. It inhibits progression of structural damage of rheumatoid and psoriatic arthritis. Reduces signs and symptoms and maintains clinical remission in Crohn disease and ulcerative colitis; reduces epidermal thickness and inflammatory cell infiltration in plaque psoriasis.

Bhopalwala. H

Detection of Cryoglobulins

Detection of cryoglobulins — To detect cryoglobulin, 10 to 20 mL of blood are drawn into syringes and/or collection tubes that have been prewarmed to 37ºC without anticoagulants. These precautions are required because failure to prewarm may lead to false-negative results, due to loss of the cryoglobulin in the clotted blood (eg, if there is cooling below 37°C during collection, clotting, or centrifugation) and because the presence of anticoagulants may produce false-positive results due to the formation of cryofibrinogen or heparin-precipitable complexes.

After clotting at 37°C for one-half to one hour, the serum is separated by centrifugation at 37°C, placed in a graduated (Wintrobe) tube, and refrigerated (4°C) to allow the precipitation of cryoglobulin. In type I cryoglobulinemia, precipitates are often seen within 24 hours (sometimes in less than 90 minutes). However, three to five days are usually allowed for complete precipitation, especially for the mixed cryoglobulins, and some type II and type III cryoglobulins require up to seven days for precipitation . Most laboratories will determine a cryocrit, which is a measure of the packed (centrifuged) volume of the precipitate as a percentage of the original serum volume at 4°C.

Further confidence that the precipitate is a true cryoglobulin is obtained by washing the precipitate three to six times in cold saline solution to reduce the possibility of precipitated salts or other proteins. In addition, the precipitate can then be redissolved in saline at 37°C to confirm the warm solubility of the cryoglobulins. At this time, cryoglobulin protein concentration can be determined by spectrophotometry. Further characterization can be accomplished by immunofixation, enzyme-linked immunosorbent assay (ELISA), or another specific immunologic assay.

Some laboratories perform further testing consisting of a measurement of absolute cryoglobulin concentration, along with a description of the components of the immune complexes, including mono- or polyclonality of IgM, IgG, IgA, IgE, kappa, and/or lambda light chains. In type II cryoglobulinemia, the monoclonal component is typically IgM kappa with rheumatoid factor (RF) activity.

The cryocrit in individuals without cryoglobulinemia is close to zero; generally, a cryocrit over 0.5 to 1 percent or cryoglobulin concentration over 50 mcg/mL is considered clinically significant . The cryocrit in affected patients may approach 50 percent or may encompass the entire serum volume in type I cryoglobulinemia under conditions in which the monoclonal protein forms a gel.

The cryocrit is generally between 2 and 7 percent in type II and between 1 and 3 percent in type III disease, but there is a poor correlation between the cryocrit and clinical symptoms and features.

When cryoglobulinemia is suspected clinically, a negative result from routine laboratory testing for cryoglobulins does not exclude cryoglobulin-mediated disease . The clinician may need to draw a new specimen after consulting with the laboratory staff or clinical pathologist to assure that procedures are in place for the appropriate handling of the patient's blood when the sample is obtained and transported and to be certain that the laboratory has the necessary equipment (particularly a temperature-controlled centrifuge) to prevent premature cooling of the sample.

Bhopalwala. H

Vision Loss in Giant Cell Arteritis

Causes of vision loss —

Permanent loss of vision in GCA results from arteritic anterior ischemic optic neuropathy (AION), central or branch retinal arterial occlusion (CRAO/BRAO), posterior ischemic optic neuropathy (PION), or, rarely, cerebral ischemia

●Anterior ischemic optic neuropathy – At least 80 percent of cases of vision loss in patients with GCA are caused by AION . The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve.

Only about five percent of the total occurrences of AION are due to GCA, the majority being nonarteritic and secondary to atherosclerotic disease . About 40 percent of patients who suffer nonarteritic AION regain some amount of visual acuity, in contrast to visual loss due to GCA, which is more often massive and irreversible .

●Central retinal artery occlusion – CRAO is responsible for approximately 10 percent of the cases of visual loss in GCA . On the other hand, approximately two percent of older patients with CRAO have underlying GCA . Bilateral CRAOs in an older adult should prompt evaluation for GCA.

●Posterior ischemic optic neuropathy – PION occurs in less than five percent of patients with GCA . It results from the interruption of blood flow to the retrobulbar portion of the optic nerve. Histopathologic examination typically reveals inflammatory occlusion of the short nutrient posterior ciliary arteries .

●Branch retinal artery occlusion – BRAO is distinctly uncommon in GCA, though it has been described.

●Cerebral ischemia — Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. The most common cause in GCA is an occipital lobe infarction resulting from a lesion in the vertebrobasilar circulation. In rare cases, bilateral occipital lobe involvement leads to bilateral homonymous field defects and to the development of cortical blindness.

Bhopalwala. H

Low Alkaline Phosphatase

Subnormal values — Extremely low serum alkaline phosphatase concentrations can be seen in patients with fulminant Wilson disease complicated by hemolysis .
Low values can also occur in patients with hypothyroidism, pernicious anemia, zinc deficiency, congenital hypophosphatemia, and certain types of progressive familial intrahepatic cholestasis in children.

Bhopalwala. H

Old Classification Criteria for Fibromyalgia

The final 1990 ACR FM classification criteria included:

●Symptoms of widespread pain, occurring both above and below the waist and affecting both the right and left sides of the body

●Physical findings of at least 11 of 18 defined tender points

These simple criteria had greater than 85 percent sensitivity and specificity for differentiating patients with FM from those with other rheumatic diseases.

In office practice, the diagnosis of FM can be made even if fewer than 11 of 18 tender points are present, provided that the history is consistent with FM and that the major differential diagnoses have been excluded . The tender points represent heightened pain perception rather than sites of inflammation or tissue pathology. Thus, they are proxies for detecting widespread pain, and the exact number necessary to diagnose FM clinically is somewhat arbitrary. It is important to recognize that the classification criteria were validated for large patient populations and should be used primarily in clinical research and epidemiologic studies of FM

Bhopalwala. H

Beighton Score for Joint Hypermobility

Beighton score for joint hypermobility —

JHM should be evaluated in all patients suspected of JHS. JHM is ascertained by determination of their Beighton score, which depends on the presence of JHM in the hands, elbows, lumbar spine, and knees using specific examination techniques . One point is awarded for the ability to perform each of nine maneuvers (including four maneuvers tested bilaterally and evaluation of the spine). A score of 4 or more points represents generalized hypermobility. The specific maneuvers include:

●Passive apposition of the thumb to the volar aspect of the ipsilateral forearm

●Passive hyperextension of fingers, demonstrated by passive dorsiflexion of the fifth metacarpophalangeal joint to at least 90 degrees

●Hyperextension of the elbow to at least 10 degrees

●Hyperextension of the knee to at least 10 degrees

●Flexion of the spine with placement of the palms flat on the floor without bending the knees

The presence of JHM can be documented by an examination limited to those areas required for calculating the Beighton score, but an examination for JHM and joint stability that is adequate for fuller assessment of the patient and the formulation of treatment plans should also encompass the other joints, including the temporomandibular joints, shoulders, hips, cervical and thoracic spine, ankles, and feet.

In addition to determination of the Beighton score based upon the examination, the presence of generalized JHM, including its presence historically, may also be suspected in patients who answer ‘yes’ to two or more questions in a simple five-part questionnaire :

●Can you now (or could you ever) place your hands flat on the floor without bending your knees?

●Can you now (or could you ever) bend your thumb to touch your forearm?

●As a child did you amuse your friends by contorting your body into strange shapes OR could you do splits?

●As a child or teenager did your shoulder or kneecap dislocate on more than one occasion?

●Do you consider yourself double-jointed?

Bhopalwala. H

Standing up & speaking out - 2

Hello people

I am glad for your support. In reality when I first chose to speak up about it , I knew none would support me, I mean why would they.
They all had nothing to gain, but a lot to loose.

I have been with my guide for a long time , there were instances which would seem impossible, I mean how can one do this?
How can someone stoop this low ?

We students were in-charge of her ot slippers. Sketchers worth 2k. As soon as the operation theatre ended we had to keep track of getting it washed and keeping it in her locker.
The ambulance was her personal vehicle, ANC and paediatric patients were made to wait for hours, while the ambulance was used to get her tiffin, drop her students at school.

Whenever she had interviews, we were asked to wear new coats and wait outside her office, and come in one by one , while the camera was rolling and ask her questions and doubts.

The operatives where we would put our hand and leg on the weighing scale to increase the weight of the tumour.

None of this can be proved but it all happened.
Her students passed out years before all have gone through this.
We were like her jewellery to make her look pretty in public , and we were thrown away and stepped on in private.

But I can't take it anymore, and I feel anger and despair that how did I even allow her to treat me like this.
This is a shout out to all those times

Simpson's Grading for Brain Tumors.

Hello Everyone!

So my Neurosurgery residency diaries continue and I continue sharing as I learn.

Learnt about the Grades of Tumor resection while operating on a Glioma.

These are Simpsons Grades of Tumor resection and are correlated as the degree of surgical resection completeness with with symptomatic recurrence. 

Grade I-complete removal including resection of underlying bone and associated dura.

9% symptomatic recurrence at 10 years

Grade II-complete removal and coagulation of dural attachment.

19% symptomatic recurrence at 10 years

Grade III-complete removal without resection of dura or coagulation.

29% symptomatic recurrence at 10 years

Grade IV-subtotal resection of the tumor.

44% symptomatic recurrence at 10 years

Grade V-simple decompression with or without biopsy

100% symptomatic recurrence at 10 years.

That was it!

Let's Learn Together!

-Medha Vyas 

Difference Between Solitary and Singular Brain Metastasis.

Hello Guys!

So we were operating on a metastatic brain lesion the other day when My Consultant happened to ask me the question-  " What is the difference between Solitary and Singular Brain Metastasis?" Well I happened to have a vague idea and managed to blabber something, the actual definition goes as-

• A solitary brain metastasis is defined as the only known metastasis of a tumour in the whole body which happens to be
localised in the central nervous system.

• A singular brain metastasis is defined as a single cerebral metastasis with additional metastases in other organ systems.

Well it's a small nugget, may save you some embarrassing moments.

Let's Learn Together!
-Medha Vyas.