Causes of Hypoventilation

Hypoventilation — 

The lung alveolus is a space in which gas makes up 100 percent of the contents. This means that once the partial pressure of one gas rises, the other must decrease. Both arterial (PaCO₂) and alveolar (PACO₂) carbon dioxide tension increase during hypoventilation, which causes the alveolar oxygen tension (PAO₂) to decrease. As a result, diffusion of oxygen from the alveolus to the pulmonary capillary declines with a net effect of hypoxemia and hypercapnia. Because the respiratory quotient (Defined as CO_{2 eliminated}/O_{2 consumed}) is assumed to be 0.8, hypoventilation affects PaCO₂more than O₂.

Hypoxemia due to pure hypoventilation (ie, in the absence of an elevated A-a gradient) can be identified by two characteristics. First, it readily corrects with a small increase in the fraction of inspired oxygen (FiO₂). Second, the paCO₂ is elevated. An exception exists when the hypoventilation is prolonged because atelectasis can occur, which will increase the A-a gradient . Abnormalities that cause pure hypoventilation include:

●CNS depression, such as drug overdose, structural CNS lesions, or ischemic CNS lesions that impact the respiratory center

●Obesity hypoventilation (Pickwickian) syndrome

●Impaired neural conduction, such as amyotrophic lateral sclerosis, Guillain-Barré syndrome, high cervical spine injury, phrenic nerve paralysis, or aminoglycoside blockade

●Muscular weakness, such as myasthenia gravis, idiopathic diaphragmatic paralysis, polymyositis, muscular dystrophy, or severe hypothyroidism

●Poor chest wall elasticity, such as a flail chest or kyphoscoliosis

Bhopalwala. H

Types of Sphenoid Sinues.

Hello Guy's!

Here's a sneak peek into the world of Neurosurgery!

In cases of Pituitary Adenomas, the general surgical approach is a TransNasal TransSphenoidal Approach for the excision of the lesion.

To know the type of sphenoid sinus is an important step in the pre-operative planning for the surgery. It also helps in estimating the site where we are most likely to encounter the tumor and the pituitary gland.

Hamburger classified 3 types of pneumatization based on its relationship to the sella turcica.

1)Conchal (rudimentary or absent sphenoid sinus)

2)Presellar (a posterior sphenoid sinus wall that is separated from sella by thick bone).

3)Sellar (a posterior sphenoid sinus wall that is adjacent to sella).

That's all for now... Time to Scrub.

Let's learn Together!

~Medha Vyas.

Restrictive vs Liberal approach to transfusion in Sepsis

Hello everyone, 

Here are some studies on approach to blood transfusion during sepsis:

One multicenter randomized study of 998 patients with septic shock reported no difference in 28-day mortality between patients who were transfused when the hemoglobin was ≤7 g/dL (restrictive strategy) and patients who were transfused when the hemoglobin was ≤9 g/dL (liberal strategy) . The restrictive strategy resulted in 50 percent fewer red blood cell transfusions (1545 versus 3088 transfusions) and did not have any adverse effect on the rate of ischemic events (7 versus 8 percent).

One randomized trial initially reported a mortality benefit from a protocol that included transfusing patients to a goal hematocrit >30 (hemoglobin level 10 g/dL) . However, similarly designed studies published since then reported no benefit to this strategy. 

Bhopalwala. H

Source: UpToDate 

Norepinephrine in ICU

Norepinephrine (noradrenaline) Levophed

8 to 12 mcg/minute (0.1 to 0.15 mcg/kg/minute)

A lower initial dose of 5 mcg/minute may be used, eg, in older adults 2 to 4 mcg/minute (0.025 to 0.05 mcg/kg/minute) 35 to 100 mcg/minute (0.5 to 0.75 mcg/kg/minute; up to 3.3 mcg/kg/minute has been needed rarely)

Initial vasopressor of choice in septic, cardiogenic, and hypovolemic shock.
Wide range of doses utilized clinically.

Must be diluted; eg, a usual concentration is 4 mg in 250 mL of D5W or NS (16 micrograms/mL).

Bhopalwala. H

Milrinone in ICU

Inotrope (nonadrenergic, PDE3 inhibitor)

Milrinone Primacor

Optional loading dose: 50 mcg/kg over 10 minutes (usually not given) 0.125 to 0.75 mcg/kg/minute

Alternative for short-term cardiac output augmentation to maintain organ perfusion in cardiogenic shock refractory to other agents.

Increases cardiac contractility and modestly increases heart rate at high doses; may cause peripheral vasodilation, hypotension, and/or ventricular arrhythmia.

Renally cleared; dose adjustment in renal impairment needed.

Must be diluted; eg, a usual concentration is 40 mg in 200 mL D5W (200 micrograms/mL); use of a commercially available pre-diluted solution is preferred.

Bhopalwala. H

Dobutamine in ICU

Dobutamine Dobutrex

0.5 to 1 mcg/kg/minute

(alternatively, 2.5 mcg/kg/minute in more severe cardiac decompensation) 2 to 20 mcg/kg/minute
20 to 40 mcg/kg/minute;

Doses >20 mcg/kg/minute are not recommended in heart failure and should be reserved for salvage therapy

Initial agent of choice in cardiogenic shock with low cardiac output and maintained blood pressure.
Add-on to norepinephrine for cardiac output augmentation in septic shock with myocardial dysfunction (eg, in elevated left ventricular filling pressures and adequate MAP) or ongoing hypoperfusion despite adequate intravascular volume and use of vasopressor agents.

Increases cardiac contractility and rate; may cause hypotension and tachyarrhythmias.
Must be diluted; a usual concentration is 250 mg in 500 mL D5W or NS (0.5 mg/mL); use of a commercially available pre-diluted solution is preferred.

Bhopalwala. H

Vasopressin in ICU

Vasopressin (arginine-vasopressin) Pitressin, Vasostrict

0.03 units per minute (alternatively 0.01 to 0.03 units/minute initially) 0.03 to 0.04 units per minute (not titrated)
0.04 to 0.07 units/minute;

Doses >0.04 units/minute can cause cardiac ischemia and should be reserved for salvage therapy

Add-on to norepinephrine to raise blood pressure to target MAP or decrease norepinephrine requirement. Not recommended as a replacement for a first-line vasopressor.
Pure vasoconstrictor; may decrease stroke volume and cardiac output in myocardial dysfunction or precipitate ischemia in coronary artery disease.

Must be diluted; eg, a usual concentration is 25 units in 250 mL D5W or NS (0.1 units/mL)

Bhopalwala. H

LMR (Last minute revision) Stuff for obstetrics and gynecology drugs

Hello Awesomites!

In LMR sessions, I will share final year MBBS Viva things on drugs and specimen.You can add your list in the comments below. 
Today I will share the Obstetric and gynaecology viva on drugs. 
Lets get started.

1.Tranexamic acid and mefanemic acid combination

Tranexamic acid:

• anti-fibrinolytic
• Amino caproic acid derivative 
• CONVERTS plasmin to plasminogen
• given during menstruation
• Adverse effect:- Intracranial thrombosis

Mefanemic Acid:

• COX inhibitor.
• Given during menstruation
• Adverse effect:- dyspepsia,gastric ulcer

USE:-

• Ovulatory cycles of DUB
• Post IUCD bleeding
• Post sterilization mennorhagia
• Fibroid

2.Doxylamine and Vitamin B6 combination

Doxylamine is anti histaminics that has effects on acetylcholine and serotonin release. And you know their receptor is present on CTZ centers.
Vitamin B6 is pyridoxine.
In pregnancy and poor diet the amount decreases.

USE:- Emesis during pregnancy at bedtime (not more than 2 tablet in a day).

3.Dinoprostone gel

• Prostaglandin E2
• 500 micro gram into the cervical canal below the level of internal os
• Or 1-2 mg in the posterior fornix 
• maximum 3 doses 6 hourly
• Applied in posterior fornix when membrane is ruptured
• applied in internal os when membrane is intact
• USE- Cervical ripening in IOL.
• Before and after CTG monitoring is must.
• C/I- Previous CS, Impending scar rupture,fetal distress,asthma,severe heart disease

S/E- hyperstimulation of uterus,fetal distress

4.L-Arginine+Folic acid+isothiocyanidin

• L-Arginine is precursor for Nitric oxide generation that will lead to vasodialtion
• USE: In IUGR, Severe oligohydroamnios, preventing pre-eclampsia

5.Misoprostol

• PGE1
• ROUTE= sublingual,vaginal,rectal (never parentral)
• S/E:Fever,chills,shivering
• Teratogenic: Mobius syndrome (Category X drug)
• USES:-

1. OBSTETRIC USES:

• Termination of pregnancy
• PPH prevention and treatment.

     2.GYNECOLOGICAL USE:

• Pe hysterectomy
• IUI
• Cervical pregnancy

    3.GIT USE:

• Treatment of peptic ulcer caused by NSAIDs.

6.Frusemide:

• Loop diuretic.
• prior to blood transfusion in severe anemia
• congestive cardiac failure
• used in complications not as anti hypertensives
• PIH with massive edema

7.Clindamycin+Clotrimazole 

• USE: Mixed bacterial and fungal vaginosis 

8.Omeprazole+Ondansetron:

• USE: GERD, peptic ulcer

9.Heparin:

• Injectable Anti-coagulant
• In 1st trimester
• Antidote: Protamine sulfate
• USE: DVT, APLA, PE, recurrent abortion (Prophylaxis:ASPIRIN+HEPARIN)

10.Iron folic acid:

• Prophylactic: 100mg elemental iron+500 micro gram folic acid daily from 2nd trimester throughout pregnancy +6 month postpartum
• Treatment: Oral  iron 200 mg elemental iron daily
• Folic acid deficiency lead to abortions, abruptio, IUGR, NTD
• In folic acid deficiency dose is 4000mg

11.Anti-D Immunoglobulin:

• IgG, intramuscular
• 300 micro gram=15 ml of D positive red cell/ 30 ml of fetal whole blood 
• If ICT -VE at 28 weeks

12.Hydrocortisone:

• 2 doses 12 mg betamethasone i/m 24 hours apart
• 4 doses 6 mg dexamethasone 12 hours apart

13.Sodium Bicarbonate:

• IV for Heart resuscitation, poor kidney function, Cocaine toxicity
• Poisoning cases
• Reviving newborn
• Preventing chemotherapy side effects
• Hyperkalemia
• metabolic acidosis

14.Diazepam:

• Central Muscle relaxant and anti convulsant, Tranquilizer
• S/E:- Maternal (Hypotension) and Fetal (Respiratory depression, hypotonia)

15.Nifedipine:

• Direct arteriolar vasodilator
• Calcium channel blocker
• USE:Tocolytics
• A/E: Flushing, Hypotension, headache, Inhibition of labor

16.Labetalol:

• Anti-hypertensive
• combined alpha and beta blocker
• orally 100mg tid to 2.4 g daily
• USE: Hypertension and hypertensive crisis
• S/E:tremor, headache, CCF.
• C/I: Hepatic disorder, asthma, CCF

17.Magnesium Sulphate:

• Top 10 series by AP Burkholderia

18.Drotaverin:

• Anti-spasmodic (PDE-4 Inhibitor)
• Enhance cervical dilatation during childbirth
• USE: Acute renal colicky, augment labor.

19.Oxytocin:

20.Methergine:

21.Prostaglandins:

More is coming up !

-Upasana Y. :)

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