Presacral myelolipomas

Presacral myelolipomas classically occur in older patients, with a female predominance of approximately 2:1 (4). Usually, they are asymptomatic and incidentally discovered; however, they may cause symptoms from mass effect on adjacent structures, including the bladder, ureters, sacral nerve plexus, and rectum (2,4,5). They are not associated with hematologic disturbances; however, they have been associated with Cushing syndrome, Addison disease, adrenal hyperplasia, and chronic exogenous steroid use (4).

Presacral myelolipomas are typically well-encapsulated round or oval masses that can vary in size (4). (Masses up to 26 cm in diameter have been described.) They may contain varying amounts of fat and interspersed soft-tissue elements that may enhance after contrast material administration. Small areas of hemorrhage within the mass can calcify, and they can adhere to the sacrum without bone invasion (1,2,6).

The characteristic finding of a presacral myelolipoma (besides its location) is the presence of fat within the mass, which would appear lucent on conventional radiographs, hyperechoic on ultrasonographic images (7), and hypovascular on conventional angiograms (8). However, the fatty tissue within a myelolipoma can be definitively diagnosed with only CT or magnetic resonance (MR) imaging. At CT, this tissue would be of low attenuation (–20 HU), while at MR imaging, it would have increased signal intensity at T1-weighted sequences and decreased signal intensity at fat-suppressed T1-weighted sequences (Fig 2) (1,9).

It may be difficult to distinguish presacral myelolipoma from liposarcoma, teratoma, extramedullary hematopoiesis, or neurogenic tumor (1,2,5,10,11). A combination of the imaging findings and the clinical scenario might be helpful in this differentiation. The most common fat-containing retroperitoneal tumor is well-differentiated liposarcoma (5,11), which typically does not have a capsule, is poorly marginated with irregular contours, and exhibits an infiltrative growth pattern (2). Extramedullary hematopoietic tissue is usually multifocal, occurs in patients with underlying hematologic disease, and typically does not contain fat (1,10). Some neurogenic tumors—such as sacrococcygeal chordomas—typically cause aggressive bone destruction and symptoms that include pain, swelling, and neurologic defects (12), while other tumors—such as neurofibromas—slowly remodel the bone and may extend into the sacral foramina. Sacrococcygeal teratomas are classically noted at birth and can be associated with vertebral anomalies.
However, there is overlap in the appearance of these different entities; therefore, they cannot be distinguished with imaging alone. Even so, myelolipomas are histologically distinct and sometimes can be differentiated from other fat-containing lesions with needle biopsy (1,4,6,10,11). When compared with myelolipomas, liposarcomas lack areas of hemorrhage and contain lipoblasts and zones of cellular atypia (11). Neurogenic tumors contain neural elements that are not present in myelolipomas. Teratomas and mesenchymal tumors may contain hematopoietic tissue and fat (similar to myelolipomas); however, they also contain other tissue subtypes (1).

Since presacral myelolipoma is benign and does not necessarily warrant surgical resection, percutaneous biopsy can be helpful in differentiating it from other presacral masses. However, if the patient is symptomatic or if the mass cannot be definitively diagnosed at needle biopsy, surgical resection may be necessary.

This patient had classic features of presacral myelolipoma. She was an older woman who had a well-defined and encapsulated presacral soft-tissue mass that contained macroscopic fatty components. Although the mass was in direct contiguity with the sacrum, it did not destroy or invade the sacrum. Even though the mass was thought to represent a presacral myelolipoma, a liposarcoma could not be excluded on the basis of the imaging findings alone. It was believed that the mass was contributing to the patient's symptoms; therefore, percutaneous biopsy was not requested and surgical resection was performed.




Kammen BF, Elder DE, Fraker DL, Siegelman ES. Extraadrenal myelolipoma: MR imaging findings. AJR Am J Roentgenol 1998;171:721–723.[Free Full Text]

Sutker B, Balthazar EJ, Fazzini E. Presacral myelolipoma: CT findings. J Comput Assist Tomogr 1985;9:1128–1130.[Medline]

Saboorian MH, Timmerman TG, Ashfaq R, Maiese RL. Fine-needle aspiration of a presacral myelolipoma: a case presentation with flow cytometry and immunohistochemical studies. Diagn Cytopathol 1999;20:47–51.[CrossRef][Medline]

Singla AK, Kechejian G, Lopez MJ. Giant presacral myelolipoma. Am Surg 2003;69:334–338.[Medline]

Prahlow JA, Loggie BW, Cappellari JO, Scharling ES, Teot LA, Iskandar SS. Extra-adrenal myelolipoma: report of two cases. South Med J 1995;88:639–643.[CrossRef][Medline]

Rao P, Kenney PJ, Wagner BJ, Davidson AJ. Imaging and pathologic features of myelolipoma. RadioGraphics 1997;17:1373–1385.[Abstract]

Asch MR, Poon PY, McCallum RW, et al. Myelolipoma: radiologic findings in seven patients. J Can Assoc Radiol 1989;40:247–250.

Chen KT, Felix EL, Flam MS. Extraadrenal myelolipoma. Am J Clin Pathol 1982;79:386–389.

Cyran KM, Kenney PJ, Memel DS, Yacoub I. Adrenal myelolipoma. AJR Am J Roentgenol 1996;166:395–400.[Abstract/Free Full Text]

Kenney PJ, Wagner BJ, Rao P, Heffess CS. Myelolipoma: CT and pathologic features. Radiology 1998;208:87–95.[Abstract/Free Full Text]

Liang EY, Cooper JE, Lam WW, Chung SC, Allen PW, Metreweli C. Case report: myolipoma or liposarcoma—a mistaken identity in the retroperitoneum. Clin Radiol 1996;51:295–297.[CrossRef][Medline]

Wetzel LH, Levine E. MR imaging of sacral and presacral lesions. AJR Am J Roentgenol 1990;154:771–775.[Free Full Text]

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India Property Goes Bust

Fri Jun 27, 2008 9:18am CDT • The Honest Truth

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Category: Real Estate

Tags: Ajit Dayal • investing in residential real estate

By Ajit Dayal

Related Articles

In July 2006, at an Equitymaster conference, I made a prediction: Indian property prices will decline by 30% over the next 6 to 12 months. Boy was I wrong! Property prices in most Indian cities increased by 50% or so between July 2006 and December 2007.

My “prediction” was a bust! If property prices were 100 in July 2006, they had reached probably 150 in most cities. And my expectation was for a “70″. Ouch! But look around you today and the only place where Indian property is still booming is in the headlines of some newspapers and lead articles on some websites.

Developers and financiers of property projects are desperate to make us believe that property prices are still increasing. They want to hold the “price line”. If potential buyers know that the supply of property is large - and sales of apartments are slow - they will wait. They will buy later - or ask for a better price now.

Any reduction in the selling price is a loss of expected profit for the developers and their financiers. Not a good thing.

News or Olds?

We get much of our information from newspapers. Note the “new” in the word “newspapers”. And what we read shapes our opinions and, eventually, our actions. But, sometimes, the “newspaper” may be carrying “oldspaper” information that, at one level, creates a false impression in our minds. And could makes us act in an incorrect manner.

So, contrast these headlines. Business Standard, in their online version, June 23rd, 2008: writes: “Booming Indian property mkt beckons UK investors”. In this article, there are a few statements of “fact”.

Indian property prices, we read, are up some 70% in 2 years. “Merrill Lynch consultants”, according to this article, “have predicted a 700 per cent increase in the Indian property market by 2015″. Quite a clever statement - its vagueness leaves room for varied interpretation. The article does not say whether this 700 per cent increase is an increase in the amount of square feet being built, or in the prices of real estate. But something to do with real estate is increasing by 700%. The mind takes that “700%” and imagines a bull market in property.

“Realty promoters pledging shares to raise funds” warns an article in the print version of the Business Standard, dated June 19th, 2008. The article lists 10 listed real estate companies whose share prices had collapsed from their 52-week high by between and -58.2% and -78.1% as of June 18th, 2008.

The large shareholder-owners of some of these listed real estate developers have apparently been pledging shares they own to financiers in exchange for loans. With sales not as brisk as in the years 2006 and 2007, cash flows are not as per expectations. And, to add to the woes of the real estate industry, many developers had already committed to larger projects. They now need to pay for this new land and the initial cost of development to get the land into some sort of “build-able” shape.

And another screaming headline, “Cash Crunch” in the Economic Times, June 15th, 2008 states that property developers are borrowing money at interest rates ranging from 35% to 50% per annum. Their “normal” interest rates range from 18% to 24% per annum. The higher borrowing, says the article, is due to the slowdown in sales and larger commitments.

A boom is a bust.

So, what happened between the “old” news of June 18th (the date of the “Realty promoters pledging shares to raise funds” article) and the “new” news of June 23rd (the date of the Booming Indian property mkt beckons UK investors” article)?

The share prices of these realtors, I assume, have declined even further - for what that is worth. The fundamentals of the industry - slow sales and large commitments for new projects - could not have changed. As these share prices decline, the “promoters” of these companies that pledged some shares will need to give more of their shares as a pledge. Additionally, if any loan is not repaid, lenders will sell the pledged shares into the stock market - probably at any price. This could result in a decline in the share prices of the real estate companies - and create a potential downward spiral of wealth destruction for investors in shares of real estate companies.

From a “buying-power” perspective, the news on inflation is worse than expected, so interest rates are likely to increase. And, under that higher interest rate scenario, the cost of borrowing money for buying a home will only increase. Not good for demand. And if demand slows down still further, sales of property will get worse and prices will decline even more.

Uh, oh - does not sound like a “boom”. Sounds more like a “thud”.

Demand stalls, supply surges.

For all the bravado of the “news” headline in the June 23rd article in Business Standard, it is more of a rear view mirror event: of what happened yesterday.

But, in a strange way, it gives a hint of what is likely to happen in the future. In 2006 and 2007, real estate buyers were in a fix. Property they wished to buy was only available at high prices. Supply was limited.

And demand for property increased due to higher incomes and the ability to borrow more from banks. The desire of many private banks and many government-owned banks to gain market share and build their retail, home loan portfolio saw this dramatic run-up in the borrowing capacity of buyers.

Sometimes these buyers were genuine buyers, and sometimes they were speculators - in for the “free” ride. After all it was a guarantee that property prices would increase every day. Just like the prices of shares increased every day when the stock markets opened. There was no need to go on a “road show” to UK to sell all the property being built.

But that was in 2006 and 2007.

Today, supply of property is more. The demand for property is lower. Demand has declined because property prices are no longer affordable. Salaries have increased - but not as much as in the recent past. Demand has also been hit by the fact that banks are closing down their home loan lending departments. Or raising interest rates for these home loans. The wealth effect from stock markets - which fuels the buying of second homes and dream homes - has evaporated.

But the supply juggernaut keeps on rolling. And building.

Whenever I ask my colleagues (who advise a real estate fund) their views on how much new construction is planned, they shake their head in disbelief. There are 50 to 70 million square feet of new construction coming up in Bangalore, Calcutta, Hyderabad, and Pune to name a few cities.

Developers who have built maybe a total of 5 million square feet in the past decade have plans to build 50 million square feet in the next 3 years. India was rising. India was shining. And a rising and shining India needed a place to live, a place to work, and a place to shop. Real estate zindabad! Stock price of real estate companies double zindabad!!

Yes, 700% correct!

All correct, and all true: India needs more property. A lot of more property. Maybe more than the 700% increase referred to in the Merrill Lynch report. But, at what price? And at what profit margin to the developer and their financiers?And will people buy any junk in any location at any price?

Our view on property has been wrong in timing. We called the “sell” on property too early.

We did not take into account the stupidity of many banks in lending money so leniently and so cheaply. Or the complete mis-pricing of risk-return by so many come-and-join-the-party property funds.

But we knew the greed of the developers. We had seen them in action in 1993 to 1995. As property prices increased in 1994, they bought more land at higher prices and thought they would sell their end product at even higher profits. Discipline was out of the door. Greed was in.

That property cycle went bust in 1995 - and stayed in bust mode till 2003. For 8 years it was a buyer’s market. Or a renter’s market. Supply was far more than demand. No one speculated on property. The actual user’s actions determined the prices. Not some bank’s desire to gain “market share”. Nor the availability of money from international sources due to the desire of a foreign fund to invest in an exotic location for an erotic return.

But demand and supply determine the price of everything. Though, they don’t tell you the value of anything. And people confuse the two and use “price” and “value” as inter-changeable words. They confuse the high price of real estate with the value of that real estate. Prices have only one way to go, I reiterate: and that is down.

And if real estate declines, so should the share prices of many of the property companies that build, and build, and build. We may shake our heads at the housing bubble in USA. But we built one right here in our own back yard.

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New Nucmed Indications

Some of the new indications for imaging systems, unveiled at the Society Of Nuclear Medicine (SNM) meeting in New Orleans earlier this month,include:

-PET scans and a radiotracer that is capable of binding to plaques found in the brain of Alzheimier's patients showed that beta-amyloid imaging can provide early detection of AD and more accurate diagnosis of other dementias by revealing the presence or absence of beta-amyloid plaques.

-Radiopharmaceuticals that bind specifically to prostate-specific membrane antigen can improve early diagnosis and staging of prostate cancer, as well as the monitoring of therapy for metastatic cancer.

-Using PET scans to see changes in coronary blood vessels offers hope that those individuals at risk can receive earlier treatment.

-Body Mass Index (BMI), instead of body weight, provides optimal dosing of a radiopharmaceutical (FDG) commonly used in oncology imaging.

-PET imaging can detect the early, so-called "silent heart" stage of disease in asymptomatic diabetic patients.

-PET and CT scans can be used as noninvasive tools for determining stages of ovarian cancer.

-Molecular imaging tracks the location of stem cells in tumors, and can potentially lead to major advances in the use of stem cell therapies to treat cancer.

-Semiconductor-based PET scanners improve PET imaging capabilities: the smaller, thinner semiconductors are easier to adjust and arrange than conventional scanners. The technology allows for even high spatial resolution and less "noise" or irrelevant images than traditional scanners.

-PET scans revealed that hormone replacement therapy may help prevent atherosclerosis. The scans showed that coronary endothelial function (the inner lining of the coronary vessels) were dilated when women used estrogen, resulting in an increase in blood flow to the heart.

-PET and CT scans significantly improve breast cancer imaging and lead to more targeted treatment options. The prototype scanner is designed to help physicians determine stages of breast cancer in patients already diagnosed with the disease.

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SWYER-JAMES SYNDROME (SYS)

Also known as the unilateral hyperlucent lung or Macleod's syndrome. It is an uncommon disease that is considered to be an acquired lesion that follows a number of lung insults, usually in infancy or childhood.

AETIOLOGY

The condition typically follows a lower respiratory tract infection in infancy or childhood. Thus it is a post infectious form of bronchiolitis obliterans following a number of lung insults;

Infections
Viral
Measles
Pertussis
Adenovirus
Bacterial
Tuberculosis
Mycoplasma
Others
Foreign body aspiration
Hydrocarbon pneumonia's
Radiation therapy
Toxic fumes
Organ transplantation

CLINICAL FEATURES

These tend to be variable and it is often an incidental finding on chest xray. Most patients are asymptomatic in adulthood. Others may complain of a cough, recurrent chest infections, shortness of breath, or hemoptysis.

PATHOGENESIS

This is not clear. Current theory favors a post infectious bronchiolitis obliterans. This follows on repeated infections in early childhood. The consequent bronchiolitis obliterans results in;

Distal airways trapping, airway distension and eventually changes characteristic of emphysema
Fibrosis of the lung with reduction in lung capacity and a compensatory reduction in pulmonary blood flow. Because the condition is usually acquired in childhood before the lungs have reached full development, the affected lung or lobe is usually small and hypo plastic
Bronchiectasis may or may not be present

FUNCTIONAL ABNORMALITY

Evidence of airway obstruction and increase in residual volume is present. There is diminished oxygen uptake in the affected lung. There is also decreased ventilation or blood flow in the affected lung.

DIAGNOSIS

The diagnosis is essentially a radiological one. The syndrome is primarily recognized by it's characteristic radiographic appearance of;

Lobar or unilateral hyperlucent lung
Small or normal lung volume on the affected side
Small hilar shadows
Sparse intrapulmonary vascular markings
Air trapping on expiration

Other diagnostic modalities such as bronchoscopy, bronchography, angiography and scintigraphy are also used to rule out other differentials such as;

unilateral agenesis or hypoplasia of a pulmonary artery
Massive pulmonary thromboembolism
Endobronchial tumor

More recently CT scans especially high resolution scans and spiral CT angiography have shown to be valuable modalities in confirming the diagnosis of SJS. It also allows for precise evaluation of vascular, bronchial and parenchymal structures.
CT scan also shows that although classically considered to affect one lung or lobe, the disease may be more heterogeneous in distribution and that contra lateral parenchymal lesions can be present.

TREATMENT AND PROGNOSIS

The prognosis is generally good. Most patients have an asymptotic course unless the opposite lung becomes diseased. The treatment is generally symptomatic. However, surgery should be considered if secondary infection or bronchiectasis become severe.

CONDITIONS THAT MAY PRESENT AS A UNILATERAL HYPERLUCENT LUNG


Technical difficulties
Pt rotation
uneven film development
Conditions that simulate a unilateral hyperlucent lung
pectoral muscle absence or wasting
absence of breast or soft tissue surgery
scoliosis
hypolucency of the contra lateral lung
Parenchymal Aetiologies
compensatory over inflation
emphysema
central obstruction of a bronchus
Vascular Aetiologies
pulmonary embolism
pulmonary artery stenosis or agenesis

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Gallstone ileus:

Gallstone ileus: Gallstone ileus refers to intestinal obstruction caused by a gallstone that has eroded/fistulized into the gastrointestinal tract. Rigler's triad on abdominal radiographs: Air in the biliary tree (pneumobilia) Partial or complete bowel obstruction; and An ectopic gallstone. (Bowel obstruction is most commonly seen. Air in the biliary tract is present in about two-thirds of patients, and the calcified stone is noted 25-50% of patients). In the majority of patients, the gallstone will pass through the intestinal tract without resulting in obstruction. Stones larger than 2.5 cm usually cause a mechanical obstruction. The point of obstruction is generally in the ileum or at the ileocecal valve (76%), in the duodenum (21%) or sigmoid colon (2%). The site of communication between the biliary tract and the intestine is most commonly at the duodenum or colon. Gallstone obstruction in the colon will usually be located at the site of disease such as sigmoid diverticulosis or at a surgical anastomosis. Gastric outlet obstruction, Bouveret's syndrome, occurs when the gallstone erodes and lodges into the stomach or duodenal bulb. Gallstone ileus is seen more commonly in the elderly ~ 70 years old. If the conventional radiographic findings are indefinite, CT or UGI-small bowel series will assist in establishing the diagnosis. Clinical management is enterolithotomy with or without cholecystectomy to prevent future occurrence. References: Zeman RK. Cholelithiasis and cholecystitis. In: Gore RM, Levine MS (eds). Textbook of Gastrointestinal Radiology, 2nd ed. Philadelphia: WB Saunders; 2000:1335-1336. Lobo DN, Jobling JC, Balfour TW. Gallstone ileus: diagnostic pitfalls and therapeutic successes. J Clin Gastroenterol 2000; 30:72-76. Day EA, Mark C. Gallstone ileus: a review of the literature and presentation of 34 new cases. Am J Surg 1975; 129:552-558. Delabrousse E, Bartholomot B, Sohm O, et a;. Gallstone ileus: CT findings. Eur Radiol 2000; 10:938-940. Loren I, Lasson A, Nilsson A, et al. Gallstone ileus demonstrated by CT. J Comput Assist Tomogr 1994; 18:262-265.

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Silent sinus syndrome

Silent sinus syndrome

Imaging features include maxillary sinus outlet obstruction, sinus opacification, and sinus volume loss with inward bowing of the maxillary sinus walls Patients often present with painless enophthalmos or diplopia rather than symptoms of sinusitis Silent sinus syndrome, or maxillary sinus atelectasis, is characterized by volume loss of the maxillary sinus after infundibular occlusion. It most often presents in the third through fifth decades of life with painless enophthalmos, facial asymmetry, and/or diplopia. Rarely do patients complain of symptoms of sinusitis. Imaging findings of silent sinus syndrome are characteristic. There is maxillary sinus volume loss with inward retraction of the sinus walls and sinus opacification. The ethmoidal infundibulum is occluded, usually due to opposition of the uncinate process against the inferomedial orbit. The sinus volume loss accounts for the corresponding increase in ipsilateral orbital volume and size of the middle meatus. The pathophysiology remains unclear. It is felt to be an acquired condition caused by chronic maxillary sinus obstruction and hypoventilation leading to negative intrasinus pressures. Chronic inflammation leads to osteolysis and thinning of the sinus walls which are retracted by the negative sinus pressure. Treatment is aimed at creating an outlet for obstructed mucous via a nasal antral window or maxillary antrostomy. The goal of surgery is to prevent disease progression and further deformity.

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Gynecologic Pelvic Mass:

Gynecologic Pelvic Mass:

• Large uterine fibroid.
• Ovarian mass.
  • Coelomic epithelial tumors: These tumors, which originate from the coelomic epithelium, constitute 80-85% of all ovarian tumors.
    • Serous cystadenoma and mucinous cystadenoma: Fifteen to 20% are malignant.
    • Endometrioid type and clear cell: Ninety-five to 98% are malignant.
    • Brenner tumor: Two percent are malignant.
  • Germ cell tumors: These tumors originate from the germ cell and constitute 10-15% of all ovarian tumors. All are malignant except mature teratomas and gonadoblastomas, which are always benign.
    • Mature teratoma.
    • Immature teratoma.
    • Dysgerminoma.
    • Gonadoblastoma.
    • Endodermal sinus.
    • Embryonal carcinoma.
    • Nongestational choriocarcinoma.
  • Gonadal-stromal cell tumors constitute 3-5% of all tumors.
    • Granulosa cell.
    • Fibroma: Fewer than 5% are malignant.
    • Thecoma: Fewer than 5% are malignant.
    • Sertoli-Leydig cell: Fewer than 5% are malignant.
    • Lipid cell type: Thirty percent are malignant.
    • Gynandroblastoma: One hundred percent are malignant.

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Meigs syndrome:

Meigs syndrome:

• Meigs syndrome is defined as the triad of benign ovarian tumor with ascites and pleural effusion that resolves after resection of the tumor. The ovarian tumor in Meigs syndrome is a fibroma.
• Pseudo-Meigs syndrome consists of pleural effusion, ascites, and benign tumors of the ovary other than fibromas. These benign tumors include those of the fallopian tube or uterus and mature teratomas, struma ovarii, and ovarian leiomyomas.
• Pseudo-pseudo Meigs syndrome includes patients with systemic lupus erythematosus and enlarged ovaries.
• Tumor marker serum levels of CA125 can be elevated in Meigs syndrome, but the degree of elevation does not correlate with malignancy.
• Etiology of ascitic fluid: Pathophysiology of ascites in Meigs syndrome is speculative: considerations include irritation of the peritoneum, secretion form the mass itself, direct pressure on surrounding lymphatics or vessels, hormonal stimulation, and tumor torsion.
• Origin of pleural effusion: The etiology of pleural effusion is unclear. Current theory is that ascitic fluid is transferred via transdiaphragmatic lymphatic channels.
• Ascitic fluid and pleural fluid in Meigs syndrome can be either transudative or exudative.
• Ovarian tumors are more prevalent in upper socioeconomic groups. Ovarian fibroma is found in 2-5% of surgically removed ovarian tumors, and Meigs syndrome is observed in about 1%. Ascites is present in 10-15% of those with ovarian fibroma and hydrothorax in 1%, especially with larger lesions.
• Although Meigs syndrome mimics a malignant condition, it is a benign disease and has a very good prognosis if properly managed. Life expectancy after surgical removal of the tumor mirrors that of the general population.
• The incidence of ovarian tumor begins to increase in the third decade and increases progressively to peak in the seventh decade. Meigs syndrome in prepubertal girls with benign teratomas and cystadenomas has been reported.

References:

1. Jones OW, Surwit EA: Meigs syndrome and elevated CA 125. Obstet Gynecol 1989 Mar; 73(3 Pt 2): 520-1[Medline].
2. Lacson AG, Alrabeeah A, Gillis DA et al: Secondary massive ovarian edema with Meigs syndrome. Am J Clin Pathol 1989 May; 91(5): 597-603[Medline].
3. Lin JY, Angel C, Sickel JZ: Meigs syndrome with elevated serum CA 125. Obstet Gynecol 1992 Sep; 80(3 Pt 2): 563-6[Medline].
4. Meigs JV, Cass JW: Fibroma of the ovary with ascites and hydrothorax: with a report of seven cases. Am J Obstet Gynecol 1937; 33: 249-267.

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Extrahepatic biliary atresia:

Extrahepatic biliary atresia:

• Extrahepatic biliary atresia is obliteration or discontinuity of the bile ducts, usually in the region of the porta (i.e., hepatic or common bile ducts).
• Usually acquired postnatally at approximately 2 – 8 weeks of age.
  • Progressive inflammation of biliary system associated with infections such as CMV, EBV, reovirus, rotavirus.
• Less often congenital and seen with other anomalies such as asplenia or situs inversus.
• Cholestasis leads to jaundice in baby several weeks old. Differential at this age is neonatal hepatitis versus biliary atresia.
• On ultrasound, may see the following:
  • No gallbladder or small, irregular gallbladder.
  • Triangular fibrous (hyper echoic) remnant measuring at least 4 mm in the region of the porta hepatis. This represents the obliterated bile duct.
  • Ultrasound is not very sensitive.
• On nuclear hepatobiliary imaging, see normal prompt homogeneous uptake in the liver (ruling out hepatitis) and NO excretion into the biliary system, even on delayed imaging.
• Patients undergo portoenterostomy (Kasai procedure).
  • If bile duct involved in anastomosis is large, greater chance of success.
  • Greater success if performed before ten weeks of age.
  • Complications include cholangitis, stenosis, and complete failure, which ultimately requires liver transplantation.

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Differential for acquired causes of intestinal obstruction in children (older) is described in Practical Pediatric Imaging: Diagnostic Radiolog

Differential for acquired causes of intestinal obstruction in children (older) is described in Practical Pediatric Imaging: Diagnostic Radiology of Infants and Children as follows: (Take AAIIMM) Adhesions (from surgery) Appendicitis (often with abscess formation) Incarcerated inguinal hernia Intussusception Malrotation with volvulus Miscellaneous causes Meckel's diverticulum Duplication Ingested foreign body Causes of pneumoperitoneum in older infants and children include the following: Bowel perforation (Meckel's, appendix, ulcer, trauma) Perforation of other organ (uterus, vagina, bladder) Iatrogenic causes (dissection from pneumomediastinum, surgery, paracentesis, biopsy, resuscitation) CT evidence of appendicitis includes the following: Enlargement of the appendix Wall enhancement Periappendiceal fat stranding Appendicolith Wall thickening of the cecum or terminal ileum Check for associated abscess. References: Donnelly, LF. Fundamentals of Pediatric Radiology. First Edition. 2001. W.B. Saunders Company. Incesu, L, Taylor, CR, et al: Appendicitis. Emedicine. June 2004. Accessed May 12, 2007. Kirks, DR; Griscom, NT. Practical Pediatric Imaging: Diagnostic Radiology of Infants and Children. Third Edition. 1998. Lippincott-Raven Publishers.

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Radiographic appearance in Osteomyelitis

• Periosteal reaction
• Thin, linear periosteal reaction
• Thick periosteal reaction
• Laminated—"onion peel"
• Codman's triangle—periosteum forms bone only at the margins of the periosteal triangle
• Bone destruction
  • Permeating bone lesion
  • Punched-out bone
  • Moth-eaten
  • Geographic
  • Aggressive osteolysis
  • Well-defined osteolytic lesion with thick sclerotic border
• Localized cortical thickening
• Involucrum
  • Reactive new bone surrounding sequestrum
• Ground-glass
• Diffusely dense bones
• CT—for evaluation of
  • Chronic disease
  • Soft tissue expansion
  • Sequestra
  • Sinus tracts
• MR—relative to X-ray
  • Increased sensitivity
  • Decreased specificity
• Nuclear Medicine
  • Tc99m-MDP bone scan
    • More sensitive than plain film
    • Negative rules out osteomyelitis
    • Phases (osteomyelitis positive through all 3 phases, cellulitis is negative on delayed)
      • Flow
      • Blood pool
      • Delayed
  • If underlying bone abnormal (i.e. diabetic foot, fractures, nonunion, pseudoarthroses, hardware) use multiple isotope scintigraphy (Tc99m-MDP combined with the agents listed below)
    • Sulfur colloid
      • Defines extent of red marrow
    • Labeled WBC's (Indium-111 or Tc99m-HMPAO)
      • Infection suggested by
        • Activity in absence of sulfur colloid activity
        • Greater activity than that of sulfur colloid
      • If activity of labeled WBC's and sulfur colloid ~equal, probably just marrow not infection
    • Gallium
      • Used in place of labeled WBCs
      • Less effective
• Risk factors
  • Penetrating trauma
  • Immunocompromised
  • IV drug abuse
  • Diabetes mellitus
  • Sickle cell disease
• Sequestrum and/or abscess
  • Antibiotics and surgical drainage
• In patients <>

References:

1. Weissleder et al, Primer of Diagnostic Imaging, 4th edition, 2007.
2. Bookstein, Medical Student's Pocket Reference, 4th edition, 2002.
3. Brant & Helms, Fundamentals of Diagnostic Radiology, 3rd edition, 2006.
4. STATdx, url: my.statdx.com (by Amirsys, Inc.).

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Thoracic outlet syndrome:

• Thoracic outlet syndrome is a clinical constellation of symptoms secondary to neurovascular compression at the level of the thoracic outlet.
• These symptoms are often exacerbated by abduction of the arms. Patients may complain of worsened symptoms when their arms are raised.
• Neurologic symptoms can include pain, numbness, paresthesias, or weakness, usually in a radicular pattern. C8 and T1 are most commonly involved.
• Vascular symptoms can include pain, no pulse, and pallor.
• Physical examination maneuvers to elicit thoracic outlet syndrome include Adson's test and the elevated arm stress test (EAST).
• The Adson's test involves abducting the arm to 90 degrees, and having the patient take a deep breath and turning his/her head away from the affected arm. A positive Adson's test results in a decrease or absence of the affected arm's radial pulse.
• The EAST test involves abducting the upper arms to 90 degrees, and flexing the elbows to 90 degrees. The patient is then asked to open and close the hands vigorously. Affected patients will be unable to continue for three minutes as this arm positioning will elicit the clinical symptoms of thoracic outlet syndrome.
• Imaging studies include a chest radiograph to evaluate for thoracic bony abnormalities, such as cervical ribs. Upper extremity dopplers and angiography are used to confirm the diagnosis.
• Patients should be anticoagulated to an INR of 2-3 to minimize the chance of subclavian artery or vein thrombosis.
• Surgical treatment includes anterior and middle scalenectomy, first rib resection, and removal of a cervical rib if present.

References:

1. Emedicine. "Thoracic Outlet Syndrome" http://www.emedicine.com/emerg/topic578.htm

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Useful link to description of Imaging exams and Prep required

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http://www.qdi.com.au/webpages.cfm?pagenumber=4

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Progression of Mild Cognitive Impairment Visualized on PET

Progression of Mild Cognitive Impairment Visualized on PET



The use of molecular imagining might help clinicians monitor the progression of mild cognitive impairment (MCI) and help to identify people at risk for Alzheimer's disease (AD), according to a study presented here at the Society of Nuclear Medicine 2008 Annual Meeting.

"We can now visualize in vivo changes in the brain that correlate with clinical testing. Not all patients with MCI progress to AD. We think we will eventually be able to determine which persons will," Chester Mathis, PhD, professor of radiology at the University of Pittsburgh, in Pennsylvania, told Medscape Radiology.

He and his colleagues evaluated molecular changes in the brains of people with MCI using positron-emission tomography (PET) and the Pittsburgh compound-B (PiB) radiotracer. PiB binds to the beta-amyloid plaques believed to be responsible for the development of AD. PiB levels above a cut-off threshold of 1.44 to 1.48 distribution volume ratio, depending on the brain region affected, were considered to be elevated (that is, PiB positive).

The longitudinal study included 23 people diagnosed with MCI (mean age, 70 years). The study also included 5 mild- to moderate-AD patients and 33 elderly controls. Subjects underwent baseline PiB scans and were followed for 2 to 4 years, either clinically or with repeat scans.

"Our hypothesis was that MCI subjects with amyloid plaque (based on PiB elevations) would develop AD, and those without plaque would not," Dr. Mathis said.

At baseline, 13 of 23 (57%) MCI subjects were PiB positive, and 10 of 23 (43%) were PiB negative. Among the 13 PiB-positive patients, 5 progressed to AD. None of the PiB-negative patients progressed; in fact, 6 remained stable and 4 actually reverted to normal. "This was probably because there were other reasons for their MCI, such as depression or drug use, which change over time," he explained.

Amyloid Plaque Burden and AD

"We found that about 60% of the MCI subjects already had plaque loads comparable to AD subjects, whereas about 35% had no detectable plaque," he said. "This means that about 15% of MCI subjects per year converted to AD."

"These are slow changes in the amyloid plaque burden from year to year, barely above the test/retest variability. The changes conform to the hypothesis generated by postmortem studies, which is that the full transition from a situation of very little plaque to substantial plaque occurs over the course of about 10 years. This is exactly what our imaging told us," he said in his presentation.

In the elderly control group, about 25% had significant plaque deposition but were asymptomatic, which indicates future risk for AD. Of the 5 people with established AD (all PiB positive at baseline), only 2 had further increases in PiB levels, indicating that "there may be a ceiling to plaque deposition," he added.

Diagnostic Value of PiB

Daniel H. Silverman, MD, head of the neuronuclear imaging research group at the UCLA School of Medicine, in Los Angeles, California, and moderator of the session, told Medscape Radiology that he has concerns about the diagnostic and prognostic utility of PiB in MCI, as opposed to fluorodeoxyglucose (FDG), which has been found to be highly sensitive, even in young adults. Although there is "overwhelming evidence" that imaging with FDG-PET can accurately identify and assess people with MCI and dementia, the role of PiB is less established, he said.

For one thing, PiB depends on the presence of extracellular amyloid plaque, which can also be observed in cognitively intact people. Furthermore, most PiB studies have not been confirmed with postmortem findings, unlike those with FDG-PET, he pointed out.

"When you try to compare the diagnostic accuracy of PiB and FDG-PET without autopsy confirmation, you are not only on shaky ground, you have buried yourself under the rubble of the ensuing earthquake," he commented, adding that, for prognostic purposes, shorter follow-up, as in this study, is acceptable. In addition, the investigators remained appropriately conservative in terms of their conclusions, he noted.

"So far, the data are insufficient to determine whether this test has prognostic utility, let alone whether it is better than FDG-PET," he said. "But PiB could expedite the development of agents aimed at reducing the amyloid plaque burden, and be useful in monitoring in this setting."


Society of Nuclear Medicine 2008 Annual Meeting: Abstract 139. Presented June 16, 2008.

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Dermoid and Epidermoid, Oral Cavity

Dermoids and epidermoids are cystic oral cavity lesions arising from congenital epithelial inclusions or rests.
Dermoids and epidermoids most commonly involve the floor of mouth in the submandibular space (SMS), sublingual space (SLS) or root of tongue (ROT).



Epidermoid and dermoid cysts are benign lesions encountered throughout the body, with 7% occurring in the head and neck area. The orbit is the most common site in the head and neck for these congenital lesions. They rarely occur within the oral cavity, representing less than 0.01% of all oral cavity cysts.

These congenital cysts are dysembryogenetic lesions that arise from ectodermal elements entrapped during the midline fusion of the first and second branchial arches between the third and fourth weeks of intrauterine life. Acquired cysts may be derived from traumatic or iatrogenic inclusion of epithelial cells or from the occlusion of a sebaceous gland duct.

The cysts can be classified as epidermoid when the lining presents only epithelium, dermoid cysts when dermal appendages are found, and teratoid cysts when other tissue such as muscle, cartilage, and bone are present. The teratoid type is the only variety that may have a malignant change.

Anatomically, these oral cavity cystic lesions most commonly involve the floor of mouth and may occur in the root of tongue (ROT), submandibular space (SMS) or sublingual space (SLS). Dermoid cysts generally present with slow and progressive growth, and even if they are congenital, the diagnosis is usually possible in the second or third decade of life. Midline cysts of the floor of the mouth present as painless subcutaneous or submucosal lesions. When large, they can displace the tongue and result in dysphagia, dysphonia or dyspnea.

Epidermoids present on imaging as low density, unilocular, well circumscribed simple cystic lesion. Dermoid cysts are usually more heterogeneous with fatty internal material and possibly calcification.

The treatment of dermoid cysts of the floor of the mouth is extracapsular excision with an intraoral or external approach, depending on the size of the lesion and the position relative to the mylohyoid muscle. The entire cyst must be removed to prevent recurrence.

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Preventing Contrast Induced Nephropathy

Preventing Contrast Induced Nephropathy

Michael Smith

Overview
Contrast induced nephropathy (CIN) is a serious concern for today’s emergency physician when ordering contrast enhanced imaging. CIN is usually defined by an increase in serum creatinine by 0.5 mg/dL or 25% from baseline that usually occurs 2-3 days after contrast administration.[1] The incidence of CIN is estimated to be 1-2% in the general population, but the relative risk is greatly increased in diabetics, the elderly, and those with intrinsic renal disease, congestive heart failure, and dehydration.[1,2] It is the duty of the emergency physician ordering the study to assess risk of developing CIN, as other care providers may not adequately identify patients at risk.[3] Careful selection of patients for contrast imaging is paramount especially in this day of frequent and profuse imaging of both medical[4] and trauma[5] patients.

Prevention
The first step in preventing CIN is determining if a contrast enhanced study is actually clinically indicated. For example, a reasonable starting point might be to employ judicious use of CT scans in trauma patients, a group in whom contrast-enhanced CT scanning is routinely ordered and whole body scanning has become rampant.[6] Screening with ultrasonography may facilitate a decrease in CT scans in both medical and trauma patients. Finally, contrast administration may prove unnecessary for certain patients. For instance, data indicates that the lack of contrast does not alter the sensitivity of an abdominal CT for appendicitis.[7]

Once it has been determined that contrast enhanced imaging is clinically indicated, a few preventative measures can be initiated. Sodium chloride hydration remains the mainstay of choice for CIN prevention.[8] Studies have also demonstrated benefit to administering sodium bicarbonate for preventing CIN.[9] Controversy remains regarding the minimal benefit of adding n-acetylcysteine (N-AC) to the treatment regimen.[10] The use of both theophylline and high dose ascorbic acid has been proposed, but no methodologically or statistically sound studies exist, making the measurement of efficacy of ascorbic acid and theophylline in preventing CIN uncertain. Unfortunately, the majority of studies address CIN induced as a result of coronary angiography. There is some thought that ED CT contrast might be slightly safer than angiography contrast, but we are only able to extrapolate based on the available data.

Application to Emergency Medicine
Prevention of contrast induced nephropathy remains as a significant challenge for today’s emergency physician. Sound clinical judgement regarding the actual need of a contrast enhanced study is essential. The responsibility of risk stratification to assess for potential development of CIN remains that of the emergency physician ordering the study. Sodium chloride and sodium bicarbonate hydration, while not risk free, remain fairly safe and reasonably effective means of preventing CIN. The utility of N-AC, ascorbic acid and theophylline is unproven at best. Most studies reflect the incidence and treatment of CIN induced by angiography contrast, rather than CT contrast. However, some extrapolation and application of the above principles may be useful.

References
Pucelikova T, et al: Contrast-induced nephropathy. Catheter Cardiovasc Interv. 2008 Jan 1;71(1):62-72. 17975790
Wong GT, Irvin MG: Contrast-induced Nephropathy. Br J Anaesth. 2007 Oct;99(4):474-83. 17681968
Reddan, D, Fishman, EK: Radiologists' knowledge and perceptions of the impact of contrast-induced nephropathy and its risk factors when performing computed tomography examinations: a survey of European radiologists. Eur J Radiol. 2008 May;66(2):235-45. 17728089
Broder J, et al: Increasing utilization of computed tomography in the pediatric emergency department, 2000-2006. Emerg Radiol. 2007 Sep;14(4):227-32. 17505849
Beck D, et al: Prospective study of the clinical predictors of a positive abdominal computed tomography in blunt trauma patients. J Trauma. 2004 Aug;57(2):296-300. 15345975
Aucar J, et al: If a picture if worth a thousand words, what is a trauma computerized tomography panel worth? Am J Surg. 2007 Dec;194(6):734-9; discussion 739-40.
Tamburrini S: Accute appendicitis: diagnostic value of nonenhanced CT with selective use of contrast in routine clinical settings. Eur Radiol. 2007 Aug;17(8):2055-61. Epub 2006 Dec 16. 17180324
Van Praet J, et al: Prevention of contrast-induced nephropathy: a critical review. Curr Opin Nephrol Hypertens. 2007 Jul;16(4):336-47.
Masuda M: Comparison of usefulness of sodium bicarbonate versus sodium chloride to prevent contrast-induced nephropathy in patients undergoing an emergent coronary procedure. Am J Cardiol. 2007 Sep 1;100(5):781-6. Epub 2007 Jun 13.
Brigouri C: Renal insufficiency following contrast media administration trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007 Mar 13;115(10):1211-7. Epub 2007 Feb 19. 17309916

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The Incidental Adrenal Mass on CT

The Incidental Adrenal Mass on CT: Prevalence of Adrenal Disease in 1,049 Consecutive Adrenal Masses in Patients With No Known Malignancy


Julie H. Song; Fakhra S. Chaudhry; William W. Mayo-Smith

Am J Roentgenol. 2008;190(5):1163-1168.
Abstract and Introduction
Abstract

Objective: The purpose of our study was to determine the nature and prevalence of adrenal lesions identified on CT in patients with no known malignancy.

Materials and Methods: A computer search of abdominal CT reports using the term "adrenal" was performed in 65,231 consecutive patients with examinations performed from January 2000 to December 2003. An adrenal mass was identified in 3,307 (5%) patients. Patients with no known malignancy and no suspicion for a hyperfunctioning adrenal mass were further isolated. Nine hundred seventy-three patients with 1,049 adrenal masses fulfilled the study criteria. The nature of each lesion was determined by histopathology; imaging characterization with CT, MRI, or washout; a minimum of 1 year of stability on follow-up imaging; or clinical follow-up of at least 2 years.
Results: One thousand forty-nine adrenal masses were characterized with the following methods: histopathology (n = 12), imaging characterization (n = 909), imaging follow-up (n = 87), and clinical follow-up (n = 41). There were 788 adenomas constituting 75% of all lesions. There were 68 myelolipomas (6%), 47 hematomas (4%), and 13 cysts (1%). Three pheochromocytomas (0.3%) and one cortisol-producing adenoma (0.1%) were found incidentally. One hundred twenty-eight lesions (12%) were presumed to be benign by imaging or clinical stability. No malignant adrenal masses were found, even among the 14 patients who later developed malignancy elsewhere.

Conclusion: In 973 consecutive patients with an incidental adrenal mass and no history of cancer, no malignant lesions were identified. Adenomas (75%) and myelolipomas (6%) were the most common lesions.


References

Hedeland H, Ostberg G, Hokfelt B. On the prevalence of adrenocortical adenomas in an autopsy material in relation to hypertension and diabetes. Acta Med Scand 1968;184:211–214

Kloos RT, Gross MD, Francis IR, Korobkin M, Shapiro B. Incidentally discovered adrenal masses. Endocr Rev 1995; 16:460 –484

Lee MJ, Hahn PF, Papanicolaou N, et al. Benign and malignant adrenal masses: CT distinction with attenuation coefficients, size and observer analysis. Radiology 1991;179:415–418

Korobkin M, Brodeur FJ, Yutzy GG, et al. Differentiation of adrenal adenomas from nonadenomas using CT attenuation values. AJR 1996; 166:531 –536

Boland GW, Lee MJ, Gazelle GS, Halpern EF, McNichols MM, Mueller PR. Characterization of adrenal masses using unenhanced CT: an analysis of the CT literature. AJR 1998;171:201–204

Mitchell DG, Crovello M, Matteucci T, Petersen RO, Miettinen MM. Benign adrenocortical masses: diagnosis with chemical shift MR imaging. Radiology 1992;185:345–351

Outwater EK, Siegelman ES, Radecki PD, Piccoli CW, Mitchell DG. Distinction between benign and malignant adrenal masses: value of T1weighted chemical-shift MR imaging. AJR 1995;165:579–583

Mayo-Smith WW, Lee MJ, McNicholas MM, Hahn PF, Boland GW, Saini S. Characterization of adrenal masses (< 5 cm) by use of chemical shift MR imaging: observer performance versus quantitative measures. AJR 1995; 165:91 –95

Korobkin M, Brodeur FJ, Francis IR, Quint LE, Dunnick NR, Londy F. CT time–attenuation washout curves of adrenal adenomas and nonadenomas. AJR 1998; 170:747 –752

Szolar DH, Kammerhuber FH. Adrenal adenomas and nonadenomas: assessment of washout at delayed contrast-enhanced CT. Radiology 1998;207:369–375
Peña CS, Boland GW, Hahn PF, Lee MJ, Mueller PR. Characterization of indeterminate (lipid-poor) adrenal masses: use of washout characteristics at contrast-enhanced CT. Radiology 2000; 217:798 –802

Abeshouse GA, Goldstein RB, Abeshouse BS. Adrenal cysts: review of the literature and report of three cases. J Urol 1959; 81:711 –718

Blake MA, Kalra MK, Sweeney AT, et al. Distinguishing benign from malignant adrenal masses: multi-detector row CT protocol with 10-minute delay. Radiology 2006;238:578–585

Caoili EM, Korobkin M, Francis IR, et al. Adrenal masses: characterization with combined unenhanced and delayed enhanced CT. Radiology 2002;222:629–633

Herrera MF, Grant CS, van Heerden JA, Sheedy PF, Ilstrup DM. Incidentally discovered adrenal tumors: an institutional perspective. Surgery 1991; 110:1014 –1021

Leifer DM, Middleton WD, Teefey SA, Menias CO, Leahy JR. Follow-up of patients at low risk for hepatic malignancy with a characteristic hemangioma at US. Radiology 2000;214:167–172

Bovio S, Cataldi A, Reimondo G, et al. Prevalence of adrenal incidentaloma in a contemporary computerized tomography series. J Endocrinol Invest 2006; 29:298 –302

Gajraj H, Young AE. Adrenal incidentaloma. Br J. Surg 1993; 80:422 –426

Barzon L, Sonino N, Fallo F, Palu G, Boscaro M. Prevalence and natural history of adrenal incidentalomas. Eur J Endocrinol 2003; 149:273 –285

Mantero F, Terzolo M, Arnaldi G, et al. A survey on adrenal incidentaloma in Italy. Study Group on Adrenal Tumors of the Italian Society of Endocrinology. J Clin Endocrinol Metab 2000; 85:637 –644

Bülow B, Ahrén B; Swedish Research Council Study Group of Endocrine Abdominal Tumours. Adrenal incidentaloma: experience of standardized diagnostic programme in the Swedish prospective study. J Intern Med 2002;252:239–246

Mansmann G, Lau J, Balk E, Rothberg M, Miyachi Y, Bornstein SR. The clinically inapparent adrenal mass: update in diagnosis and management. Endocr Rev 2004;25:309–340

Benitah N, Yeh BM, Qayyum A, Williams G, Breiman RS, Coakley FV. Minor morphologic abnormalities of adrenal glands at CT: prognostic importance in patients with lung cancer. Radiology 2005; 235:517 –522

Heinz-Peer G, Hönigschnabl S, Schneider B, Niederle B, Kaserer K, Lechner G. Characterization of adrenal masses using MR imaging with histopathologic correlation. AJR 1999;173:15–22

Paulsen SD, Nghiem HV, Korobkin M, Caoili EM, Higgins EJ. Changing role of imaging-guided percutaneous biopsy of adrenal masses: evaluation of 50 adrenal biopsies. AJR 2004;182 :1033 –1037

Lam KY, Lo CY. Adrenal lipomatous tumours: a 30 year clinicopathological experience at a single institution. J Clin Pathol 2001; 54:707 –712

Olsson CA, Krane RJ, Klugo RC, Selikowitz SM. Adrenal myelolipoma. Surgery 1973; 73:665 –670

Mayo-Smith WW, Boland GW, Noto RB, Lee MJ. State-of-the-art adrenal imaging. RadioGraphics 2001;21:995–1012
Sevitt S. Post-traumatic adrenal apoplexy. J Clin Pathol 1955; 8:185 –194
Burks DW, Mirvis SE, Shanmuganathan K. Acute adrenal injury after blunt abdominal trauma: CT findings. AJR 1992; 158:503 –507
Rana AI, Kenney PJ, Lockhart ME, et al. Adrenal gland hematomas in trauma patients. Radiology 2004;230:669–675
Lee JE, Evans DB, Hickey RC, et al. Unknown primary cancer presenting as an adrenal mass: frequency and implications for diagnostic evaluation of adrenal incidentalomas. Surgery 1998; 124:1115 –1122
Caplan RH, Strutt PJ, Wickus GG. Subclinical hormone secretion by incidentally discovered adrenal masses. Arch Surg 1994; 129:291 –296
Motta-Ramirez GA, Remer EM, Herts BR, Gill IS, Hamrahian AH. Comparison of CT findings in symptomatic and incidentally discovered pheochromocytomas. AJR 2005;185:684–688
Grumbach MM, Biller BM, Braunstein GD, et al. Management of the clinically inapparent adrenal mass ("incidentaloma"). Ann Intern Med 2003;138:424–429
Bernini GP, Moretti A, Oriandini C, Bardini M, Taurino C, Salvetti A. Long-term morphological and hormonal follow-up in a single unit on 115 patients with adrenal incidentalomas. Br J Cancer 2005; 92:1104 –1109

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Now US radiology jobs for India

Now US radiology jobs for India

Arvinder Kaur in New Delhi | PTI | March 28, 2006 | 13:51 IST

With a large pool of well-trained doctors and high-tech infrastructure, India is fast emerging as a tele-radiology hub, providing offshore X-ray reporting services to the United States, Europe, Singapore and the Middle East.

In fact, with tele-radiology, there are no geographic boundaries!

According to estimates, the US is facing a shortage of radiologists with 20 per cent of vacancies going unfilled in hospitals.

"There is worldwide shortage of qualified radiologists and tele-radiology counters this by providing services from one area to another. It can be used to cover the night shift from another geographic zone or to cover remote areas where there are CT (computerised tomography) or other scanners but no radiologists to interpret the results," said Sunita Maheshwari, director, Telerad Solutions, Bangalore, which is pioneer in tele-radiology.

Outsourcing and India: Complete Coverage

"India has an optimal time advantage with the US in terms of providing emergency night shift services to the American hospitals. We also possess high technology infrastructure base, a large pool of well-trained doctors, skilled manpower and a lower cost of living," Maheshwari told PTI.

Tele-radiology means electronic transmission of radiological images, such as X-Rays, CTs and MRIs from one location to another for the purpose of interpretation and consultation.

The doctors here are thus providing diagnostic interpretation of all emergently and non-emergently performed non-invasive imaging studies, including compound tomography, MRI (Magnetic Resonance Imaging), ultrasound, X Ray, nuclear medicine studies and conventional plain films. In emergency setting, these services are provided with a turnaround time of less than 30 minutes.

"The scope of tele-radiology is enormous. One doctor sitting in a centralised reading facility can cover several hospitals at the same time making this a very efficient use of a radiologists time and skill," said Maheshwari.

However, Yatish Agarwal, a medical specialist at Safdarjung Hospital in New Delhi said "The scope has become limited because of certification problems. Only those doctors who have relocated from the US, can do offshoring to America. Such restrictions also exist in many European countries."

"Thus Indian doctors who have relocated from these countries can only do this job, which is limiting the scope of this work. However, as said tele-radiology knows no boundaries. It has immense scope even in Indian conditions. A doctor sitting in a remote area can discuss the results of an MRI or CT scan with a specialist in Mumbai or Delhi," points out Agarwal.

Agrees Maheshwari, but said "the US has around 20 per cent Indian doctors. And with telemedicine becoming popular, they can easily come back and start working from here. Five Indian radiologists from the US will be back in Bangalore by this year end."

Licensing barriers are there but they can be easily overcome. American doctors too come here and apply for a working licence. There are many FRCS (Fellow of the Royal College of Surgeons) doctors practising here. They all can work for the UK and countries, which recognise British degrees. Singapore has recently awarded recognition to our doctors, she added.

Within India also, the scope of tele-radiology is immense. The remote areas have limitations of infrastructure. There it can make the greatest impact. If a patient gets right diagnosis, he can be treated in the right manner, she said.

Tele-radiology is already working in Bijapur, Raipur and some backward areas also. "We have also started the service for a hospital in Kerala and remote areas in Karnataka," she said.

There are three main challenges facing healthcare -- quality, cost and time delivery. The goal of tele-radiology is to optimise the use of technology to tackle these challenges head on, said Maheshwari, noting, "We leverage technology every day as we work with hospitals that extend halfway around the world literally from Bijapur to Philadelphia."

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Negotiating salary? 4 important tips

Negotiating salary? 4 important tips

Meenakshi Subramaniam | BS | May 05, 2008 | 10:09 IST

When Sanjeev Verma took the offer to join a new company, he was quite happy with the cost-to-company salary that was offered to him.

However, after the first month, when the salary cheque came, he was shocked with the numbers. His actual take-home was slightly more than his previous salary. And,Verma is not alone.

There are many of us who get lured with the numbers that show in our CTC package, but when the actual take-home salary comes in our hand, it causes a lot of heartache. It is therefore very important that when you are negotiating the salary, you should have a clear idea about numbers. A good way to achieve this is by using tax saving strategies that would reduce your burden.

Ah! those slips that snip

The first thing to look for is the different heads in your salary package. Heads like performance incentive sound challenging, but they are always taxed. Special allowances, added with conveyance and phone reimbursement, also attract tax.

Often, there is a notion among salary-earners that a lesser basic pay and high allowances may bring down income tax burden. However, it is best if you avoid this approach. A reduced basic salary leads to a lower provident fund, which is a forced saving for your future.

Anyone who gets many allowances must combine all of them under a single head. Put car allowance, books reimbursement, house rent allowance, office travel allowance, phone, vehicle and staying in hotels under on head, which straight away lowers your tax bill. Call this consolidated allowance.

Allowances that help

Always go for conveyance allowance. A sum of Rs 800 a month is tax-free. Even if your office does not give conveyance allowance, you can ask for a reduced basic pay and additional conveyance allowance. This move can cut down tax outgo.

Daily allowance, wherever allowed, must be grabbed with both hands because it carries total tax exemption. Professional tax, up to Rs 2,500, is also unencumbered by tax. Also, office loans for car or personal reasons can be used to avoid taxation to a great extent.

Policies that pay

Employees State Insurance Scheme, if available, must be compulsorily availed. Unlike LIC schemes, the amount is absolutely free from income tax. Fidelity Guarantee Scheme is another insurance plan that is completely tax-free.

Even if you are contributing to a Public Provident Fund, a salaried individual must also opt for Employers Provident Fund, because this also doesn't attract tax. Many salaried people are unaware that a loan for medical treatment is exempt from income tax under Rule 3 A, but make sure that your medical insurance policy is not utilised.

Avoiding FBT

The fringe benefit tax can be avoided if you own a car and the company pays for maintenance and petrol bills. The most profitable way to claim HRA is to ask the company to take a house on lease, which is owned by any of your relatives. If it's your parents, who don't have any income, it works completely to your advantage.

It is because, on one hand, you claim HRA and they, having zero income, don't have to pay any tax. In fact, even if they have some income, but less than the stipulated base limit of Rs 220,000 a year (assuming they are retired), they would gain from the situation. The maximum benefit occurs when the rent is over 20 per cent of your salary.

When gift vouchers are given, insist on taking them under the employee welfare scheme.

Mobile phone bills are considered a perquisite and taxed, causing your office to fret a lot. You can again offer tax counselling by suggesting a simple trick.

The mobile phone bills can be placed under "recurring operative expenditure" head. All taxes are eliminated at one stroke. At home, leased phone landlines installed at the company's behest and cost, allows you to get rid of paying tax on calls.

Travel expenses and hotel stays are taxed under FBT. In fact, even a conference to discuss reducing tax incidence on perquisites will also be taxed! However, by not showing the expenditure as conference/seminar and calling it "convention" would remove the tax burden.

The office may want to give meals, breakfast or tiffin, but FBT fear precludes an employer from extending this perquisite to staff. Why not have an office "food and beverage" account? Show the claim in the income tax return.

The FBT will not apply, at all. Finally, soft furnishings for a house (such as curtains and table cloth), which give the abode a decent appearance for entertaining guests who drop in for official duties, can be shown as expenses. They also qualify for tax exemption.

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