Let me begin by acknowledging that the causes of acute right upper quadrant abdominal pain are many. The 3 modalities you mentioned possess varying diagnostic powers in revealing the different causes of such pain, cholescintigraphy being the least specific of them in identifying non-cholecystic causes, while CT scan has greater ability in demonstrating such etiologies but less sensitivity for acute cholecystitis. It has no role in verifying acute cholecystitis. Sonography boasts equal diagnostic accuracy with scintigraphy with the additional peck of demonstrating some non-gallbladder reasons for acute right upper quadrant pain.

The fundamental problem in acute cholecystitis is obstruction of the cystic duct, which prevents the evacuation of bile from and its entrance into the gallbladder. Bile stasis in the viscus then induces bacterial superinfection resulting in intravesical accumulation of inflammatory exudate, raised intraluminal pressure, edema of the wall of the gallbladder, and, in extreme cases, suppuration, gangrene, and perforation. There is, in 90% to 95% of patients, a stone responsible for the obstruction; in the remaining 5% to 10% there is no such cause, rather ischemia and infection are present. This is acalculous cholecystitis and is common in bedridden, debilitated, intensive-care-unit patients.

In cholescintigraphy the patient receives an intravenous dose of Tc99m-labelled derivative of iminodiacetic acid, which is rapidly cleared from the circulation and excreted into the biliary tree by the hepatocytes. Timed hepatobiliary scintigraphy is obtained over 60 minutes. Radiotracer activity in the lumen of the gallbladder indicates absent cystic duct obstruction and has an overall accuracy of 95% to 98% in declaring that acute cholecystitis is not present. Intravenous morphine may be given on occasion to induce spasm of the sphincter of Oddi and raise intracholedochal pressure, which refluxes bile into the gallbladder, enhancing the specificity of the test. Sometimes it is necessary to obtain 2, 4, or even 24-hour delayed views when the gallbladder fails to fill immediately. Cholescintigraphy, though quite specific in diagnosing acute cholecystitis, may be falsely positive in patients with liver cirrhosis, acute pancreatitis, chronic cholecystitis, prolonged fasting, or in those on hyperalimentation.

Sonography has, in some studies, comparable diagnostic powers to scintigraphy in revealing acute cholecystitis. It also, unlike scintigraphy, has the ability to demonstrate some other causes of right upper quadrant abdominal pain. It is easy and quick to perform and can be done at a patient’s bedside. The 2 most reliable sonographic signs of acute cholecystitis are the presence of a gallstone and demonstrable sonographic equivalent of clinical Murphy’s sign. There are other less specific signs, too: thickening of the wall of the gallbladder (>4-5mm) which can be caused by ascites, congestive heart failure, hepatitis, hypoproteinemia, chronic cholecystitis, and gallbladder carcinoma; the other is pericholecystic fluid, which shows as pericholecystic echopenia (gallbladder halo sign) and is a more specific though less frequent finding than wall thickening. In reality, the more signs present the better the reliability of sonographic diagnosis of acute cholecystitis.

In summary, when the cause of acute right upper quadrant abdominal pain is unclear, CT of the abdomen with and without contrast enhancement will help identify or eliminate non-cholecystic causes of such pain. If suspicion for acute cholecystitis is strong, then the choice between cholescintigraphy and sonography should be influenced by the availability of personnel and technology as well as the necessity for bedside diagnosis.

It sounds like your patient has classic features of acute gallstone pancreatitis, which has a high recurrence rate if you delay cholecystectomy (the recommendation is cholecystectomy before hospital discharge). You must then focus your attention on confirming your clinical impression before surgery.

Stones typically form in the gallbladder (cholelithiasis) and may migrate out into the biliary tree (choledocholithiasis). On occasion they form de novo in the biliary system. Gallstones are the commonest cause of initial acute pancreatitis. Stones in the gallbladder are easy to detect but those in the biliary tree can be hard to find.

You have at your disposal abdominal sonography, endoscopic ultrasonography, abdominal and pelvic contrast-enhanced CT scan, hepatobiliary scintigraphy (HIDA scan), magnetic resonance cholangiopancreatography (MRCP), and endoscopic retrograde cholangiopancreatography (ERCP).

Abdominal ultrasound in this instance simply answers the specific question, “Does the patient have gallstones”? Compared to CT scan, sonography shows gallstones and sludge better both of which can be missed by CT scan. In addition sonography is capable of evaluating the pancreas but not as well as CT scan especially when sonopenetration is impeded.

Abdominal sonography has a sensitivity of 30% to 50% for detecting choledocholithiasis, while endoscopic sonography detects them more than 90% of the time. So it is a useful tool in the occasional patient with post-cholecystectomy choledocholithiasis and gallstone pancreatitis. It requires expertise and equipment that may not be available to all.

CT scan, which, by the way, should be performed with intravenous and luminal contrast enhancement if you chose to walk down this lane, has the advantage of global inspection of the abdomen and pelvis but at the cost of radiation and more money. Since your clinical and biochemical investigation thus far strongly indicate uncomplicated acute gallstone pancreatitis I see no utility in obtaining a CT scan of the abdomen and pelvis.

MRCP in this case will be an overkill because it is expensive. It also requires technical and interpretive skills that are not universally available. Not all institutions own MRI machines. If, however, sonography is not helpful, MRCP would probably serve a more useful diagnostic role than CT scan in this specific need to confirm the presence of cholelithiasis.

HIDA scan is an excellent alternative modality for evaluation of obstructions of the cystic duct (acute and chronic cholecystitis), but it will not show gallstones. Since our objective here is not to confirm or exclude cholecystitis but to confirm the presence of gallstones HIDA scan has no place in your patient’s investigation.

ERCP should be your choice if your patient is not fit for or disagrees with surgery because in addition to confirming your clinical impression, the endoscopist can perform therapeutic sphincterotomy at the same time. The caveat though is that the patient retains her stone-filled gallbladder and is prone to future recurrences of pancreatitis. If on the other hand the abdominal sonography reveals a normal gallbladder and gallstone pancreatitis remains a prime suspect in your differential diagnosis, then ERCP is your next diagnostic/therapeutic tool.

First, you must try to stabilize the patient’s hemodynamics through infusions of crystalloids and blood products and you should keep count of how much of these she requires because the information has prognostic value. More of them portents worse outcome.

You must then notify your surgeon, gastroenterologist, and interventional radiologist about the patient.

If the patient is actively pouring blood per rectum she is most likely to benefit from mesenteric angiography with intention to treat abnormalities it uncovers. Delaying for nuclear scan, surgical consult, and endoscopy will only waste valuable time and allow the bleeding to cease when angiography is likely to be unrewarding.

If blood loss is less torrential and the patient’s hemodynamics stable, a tagged red blood cell nuclear scan or endoscopy is in order. Endoscopy has the advantage of direct visualization of abnormalities and the opportunity to treat them instantly. Its downside is that it may be negative or indeterminate on account of blood in the bowel. Nuclear scintigraphy is non-invasive and very sensitive to small amounts of blood loss (0.05-0.1mL/min loss compared to 0.5 – 1mL/min loss required for a positive digital subtraction angiography). A positive scan directs a surgeon or an interventional radiologist to the site of bleeding, saving time and procedural morbidity and cost. Its downside is that sometimes the yo-yo movement of blood in the bowels due to peristalsis and antiperistalsis make accurate identification of the site of bleeding less easy. At least the test provides a general sense of where the problem lies. Surgery plays a more definitive role in that it allows resolute correction of the underlying problem when known or total colectomy if the answer is nebulous. It carries the burden of invasiveness, significant morbidity and even mortality.

The interventional radiological therapeutic options are:

Vasopressin infusion into the main trunk of the artery supplying the bleeding site.

Highly selective microcoil embolization of the bleeding vessel.

If the above 2 fail or are not possible, providing a roadmap for surgical treatment by infusing the bleeding vessel with methylene blue. The surgeon is guided by the bluish stain of the gut in removing the diseased bowel.

Though it has a high success rate (80%), vasopressin infusion also has a reasonable recurrence rate (30%) and may not be appropriate for patients with certain cardiovascular problems. Additionally, it may infarct the bowel. Coil embolization is highly technical but effective. It, too, carries a risk of infarction. Nonetheless, these two alternatives are less invasive while effective in the management of patients with active lower gastrointestinal bleeding when compared to the other forms of therapy.

Because in a patient with a history of malignant disease metastasis is the most common cause of an incidental adrenal mass regardless of its size, and because melanoma is one of the tumors that commonly metastasize to the adrenal gland, it is reasonable to assume that your patient has an adrenal metastasis from his melanoma. It is not necessary to perform CT-guided fine-needle aspiration of the mass. The presumption is even more secure if there are other sites of metastatic disease in the patient.

If it is necessary to characterize the mass for any reason, contrast-enhanced CT or MRI or repeating the present study in 3 months might confirm the mass is malignant from the changes that will be apparent because of its biologic behavior.

The dilemma you face is not uncommon in clinical medicine and it is so for 2 reasons: the adrenal gland is a common site for metastasis from some common epithelial malignancies (lung, breast, colon, melanoma, for example) and the gland is source for primary tumors of its own cells such as adenomas, adrenal hyperplasia, adrenal carcinoma, and pheochromocytoma. To confuse matters more, not all adrenal masses are tumors, some being infections, artifacts, or inflammatory masses and others infiltrative diseases.

The frequent use of high-resolution cross sectional imaging (CT scan with and without contrast enhancement and MRI) has resulted in the identification of small adrenal lesions in patients without symptoms, signs, or biochemical indices of adrenal disease – ‘adrenal incidentalomas’. The key then is to know what to ignore and what to investigate and treat.

An adrenal incidentaloma is an adrenal mass 1 cm or more in diameter discovered by chance during radiologic imaging in a patient who has no symptoms, clinical signs, or biochemical indices of adrenal disease.

At least 38 different diagnoses have been reported for incidentally-discovered adrenal masses, most of them being nonhypersecretory adrenal cortical adenoma. But some incidental adrenal masses are hyperfunctional or autonomously overproduce adrenal hormones. In fact, current evidence recommends screening for the following forms of adrenal hyperfunction or autonomous function in all patients with ‘adrenal incidentalomas’: autonomous cortisol secretion, pheochromocytoma, and primary aldosteronism in patients with hypertension. The absence of signs and symptoms of adrenal disease must not dissuade the physician from doing so, since some forms of these diseases, for instance pheochromocytoma, though silent remain potentially lethal. This responsibility for biochemical discernment of an adrenal incidentaloma may be borne by the primary care provider or a consultant endocrinologist.

The most troubling thought to a patient with an ‘adrenal incidentaloma’ and their physician is whether the mass is malignant and this is where the role of the imaging characteristics and the size of the mass come in; hormonal evaluation does not predict malignancy.

The principal tumors of concern are an adrenal cortical adenoma (benign) and an adrenal carcinoma, a pheochromocytoma, and a metastasis (the last 3 are malignant). In other words, is the mass a radiologist incidentally identified on a recent imaging study an adenoma or a malignancy? CT, enhanced and unenhanced, and MRI with chemical shift imaging are very useful tools in the imaging of adrenal tumors. With them a reasonable prediction can be made about the benign or malignant nature of an adrenal mass, saving unnecessary biopsy and alleviating anxiety. The following observations about them are pertinent:

An adrenal mass with zero (0) attenuation units on unenhanced CT scan has a likelihood of being an adenoma close to 100% and so may be watched or left alone.

Adrenal adenomas show much earlier washout than non-adenomas on post contrast CT examination; a lesion with such characteristic may be watched in the right clinical setting.

Many adrenal masses are indeterminate on T1 and T2-weighted MRI; their behavior after gadolinium enhancement and on chemical shift imaging compliments their T1 and T2 characteristics.

On post-gadolinium MRI, adenomas enhance mildly but wash out rapidly, while malignant masses enhance rapidly and intensely but wash out slowly; there is more angiogenesis in malignant tumors that traps more gadolinium-laden blood.

On chemical shift imaging, adenomas are brighter on the in-phase sequence but drop in signal intensity on the opposed-phase sequence because they are composed of a disproportionate amount of fat and parenchymal cells, whereas malignancy contain less fat.

Because in a patient with a history of malignant disease metastasis is the most common cause of an incidental adrenal mass regardless of its size, and because melanoma is one of the tumors that commonly metastasize to the adrenal gland, it is reasonable to assume that your patient has an adrenal metastasis from his melanoma. It is not necessary to perform CT-guided fine-needle aspiration of the mass. The presumption is even more secure if there are other sites of metastatic disease in the patient.

If it is necessary to characterize the mass for any reason, contrast-enhanced CT or MRI or repeating the present study in 3 months might confirm the mass is malignant from the changes that will be apparent because of its biologic behavior.

The dilemma you face is not uncommon in clinical medicine and it is so for 2 reasons: the adrenal gland is a common site for metastasis from some common epithelial malignancies (lung, breast, colon, melanoma, for example) and the gland is source for primary tumors of its own cells such as adenomas, adrenal hyperplasia, adrenal carcinoma, and pheochromocytoma. To confuse matters more, not all adrenal masses are tumors, some being infections, artifacts, or inflammatory masses and others infiltrative diseases.

The frequent use of high-resolution cross sectional imaging (CT scan with and without contrast enhancement and MRI) has resulted in the identification of small adrenal lesions in patients without symptoms, signs, or biochemical indices of adrenal disease – ‘adrenal incidentalomas’. The key then is to know what to ignore and what to investigate and treat.

An adrenal incidentaloma is an adrenal mass 1 cm or more in diameter discovered by chance during radiologic imaging in a patient who has no symptoms, clinical signs, or biochemical indices of adrenal disease.

At least 38 different diagnoses have been reported for incidentally-discovered adrenal masses, most of them being nonhypersecretory adrenal cortical adenoma. But some incidental adrenal masses are hyperfunctional or autonomously overproduce adrenal hormones. In fact, current evidence recommends screening for the following forms of adrenal hyperfunction or autonomous function in all patients with ‘adrenal incidentalomas’: autonomous cortisol secretion, pheochromocytoma, and primary aldosteronism in patients with hypertension. The absence of signs and symptoms of adrenal disease must not dissuade the physician from doing so, since some forms of these diseases, for instance pheochromocytoma, though silent remain potentially lethal. This responsibility for biochemical discernment of an adrenal incidentaloma may be borne by the primary care provider or a consultant endocrinologist.

The most troubling thought to a patient with an ‘adrenal incidentaloma’ and their physician is whether the mass is malignant and this is where the role of the imaging characteristics and the size of the mass come in; hormonal evaluation does not predict malignancy.

The principal tumors of concern are an adrenal cortical adenoma (benign) and an adrenal carcinoma, a pheochromocytoma, and a metastasis (the last 3 are malignant). In other words, is the mass a radiologist incidentally identified on a recent imaging study an adenoma or a malignancy? CT, enhanced and unenhanced, and MRI with chemical shift imaging are very useful tools in the imaging of adrenal tumors. With them a reasonable prediction can be made about the benign or malignant nature of an adrenal mass, saving unnecessary biopsy and alleviating anxiety. The following observations about them are pertinent:

An adrenal mass with zero (0) attenuation units on unenhanced CT scan has a likelihood of being an adenoma close to 100% and so may be watched or left alone.

Adrenal adenomas show much earlier washout than non-adenomas on post contrast CT examination; a lesion with such characteristic may be watched in the right clinical setting.

Many adrenal masses are indeterminate on T1 and T2-weighted MRI; their behavior after gadolinium enhancement and on chemical shift imaging compliments their T1 and T2 characteristics.

On post-gadolinium MRI, adenomas enhance mildly but wash out rapidly, while malignant masses enhance rapidly and intensely but wash out slowly; there is more angiogenesis in malignant tumors that traps more gadolinium-laden blood.

On chemical shift imaging, adenomas are brighter on the in-phase sequence but drop in signal intensity on the opposed-phase sequence because they are composed of a disproportionate amount of fat and parenchymal cells, whereas malignancy contain less fat.

If you have managed patients who require central venous accesses long enough you will find out that this is a common problem. Total chronic occlusion of central veins can be due to infections, injection of vesicants, extrinsic tumor compression, radiation therapy, hypercoagulable states, or other reasons. When it happens an inspection of the patient’s chest will identify large vessels returning blood to the heart by alternate routes and this may be confirmed by venous mapping using duplex venous ultrasound, CT venography, digital subtraction venography or magnetic resonance venography.

Sometimes these examinations will show, not only chronic occlusions of the superior vena cava and its tributaries, but similar occlusions of the inferior vena cava and its tributaries.

Depending upon the locations of the obstructions, there are fortunately alternative routes for venous cannulation, albeit a little more invasive than the conventional avenues. They include:

1. Percutaneous translumbar catheter insertion, in which the catheter is introduced from the back, through the lumbar muscle, into the inferior vena cava,

2. Percutaneous transhepatic catheter insertion, in which the catheter is advanced through the liver into a hepatic vein,

3. Percutaneous catheter insertion using a number of inguinal routes ( the common, superficial, and deep femoral veins to enter the inferior vena cava),

4. Use of various enlarged collaterals to access the central veins (the azygos and hemiazygos systems, the intercostal veins, or the internal mammary vein to gain purchase into the superior vena cava, or the inferior epigastric vein, the lumbar vein, or the gonadal vein to enter the inferior vena cava).

Securing access into some of these alternative routes can be quite aggressive and invasive but it ultimately affords patients much needed access in desperate times.

The main clinical concerns which should inform our choice(s) of imaging modality in the investigation of cardiac masses are:

Does the patient have a cardiac mass?

If she does what could it be, where is it located and what effects does it have on cardiac function?

The first question deals with detection or verification of the existence of a mass, the second, its characterization. In this instance we know, or at least suspect, that the patient has a mass.

The principal modalities in current clinical practice that can answer these questions with varying powers and abilities are contrast-enhanced CT scan (CECT), echocardiography, and MRI.

CECT will reveal most cardiac masses but lacks clarity in characterizing them. Original CT images are acquired axially and reformatted in different planes, which saddles it with problems with volume averaging. Finally, there is the problem of exposure to radiation and the nephrotoxic effects of iodinated contrast materials.

Echocardiography is excellent for detecting most cardiac masses but is limited by narrow acoustic windows, operator dependability, and inability to characterize lesions. It is, however, readily available and saves the patient exposure to radiation and iodinated contrast.

Of all the available modalities MRI is the most robust and capable imaging modality for the investigation of cardiac masses for these reasons:

Its ability to acquire its source images in multiple planes eliminates artifacts related to volume averaging.

This multiplanar ability also expands its panoramic capabilities, affording it a much wider area of coverage.

Using the signal characteristics of lesions it detects MRI is able to predict the tissue composition of most masses and, thus is able to characterize thrombi, lipomas, melanomas, cysts, and other solid masses. It is unable to classify lesions as malignant or benign; this requires the interplay of such characteristics of the lesion as, location, the age of the patient, existing diagnosis, and, possibly, biopsy.

Except in patients with impaired renal function it lacks the nephrotoxic burden that CT scan has and avoids exposure to radiation.

It has the ability to determine various cardiac functions and show the relationship of the mass to the cardiac chambers and its effects on cardiac function.

Recommended modality, in order of preference and capability:

MRI

Echocardiography

CECT scan

You may be dealing with one of four possibilities:

1. Snapping iliopsoas tendon
2. Iliotibial band friction syndrome
3. Loose bodies
4. Acetabular labral tear.

Each of these may be evaluated with either CT or MRI but the sensitivity of CT for some of the abnormalities is low, while MRI, though costlier, universally has higher sensitivity. Considering that a negative or equivocal CT result will lead to MRI evaluation, obtaining MRI in the first place is your most sensible and cost-effective approach, unless your patient has contraindications to MRI.

Your patient’s presentation suggests inferior vena caval obstruction or stenosis, a complication that occurs in 1 – 2% of liver transplant patients. A clot, an anastomotic stricture, retroperitoneal fibrosis, caval compression by the transplanted liver, caval kink or bending, or inadvertent ligature of the IVC during surgery are some reasons this happens.

The way the patient presents depends on where the obstruction lies, their other diseases, and the acuity of the obstruction.

Ultrasonography, CT, CTA, MRA and conventional venography can each be used to evaluate the patient.

Sonography is cheap, commonplace, and easy to perform. It shows indirect signs of caval obstruction such as loss of transmitted waveforms of cardiac rhythm but lacks the ability to characterize the obstruction for treatment planning. It may not show its location.

CT, CTA and MRA have cross-sectional powers that not only demonstrate the obstruction but also allows the identification of other problems.

Venography, CT, CTA and MRA each possesses the ability to demonstrate direct and indirect signs of inferior vena caval obstruction, but venography is more robust in this regard because it allows documentation of pressure gradients across obstructions, thus allowing planning for interventions. Additionally, although the standard treatment for post transplant caval obstruction is surgery, successful endoluminal management of such cases has been reported and this can be done at the time of diagnosis. For this reason, venography holds sway over its competitors.

Your concern, understandably, is whether you are dealing with a benign or malignant (primary or secondary) hepatic mass. This is a common scenario.

A cavernous hemangioma of the liver is the commonest benign hepatic mass (0.4% -7.3%) and often is found incidentally. It is a collection of tubular vascular channels lined with low-column endothelial cells and supported by a fibrous stroma. The flow of blood through these channels is comparable to the flow of water through a swamp, not a river; it is slow with no clear inflows or outflows. The collection is bound by a pseudocapsule.

Hepatomas are the commonest primary cancers of the liver, which like secondary hepatic malignancies, are composed of solid malignant cells often supported by a vascular stroma; the vascularity of hepatic metastases is variable and depends on the primary disease.

The probability that a lesion with benign imaging characteristics is not cancerous is 95% in a patient with no known primary cancer. This value drops to 80% if there is a primary malignancy elsewhere in the body. So the need to verify the nature of your patient’s mass depends, to some extent, on his history. Fortunately you have a number of diagnostic options to choose from, each with its pros and cons: sonography, hepatobiliary scintigraphy, CT scan, MRI, angiography, and percutaneous imaging-guided biopsy. The last is the most definitive and the most invasive of the options.

Sonography can reliably predict a lesion to be a hemangioma based on its appearance, especially when there is no cancer elsewhere in the body. This, however, is confounded by the shared appearance of some malignant liver masses with the sonographic appearance of hemangiomas, particularly the large hepatic malignancies.

Hemangiomas on delayed scintigraphic images show increased radiotracer activity but decreased activity on dynamic flow images, an expression of the sluggish blood flow through their rich vascular channels. Hepatomas and vascular metastases display increased radiotracer activity on both flow and blood pool studies because of their rich blood supply.

Hemangiomas and hepatic malignancies may look similar on unenhanced CT scans – low-attenuation masses. The way they enhance after the administration of a bolus of contrast agent on dynamic imaging can be decisive. Hemangiomas exhibit a nodular pattern of centripetal enhancement while malignancies, sometimes capable of centripetal enhancement, lack the nodular pattern. This is due to the slow opacification of the vascular channels filled with blood in hemangiomas while in malignancies contrast enhancement depends on the richness of vascular branches and the accumulation of the contrast agent in the tumor interstices.

On MRI hemangiomas behave like most solid masses on the T1-weighted and inversion recovery sequences; it is hypo- or isointense to muscle. On the T2-weighted sequence while hepatic malignancies and hemangiomas are bright in signal, hemangiomas become brighter as the time to echo (TE) is prolonged because of their rich constituent of free water spins while hepatic malignances diminish in intensity on account of the lattice framework within which their spins operate.

Although we do not use angiography much anymore in clarifying the nature of hepatic masses except in difficult cases it is still regarded as the ‘gold-standard’ method for that purpose.

Percutaneous biopsy of a hepatic mass may be your final choice when you run out of cross-sectional imaging options. It is possible and safe to biopsy cavernous hemangiomas with 20-gauge to 22-gauge needles although the specimens you obtain with such small needles reveal endothelial and blood cells and may miss malignant foci. You can employ larger-bore needles but must be prepared to risk significant bleeding.

In summary then, if a patient currently harbors a malignancy or did so in the past and presents with a new hepatic mass it should be biopsied because the risk of metastatic malignancy is high. If, on the other hand, there is no such history then such factors as availability of technology and skill and your preference and level of comfort should guide your choice of diagnostic modality in investigating such serendipitous mass.

Osteoid osteoma is a benign lesion of bones, composed of a nidus and a sclerotic rim. The nidus is made up of an osteoid matrix and a vascular fibrous connective tissue. It usually occurs in the femur and the tibia but can occur in other bones. When it measures greater than 2cm it is referred to as an osteoblastoma. Typically an osteoid osteoma causes pain responsive to non-steroidal anti-inflammatory agents presumably because of the high levels of prostaglandins in the nidus.

Your radiologic choices for investigating an osteoid osteoma are:

1. Plain radiography.

2. Triple-phase bone scan.

3. CT scan.

4. Magnetic resonance imaging.

Plain radiography will suggest the lesion but its sclerotic rim may overshadow the nidus.

CT is the imaging modality of choice for the detection of osteoid osteomas because it displays the nidus and the sclerotic rim well.

The MRI features of the osteoid osteoma are not specific. There are other abnormalities that resemble osteoid osteoma on MRI.

Nuclear scintigraphy will show the lesion in all 3 phases and the double-density sign is distinct for osteoid osteoma.

The approach I recommend is:

Determine the response of the lesion to NSAIDs; if this response suggests osteoid osteoma, perform CT scan.

Perform MRI if doubt remains or the lesion seems more aggressive.

Beware of these conditions that may resemble osteoid osteoma – Brodie’s abscess and Langerhans’ cell histiocytosis.

Imbalance of the fluid and electrolytes of the internal milieu is a common component of the conundrum of hepatic cirrhosis. It is due to a combination of hypoalbuminemia, portal hypertension, and the revving up of the renin-angiotensinogen-aldosterone axis by the prevailing diminished intravascular volume: hypoalbuminemia diminishes the oncotic pressure, which allows egress of fluid into the interstitial space, reducing the intravascular capacity. This stimulates the juxtaglomerular apparatus to go leading to retention of salt and water.

Frequently, the use of restriction of dietary salt and fluid consumption along with diuretics helps to control the problem, but it fails in 10% of patients. In such cases tense ascites and hepatic hydrothorax (usually right-sided) occur and significantly discomfort patient. They also can precipitate infection, respiratory discomfort or hepatorenal syndrome. Traditional teaching is to manage such patients with frequent large-volume paracentesis and thoracentesis, the placement of a Levine or Denver shunt, or to surgically fashion a porto-systemic venous anastomosis to decompress the portal system. Ultimately, the patient may require a liver transplant.

The situation, however, can be managed less invasively with a percutaneously-created intrahepatic shunt that connects a portal vein to a hepatic vein, which provides complete or partial relief in 60% to 92% of patients with refractory ascites and in 58% to 83% of those with hepatic hydrothorax. This shunt, commonly done by interventional radiologists, is called Transjugular Intrahepatic PortoSystemic Shunt (TIPS) and may serve your patient well. It is safe and effective.

The goal of TIPS is to reduce the pressure gradient between the portal venous system and the right atrium, without precipitating hepatic encephalopathy. The normal gradient is < 5mmHg. Pressures above this suggest portal hypertension, and when greater than 12mmHg are associated with variceal hemorrhage. By using stents of the right dimensions (the trend now is to use stents covered with Dacron or polytetrafluorethylene (PTFE) material to prolong the life of the stent) to line the intrahepatic tract, it is possible to reduce the portosystemic pressure gradient without causing encephalopathy. In the patient with refractory variceal hemorrhage the shunt also affords a path for embolization of the culprit esophageal varices.

Integral to this management strategy is the periodic surveillance of the patient with shunt ultrasonography or portal venography to detect and treat ensuing stenosis of the shunt.

There are 3 parts to your inquiry:

1. The incidence of simultaneous stenting of the iliacs. ( I assume you mean the common iliac arteries.)

2. The impact of such stenting on the ease of accessing the arteries in the future.

3. My wish for the development of endovascular materials that facilitate such stenting while reducing any adverse influence it may have on accessing the vessels in the future.

1. I do not have exact statistics on the commonality of bilateral common iliac artery stenting, but know that it is not infrequent in my practice. Common iliac arterial disease is common and I have addressed it unilaterally and bilaterally. I am more inclined to use the ‘kissing technique’ when I treat bilateral disease in that area, but have successfully treated unilateral disease without a second balloon in the contralateral vessel. Much of the outcome of interventions in that region, like in many areas of interventional radiology, depends on technique, experience, and finesse of an operator.

2. Again, technique determines whether accessing the vessels in the future will be impacted or not when the common iliac arteries are stented. The more the proximal end of a stent juts into the distal abdominal aorta, the more problematic accessing the contralateral iliac will be from a groin approach in the future. Approach from a brachial or radial puncture may not be difficult.

3. Certainly, any novel idea that improves past or existing deficiencies of what we do is welcome. For instance, it would be wonderful to have a unimodular bifurcated iliac conduit that can be deployed through a single femoral arterial puncture followed, of course, by tandem bilateral balloon inflation to appose the stent against the arterial wall well. Such unimodular conduit would have an aperture on its side that should be aligned with the lumen of the distal abdominal aorta to allow blood to flow into the iliacs. By straddling the aortic crutch with the stent one safeguards it against dissection or rupture during balloon inflation and a single balloon may be used for the inflation. This would even be better if the stent is mounted on the balloon, simplifying the entire process while making it safer and cheaper..

Yes.

As a group, splanchnic arterial aneurysms are rare. Splenic artery aneurysm represents 60% of these aneurysms and is 4 times commoner in women than men. Medial degeneration and fibrodysplasia in the face of sustained exposure to hormonal influences of pregnancy contribute to this higher prevalence of the disease among women. There are other causes of the disease, such as trauma, infection, pancreatitis, and autoimmune disease. When atherosclerosis is present it is more likely a secondary phenomenon.

These aneurysms are typically quiet, frequently coming to attention as incidental observations, during examination for other reasons. When they cause symptoms, which they do in 20% of patients, they do so as epigastric or left upper quadrant abdominal pain. Sometimes they rupture into the bowels or the peritoneal cavity proving more deadly. Fortunately, the latter occurs in less than 2% of patients and does so especially in pregnant moms (in whom there is a 95% chance of rupture during cyesis with 70% maternal mortality and 95% fetal mortality) and women of child-bearing age as a group, because of the effects of progesterone on arterial elastic tissues. For this reason, it is prudent and recommended that splenic artery aneurysms in symptomatic or pregnant patients be treated. Other situations that justify proactive management of these aneurysms include: women of child-bearing age because sooner or later they will become pregnant, when aneurysms are associated with inflammatory processes such as pancreatitis, or in low-risk patients whose aneurysms are greater than 2cm in diameter. In other situations the aneurysm may be watched for growth.

Percutaneous obliteration of splenic aneurysms is safer and more expeditious than surgical extirpation and is currently favored over surgery. Typically, coil embolization is used and this can be done while saving splenic tissue. Its pitfalls are postembolization syndrome (fever, left upper quadrant pain, leukocytosis, nausea, vomiting) that usually responds to treatment, splenic infarction and abscess formation.

Options in surgery include excision of the aneurysm, endoaneurysmal exclusion of feeding vessels with proximal and distal ligation of the aneurysm, and laparoscopic or open splenectomy with or without distal pancreatectomy, which are more herculean than percutaneous treatment.