eMedicine Specialties > Radiology > Gastrointestinal

Cholecystitis, Acute

Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Coauthor(s): Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute; Tufail Ahmed Patankar, MBBS, FRCR, PhD, DMRD, DMRE, DNBE, Consulting Neuroradiologist and Interventional Neuroradiologist, Department of Neuroradiology, Royal Preston Hospital, Lancashire Teaching Hospitals NHS Foundation Trust; Lalam Radhesh Krishna, MBBS, MRCS, Specialist Registrar, Department of Radiology, North Manchester General Hospital; Hemalatha Chandramohan, MBBS, Staff Physician, Department of Geriatric Medicine, Stepping Hill Hospital, United Kingdom; David Sherlock, MBBS, FRCS, Consulting Staff, Department of Surgery, North Manchester General Hospital, Christie Hospital; Ravi Devidas Kadasne, MBBS, MD, Specialist in Radiology, Emirates International Hospital, UAE
Contributor Information and Disclosures

Updated: Feb 4, 2009

Introduction

Background

Acute cholecystitis (AC) occurs as a result of inflammation of the gallbladder (GB) wall, usually as a result of obstruction of the cystic duct. In 90% of cases, AC is initiated by the impaction of a calculus in the neck of the GB or in the cystic duct.1 Acute acalculous cholecystitis (AAC) represents inflammation of the GB in the absence of GB calculi. AAC occurs more commonly in children and adults who are critically ill or in those who have recently undergone the stress of severe trauma, burns, or major surgery.

Plain abdominal radiograph of a 68-year-old woman...

Plain abdominal radiograph of a 68-year-old woman who presented with acute abdominal pain. There are multiple calculi distributed in a pyriform shape in the right upper quadrant; these are suggestive of gallstones. Gallstones were diagnosed during sonography several months earlier. A clinical diagnosis of acute cholecystitis was made. However, the plain radiograph also shows features of a pneumoperitoneum. At laparotomy, a perforated cecal carcinoma was found. There were no findings of acute cholecystitis.

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Plain abdominal radiograph of a 68-year-old woman...

Plain abdominal radiograph of a 68-year-old woman who presented with acute abdominal pain. There are multiple calculi distributed in a pyriform shape in the right upper quadrant; these are suggestive of gallstones. Gallstones were diagnosed during sonography several months earlier. A clinical diagnosis of acute cholecystitis was made. However, the plain radiograph also shows features of a pneumoperitoneum. At laparotomy, a perforated cecal carcinoma was found. There were no findings of acute cholecystitis.


Acute emphysematous cholecystitis is characterized by the presence of gas within the wall of the GB, the lumen of the GB, or both. It occurs more commonly in diabetic men; less frequently, it occurs in association with cholelithiasis. Emphysematous cholecystitis is considered either a complication of AC or a separate entity.

For excellent patient education resources, see eMedicine's Liver, Gallbladder, and Pancreas Center. Also, visit eMedicine's patient education article Gallstones.

  

Pathophysiology

Acute cholecystitis (AC) represents an acute inflammation of the gallbladder (GB), caused in most instances by obstruction of the cystic duct, resulting in acute inflammation of the GB wall; the usual cause of the obstruction is a gallstone. AC is one of the major complications of cholelithiasis. The inflammatory process begins with a calculous obstruction of the cystic duct or GB neck. The exact mechanism by which GB inflammation is initiated is unknown.

Microorganisms are identified in 80% of cases early in the course of disease; Escherichia coli is the primary organism found; other organisms include gram-negative aerobic rods, enterococci, and a number of anaerobes. The bacterial invasion is not considered to be a primary event, because in 20% of patients, no bacterial growth occurs in surgical specimens.2 The general consensus is that bacterial infection is a secondary event, not an initiating one.

Factors that may initiate the inflammatory process include the formation of inflammatory mediators (eg, lysolecithin and prostaglandins); an increase in intraluminal pressure in association with compromise of the blood supply; and chemical irritation by bile acids.

Spontaneous resolution of AC may occur within 5-7 days after onset of symptoms, because of the reestablishment of cystic duct patency. In the majority of such cases, fibrotic wall thickening of the GB occurs; this is characteristic of chronic cholecystitis. In more than 90% of cholecystectomy specimens, the histologic pattern is one in which AC is superimposed on chronic cholecystitis. If cystic duct patency is not reestablished, inflammatory cell infiltration of the GB wall in association with mural and mucosal hemorrhagic necrosis follows. Gangrenous cholecystitis may be seen in as many as 21% of cases.3

Acalculous cholecystitis occurs in a different clinical setting. It occurs more often in males (usually children) and in persons older than 65 years. The pathophysiology of acalculous cholecystitis is not well understood but is probably multifactorial. It is probable that acalculous cholecystitis occurs through the combined effects of the actions of systemic mediators of inflammation; localized or generalized tissue ischemia; and bile stasis.

Often, predisposing factors place persons at risk for bile stasis; such factors include starvation; use of parenteral nutrition; use of narcotic analgesics; and a lack of mobility in postoperative states. Hypovolemia and shock predispose patients to tissue ischemia. Ischemia, such as occurs in association with small-vessel vasculitis, may be a primary cause of acalculous AC; ischemia may also occur as a complication of hepatic chemoembolization. Often, functional cystic duct obstruction is present; such obstruction is related to inflammation and viscous bile. Extrinsic compression may play a role in the development of bile stasis.

In the majority of patients with acalculous AC, secondary infection with gram-negative enteric flora occurs4 ; however, in patients with typhoid fever, infection with Salmonella organisms has been identified as a primary event. AIDS-related cholecystitis and cholangiopathy may occur secondary to cytomegalovirus (CMV) infection and infections with Cryptosporidium organisms.

In patients who have emphysematous cholecystitis, ischemia of the GB wall is followed by infection with gas-forming organisms that produce gas in the GB lumen, in the GB wall, or both. In 30-50% of patients, preexisting diabetes mellitus is present; the male-to-female ratio is 5:1.1 Gas may be confined to the GB; however, in 20% of cases, gas is also seen in the rest of biliary tree. Gallstones are not present in 30-50% of cases, and the mortality rate is 15%.1  There is a predisposition for gangrene formation and perforation, but clinical symptoms are mild; such symptoms can be deceptive. Emphysematous cholecystitis may occur after chemoembolization performed as palliation for hepatocellular carcinoma; after atheromatous embolism during aortography; and after GB hypoperfusion during cardiorespiratory resuscitation.

Opiate narcotic addiction has been found to be a major risk factor for the occurrence of acute calculous cholecystitis.5

The following factors have been associated with acalculous cholecystitis6 :

  • Surgery, particularly abdominal
  • Severe burns
  • Gastroenteritis
  • Severe trauma
  • Total parenteral nutrition (TPN)
  • Mechanical ventilation
  • Blood transfusion reactions
  • Dehydration
  • Narcotic analgesia
  • Diabetes mellitus
  • Antibiotics, particularly broad spectrum
  • Hepatic arterial embolization (islet cell tumors and hepatocellular carcinoma)
  • Postpartum complications
  • Vascular insufficiency and vasculitis, such as systemic lupus erythematosus (SLE) and Sjögren syndrome
  • Arteriostenosis/hypertension
  • AIDS, CMV, Cryptosporidium infections
  • Typhoid

Empyema of the GB may develop as a complication of AC. In AC, the GB is usually distended as a result of the mixture of inflammatory cells with bile and calculi. The bile becomes infected as the disease progresses. In 85% of patients, disimpaction of the cystic duct occurs, and inflammation in the GB settles. If the cystic duct remains obstructed, the inflammatory process may progress to GB empyema and eventually result in perforation.

Frequency

United States

Because of the close relationship between gallstones and acute cholecystitis (AC), the distribution and the incidence of AC follow that of cholelithiasis. Gallstones are present in more than 20 million persons in the United States, resulting in 500,000 cholecystectomies annually. In 10-20% of patients, AC occurs as a complication in cases of symptomatic gallstones.1  

Acute acalculous cholecystitis (AAC) accounts for 5-15% of cases of AC1 ; the incidence is higher in ICU patients, particularly those with burns and trauma. Most cases of AC in the ICU are acalculous; in this setting, the overall incidence of acalculous AC is only 0.2%. In the majority of postoperative cases (90%), AC is acalculous.7

International

The incidence rates of acute cholecystitis are approximately the same in Western Europe and the United States. Worldwide, the exact incidence is not known.

Mortality/Morbidity

Mortality associated with acute cholecystitis is 5-10%; death mostly occurs in patients older than 60 years.

Acute cholecystitis (AC) may be complicated by empyema, gangrenous cholecystitis, gallbladder (GB) perforation, pericholecystic abscess, and bilioenteric fistula. Gangrenous cholecystitis is a frequent cause of GB perforation. Suppurative complications are more frequent in the elderly. Most localized perforations may be satisfactorily treated by means of surgery.

Although free intraperitoneal perforation is rare, it is associated with a mortality of 25%. Necrosis of the GB wall occurs in about 60% of cases of acalculous cholecystitis because gangrene and perforation are frequent occurrences. Mortality ranges from 9-66%.8

The higher mortality in acute acalculous cholecystitis (AAC) has been attributed to delayed diagnosis and comorbidities. The morbidity associated with emphysematous cholecystitis is higher, because of GB wall gangrene and perforation.

Recurrent symptoms are common in patients with AC who are treated expectantly; most patients need elective cholecystectomy.

Race

Because of the close relationship between gallstones and acute cholecystitis (AC), the incidence of AC is higher in populations in which the incidence of gallstones is higher. Such populations include Native Americans and persons of Chinese or Japanese descent.

Sex

The male-to-female ratio of acute cholecystitis is 1:3. Acute acalculous cholecystitis (AAC) is more common in men than in women; the male-to-female ratio of AAC is 2-3:1. Acute emphysematous cholecystitis is also more common in men than in women.

Age

Acute cholecystitis affects persons of any age group; the peak incidence is in persons 40-60 years of age. Approximately 50% of cases of AC in children are acalculous.

Anatomy

The gallbladder (GB) stores and concentrates bile, and the ducts function as a bile drainage system. The flow of bile through the bile ducts is affected by several factors, including hepatic secretory pressure, the tone in the sphincter of Oddi, the rate of GB fluid absorption, and GB contraction.

Anatomically, the GB is a pear-shaped musculomembranous reservoir lying in the GB fossa on the inferior aspect of the liver. The fundus of the GB lies close to the anterior abdominal wall, near the hepatic flexure of the colon. The surface marking of the GB fundus is in the region of the costal cartilage. At this point, it is covered by peritoneum; its appearance may be obscured, owing to its proximity to the hepatic flexure of the colon. The body of the GB is adjacent to the duodenum, which indents and produces a frequent ultrasonographic artifact that mimics gallstones or a mass in the GB.

An inflamed GB may perforate the colon or duodenum because of the close proximity of the GB to these structures. The mucosa of the GB neck is thrown into folds, giving an echogenic appearance that may also mimic gallstones. A small pouch, known as the Hartmann pouch, projects from the right side of the GB neck. In patients in whom the Hartmann pouch is visible, pathology, particularly dilatation, is often present. The GB fundus is often folded over; in such cases, the GB then assumes a double-barrel appearance.

In 2-6% of the GBs, pseudoseptation of the GB fundus is seen. This pseudoseptation is usually the result of kinking; occasionally, a true septum, called the phrygian cap, is seen. The phrygian cap is of no pathologic significance. A cystic artery supplies the GB; it is usually a branch of the right hepatic artery. The artery lies in the triangle made by the liver, the cystic duct, and the common hepatic duct (CHD). Other, smaller tributaries supply the GB through the right hepatic artery via the GB bed through the liver. Usually, the right hepatic artery passes behind the CHD, and the cystic artery crosses behind the cystic duct. In 25% of cases, the common hepatic artery passes in front of the CHD, and the cystic artery passes in front of the cystic duct.

The recognition of GB blood supply is becoming increasingly important, owing to the use of vascular intervention in the liver, particularly chemoembolization. Catheters should be placed distal to the cystic artery to prevent embolic material from entering the cystic artery and causing GB ischemia.

Ultrasonographic anatomy

The GB is a pear-shaped anechoic structure indenting the inferomedial aspect of the right lobe of the liver. A linear echogenic line representing fat in the main interlobar fissure is interposed between the GB and the right main portal vein. The GB mucosa is hyperechoic; the submucosa and the muscle layer are hypoechoic; and the serosal surface fatty layer is hyperechoic.

A linear fold known as the junctional fold is present on the posterior GB wall at the junction of the body and neck. This structure is of no pathologic significance.

Sound waves from the spiral valve of the neck may cast an acoustic shadow and may mimic a gallstone. The normal thickness of the GB wall is usually less than 3 mm. Provided that the patient has been fasting for 8-12 hours, visualization of the normal GB should be nearly complete. Nonvisualization of the GB is a pathologic finding in 96% of cases involving truly fasting patients.

GB dimensions

The normal gallbladder usually measures 7-10 × 2-3.5 cm. In the fasting patient, the normal dimensions of the GB seldom exceed 4 × 10 cm. The size of the GB generally increases with age, but the GB wall thickness is unaffected by age. The normal wall thickness is 2-3 mm. In neonates, the GB measures 0.5-1.6 cm (mean, 0.9 cm) × 2.5 cm; the wall thickness is usually 1 mm.

GB anomalies

Many anatomic anomalies affect the GB. The recognition of these anomalies is important in the context of GB disease. Errors in GB surgery are frequently a result of the failure to appreciate variations in the anatomy of the biliary system.

Anomalous positioning or orientation of the GB includes situs inversus, in which the GB is in the left upper quadrant. It is rare that a GB occurs in the left lobe of the liver in the absence of situs inversus. Heterotaxia, which represents an intermediate situs in which GB is located in the midline, may be associated with asplenia, polysplenia, pulmonary isomerism, and congenital heart disease.

The GB may be anomalously located in a vertical or horizontal orientation. It may descend into the right iliac fossa, particularly in the presence of the Riedel lobe.

Unusual locations include intrahepatic, suprahepatic, lateral, anterior abdominal wall, and retrorenal sites. The GB may also be present in the thorax; in the falciform ligament, the interlobular fissure, or both; and in the transverse mesocolon.

A wandering GB results when the GB is suspended on its own mesentery. Recognition of this anomaly is important because such a GB is prone to torsion.

Agenesis is a rare anomaly found in 0.04-0.07% of cases at autopsy. Agenesis may be associated with biliary atresia, imperforate anus, CHD, and anomalies of the common bile duct (CBD). Rarely, the GB opens separately into the duodenum.

The most common anomalous shape is that involving the phrygian cap, in which the fundus of the GB is folded back on itself, producing a kink in the fundus. Rarely, the GB appears as a diverticulum with no cystic duct. Other anomalies include a fishhook, a siphon, and an hourglass configuration. A diverticulum of the GB is extremely rare; it is usually located at the neck of the GB. This is rarely symptomatic unless it is complicated by calculus disease.

True duplication of the GB is rare, but it has been reported in as many as 1 in 3000-4000 people; the male-to-female ratio is 2:1. Triplication is even rarer; it may be an incidental finding at autopsy. In duplication, each GB may have a separate cystic duct, or the GBs may share 1 cystic duct. A septate GB may have an isolated transverse septum. In true duplication, a longitudinal septum is present.

A multiseptate GB is extremely rare; it is characterized by multiple loculi connected by small pores. Patients with this condition are particularly prone to bile stasis and calculus formation.

In cases of anomalous cystic duct insertion, the cystic duct inserts into the CBD or CHD, either high or low. The cystic duct is often intramural, running for some distance in the wall of the CBD within a common sheath. Congenital stenosis of the cystic duct is extremely rare; calculus disease may occur as a complication in such cases.

Heterotopic tissue may be present within the GB; there are reports of gastric or pancreatic tissue occurring within the GB wall. This tissue may mimic tumors.

Presentation

Clinical findings

Acute cholecystitis usually occurs with right upper quadrant pain and tenderness. The abdominal pain increases with time. The site of pain is usually the right subcostal region, although the pain may begin in the epigastrium or the left upper quadrant and then shift to the right subcostal region to the area of the gallbladder (GB) inflammation. Referred pain to the right shoulder or the interscapular region may be experienced. Approximately 70% of patients have had previous attacks of similar pain that spontaneously resolved. Anorexia, nausea, and vomiting may occur, but vomiting is seldom severe. Most patients are afebrile and have no leukocytosis.

When fever occurs, the patient's temperature is seldom higher than 38°C. Chills are unusual; their presence suggests a case of complicated cholecystitis (abscess or associated cholangitis).

Palpation of the right subcostal area reveals muscle spasm. During deep inspiration, the tenderness becomes suddenly worse and produces an inspiratory arrest called the Murphy sign. The Murphy sign may be elicited with an ultrasound probe.

In approximately 35% of patients, a distended, tender GB may be palpable as a distinct mass. This is an important clinical finding and may confirm the diagnosis.

Approximately 20% patients with acute cholecystitis (AC) have mild jaundice, which may be related to common hepatic edema, bile duct edema, or both, or to the presence of calculi within the CBD.1 In most patients, improvement occurs within 24 hours after hospitalization, and signs and symptoms gradually subside. Persistent pain, fever and leukocytosis, chills, and more severe localized or generalized tenderness may indicate complicated disease, such as abscess formation or GB perforation. The development of empyema of the GB may produce systemic toxicity, and it may be predictive of GB perforation.

Leukocytosis is pronounced in cases of empyema; it is usually in the range of 10,000-15,000/μ L. The clinical differential diagnosis includes acute pancreatitis; perforated peptic ulcer; gonococcal perihepatitis (Fitz-Hugh-Curtis syndrome) in women; acute hepatitis; pneumonitis; pyelonephritis; cardiac disease; sickle cell crises; and leptospirosis.

Acute acalculous cholecystitis (AAC) is difficult to diagnose clinically. It often occurs in children (50%) and in patients who are critically ill or who have recently undergone stress from severe trauma, burns, or surgery. Predisposing factors include prolonged fasting, immobility, and hemodynamic instability. Often, these patients cannot express pain; however, fever, jaundice, vomiting, abdominal tenderness, leukocytosis, and hyperbilirubinemia are highly suggestive findings.

Children with AAC more often present in the outpatient setting than in other settings. They usually present with right upper quadrant pain in the absence of gallstones. These patients are usually treated with cholecystectomy.

Some elderly patients with AC present with few signs. A minority of adult patients, mostly elderly patients with AAC, present in the outpatient setting. These cases are diagnosed and treated early and are associated with a good prognosis.

Causal factors

  • Hemolytic
    • Hemolytic anemias, such as congenital spherocytosis (43-85%), sickle cell disease (7-37%), and thalassemia
    • Cardiac causes, such as mitral valve stenosis and prosthetic heart valves
    • Pernicious anemia
    • Aortic aneurysm
    • Hypersplenism
  • Metabolic
    • Overweight, female sex, fair complexion, fertile, and age of 40 years or older
    • Diabetes mellitus
    • Obesity
    • Hemosiderosis
    • Pregnancy
    • Prolonged use of estrogen/progesterone
    • Hyperparathyroidism
    • Cystic fibrosis
    • Pancreatitis
    • Hypothyroidism
    • Muscular dystrophy
    • Crohn disease
    • Ileal resection and intestinal malabsorption
    • Type IV hyperlipidemia
    • Surgical bypass for obesity
    • Cholestasis
  • Miscellaneous
    • Chronic hepatitis
    • Cirrhosis
    • Congenital biliary malformation (eg, Caroli disease)
    • Parasites (eg, ascariasis, liver flukes), which form a nidus for development of calculi
    • Drugs such as methadone
    • Biliary strictures (eg, oriental cholangiohepatitis [bile stasis])
  • Genetic
    • Genetic predisposition in some populations, such as Native Americans
    • Higher incidence of intrahepatic gallstones in Chinese and Japanese populations

Preferred Examination

Clinically, few signs differentiate uncomplicated acute cholecystitis (AC) from complicated AC. Complications of AC may have serious clinical implications. These complications include perforation, pericholecystic abscess, empyema, and bilioenteric fistula. Therefore, radiologic imaging makes a substantial contribution to the differential diagnosis. Ultrasonography significantly aids in the diagnosis of AC, although most ultrasonographic signs are not typical but are suggestive of AC. Inflammatory pericholecystic reaction in the GB fossa is better depicted with CT than with other modalities. CT is also useful in making the differential diagnosis when obesity or gaseous distention limits the use of ultrasonography.

MRI may demonstrate the same morphologic changes as CT, displaying inflammatory changes in the GB wall, pericholecystic fat, and intrahepatic periportal tissues. Plain radiography greatly contributes to the diagnosis of emphysematous pyelonephritis; ultrasonography and CT findings may further confirm the diagnosis (although CT scanning is not strictly needed to make the diagnosis). Cholescintigraphy is an extremely sensitive diagnostic modality in diagnosing AC, although the findings are nonspecific. Oral cholecystography is of historical interest and has no role in the diagnosis of AC. Arteriography is seldom required for AC.6,9,10,11,12,13,14

Limitations of Techniques

For patients with acute cholecystitis (AC), plain radiographic findings may be entirely normal. Radiolucent calculi are visible. Opaque calculi in the right upper quadrant on plain abdominal radiographs may be an incidental finding and is not necessarily related to AC.

Oral cholecystography is of historical interest and has a low sensitivity and specificity in the diagnosis of AC.

The main features of AC on ultrasonography are all nonspecific findings. Examples include gallbladder (GB) thickening, calculi in the GB, a positive ultrasonographic Murphy sign, and pericholecystic fluid. The sonographic Murphy sign is negative in as many as 70% of patients with AC. In cases of perforated GB, the wall of the GB is not well delineated, and a localized interruption of the wall may not be noted at the site of perforation. The diagnosis is difficult to make with ultrasonography in obese patients and in patients with gaseous distention. Ultrasonography remains operator dependent.

CT exposes the patient to a radiation burden, which may not be necessary.

Arteriography is invasive and is seldom indicated.

MRI has limited availability, and it is expensive. In addition, in patients with certain prosthetics, surgical clips, cardiac pacemakers, or claustrophobia, the diagnosis is difficult to make with MRI.

Although cholescintigraphy is sensitive, it has low specificity and involves the use of ionizing radiation.

Differential Diagnoses

Cholecystitis, Acalculous
Cholelithiasis
Pancreatitis, Acute

Other Problems to Be Considered

Cholangitis
Cholecystitis, chronic
Peptic ulcer perforation
Acute hepatitis
Perihepatitis

The differential diagnosis is broad, both on clinical and imaging examination, because specific signs are few and because the diagnosis is made on the basis of a constellation of imaging findings. The differential diagnosis of acute acalculous cholecystitis is particularly extensive because of the broad range of comorbidities present in affected patients.

More on Cholecystitis, Acute

Overview: Cholecystitis, Acute
Imaging: Cholecystitis, Acute
Follow-up: Cholecystitis, Acute
Multimedia: Cholecystitis, Acute
References
Further Reading
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Keywords

acute cholecystitis, acute acalculous cholecystitis, acalculous cholecystitis, AC, AAC, necrotizing cholecystitis, emphysematous cholecystitis

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Contributor Information and Disclosures

Author

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP is a member of the following medical societies: American Institute of Ultrasound in Medicine, Radiological Society of North America, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Coauthor(s)

Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR is a member of the following medical societies: British Medical Association, Royal College of Physicians, and Royal College of Radiologists
Disclosure: Nothing to disclose.

Tufail Ahmed Patankar, MBBS, FRCR, PhD, DMRD, DMRE, DNBE, Consulting Neuroradiologist and Interventional Neuroradiologist, Department of Neuroradiology, Royal Preston Hospital, Lancashire Teaching Hospitals NHS Foundation Trust
Tufail Ahmed Patankar, MBBS, FRCR, PhD, DMRD, DMRE, DNBE is a member of the following medical societies: British Society of Neuroradiologists and Royal College of Radiologists
Disclosure: Nothing to disclose.

Lalam Radhesh Krishna, MBBS, MRCS, Specialist Registrar, Department of Radiology, North Manchester General Hospital
Disclosure: Nothing to disclose.

Hemalatha Chandramohan, MBBS, Staff Physician, Department of Geriatric Medicine, Stepping Hill Hospital, United Kingdom
Disclosure: Nothing to disclose.

David Sherlock, MBBS, FRCS, Consulting Staff, Department of Surgery, North Manchester General Hospital, Christie Hospital
Disclosure: Nothing to disclose.

Ravi Devidas Kadasne, MBBS, MD, Specialist in Radiology, Emirates International Hospital, UAE
Disclosure: Nothing to disclose.

Medical Editor

John L Haddad, MD, Clinical Associate Professor, Department of Radiology, Weill Medical College of Cornell University; Director of Body MRI, Department of Radiology, Methodist Hospital in Houston
John L Haddad, MD is a member of the following medical societies: American College of Radiology, American Medical Association, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Arnold C Friedman, MD, FACR, Associate Chairman, Department of Radiology, University of Florida Health Science Center; Chief, Department of Radiology, Shands-Jacksonville Hospital
Arnold C Friedman, MD, FACR is a member of the following medical societies: American College of Radiology, American Institute of Ultrasound in Medicine, American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

John Karani, MBBS, FRCR, Consulting Staff, Department of Radiology, King's College Hospital, London
Disclosure: Nothing to disclose.

 
 
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