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Reporting errors happen in radiology. Certainly they are not intentional, and many have little or no consequence to patients; others are significant. In an effort to be helpful, I would like to share four strategies to help reduce reporting errors in radiology. They are not intended to be in any way comprehensive, but they are actions that might help to increase accuracy.

It’s important to emphasize that I prefer the term “discrepancy” rather than error for much of what we’re considering. The term error implies a mistake, and that a clear-cut diagnosis and correct report are possible. However, as radiologists we know that there is not always a single definitive outcome from an imaging study. Imaging is rarely binary – “normal” or “abnormal”. We render an interpretation that is based on our understanding of the patient’s condition at the time of the exam. Often an “error” is determined later in the light of additional information and a developing clinical picture. The concept of necessary fallibility must be accepted. However, I will use the term “error” for the purpose of this blog, as it is the label most frequently used in literature and discussion.

How prevalent are errors? It seems that 3-5 % is the best minimum error rate achievable even when working in the best of circumstances (1). Knowing that one billion radiologic imaging exams are read annually worldwide, and assuming an average error rate of 4 percent, that equals approximately 40 million radiologist errors annually (2).

Strategy: address cognitive biases in radiology

We all have cognitive biases. They are the result of our brains’ attempts to simplify information processing. We cannot rid ourselves of these biases, but we need to be aware of them and take corrective actions to minimize their influence on our reporting (3). The following are only a selection of the many recognized biases to which radiologists are prone, with some suggested corrective measures of varying practical applicability. Admittedly, some of the suggested correction strategies are not feasible in usual radiology practice.

Strategy: address cognitive biases in radiology

We all have cognitive biases. They are the result of our brains’ attempts to simplify information processing. We cannot rid ourselves of these biases, but we need to be aware of them and take corrective actions to minimize their influence on our reporting (3). The following are only a selection of the many recognized biases to which radiologists are prone, with some suggested corrective measures of varying practical applicability. Admittedly, some of the suggested correction strategies are not feasible in usual radiology practice.

  • Anchoring bias – this is the tendency to rely on our initial impression and fail to adjust it in the light of subsequent information. Correction: avoid early guesses, and seek to disprove your initial diagnosis rather than confirm it. In some cases, you might want to get a second opinion.
  • Framing bias – this is the result of being influenced by the way a problem is framed. For example, if a referrer states, “the patient may have leprosy,” then your interpretation will be influenced by that statement, even though the likelihood of imaging findings being due to leprosy may be remote. Correction: initially review the study blindly before reading the clinical information.
  • Availability bias – this is the tendency to consider a diagnosis more likely if it readily comes to mind. For example, you are more likely to consider a pathology that you saw on a study the previous day, even if its likelihood is very small. Correction: try to use objective information to estimate the true base rate of that diagnosis, rather than relying on a quick initial impression.
  • Satisfaction of search – this is the tendency to stop searching for abnormalities once a likely diagnosis or first abnormality is found. Correction: use a systematic interpretation strategy, perhaps relying on a checklist or algorithmic approach, to help ensure a thorough review. Additionally, do a secondary search after initial abnormality detection, and also consider known combinations (e.g associated multiple injuries that commonly occur together in the knee).
  • Premature closure – this is the tendency to accept a diagnosis before full verification. Correction: always give a differential diagnosis. Never make a working diagnosis absolute without pathological confirmation. It’s important to make clear that I DON’T advocate this suggested corrective strategy; it would diminish the value created by radiology in patient care).

Strategy: probe for more patient information

I realize that it can be difficult to find time for clinical consultations with our referring colleagues, and for direct interaction with our patients. But I strongly believe that these activities are essential to improving our clinical practice. Also, their value is supported by several studies that show a higher percentage of errors occur when reporting is done by off-site reporters who had no opportunity to interact with the referrers or patients, and were presented with only a limited amount of clinical information (4). It is part of the job of radiologists to probe for more information when our instincts tell us the picture we have been given is incomplete.

A few helpful actions are:

• Discussing the appropriateness and justification of scans

• Tailoring studies to the specific clinical question

• Asking for appropriate missing snippets of history, rather than just proceeding because of time pressures

• Having direct discussions with referrers (including within multidisciplinary team meetings) about the significance of the scan results

Strategy: improve report writing

Sometimes we may interpret imaging studies accurately but be unclear in how we convey our meaning in the written report. From the patient’s perspective, the outcome can be the same whether we miss a potential diagnosis or we identify the relevant abnormalities but fail to effectively communicate the key findings and/or their meaning in a poorly-written report. If our reports are incoherent, rambling, and verbose – and if it’s impossible for the referrer to clearly understand what is most important in them – then we have failed to communicate, and are as guilty of “error” as if we missed the relevant findings entirely.

In fact, communication failure in general is the fourth most common reason for radiologists in the U.S. being sued, and 60% of these cases were due to a failure to highlight an urgent or unexpected abnormal finding and to emphasize it appropriately in reports.

I recommend you take a look at your own past reports with a fresh set of eyes, or perhaps ask a trusted colleague to read them. Look closely at your report structure, its organization, and your vocabulary choices. Are there mistakes in grammar or punctuation? Have you failed to correct errors in voice-recognition transcription, leading to confusion about your meaning?

I personally am not a huge fan of structured reporting, but I acknowledge that using them, especially for complex imaging studies, increases thoroughness and accuracy.

My recommendation: make your reports simple and clear, correct typographical errors, include what matters, do not include the irrelevant.

Strategy: ease mental and visual fatigue

Visual fatigue results from prolonged focusing on a workstation, and can be  alleviated (in part) by accommodative relaxation, shifting your visual focal point from near to far (e.g. looking at a distant object for 15-30 seconds) every 15 minutes.

Prolonged focus on a workstation causes visual and mental fatigue.

Mental fatigue is the consequence of continuous and prolonged decision making. We need to be aware that our cognitive processes respond to this mental strain by taking short cuts that might result in poor judgement and diagnostic errors. Here are a few suggestions that that might help you ease your mental fatigue (5):

  • Read the most difficult cases at the beginning of your shift when you are fresh.
  • Switch periodically between modalities.
  • Take structured breaks.
  • Reduce unnecessary interruptions and distractions

It is impossible to expect 100 percent accuracy 100 percent of the time, even under the best of circumstances. Our working environments in this current era of expected hyper-efficient radiology are far from ideal. Radiologist “error” may arise from personal issues, such as the visual and mental fatigue mentioned above, but systemic issues beyond our control (staff shortages, excessive workload, inadequate equipment, poor lighting conditions, lack of availability of previous studies etc.) are also frequent contributors, and they are unlikely to ever be completely eliminated.

Shifting to a system-centered view of errors

In addition to taking steps to minimize the occurrence of errors, we should also consider our reaction when they do happen. The traditional approach within medicine has been  person-centered, with errors viewed as indicative of a personal or professional failure. This culture of “naming, shaming and blaming” can result in suppression of error reporting as well as missed opportunities to learn from each other’s mistakes, and to make process improvements. We need understanding and support from each other and from others in healthcare when mistakes happen.

I believe we should shift our focus to the system, rather than the individual. A system-centered approach facilitates exploration of why an error happened and what can be done to prevent it from happening again. The National Radiology Quality Improvement Programme of the Faculty of Radiologists of the Royal College of Surgeons in Ireland is an example of an effort to embed in practice this more-enlighted and more-beneficial approach to errors. (6)

I also believe that we as a profession need to educate our patients about error rates. As leaders in radiology like Giles Maskell have emphasized, there is a yawning gap between what we know to be our error rate and what our patients believe it to be. The discovery in hindsight of an error in interpretation of a radiological image is often perceived by the patient as something shocking and exceptional, calling into question the competence of the radiologist and the overall care they are receiving. It would benefit radiologists if patients, referrers, and others in healthcare better understood the pervasive nature of radiological “error”, the inherent uncertainty in much of what we do,  and the measures we take to avoid it, while also emphasizing the enormous benefit that radiology – despite its inherent flaws – continues to bring to patient care.

In closing, I will share this quote from Sir William Osler, English/Canadian physician, who said, “Errors in judgement must occur in the practice of an art which consists largely in balancing probabilities.”

What are your thoughts and strategies for reducing errors in radiology? Please comment below.

This content was originally presented by Dr. Brady at ECR 2023.


Esr president Adrian Brady recently sat down with Carestream to discuss the 4 best  Strategies for reducing reporting errors in radiology.

We would like to thank https://www.myesr.org/ for providing valuable information and resources for this article.



HBV and HCV are major causes of viral hepatitis that lead to the development of cirrhosis and HCC. HBV gains entry into liver cells through a receptor mediated pathway. HBV-DNA integration into host genetic machinery causing DNA methylation resulting in oxidative stress and formation of HBx protein(1). The risk of developing HCC has been shown to be proportional to HBV-DNA level in liver cells. Chronic illness results from persistence of the virus in the host cells via various mechanisms that include infection of immune defense control centers, viral inhibition of antigen presentation,selective immune suppression, down-regulation of viral gene expression, and viral mutations that functionally incapacitate virus-specific T cells from recognizing HBV antigen(2)

HCV hijacks host cellular machinery to increase cellular proliferation, steatosis, inflammatory processes, mitochondrial dysfunction, insulin resistance, all leading to oxidative stress, genetic instability and DNA damage with cirrhosis and HCC as a likely outcome(3)


Diabetes mellitus, alcohol abuse, cardiovascular disease, liver inflammation, obesity, dyslipidemia and non-alcoholic fatty liver disease (NAFLD) are some other major contributors to HCC development(4)

Accumulation of iron in the liver of NASH and HCC patientsis correlated with progression of fibrosis and HCC. NAFLD provides the metabolic environment to induce insulin resistance a known etiological factor for HCC(4,5).

Obesity impairs metabolism, induces inflammation and is an etiological factor for NAFLD, steatosis, NASH, hepatic fibrosis, cirrhosis, and ultimately HCC.

Toxic by-products of alcohol catabolism such as accumulation of acetaldehyde and free radicals can influence oxidative stress, apoptotic cell death, necrosis and necroptosis(6).Reactive oxygen species (ROS) generation is the result of increased inflammatory cytokine. ROS-induced DNA damage, genomic vulnerability of hepatocytes and T-lymphocyte suppression contribute to HCC development. Alcohol diet have shown exacerbation of inflammation, epithelial-mesenchymal transition (EMT) andfibrosis, and consequent progression to HCC (3).

Other possible risk factors include genetic predisposition and congenital abnormalities, toxic exposures (aflatoxin or arsenic contaminated food), and autoimmune diseases of the liver. The pathogenesis of aflatoxin B1 (AFB1) – induced HCC includes several mechanisms, including the formation of mutagenic and carcinogenic intermediates and adducts. These adducts and intermediates can also directly induce a mutation at codon 249 of the p53 tumor suppressor gene. This replaces arginine with serine, a change that reverses the tumor suppressing ability of the gene. There are reports that suggest that AFB1 acts synergistically with HBV to induce HCC(7).




  • Small focal HCC appears hypoechoic compared with normal liver.
  • Larger lesions appear heterogeneous due to fibrosis, fatty change, necrosis and calcification.
  • A peripheral hypoechoic halo may be seen with focal fatty sparing
  • Contrast-enhanced ultrasound 1

o arterial phase-arterial enhancement from neovascularity

o portal venous phase

 Decreased echogenicity relative to background liver ie wash out.

 Tumour thrombus may be visible.(8)

Figure 1:Two different HCC lesions (arrows) in gray-scale ultrasound (a,c)
and in late phase of contrast-enhanced ultrasound (b,d)(9)


Imaging protocols are

  1. The patient was positioned in the supine position.
  • Technical parameters were X-ray tube current 160 to 220 mA; tube voltage 120 kV;

collimation 5mm; rotation speed 0.75 s; matrix 512×512. Iohexol (350 g/L) was used to

perform the contrast-enhanced scanning.

  • A high-pressure syringe was used to inject 1.2-2 ml/kg of contrast agent at injection rate

of 3.5- 4.0mL/s. Twenty millilitre saline were later injected at the same rate.

  • Scanning range was set to from the lower chest to the to lower abdomen level.
  • All image data were transmitted directly to our picture archiving and communication

system. Sagittal and coronal reformats of images were also obtained(10).

Imaging of FLLs in CT requires the use of a multi-phase study protocol.

  • Includes a phase prior to the intravascular administration of contrast agent.
  • Phases obtained after intravascular administration of contrast medium – Hepatic arterial

phase(HAP), Portal Venous Phase(PVP) and Equilibrium phases(EP) obtained routinely

40, 60 and 180 seconds post contrast administration respectively in a multi-row CT unit

  • EP may be also referred to as an early delay phase in comparison to the late delay phase,

obtained after 10 to 15 minutes after administration of contrast medium, acquired if the

imaging protocol is extended to detect lesions with a high content of fibrous tissue(9).

Figure 2:Multiphase CT. Native examination (a), hepatic arterial phase with contrast agent in
hepatic arteries and slight enhancement in portal vein (b), portal venous phase (c) equilibrium
phase (d).

Imaging features in Hepatocellular carcinoma

  • HCCs enhance strongly in the HAP, depending on the size of the tumor and the presence

of regressive changes homo- or heterogeneously. Large tumors will typically present with

heterogeneous enhancement, often with so-called mosaic pattern as opposed to small,

early forms of hepatocelullar carcinomas

2. Washing-out of the contrast agent in PVP (the phase of the strongest enhancement of the

liver parenchyma) or/and EP is a sine qua non for diagnosing HCC with specificity of 95-


3. If tumor pseudo-capsule is present, it is more clearly visible in the PVP and EP than in

HAP, with delayed enhancement in EP. Tumors with pseudo-capsule show better


Figure 3: Schematic presentation of pattern of enhancement of HCC lesion with strong enhancement
in HAP and wash-out of contrast agent in subsequent PVP and EP(12)
Figure 4:CT axial images. HCC in hepatic arterial phase (a) and equilibrium phase (b). Wash-out
feature and enhancing tumor pseudo-capsule is visible in the latter(9).


Standard MRI protocol consists of

  • Patients were positioned supine head first on the MRI table, then the MRI was

performed including T2 weighted fast spin-echo (T2-FSE) and DIXON, Duel echo

sequence(TE 90 and 180 ms), chemical shift imaging (in- and opposed-phase) and

diffusion-weighted image (DWI) map was performed for using b value of 500 (with

TR 1300 ms & TE 64 ms), with corresponding ADC mapping.

  • CE-MRI was performed afterward using gadopentetate dimeglumine

(Omnivist)/gadoterate meglumine(Clariscan) injected through an antecubital

intravenous catheter at a rate of 1.2 ml/min over 15 s and a dose of 0.2 ml/kg followed

by saline chaser of 20 ml at a rate of 1–2 mL/s

  • Dynamic contrast-enhanced sequences were acquired using DIXON sequence

acquired before (pre-contrast) and after contrast injection at 15-20 s (arterial phase), 40

s (portal phase), 60s (venous phase), and 180s (delayed phase). All contrast sequences

were acquired at the axial plane(13).

Imaging features in Hepatocellular carcinoma

  • Pre-contrast MRI sequences the majority of large HCCs show decreased signal intensity

in T1-weighted and increased signal intensity in T2-weighted images.

Small lesions tend to remain isointense to the adjacent liver parenchyma in T1-weighted

images Presence of intracellular fatty components may be easily confirmed in phase and

out of phase sequences.

  • Decrease in signal intensity in T2-weighted images is seen in case of fibrous tissue,

while areas of necrosis present especially within large foci cause an increase in signal

intensity and lead to heterogenous enhancement.

  • Low signal intensity of regenerative nodules in T2-weighted images resulting from

characteristic iron deposits, facilitate differential diagnosis with usually hyperintense

HCC foci.

  • Pseudocapsule is hypointense in T2-weighted images and shows delayed enhancement

in EP, similarly to CT.

  • DCE-MRI shows a similar enhancement pattern in majority of HCCs as observed in

multiphase CT with early strong enhancement in HAP and washing-out in the following


Figure 8:

Stepwise carcinogenesis of HCC in cirrhosis

Table 1: Various imaging appearance of cirrhotic nodules to frank HCC in MRI
  • Early washout can be seen in high grade or undifferentiated hepatocellular carcinoma

since the lesion is entirely supplied by hepatic artery. So the phase of washout will

help in diffentiation the grade of hepatocellular carcinoma.

  • Hepatocellular carcinomas have fat within it where as dysplastic and regenerative

nodules do not contain fat within it.

  • HCC directly invades the vessel and enhances on arterial phase.
  • Collateral formation and prominent adjacent vessel are the additional imaging features seen in HCC.
  • Intratumoural psuedoaneurysms are common in HCC(9).
Figure 5:Large HCC with degenerative changes in coronal T1-weighted image with fat saturation

(a) and in coronal T2-weighted image (b). Dynamic contrast-enhanced sequences in axial T1-

weighted images with fat saturation after administration of hepatocyte-specific contrast agent in

hepatic arterial phase (c), portal venous phase (d) and hepatobiliary phase (e). Heterogenous

enhancement of the lesion is seen with areas of non-enhancing focal necrosis (c) with subsequent

washing out of the contrast agent (d). Lesion shows low signal intensity in comparison to adjacent

liver parenchyma in hepatobiliary phase (e) (9).


LABORTARY TESTS-Serum AFP is the most widely used tumor biomarker in

diagnosis of HCC. An increase of serum AFP levels in cirrhotic patients, however its

value is often considered insufficient(14)

HISTOPATHOLOGY- Well vascularized tumors with wide trabeculae (> 3 cells),

prominent acinar pattern, small cell changes, cytologic atypia, mitotic activity, vascular

invasion, absence of Kupffer cells and the loss of the reticulin network(12).