Scope. Point-of-care ultrasonography in cystic fibrosis does not replace computed tomography, formal radiology-performed ultrasonography, magnetic resonance imaging, endoscopic ultrasonography, pulmonary function testing, laboratory assessment, or specialist CF care. Its role is to answer focused clinical questions and to provide repeatable, radiation-free assessment of pulmonary, diaphragmatic, hepatobiliary, pancreatic, and intestinal abnormalities at the bedside. Published 20.09.2026
Abstract
Cystic fibrosis is a multisystem disorder in which point-of-care ultrasound (POCUS) can complement HRCT, chest radiography, and comprehensive diagnostic imaging without exposing the patient to ionising radiation. Lung ultrasound may demonstrate peripheral loss of aeration through pleural-line abnormalities, B-lines, and subpleural consolidations; it may help distinguish mucus-plug-related atelectasis from inflammatory consolidation, quantify diaphragmatic excursion, and support the rapid diagnosis of pneumothorax. Abdominal POCUS can identify features of CF hepatobiliary involvement, portal hypertension, microgallbladder, gallstones, distal intestinal obstruction syndrome, and intussusception. Pancreatic assessment is particularly relevant in adults, in whom inspissated secretions, chronic ductal obstruction, and acinar destruction may produce atrophy, fibrosis, fatty replacement, cysts, and calcifications. A technically adequate examination includes assessment of pancreatic size and echogenicity, the main pancreatic duct, focal lesions, and calcifications using epigastric views, the splenic acoustic window, Fowler positioning, and, when appropriate, a fluid-filled stomach. The greatest value of POCUS lies in serial comparison with the individual patient’s baseline while recognising that a normal examination does not exclude central pulmonary disease, pancreatic dysfunction, or a CF exacerbation.
Cystic fibrosis as a multisystem disease: the role of POCUS
Cystic fibrosis results from dysfunction of the cystic fibrosis transmembrane conductance regulator. Impaired chloride and bicarbonate transport dehydrates secretions, impairs mucociliary clearance, and promotes chronic inflammation. In the lungs, the resulting process includes mucus plugging, bronchiectasis, recurrent infection, atelectasis, remodelling, and air trapping. Clinically relevant extrapulmonary manifestations involve the pancreas, liver, biliary tract, and bowel.
HRCT remains the reference imaging method for structural lung disease. It demonstrates bronchiectasis, mucus plugging, mosaic attenuation, and air trapping more accurately than ultrasound. It cannot, however, be repeated without limitation at every deterioration because examinations require transport and add to cumulative lifetime radiation exposure. Chest radiography uses a lower dose but has limited sensitivity for early or small peripheral abnormalities [1].
POCUS uses a different diagnostic model. It does not provide a complete structural map of the lungs; instead, it assesses the pleural surface, regional loss of aeration, diaphragmatic motion, pleural fluid, pneumothorax, and selected abdominal complications in real time. The examination can be repeated before and after antibiotics, airway-clearance therapy, or relief of airway obstruction. Findings must be interpreted together with symptoms, oxygen saturation, work of breathing, spirometry, inflammatory markers, and previous imaging.
The principal limitation of lung ultrasound is the physics of sound transmission. Ultrasound does not penetrate normally aerated lung. Most visible findings are artefacts arising from the pleural interface or abnormalities that extend to the lung surface. Central bronchiectasis, deep mucus plugging, and non-peripheral inflammatory foci may remain invisible. A normal lung ultrasound therefore does not exclude pulmonary exacerbation.
Lung ultrasound in cystic fibrosis
Examination technique
A 7–15 MHz linear transducer provides the best depiction of the pleural line and small subpleural consolidations. A 2–6 MHz convex or microconvex transducer provides greater penetration in adults, patients with obesity, and when evaluating larger consolidations or the diaphragm. A phased-array transducer can be useful in narrow intercostal spaces and emergencies.
Whenever the clinical condition permits, the patient should be examined sitting upright. Anterior, lateral, and posterior regions should be scanned symmetrically. Reproducibility is improved by dividing each hemithorax into anterior, lateral, and posterior regions and then into superior and inferior zones, creating a 12-zone protocol. A short cine loop should be stored from each zone. When assessing B-lines, tissue harmonics and artefact-reduction algorithms should be disabled, the focal zone should be placed at the pleural line, and equivalent settings should be used during follow-up examinations.
Pleural line
A normal pleural line is thin, smooth, hyperechoic, and demonstrates respiratory lung sliding. In CF it may appear thickened, irregular, fragmented, or locally immobile. Vertical artefacts and small subpleural consolidations may coexist.
These findings do not directly depict bronchiectasis. They more likely reflect peripheral inflammation, oedema, microatelectasis, fibrosis, and scarring adjacent to the pleura. The pattern is not specific to CF and can also occur after pneumonia, in interstitial lung disease, and after thoracic procedures. Assessment of pleural irregularity is operator dependent.
B-lines and loss of aeration
A B-line is a vertical hyperechoic artefact arising from the pleural line, extending to the bottom of the screen without fading, erasing A-lines, and moving with lung sliding. One or two B-lines in a single intercostal space, particularly at the lung bases, may occur in healthy individuals. Three or more B-lines in one space, or a clear increase from the patient’s baseline, is generally considered abnormal.
Separated B-lines usually represent a smaller reduction in aeration. With increasing tissue density, B-lines become numerous and may merge into a broad bright band described as coalescent B-lines or white lung. In some LUS scoring systems, confluent artefacts occupying more than half of the intercostal space represent a higher grade of aeration loss.
A mucus plug does not generate a B-line directly. Obstruction of a small airway causes distal hypoventilation, gas resorption, focal atelectasis, and inflammation. The resulting increase in peripheral tissue density and altered air-to-fluid ratio generates vertical artefacts. In CF the distribution is often patchy, focal, and associated with an irregular pleural line. This differs from the more symmetrical distribution of hydrostatic pulmonary oedema, where the pleural line may remain smooth. Paediatric studies have found B-lines and small subpleural consolidations more frequently in CF, but current correlations with HRCT and lung function are insufficient to replace standard monitoring [2,3].
Subpleural consolidations
A consolidation becomes visible only when it reaches the pleural surface. A small subpleural consolidation measuring less than 1 cm is usually hypoechoic, wedge-shaped, or irregular. Its deep border may be ragged, producing the shred sign, and isolated B-lines may arise from its margins. This appearance may represent focal atelectasis, a small inflammatory infiltrate, or scarring; size alone does not establish aetiology.
A larger consolidation develops a tissue-like or liver-like appearance known as hepatization. The operator should look for air and fluid bronchograms. Dynamic air bronchograms move centrifugally during inspiration and support patent airways within inflammatory consolidation. Static air bronchograms can occur in both pneumonia and atelectasis. Anechoic or hypoechoic branching structures may represent fluid bronchograms and retained secretions.
Mucus-plug-related atelectasis more often shows volume loss, relatively smooth margins, a static bronchogram, or no visible air bronchogram. Pneumonic consolidation more often has an irregular deep border, dynamic air bronchograms, and adjacent focal B-lines. Overlap is common. Suspected central airway obstruction, abscess, unexplained focal change, or failure to improve should prompt escalation to cross-sectional imaging or bronchoscopy, as clinically appropriate.
Diaphragm and air trapping
Diaphragmatic excursion can be assessed with a convex transducer in M-mode. The patient should be supine or positioned with the torso elevated by 20–30 degrees; the same position should be used for follow-up. On the right, the transducer is placed below the costal margin between the midclavicular and anterior axillary lines, using the liver as an acoustic window. The beam is directed cranially and posteriorly, as perpendicular as possible to the posterior dome. After identifying the diaphragm in B-mode, the M-mode cursor is aligned with the actual direction of motion. Excursion is measured from end-expiration to peak inspiration over several quiet breaths. Deep inspiration and a sniff manoeuvre can be assessed separately. On the left, the spleen serves as the acoustic window, although measurements are usually more difficult.
Air trapping and hyperinflation flatten the diaphragm, shorten the zone of apposition, and place muscle fibres at a mechanical disadvantage. Excursion and inspiratory reserve may decrease. A single value has limited meaning because it depends on age, body size, position, effort, and cooperation. Serial measurements obtained with an identical technique are more informative [4].
Abdominal POCUS
Liver and portal venous system
CFTR dysfunction in cholangiocytes promotes inspissated bile, small-duct obstruction, portal inflammation, fibrosis, nodular remodelling, and portal hypertension. Current terminology distinguishes broad CF hepatobiliary involvement (CFHBI) from advanced CF liver disease (aCFLD), which includes a nodular liver, advanced fibrosis, multilobular cirrhosis, or non-cirrhotic portal hypertension [5].
A convex transducer is used to assess both hepatic lobes, surface contour, echotexture, portal vein, bile ducts, spleen, and ascites. Early steatosis appears as diffuse increased echogenicity, posterior beam attenuation, and reduced visualisation of vessel walls and the diaphragm. The surface may remain smooth. Advanced fibrosis may produce a coarse heterogeneous echotexture, periportal bands, nodular remodelling, an irregular contour, and altered lobar proportions.
CF-related disease may be patchy; a normal-appearing region does not exclude clinically relevant involvement. Splenomegaly, portosystemic collaterals, recanalisation of the umbilical vein, ascites, reduced portal velocity, bidirectional flow, or hepatofugal flow support portal hypertension. Portal vein diameter alone is nonspecific and varies with age and respiration. Doppler velocity measurements should use an insonation angle no greater than 60 degrees.
The Cystic Fibrosis Foundation recommends abdominal ultrasound including liver and spleen assessment at least every two years from age three through late adolescence. People with CFHBI or aCFLD should undergo periodic liver stiffness assessment where available. POCUS may contribute to surveillance but does not replace a standardised hepatology examination [5].
Gallbladder and biliary tract
The gallbladder should be examined after fasting. A microgallbladder is a persistently small gallbladder, classically less than 2–3 cm long and less than 0.5–1.5 cm wide. It must be distinguished from physiological postprandial contraction. Proposed mechanisms include inspissated bile, cystic duct stenosis, and secondary gallbladder atrophy [6].
Thick bile promotes sludge and gallstones. Sludge produces low-level dependent echoes and usually does not shadow. A gallstone is hyperechoic, usually mobile, and commonly produces posterior acoustic shadowing. Small stones may lack a complete shadow but may generate a twinkling artefact on colour Doppler. The common bile duct, gallbladder wall, sonographic Murphy sign, and pericholecystic fluid should also be assessed [7].
Pancreas in an adult with cystic fibrosis
Mechanism of fatty replacement and increased echogenicity
Pancreatic abnormalities are among the most frequent extrapulmonary manifestations of CF. Reduced chloride and bicarbonate secretion produces thick, poorly hydrated pancreatic juice. Small ducts and acini become obstructed and dilated, with retention of secretions, inflammation, and progressive destruction of exocrine tissue. Acinar atrophy, fibrosis, fatty replacement, cysts, and calcifications may follow [8,9].
A normal pancreas in a young person is usually homogeneous and similar in echogenicity to the liver. In an adult with CF it may become markedly hyperechoic. This is not necessarily simple metabolic fat accumulation. In many patients, destroyed exocrine parenchyma is replaced by adipose and fibrous tissue. Multiple interfaces between residual lobules, fibrosis, and adipocytes increase ultrasound backscatter. Advanced fatty replacement can make the gland difficult to distinguish from retroperitoneal fat [7,10].
The pancreas should not be compared only with the liver because hepatic steatosis may coexist. Comparison with the spleen, renal cortex, and retroperitoneal fat is useful, as is assessment of the splenic vein, mesenteric vessels, and pancreatic duct. Studies comparing ultrasound with Dixon MRI confirm that marked pancreatic hyperechogenicity is common in CF with exocrine pancreatic insufficiency, although ultrasound cannot replace functional testing [10,11].
Remodelling does not always reduce gland size. Lipomatous pseudohypertrophy may enlarge the pancreas because extensive fat replaces exocrine tissue. Cystic and macrocystic patterns have also been reported. Apparent enlargement of the pancreatic head can therefore reflect fatty replacement, cystic change, or inflammation, but it should not automatically be accepted as a benign CF pattern. Focal asymmetry, segmental duct dilatation, abrupt duct cut-off, cholestasis, or new pain requires cross-sectional imaging and exclusion of neoplasia [7,9,12].
High-resolution magnification may reveal hyperechoic fibrous strands, lobular irregularity, and small calcifications. These resemble chronic pancreatitis, but isolated strands or echogenic foci are nonspecific, particularly in older adults, patients with obesity, and people with metabolic pancreatic steatosis. Their significance increases when they coexist with atrophy, an irregular main duct, visible side branches, or shadowing calcifications [13].
How to visualise the pancreas
The patient should ideally fast before examination. A 2–6 MHz convex transducer is used initially. The standard view is a transverse epigastric section. The splenic vein is an important landmark behind the pancreatic body; the superior mesenteric artery and vein lie inferiorly. The pancreatic head is assessed near the duodenum and inferior vena cava, while the neck lies anterior to the portal venous confluence. Longitudinal and oblique views improve assessment of the head, uncinate process, and relationship with the biliary tract.
If bowel gas obscures the gland, graded compression, the left hepatic lobe as an acoustic window, deep inspiration, and a short breath hold may improve visualisation. Elevating the head of the bed to a semi-upright or Fowler position can displace bowel gas and improve assessment of the body and tail. Standing, slight right-side-down positioning, or right lateral decubitus may also help [14].
The pancreatic tail can be approached through a left intercostal or subcostal view using the spleen as an acoustic window. This is particularly useful in CF because atrophy and fatty replacement may make the tail almost invisible from the anterior approach.
A fluid-filled stomach can provide an additional acoustic window. In a patient who can safely drink, the examination can begin with approximately 300 mL of still water, increasing the volume according to body habitus and image quality. Some practical protocols use 600–800 mL, but this volume is not required or appropriate for every patient. After drinking, the patient can be placed in Fowler position or slight right lateral decubitus to move fluid into the antrum and partially into the duodenal bulb. Large fluid loads should be avoided in patients with vomiting, high aspiration risk, complete obstruction, or cardiorespiratory intolerance [14].
Main pancreatic duct
The main pancreatic duct is a thin anechoic tubular structure running along the gland. It is usually easiest to identify in the body, slightly anterior to the splenic vein on a transverse epigastric view. The diameter should be measured perpendicular to the duct from inner wall to inner wall. Oblique measurement falsely increases the value.
In a classic ultrasound study, the mean normal diameter was approximately 1.3 mm and a duct greater than 2 mm was considered dilated [15]. Contemporary practice allows for age-related enlargement and uses approximate upper values of 3 mm in the head, 2 mm in the body, and 1 mm in the tail. The pattern is more important than a single measurement. Irregular contour, segmental dilatation, visible side branches, intraductal material or stones, and abrupt cut-off are concerning. New duct dilatation in an adult with CF, particularly with distal atrophy, should prompt CT, MRI/MRCP, or EUS.
Calcifications and the twinkling artefact
Macrocalcifications are strongly hyperechoic and commonly produce clean posterior acoustic shadowing. Smaller deposits may not shadow and can be difficult to distinguish from fibrosis. The twinkling artefact is a rapidly alternating mosaic of red and blue pixels on or immediately behind a rough, strongly reflecting interface. It does not represent blood flow; it reflects unstable Doppler phase estimates. It has been described with pancreatic parenchymal calcifications and ductal stones in chronic pancreatitis and can support recognition of similar chronic destructive change in CF [16,19].
The examination begins in B-mode. Magnify the target, reduce depth, and place a single focal zone at or just below the suspected calcification. Activate colour Doppler and use the smallest practical colour box encompassing the reflector and a short segment behind it. A small box improves frame rate and makes the rapidly changing mosaic easier to recognise.
PRF or velocity scale must be adjusted actively. A low or moderately low scale similar to slow-flow settings can be used initially, then swept gradually in both directions. Lower PRF often increases twinkling conspicuity but also increases vascular aliasing, motion artefact, and random tissue colour. Higher PRF suppresses slow flow and motion and may isolate strong twinkling near vessels. There is no universal PRF value because the optimum depends on the scanner, transducer, depth, and reflector surface. A practical approach is to sweep slowly from low to higher scale while holding the transducer still and checking whether the signal remains tightly coupled to the reflector [19].
The wall filter should initially be low. Colour gain is increased until random colour begins to appear in adjacent tissue and then reduced slightly. Excessive gain causes blooming and can mimic twinkling. Colour-write priority should permit colour to overwrite the bright reflector without flooding the field. The transducer should be kept still, and a brief breath hold may reduce respiratory motion artefact.
After colour twinkling is identified, pulsed-wave Doppler can be used for confirmation. A small sample volume is placed on the calcification or immediately behind its posterior surface. Angle correction is not relevant because no true velocity is being measured. Instead of a reproducible vascular waveform, the spectral display shows dense, bright, nearly vertical bands or broadband noise on both sides of the baseline. Moving the sample volume a few millimetres away from the reflector should abolish the signal. Persistence of an organised arterial or venous waveform indicates a true vessel rather than a calcification-related artefact.
A robust diagnosis of macrocalcification should be based on concordant B-mode echogenicity, posterior shadowing or colour twinkling, and the PW appearance. Twinkling supports but does not prove calcification, and absence of the artefact does not exclude it. Particular care is required near the splenic and mesenteric vessels to avoid misclassifying true-flow aliasing.
Clinical reporting of the pancreas
The report should describe visualisation and size of the head, body, and tail; echogenicity and homogeneity; fibrous strands, cysts, and calcifications; main duct calibre and course; focal lesions; the biliary tract; and the splenic vein. Findings should be correlated with pain, lipase, faecal elastase, nutritional state, and glucose metabolism. A normal or mildly abnormal appearance does not exclude exocrine pancreatic insufficiency, and extensive fatty replacement does not independently quantify functional loss.
Bowel complications
Distal intestinal obstruction syndrome
Distal intestinal obstruction syndrome (DIOS) is partial or complete obstruction of the terminal ileum and caecum by viscid, dehydrated faecal and mucoid material. Ultrasound may show dilated fluid-filled small-bowel loops and granular echogenic content in the right lower quadrant, sometimes with gas and dirty shadowing. Early mechanical obstruction may show increased to-and-fro peristalsis; peristalsis may decline as mural oedema, ischaemia, and muscular fatigue progress.
Ultrasound supports but does not establish the diagnosis. Differential diagnoses include constipation, appendicitis, Crohn disease, adhesions, volvulus, and intussusception. Peritoneal signs, interloop fluid, impaired mural perfusion, complete obstruction, or an indeterminate examination require urgent cross-sectional imaging and surgical assessment [17].
Intussusception
On a transverse view, intussusception produces the target or doughnut sign, with concentric rings of alternating echogenicity. Hypoechoic layers represent oedematous bowel wall; the echogenic centre contains invaginated mesentery and fat. On a longitudinal view, the lesion resembles a kidney, producing the pseudokidney sign. Doppler is used to assess mural perfusion. Absent flow, free fluid, and fluid trapped between layers increase concern for ischaemia, although preserved flow does not exclude it.
Emergency assessment: pneumothorax
Advanced obstructive lung disease, hyperinflation, and parenchymal remodelling promote subpleural blebs. Rupture during coughing, exertion, or positive-pressure ventilation may cause pneumothorax.
In a supine patient, scanning begins over the most anterior non-dependent chest. Absent lung sliding raises suspicion but is not diagnostic; adhesions, apnoea, mainstem intubation, severe hyperinflation, and consolidation can produce the same finding. Absence of B-lines supports pneumothorax, whereas a genuine B-line excludes it at the exact scanning point. In M-mode, absent sliding produces the barcode or stratosphere sign rather than the normal seashore sign.
The most specific finding is the lung point, where sliding and non-sliding pleura alternate with respiration. It approximately marks the extent of pneumothorax. It may be absent in complete pneumothorax or extensive pleural adhesions. Chronic pleural irregularity in CF increases the risk of false-positive diagnosis based only on absent sliding. Treatment of haemodynamically unstable tension pneumothorax must not be delayed for a complete ultrasound examination [18].
Practical summary and organ-based review
The quality of POCUS in CF depends not only on recognising signs but also on obtaining and deliberately optimising the image. Selecting a transducer appropriate to depth, repositioning the patient, using solid organs as acoustic windows, setting depth and focus correctly, and understanding M-mode and Doppler directly improve report quality. A protocol-based examination should not end with statements such as “B-lines present” or “hyperechoic pancreas.” It should describe location, extent, symmetry, dynamics, technical limitations, and relationship to symptoms. This approach helps distinguish the patient’s chronic CF phenotype from new pathology and enables meaningful serial comparison.
In the lungs, the operator may encounter pleural-line irregularity, focal B-lines, small subpleural consolidations, and larger areas of aeration loss. The report should identify the affected zones, B-line density, consolidation size, bronchogram characteristics, and pleural fluid, with explicit comparison to prior imaging.
In the pleura and emergency examination, lung sliding, B-lines, lung pulse, and the lung point should be documented. The report should not diagnose pneumothorax from absent sliding alone, particularly in a patient with chronic scarring or adhesions.
For the diaphragm, reduced excursion may reflect hyperinflation and mechanical flattening. The report should specify side, patient position, breathing manoeuvre, number of analysed cycles, and comparison with earlier measurements. Aligning the M-mode cursor with true motion prevents falsely low excursion values.
In the liver and portal system, expected abnormalities include steatosis, heterogeneity, periportal echogenicity, nodular surface remodelling, splenomegaly, collaterals, and altered portal flow. The report should distinguish steatosis from suspected fibrosis and should not infer portal hypertension from vessel diameter alone.
In the gallbladder and biliary tract, possible findings include microgallbladder, sludge, small stones, and cholelithiasis. A fasting examination and changes in patient position improve assessment of mobility and help distinguish dependent sludge from mural lesions.
In the pancreas, common patterns include increased echogenicity, fatty replacement, atrophy, poorly defined borders, fibrous strands, lobular irregularity, cysts, lipomatous pseudohypertrophy, and calcifications. The head, body, and tail should be assessed separately. Fowler positioning, the splenic window, graded compression, and a water-filled stomach reduce the number of examinations ending with the imprecise statement “pancreas not visualised.” Deliberate adjustment of PRF, wall filter, and colour gain can support identification of calcifications through twinkling, while PW Doppler helps distinguish artefact from true flow.
In the bowel, DIOS may present as dilated loops, echogenic material in the terminal ileum and caecum, and to-and-fro movement. The report should describe loop diameter, wall thickness and perfusion, luminal content, peristalsis, free fluid, and a possible transition point. Suspected intussusception should be documented in transverse and longitudinal planes with Doppler perfusion assessment.
A practical POCUS report should end with a synthesis rather than a list of abnormalities. It should state which findings appear chronic, which are new or progressive, whether an acute complication is suspected, and what the technical limitations were. The conclusion may identify new focal aeration loss requiring correlation with pulmonary exacerbation, stable pancreatic fatty replacement without duct dilatation, or features of DIOS requiring urgent investigation. POCUS remains complementary to HRCT, MRCP, EUS, elastography, and comprehensive CF-centre care.
Quick-reference table
| Organ or target | Key POCUS appearance | Relevance in CF | Technique and principal pitfall |
| Pleural line | Thickening, irregularity, fragmentation | Peripheral inflammation, scarring, microatelectasis | Linear 7–15 MHz transducer; nonspecific and operator dependent |
| B-lines | Numerous or coalescent B-lines | Peripheral loss of aeration distal to obstruction, inflammation, or oedema | Mucus does not create B-lines directly; disable harmonics and artefact suppression |
| Small consolidation | Hypoechoic lesion <1 cm, shred sign | Atelectasis, inflammation, or scar | Only lesions reaching the pleura are visible |
| Large consolidation | Hepatization and bronchograms | Pneumonia or obstructive atelectasis | Dynamic air bronchograms support pneumonia but are not absolute |
| Diaphragm | Reduced M-mode excursion | Hyperinflation and mechanical flattening | Compare measurements obtained in an identical position |
| Liver | Bright liver, heterogeneity, nodularity, irregular surface | Steatosis, CFHBI, or aCFLD | Assess spleen, collaterals, and portal flow; normal ultrasound does not exclude disease |
| Microgallbladder | Length <2–3 cm and width <0.5–1.5 cm | Inspissated bile, cystic duct narrowing, and atrophy | Examine fasting; distinguish from postprandial contraction |
| Pancreatic fatty replacement | Diffuse hyperechogenicity and loss of borders | Replacement of damaged exocrine tissue by fat and fibrosis | Compare with spleen and retroperitoneal fat, not only with liver |
| Pancreatic atrophy | Reduced size and poorly seen tail | Advanced chronic exocrine injury | Use Fowler position, splenic window, and fluid-filled stomach |
| Main pancreatic duct | Dilatation, irregularity, visible side branches, or abrupt cut-off | Chronic obstruction, ductal stone, or focal lesion | Measure inner-to-inner in the body; new focal change requires MRCP, CT, or EUS |
| Pancreatic calcifications | Bright focus, shadowing, and twinkling | Chronic destructive change | Small colour box, active PRF adjustment, low wall filter, and PW confirmation |
| DIOS | Dilated loops, echogenic material, and to-and-fro motion | Obstruction of terminal ileum and caecum by viscid content | Ischaemic signs require urgent escalation |
| Intussusception | Target sign and pseudokidney sign | Invaginated bowel and mesentery | Linear transducer, graded compression, and Doppler perfusion |
| Pneumothorax | Absent sliding and B-lines, barcode sign, lung point | Rupture of a subpleural bleb | Absent sliding alone is insufficient; lung point may be absent in complete pneumothorax |
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