Acute complications after hematopoietic stem cell transplantations – a radiological perspective

Abstract

Background

The number of stem cell transplants for hematologic malignancies has doubled since 2000 and continues to rise. Acute complications within the first 100 days post-transplant are linked to high morbidity and mortality of up to 30%. Since all organ systems can be affected and symptoms may be subtle, imaging plays a central role in early detection and monitoring of these complications. In response to increasing transplant numbers, expanding indications, and rapid therapeutic advances, the European Society for Blood and Marrow Transplantation (EBMT) revised its handbook in 2024. Most existing reviews on imaging acute complications post-transplant are five to ten years old. This article aims to provide an updated overview for radiologists increasingly confronted with acute complications after stem cell transplantation.

Method

The structure of this systematic review follows the updated EBMT Handbook. A systematic search was conducted in the PUBMED database to identify original studies on imaging of acute post-transplant complications from the past five years. A supplementary selective search helped to integrate the findings into the EBMT-handbook-aligned framework. A total of 29 original studies published in the last five years were included, providing new insights into imaging of acute complications post-HSCT.

Conclusion

This review offers a concise overview of typical acute organ-specific complications following stem cell transplantation and highlights recent advances in imaging.

Key Points

• Acute complications after stem cell transplantation are still associated with high mortality.

• Imaging is essential for early diagnosis and management.

• This review presents an updated, guideline-based overview of typical acute post-transplant complications.

Citation Format

• Brandt J, Helfen A. Acute complications after hematopoietic stem cell transplantations – a radiological perspective. Rofo 2026; DOI 10.1055/a-2787-4646

Zusammenfassung

Hintergrund

Die Zahl der Stammzelltransplantationen zur Behandlung hämatoonkologischer Erkrankungen hat sich seit dem Jahr 2000 verdoppelt und steigt weiter kontinuierlich an. Akute Komplikationen innerhalb von 100 Tagen nach der Transplantation sind mit einer erheblichen Morbidität und Sterblichkeit bis zu 30% assoziiert. Da alle Organsysteme betroffen und Symptome subtil sein können, kommt der Bildgebung eine zentrale Rolle bei der Früherkennung und Verlaufskontrolle von Komplikationen zu. Vor dem Hintergrund wachsender Fallzahlen, neuer Indikationen und therapeutischer Innovationen hat die europäische Gesellschaft für Stammzelltransplantationen (EBMT) ihr Handbuch 2024 grundlegend überarbeitet. Viele Übersichtsarbeiten zur Bildgebung solcher Komplikationen sind bereits fünf bis zehn Jahre alt. Ziel dieser Arbeit ist es daher, eine aktualisierte Studienübersicht zur Bildgebung akuter Komplikationen nach Stammzelltransplantationen für die zunehmende Zahl an RadiologInnen bereitzustellen, die Patienten im Verlauf nach Stammzelltransplantationen bildgebend betreuen.

Methode

Die Gliederung folgt dem aktualisierten EBMT-Handbuch. Für dieses systematische Review wurde eine systematische Literaturrecherche in der Meta-Datenbank PUBMED durchgeführt, die Originalarbeiten der letzten fünf Jahre zur Bildgebung akuter Komplikationen nach Stammzelltransplantationen identifizierte. Eine ergänzende selektive Suche diente der Einbettung in den an das EBMT-Handbuch angelegten Rahmen der Arbeit. Insgesamt wurden 29 Originalarbeiten eingeschlossen, die neue Erkenntnisse zur Bildgebung akuter Komplikationen nach Stammzelltransplantation lieferten.

Schlussfolgerung

Diese Arbeit bietet einen Überblick über typische, akute, verschiedenen Organsystemen zugeordnete Komplikationen nach Stammzelltransplantationen und fasst aktuelle Entwicklungen der Bildgebung auf diesem Gebiet zusammen.

Kernaussagen

• Akute Komplikationen nach Stammzelltransplantation sind weiterhin mit hoher Mortalität verbunden.

• Bildgebung spielt eine zentrale Rolle bei Erkennung und Management dieser Komplikationen.

• Die Übersicht bietet eine aktuelle, leitlinienbasierte Zusammenfassung typischer akuter Komplikationen nach Stammzelltransplantationen.

Keywords

hematopoietic-stem-cell-transplantation - acute - complications - imaging - European Society for Blood and Marrow Transplantation

Introduction

In Europe, approximately 140,000 people are diagnosed with hematologic malignancies per year [1]. The number of hematopoietic stem cell transplantations (HSCT) as a therapeutic approach has nearly doubled since 2000 and increased by 20% over the past decade in Europe. In 2023, approximately 48,000 HSCTs were performed across 700 European centers [2]. Acute complications after HSCT are associated with high morbidity and mortality, with 100-day post-HSCT mortality rates exceeding 15% due to non-infectious as well as infectious complications [3]. These complications are typically categorized into the pre-engraftment/neutropenic phase (phase 1: weeks 1–4 post-HSCT) and the early post-engraftment phase (phase 2: engraftment to day 100) [4]. Patients are especially vulnerable around the time of engraftment in phase 1 and, therefore, the threshold for initiating imaging during this phase should be lower. Since complications can affect all organ systems and symptoms may be subtle, atypical, or absent, imaging plays a crucial role in their identification and management. In order to adequately address the rapid development of HSCT, specific training for the management of complications is paramount for specialists, including radiologists. Accordingly, the European Society for Blood and Marrow Transplantation's (EBMT) handbook on HSCT and cellular therapies was thoroughly revised in 2024, incorporating insights from over 200 experts on transplant indications, procedural advancements, and the management of complications [5]. An analysis of the current literature on imaging of complications after HSCT revealed that most reviews focus on specific organ systems and date back five to ten years. Therefore, we aimed to provide an updated review of common complications within the first 100 days after HSCT affecting different organ systems guided by the updated EBMT handbook, with a particular focus on novel imaging insights ([Fig. 1]).

Fig. 1 Structure of the conducted systematic literature search and overview of the selected studies. The scheme is adapted from the PRISMA 2020 guidelines for reporting systematic reviews (DOI: 10.1136/bmj.n71).

Complications after hematopoietic stem cell transplantation

Thoracic complications

Pulmonary edema

Pulmonary edema is one of the earliest complications after HSCT, typically occurring immediately prior to transplantation or in the pre-engraftment phase in 20% of patients [6]. Risk factors include intravenous fluid overload, increased capillary permeability, and cardiac, renal, or hepatic failure. Diagnosis can be established based on chest X-ray (CXR) findings. Characteristic imaging features visible on CXR and native chest CT are enlarged pulmonary vessels, peribronchial cuffing, interlobular septal thickening, bilateral ground glass opacities (GGO), and pleural effusions, predominantly in dependent lung regions [4] [7].

Pneumonia

Pneumonia is the most common complication after hematopoietic stem cell transplantation (HSCT), typically occurring during the pre-engraftment and early post-engraftment phases, and accounts for approximately 50% of non-relapse-related deaths [3] [4]. Patients after HSCT are prone to a wide range of viral, bacterial, fungal, and atypical pulmonary infections [8] ([Fig. 2], [Fig. 3]). Among these, fungal infections represent the leading cause of infection-related mortality after HSCT [9]. Although imaging rarely allows identification of a specific pathogen, it plays a crucial role in narrowing the differential diagnosis to a potential pathogen group and in guiding bronchoalveolar lavage (BAL) to the most representative lesion sites [9] [10]. When pneumonia is suspected, native chest CT should be performed promptly, as patients in the aplastic phase after HSCT often fail to mount a normal inflammatory response. This results in subtle or absent radiographic findings on CXR, which limits its diagnostic value and reliability for ruling out pneumonia [9] [10].

Fig. 2 Native low-dose chest CT in a patient with ventilator-associated Stenotrophomonas maltophilia pneumonia. A, B Axial and coronal CT reformations obtained 24 days after transplantation due to acute myeloid leukemia (early post-engraftment phase) show patchy, confluent peribronchovascular consolidations with a positive bronchopneumogram and bilateral pleural effusions. C, D Axial and coronal CT reformations 35 days after transplantation demonstrate progression of the peribronchovascular consolidations, while the pleural effusions have regressed following drainage. The patient died 39 days after transplantation due to respiratory failure secondary to pneumonia.

Fig. 3 CT pulmonary angiogram in a patient with advanced angioinvasive pulmonary aspergillosis. A Axial reformation demonstrating multiple pulmonary nodules with central cavitation and surrounding ground-glass halos, consistent with fungal invasion of pulmonary vessels and associated hemorrhage. B Coronal reformation highlighting direct fungal infiltration (white asterisk) of the right lower lobe pulmonary artery, resulting in subtotal stenosis of the remaining vessel lumen. C Axial maximum intensity projection revealing occlusion of two subsegmental pulmonary arteries in the right lower lobe (arrow heads), accompanied by a wedge-shaped area of pulmonary infarction.

Pulmonary infections also tend to occur at characteristic time points following HSCT. Bacterial and fungal pneumonias, particularly Aspergillus infections, are most frequent in the pre-engraftment phase, whereas Pneumocystis jirovecii, cytomegalovirus (CMV), and adenovirus pneumonias are more commonly observed in the early post-engraftment phase [9]. Imaging features of pulmonary infections after HSCT are best visualized on native chest CT, although some findings may also be detectable on CXR [9].

Bacterial pneumonia typically presents with airspace consolidation and extensive GGOs, sometimes accompanied by centrilobular opacities [9].

Pulmonary aspergillosis may present in two major forms. Angioinvasive aspergillosis is characterized on native chest CT by a halo sign – a necrotic nodule surrounded by ground-glass opacity (GGO) representing hemorrhagic infarction as an early manifestation – and later by an air crescent sign, which appears 2–3 weeks after neutropenia resolves. The latter corresponds to cavitation with residual solid components and an intracavitary air crescent and is generally associated with a favorable prognosis. Airway invasive aspergillosis on the other hand corresponds pathologically and on imaging to bronchiolitis or bronchopneumonia [9].

Pneumocystis jirovecii pneumonia (PJP) typically demonstrates diffuse GGOs on native CT predominantly in the perihilar regions, often with a characteristic “geographic” or “mosaic” pattern due to patchy lobular sparing. Centrilobular nodules are uncommon, but can be observed more often in patients after HSCT compared to patients, who did not undergo HSCT [9] [11].

CMV pneumonitis usually presents with patchy or diffuse GGOs, airspace consolidation, and randomly distributed or centrilobular nodules, with a tendency toward the lower lobes [9].

Deep learning models could aid in distinguishing rare pneumonia types as shown in a proof-of-concept study on post-HSCT CMV-pneumonia [12]. Improvements in dedicated MRI sequences increasingly enable radiation-free assessment of pulmonary complications and therefore are promising, especially for pediatric patients, but do not yet match the diagnostic performance of CT, especially regarding the identification of GGOs [13].

Noninfectious pulmonary complications and idiopathic pneumonia syndrome

Idiopathic pneumonia syndrome (IPS) is defined by the American Thoracic Society as an idiopathic pneumopathy after HSCT and can be diagnosed in cases of widespread alveolar injury (indicated by multilobular infiltration on imaging (mainly CXR and native CT), signs and symptoms of pneumonia, increased A–a gradient, or restrictive pattern on pulmonary function tests) in the absence of a concurrent infection, iatrogenic fluid overload, cardiac or renal dysfunction [3]. IPS typically occurs in the pre-engraftment phase and early post-engraftment phase 14–90 days after HSCT in 2–15% of patients with high mortality (60–80%) [4]. Histopathologic findings include interstitial pneumonitis, diffuse alveolar damage, lymphocytic bronchiolitis, and bronchiolitis obliterans [4] [14]. Several subtypes of IPS exist [3]:

Peri-engraftment respiratory distress syndrome

Neutrophil engraftment occurs 5–15 days after HSCT and may cause a massive release of cytokines, leading to diffuse capillary leakage and peri-engraftment respiratory distress syndrome (PERDS) at the transition from the pre-engraftment to the early post-engraftment phase [3] [4]. The diagnosis of PERDS can be supported by characteristic findings on CXR. Imaging features, visible on CXR or native chest CT, include diffuse vascular redistribution, smooth interlobular septal thickening, hilar/peribronchial bilateral GGOs, and consolidations as well as pleural effusions ([Fig. 4]) [7] [15]. A recent study revealed that radiographic changes precede engraftment in roughly 80% of cases, indicating the value of CXR in the early detection and treatment of PERDS [15].

Fig. 4 Low-dose CT of the thorax in a 12-year-old child with periengraftment respiratory distress syndrome. A Coronal and B axial reformations demonstrating mild, smooth interlobular septal thickening and bilateral peribronchial ground-glass opacities, consistent with interstitial and alveolar involvement. C Axial reformation revealing a small pericardial effusion along with bilateral pleural effusions, predominant on the right side.

Diffuse Alveolar Hemorrhage

Diffuse alveolar hemorrhage (DAH) occurs in 1–21% patients with a median onset of 19 days after HSCT at the transition from the pre-engraftment to the early post-engraftment phase, often during granulocyte recovery [3] [7]. Mortality is high with 15% of patients dying as a direct consequence of DAH and 60% of patients from progression to multiorgan failure [6]. DAH is suspected to be caused by a strong immune response to alveolar epithelial damage [3] [6]. Hemoptysis may occur but is not mandatory [3]. Radiographic features are best visualized on native chest CT but are also potentially detectable on CXR and include diffuse GGOs with an alveolar pattern and predilection to the perihilar regions and mid to lower lung zones ([Fig. 5]). Interlobular septal thickening may superimpose, resulting in a “crazy paving” appearance on native chest CT [3] [4]. Diagnosis heavily relies on progressive bloodier return in BAL [6].

Fig. 5 Native low-dose chest CT in a patient with diffuse alveolar hemorrhage in the middle lobe. A, B Axial and sagittal CT reformations obtained approximately 2 years after transplantation due to acute myeloid leukemia (late post-engraftment phase) show diffuse ground-glass opacities in the perihilar regions with an alveolar pattern, during persistent thrombocytopenia secondary to toxic graft insufficiency with pancytopenia.

Drug-induced lung injury and organizing pneumonia

Drug-induced lung injury shows a wide range of morphological features, the most common being DAH, nonspecific interstitial pneumonia (NSIP) and organizing pneumonia (OP) [7]. OP commonly presents during the transition from the early to the late post-engraftment phase [4] and is characterized by inflammation and obliteration of alveolar ducts and alveoli [16]. The diagnosis of OP can be supported by characteristic findings on native chest CT, including thickening of the distal bronchi, migratory alveolar opacifications with peribronchovascular and/or subpleural distribution, GGOs, and linear bands [4] [16]. A recent study revealed a strong correlation between OP presence and increased wall thickness of distal bronchi and elevated alveolar NO concentrations, a marker for airway inflammation [16]. Furthermore, patients have a higher risk for air leak syndrome, including pulmonary interstitial emphysema, pneumomediastinum, and pneumothorax, detectable on CXR and native chest CT, likely being caused by bronchiolitis obliterans and a treatment related increase in alveolar wall fragility and lung compliance decrease [17].

Cardiac complications, sarcopenia, and body composition

Acute cardiac complications, aside from frequently observed hypertension, are relatively uncommon. The most frequent abnormalities – arrhythmias, pericardial effusion and congestive heart failure – affect less than 5% of patients and can be assessed using echocardiography and CXR [18] [19] [20]. Recent studies highlighted the utility of semiautomated assessment of CT-defined sarcopenia and adipopenia prior to HSCT, two parameters indicating poor prognosis after transplantation [21] and ultrasound (US) for quantifying obesity and visceral fat, both associated with higher mortality rates 100 days after HSCT [22]. Moreover, native chest CT scans can help diagnose anemia non-invasively by assessing the left ventricular cavity and interventricular septum attenuation [23].

Abdominal complications

Gastrointestinal tract

Gastrointestinal affection after HSCT is mainly caused by toxic effects of conditioning regimes leading to transmural bowel wall necrosis, normally occurring during the pre-engraftment phase. When occurring during neutropenia, it is termed neutropenic enterocolitis ([Fig. 6]) [24] [25] [26] with a predilection for involvement of the caecum and colon ascendens [24] [26]. Symptoms include bloody diarrhea and right lower quadrant abdominal pain [24] [26]. Common imaging features, assessable on baseline ultrasound (US) and more comprehensively on contrast-enhanced (CE) CT or MRI, are thickened bowel walls, “accordion sign” (thickened haustral folds), mesenteric fat stranding, ascites, and the “target sign” (combination of submucosal edema and mucosal enhancement) on contrast-enhanced cross-sectional imaging [24]. In adults, these features are best visualized on contrast-enhanced CE-CT, while US (and MRI) are preferable in children [24]. A recent study evaluating 990 pediatric patients showed that pneumatosis intestinalis following HSCT occurs in roughly 5% of patients with steroid therapy as the main risk factor. In the majority of cases, pneumatosis and pneumoperitoneum (observed in 25% of patients with pneumatosis), resolved spontaneously within 3–61 days [27]. Surgical intervention was not necessary in any of the cases. Whether these observations can be applied to the adult population remains unclear. Impairment of the gastrointestinal barrier increases the risk for infection, with pseudomembranous colitis (PMC) and cytomegalovirus (CMV)-associated colitis being common. PMC may progress to toxic megacolon and rarely colonic perforation. Wall nodularity and sparing of the small bowel are associated imaging features for cross-sectional imaging of PMC [24]. CMV, the leading cause of gastrointestinal infections in the early post-engraftment phase, leads to occlusive vasculitis, especially in the colon ascendens, leading to necrosis, ulceration, hemorrhage, and finally perforation [24].

Fig. 6 Abdominal CT in a patient with findings consistent with neutropenic colitis. A Coronal reformation demonstrating marked wall thickening of the cecum and ascending colon, accompanied by mesenteric fat stranding and engorgement of the vasa recta. B Coronal reformation showing thickening of the hepatic flexure (white arrow head), prominent fat stranding and dilated small bowel loops suggestive of a paralytic ileus. C Axial reformation revealing circumferential wall thickening and submucosal edema of the ascending and transverse colon, along with associated mesenteric fat stranding.

Hepatobiliary complications

Sinusoidal Obstruction Syndrome and Veno Occlusive Disease

Obstruction of the small liver veins is termed Sinusoidal Obstruction Syndrome (SOS) or Veno Occlusive Disease (VOD). SOS affects 10–60% of patients, typically in the early post-engraftment phase with a mean onset of 4–5 weeks after HSCT. Mortality rates reach up to 80% [24] [28]. During conditioning, cytotoxic metabolites damage sinusoidal endothelial cells, causing gap formation in the sinusoidal barrier. Passing of blood cells and debris through these gaps leads to progressive reduction of sinusoidal venous outflow and post-sinusoidal portal hypertension [28]. Established diagnostic criteria for SOS are the “Seattle”, “Baltimore”, and “revised criteria of the EBMT” [28]. Radiographic features of SOS are hepatic vessel flow abnormalities, portal vein dilatation, periportal edema, narrowing of hepatic veins, hepatomegaly, ascites, thickening of the gall bladder wall visible on US, and additionally geographic reduction of parenchymal contrast enhancement visible on CE-CT or MRI ([Fig. 7]) [24] [29] [30] [31] [32]. There are numerous recent studies highlighting advantages of US in SOS assessment compared to CE-CT and MRI (bedside application, availability, cost-effectiveness and lack of ionizing radiation). Regular US monitoring should, therefore, be the first-line imaging method for SOS assessment, facilitating early detection of abnormal blood flow in liver vessels and the prediction of SOS development [33] [34] [35]. The recently developed Hokkaido US-based scoring system (HokUS-10 and HokUS-6) enables diagnosis of SOS with high sensitivity and specificity, as well as outcome prediction [29] [36] [37]. Increases in liver stiffness observed through US elastography have also been shown to accurately predict the development of SOS [38] [39] [40] [41] [42] [43] [44].

Fig. 7 Abdominal CT and ultrasound in a patient with typical radiographic features of sinusoidal obstruction syndrome. A Axial CT reformation demonstrating narrowed hepatic veins. B Axial CT reformation depicting gallbladder wall thickening and associated perihepatic ascites. C Coronal CT reformation showing periportal edema and perihepatic ascites, typical of early hepatic outflow obstruction. D Doppler ultrasound revealing loss of the normal triphasic waveform in the hepatic veins, indicating impaired hepatic venous flow.

Infection

In severely immunocompromised patients, fungal dissemination occurs in approximately 20–40% of cases during the pre-engraftment and the early post-engraftment phase, most commonly caused by Candida, Aspergillus, and Cryptococcus species [24] [45]. Early recognition of hepatic fungal infection is critical to initiate timely therapy and prevent fatal complications. However, imaging rarely enables identification of the specific pathogen, as many fungal diseases share overlapping features across US, CT, and MRI [45]. US is readily available and can be performed bedside in the BMT ward. The typical US features of hepatic candidiasis, the most common form of hepatic fungal disease, include [45]: The “wheel-within-a-wheel” pattern, with a hypoechoic center representing necrotic fungal debris, an inner hyperechoic ring of inflammatory cells, an outer hypoechoic rim corresponding to fibrosis and the “bull’s-eye” pattern, similar in appearance but lacking the central hypoechoic nidus, consisting only of the inner hyperechoic and outer hypoechoic rings. CE-CT with both arterial and portal venous phase acquisition provides an optimal balance between sensitivity and availability. Approximately 30% of hepatic fungal lesions are detectable only in the arterial phase. Typically, fungal lesions are visualized as hypoattenuating lesions on CT (supplemental Figure 1). Homogeneous or rim enhancement during the arterial phase may be observed, sometimes accompanied by associated wedge-shaped regions of increased enhancement. Small central foci of high attenuation may also be seen, likely representing pseudohyphae [24] [45]. MRI demonstrates superior sensitivity and specificity (100% and 96%, respectively) compared to CT, although it is less widely available. Lesions typically appear mildly T1-hypointense and markedly T2-hyperintense [45]. With neutrophil recovery, intense ring enhancement may appear on early gadolinium-enhanced arterial phase images, and fungal abscesses may show diffusion restriction on diffusion-weighted imaging (DWI) [45].

Cholecystitis

Acute cholecystitis has an incidence of roughly 5%, mainly occurring in the early post-engraftment phase with a median onset of 57 days after HSCT and is associated with an increased 1-year mortality rate (60% vs. 20% in healthy controls after HSCT) [46]. US is the first-line imaging method for detecting cholecystitis after HSCT, with typical features including gallbladder wall thickening, wall hyperemia, and pericholecystic fat inflammation. However, equivocal findings are more common than in the non-HSCT population, making CE-CT, MRI, and hepatobiliary iminodiacetic acid (HIDA) scans valuable complementary tools [46].

Urogenital complications

Hemorrhagic cystitis

With a cumulative incidence of approximately 20%, hemorrhagic cystitis (HC) is a common complication after HSCT, typically occurring during conditioning or in the pre-engraftment phase [47] [48]. US with Doppler imaging is a well-suited and readily available modality for both diagnosis and follow-up. Characteristic US findings include segmental or diffuse bladder wall thickening, bladder wall hypervascularization on Doppler imaging, and intravesical blood clots ([Fig. 8]) [47]. HC is associated with an increased risk of urinary bladder tamponade, hydronephrosis, and subsequent renal impairment [47] [48].

Fig. 8 Abdominal CT in the portal venous phase in a patient with hemorrhagic cystitis due to BK virus infection. A, B Axial and coronal CT reformations obtained 90 days after transplantation due to acute myeloid leukemia (early post-engraftment phase) show moderate, irregular thickening of the urinary bladder wall and inhomogeneous bladder content due to intravesical coagula. C, D Axial and coronal CT reformations obtained 104 days after transplantation demonstrate progression of the infectious bladder wall thickening and complete regression of the intravesical coagula.

Neurological complications

Neurological complications after HSCT occur with an incidence of 8–65% [49] [50]. Imaging plays a key role and has prognostic value, as abnormal enhancement, ventriculomegaly, cortical changes, deep grey matter, and cerebellar abnormalities are associated with a poor outcome [49] [51].

Drug toxicity

Drug toxicity may lead to posterior reversible encephalopathy syndrome (PRES), acute toxic leukoencephalopathy or progressive multifocal leukoencephalopathy (PML) after HSCT, best evaluated by CE-MRI.

PRES typically occurs in the pre-engraftment phase, affects 1–10% of patients after HSCT and reflects reversible subcortical vasogenic brain edema caused by endothelial injury, leading to headache, visual disturbances, seizure, encephalopathy, or focal neurological deficits [49] [52] [53]. MRI typically shows bilateral subcortical parietooccipital T2-hyperintense white matter lesions and less often a holohemispheric watershed pattern ([Fig. 9]) [49] [54] [55]. Involvement of the cortex, diffusion restriction, and contrast enhancement may be noted [49] [52] [54]. Isolated involvement of the bilateral frontal lobes, cerebellar vermis and basal ganglia, as well as subcortical microhemorrhage is rare and mainly described in children [52] [56]. PRES lesions persist in a minority of cases [52].

Fig. 9 MRI in a patient with posterior reversible encephalopathy syndrome (PRES). A Axial T2-weighted TSE sequence demonstrating hyperintense signal alterations in the frontal and parietal cortices and subcortical white matter, consistent with vasogenic edema. B Sagittal T1-weighted TFE post-gadolinium administration revealing discrete, patchy leptomeningeal and cortical enhancement (white arrow heads). C Coronal T2/FLAIR-weighted image showing cortical and subcortical edema involving the parieto-occipital regions and cerebellum. D Sagittal T2/FLAIR-weighted imaging demonstrates widespread cortical and subcortical edema in the frontal, parietal, occipital, and cerebellar regions. E Follow-up sagittal T2/FLAIR-weighted imaging five days after the initial scan (A–D) showing regression of the cortical and subcortical edema, consistent with the reversible nature of PRES.

Acute toxic leukoencephalopathy commonly presents in the pre-engraftment phase with similar initial symptoms as PRES, but has a median overall survival of two months [49]. MRI typically shows bilateral periventricular T2-hyperintense white matter lesions that persist on follow-up imaging [49] [56]. In the initial setting, differentiating acute toxic leukoencephalopathy from PRES might be challenging. Features favoring acute toxic leukoencephalopathy include a periventricular predominance of T2-hyperintense lesions, in contrast to the predominantly subcortical and parietooccipital involvement seen in PRES, as well as the persistence of these lesions on follow-up imaging [49].

PML is a demyelinating CNS disease due to JC virus reactivation, potentially occurring in the early post-engraftment phase one month to years after HSCT [49] [55]. MRI typically shows juxtacortical and periventricular T2-hyperintense white matter lesions and no contrast enhancement. Peripheral patchy diffusion restriction is possible. Immune reconstitution can lead to contrast enhancement of lesions and progressive edema [55]. Differentiation from PRES and acute toxic leukoencephalopathy can be made based on the timing of onset, imaging characteristics, and disease course. PRES and acute toxic leukoencephalopathy typically occur in the pre-engraftment phase, whereas PML arises during the early post-engraftment phase. PRES is characterized by predominant T2-hyperintense white matter lesions in the parietooccipital regions, which usually resolve over time, in contrast to the progressive course seen in PML [55].

Infection

HHV6 and EBV are common pathogens in infectious CNS diseases after HSCT, compared to rare infections with Aspergillus, Toxoplasma, and bacteria [49] [55] [57]. Although rare during the pre-engraftment period, it is notable that due to the impaired host inflammatory response symptoms, rim enhancement, edema, and mass effect may be absent in this phase [55].

HHV6 reactivation occurs in 30–50% of patients leading to encephalitis and myelitis in up to 12% of patients 2–6 weeks after HSCT at the transition from the pre-engraftment to the early post-engraftment phase [57] [58] [59] [60]. Typical symptoms of HHV6-encephalitis are short-term memory loss, disorientation, impaired consciousness, and seizure [58] [60]. Radiographic features of HHV6 encephalitis visible on MRI are symmetrical T2-hyperintense lesions in the mesial temporal lobes with associated faint diffusion restriction, but might not be present when MRI is performed shortly after symptom onset (supplemental Figure 2) [57] [58] [60] [61]. Imaging features of HHV-6 myelitis seem to be nonspecific [58].

Encephalitis and meningoencephalitis are common CNS manifestations of EBV [62]. Imaging features of EBV encephalitis on MRI include T2-hyperintense lesions of the cortex, white matter, basal ganglia, and less frequently the thalamus, brainstem, cerebellum, and spinal cord. Associated diffusion restriction, hemorrhage, and leptomeningeal enhancement may be apparent [62].

Cerebrovascular diseases

Subdural hematoma is the most frequent cerebrovascular pathology after HSCT with an incidence of roughly 3% [49] [56]. Risk factors are falls, thrombocytopenia, graft-versus-host disease (GvHD), and hypertension. Active infection, atrial fibrillation, hypercoagulative states and corticosteroid treatment favor thromboembolism and ischemic stroke [49] [55].

A rare but potentially fatal complication after HSCT is transplantation-associated thrombotic microangiopathy (TA-TMA), which typically occurs in the early post-engraftment phase [63] [64]. The pathophysiology of TA-TMA is thought to result from multifactorial endothelial injury – related to factors such as age, conditioning regimen, and post-transplant infections – along with complementary system dysregulation [63] [64]. This leads to endothelial damage, microvascular thrombosis, and subsequent tissue injury. TA-TMA can affect multiple organs – most commonly the kidneys, but also the gastrointestinal tract, brain, heart, and lungs – each exhibiting distinct manifestations of vascular injury [63]. Definitive diagnosis is established via biopsy, which can be challenging in some patients due to coagulopathy or the location of the affected organ [64]. Neurological involvement may present with altered mental status, memory impairment, confusion, headache, hallucinations, or seizures. Brain imaging, may reveal multifocal hemorrhages of varying size, siderosis, or features of PRES, best seen on MRI [63]. In patients presenting with neurological symptoms after HSCT, differentiation of TA-TMA from infectious etiologies (bacterial, fungal, viral, or parasitic) is essential [64].

Immune-mediated causes

Immune-mediated neurological complications after HSCT are rare and include demyelinating polyneuropathy, myositis, and autoimmune limbic encephalitis. Cytokine release syndrome and myasthenia gravis can also occur, but do not typically require imaging [49] [65] [66] [67].

Polyneuropathies like Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy occur in 1–4% of patients within the early post-engraftment phase and 3 months after HSCT [49], their imaging features after HSCT are not yet addressed in the literature.

Myositis has a prevalence of roughly 5% and a median onset of 660 days after HSCT. However, onset in the early post-engraftment phase as soon as 60 days is possible. The suspected pathomechanism is muscle fascia involvement of GvHD [68]. MRI helps to guide muscle biopsy for histopathologic confirmation. Typical MRI findings include muscle fascia thickening and patchy and diffuse hyperintense signals on STIR and fat-saturated post-gadolinium T1-weighted sequences. Hyperintense unenhanced T1 signals indicate exudation from rhabdomyolysis. FDG-PET imaging can reveal areas of increased FDG uptake in regions of inflammatory activity and may be useful for monitoring treatment response [68] [69].

Graft-versus-host disease

Acute GvHD after allogeneic HSCT has an incidence of 30–40%, typical onset within the early post-engraftment phase, and a one-year survival rate of 40% for patients with Grade III-IV acute GvHD [70] [71] [72] [73] [74]. Its pathophysiology involves tissue damage due to drug toxicity, release of inflammatory cytokines, activation of host immune cells and apoptosis, marked in stem cell niches [72] [73]. Consequently, the target organs are the skin, gastrointestinal tract, and liver [72] [73] [75]. Diagnosis of skin GvHD is associated with organ site GvHD [72], making it a critical clue in the patient's history for radiologists.

Gastrointestinal tract

In general, all segments of the gastrointestinal tract can be affected, but there is a predominance for the small bowel due to injury of intestinal stem cells, Paneth cells, and goblet cells, which are more abundant in this segment [72]. Common imaging features, detectable on baseline US and more comprehensively on CE-CT or MRI, include dilated, fluid-filled bowel loops, moderate bowel wall thickening (<7–10 mm), and ascites. On contrast-enhanced cross-sectional imaging, additional findings may include multifocal or generalized mucosal hyperenhancement, submucosal edema with mucosal hyperenhancement (“target sign”), and engorgement of the vasa recta (“comb sign”; [Fig. 10]) [24] [75] [76]. Mesenteric fat stranding and lymphadenopathy are uncommon [24]. US has high sensitivity and a good predictive value for the diagnosis of GvHD [77]. In a novel nomogram model, the concurrent presence of the “target sign”, multifocal intestinal inflammation (on CT or MRI), other GvHD manifestations, and elevated serum bilirubin levels had a strong predictive value for gastrointestinal GvHD [76]. MRI shows high sensitivity and specificity (up to 85% and 100%), emphasizing possible partial replacement of endoscopy by MRI [78]. ¹⁸F-FDG-PET-MRI allows for a highly reliable assessment of acute gastrointestinal GvHD with potentially even higher sensitivity and correlates with the clinical stage [75] [79]. Furthermore, a predictive value of bowel wall thickness estimated by US for steroid-refractory GvHD was demonstrated [80].

Fig. 10 F18-FDG-PET-MRI in a patient with severe gastrointestinal Graft-versus-Host-Disease (GvHD). A Maximum intensity projection (MIP) image revealing intense FDG uptake throughout the small intestine and colon, indicating active inflammation. B, C Axial fused PET and T2-HASTE images showing marked FDG uptake in the ascending, transverse, and descending colon (B), as well as in the sigmoid colon and rectum (C), consistent with widespread colonic involvement. D Axial T2-HASTE sequence demonstrating significant wall thickening and submucosal edema in the sigmoid colon as well as discrete ascites. E, F Axial T2-HASTE (E) and axial post-contrast T1-weighted mDixon sequence (F) showing pronounced wall thickening, submucosal edema, mucosal hyperenhancement, and mesenteric fat stranding in the descending colon as features characteristic of acute GvHD.

Liver

Hepatic GvHD affects approximately 50% of patients with acute GvHD and usually develops in the early post-engraftment phase 2–10 weeks after HSCT [24]. Histopathologically bile duct damage, periportal and midzone hepatocellular necrosis, and minimal periportal lymphocytic infiltration are common [24] [72]. Radiographic features are similar to hepatic SOS, including ascites, gallbladder and small bowel wall thickening [24] [72]. Small bowel wall thickening, however, is more indicative for GvHD than SOS, indicating concordant gastrointestinal GvHD [24]. Definitive diagnosis is made by histopathological confirmation obtained through imaging-guided biopsy, typically performed under ultrasound or CT guidance. However, due to the high prevalence of thrombocytopenia early after transplantation, biopsy is not feasible in all cases [72]. When tissue sampling is clinically indicated despite severe thrombocytopenia, a transjugular liver biopsy may be considered as a safer alternative. Preclinical data on contrast-enhanced US suggest that liver parenchymal enhancement alterations could be promising in the early detection of hepatic GvHD [81].

Brain

GvHD of the brain is rare and diagnosis should only be made as a diagnosis of exclusion [49] [82]. Three distinct types are recognized: demyelinating disease, cerebrovascular disease, and immune-mediated encephalitis [49] [82]. Typical MRI findings of the demyelinating type are white matter lesions similar to those seen in multiple sclerosis [82]. Vasculitis in CNS-GvHD affects small to large-sized arteries and can lead to ischemic lesions, microhemorrhages, and multifocal T2-hyperintense white matter lesions [49]. Immune-mediated encephalitis in CNS-GvHD is extremely rare [49].

Conclusion

This systematic review provides a comprehensive, up-to-date overview of the wide clinical spectrum of complications affecting various organ systems within the first 100 days following HSCT, as outlined in the recently updated EBMT handbook. It underscores the crucial role of imaging in the early detection and characterization of these complications, highlighting its value with respect to guiding timely diagnosis and treatment.

Conflict of Interest

The authors declare that they have no conflict of interest.

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Publication History

Received: 12 June 2025

Accepted after revision: 04 January 2026

Article published online:
10 February 2026