Key words
COVID-19 - COVID-19 pneumonia - SARS-CoV-2 - CO-RADS - extrapulmonary manifestations
- pneumonia
Introduction
More than one year after the identification of the first case in Germany on 1/28/2020,
COVID-19 (coronavirus disease 2019) is more relevant than ever. Since the outbreak
of the disease in Wuhan (Hubei province, China) in December 2019, SARS-CoV-2 (Severe
Acute Respiratory Syndrome Coronavirus 2), the pathogen causing COVID-19, has infected
over 151 million people worldwide (as of 5/2/2021). Over 3.1 million have died of
or with the disease [1]. More than 3.4 million infections and over 83 000 deaths have been recorded in Germany
(as of 5/2/2021). 88 % of those who died were over the age of 70 [2]. Over 129 000 medical articles on a wide range of aspects of the disease (including
radiology), (PubMed search for “COVID-19” on 5/2/2021) have been published. In addition
to the dominant pulmonary changes, systemic complications and manifestations in various
other organ systems have increasingly become the focus of scientific interest.
Pathophysiology and symptoms
Pathophysiology and symptoms
SARS-CoV-2 is an enveloped single-stranded (positive-sense) RNA virus that is primarily
transmitted on an airborne-basis by inhaling viral particles emitted during breathing,
coughing, and speaking; to a lesser degree it is transmitted by direct contact [3]
[4]. The most common symptoms are fever (80.4 %), cough (63.1 %), fatigue (46 %), expectoration
(41.8 %), anorexia (38.8 %), tightness in the chest (35.7 %), shortness of breath
(35 %), dyspnea (33.9 %), and muscle soreness (33 %) [5]. Loss of taste and smell has also been frequently described [6]. In addition to the upper respiratory tract, the virus mainly affects the lungs,
with pneumonia requiring inpatient care being seen in approximately 2–3 % of those
infected [7]
[8]. This organotropism can be explained by the high expression of the angiotensin-converting
enzyme 2 (ACE2) receptor on the alveolar epithelial cells: The cellular serine protease
TMPRSS and other proteases prime the spike protein of SARS-CoV-2, which binds to the
ACE2 receptor and enters the host cells [9]. In addition to the lung, other organ systems are affected to varying degrees of
frequency and severity, including the vascular system, the heart, the nervous system,
the gastrointestinal tract, the hepatobiliary system, and the kidneys [9]. Some of these disease manifestations can be attributed to direct viral toxicity:
Viral RNA as well as a co-expression of ACE2 and TMPRSS2 were detected in the indicated
organs [9]. Damage to endothelial cells with resulting inflammation and formation of a prothrombotic
milieu seems to be another important component in the pathogenesis of COVID-19. The
expression of ACE2 has been detected in arterial and venous endothelial cells of various
organs, and histopathological studies have shown microthrombi in small vessels of
the lung among other organs [9]
[10]. Dysregulation of the immune response with a cytokine storm is a further pathophysiological
characteristic of severe COVID-19 [9]. Not least, a disruption of the renin-angiotensin-aldosterone system plays a pathogenetic
role [9]. The role of these individual mechanisms in the overall pathophysiology of COVID-19
has not yet been sufficiently clarified. In severe cases, general pathophysiological
processes of systemic infection and inflammation including changes in the coagulation
system are also seen [9].
Pulmonary manifestations
COVID-19 pneumonia on CT
Typical signs of COVID-19 pneumonia are rounded, polycyclic, or geographic confluent
ground-glass opacities and/or consolidations with peripheral (subpleural and perifissural)
or both peripheral and peribronchovascular distribution. The immediate subpleural
space can be spared ([Fig. 1], [2], [3], [4]) [11]
[12]
[13]. The ratio between ground-glass opacities and consolidations varies and ranges from
presentations with only ground-glass opacities to presentations with only consolidations
[11]
[12]
[13]. At the onset of pneumonia, ground-glass opacities usually dominate, while consolidations
increase as the disease progresses [14]
[15]
[16]
[17]
[18]. In later stages of the disease, consolidations frequently show a band-like or irregular
configuration ([Fig. 4]). In the recovery phase, ground-glass opacities prevail again [14]
[15]
[16]
[17]
[18]. COVID-19 pneumonia typically has a multifocal appearance with bilateral lesions
in all lobes. Predominant occurrence of changes in the dorsal and basal pulmonary
segments is frequently, but not necessarily, seen [11]
[12]
[13]. Further, less common, but highly typical changes include reticular consolidations
that – in combination with ground-glass opacities – result in a “crazy paving” pattern
([Fig. 3]). Moreover, the halo sign and the reversed halo sign (ground glass opacity surrounded
by a ring-shaped consolidation) as well as slight dilatation of the vessels in the
affected lung areas have been reported [11]
[12]
[13]
[19]. In rare cases, the “ring of fire sign” (peripheral ring-shaped opacification consisting
of consolidation and ground-glass opacity surrounding lung parenchyma with normal
transparency) and the “target sign” (ring-shaped opacity around lung parenchyma with
normal transparency containing a central hyperdensity reminiscent of a target) have
been described as specific imaging findings [20]
[21]
[22].
Fig. 1 Mild COVID-19 pneumonia. 83-year-old female, approx. 24 hours after onset of symptoms:
dry cough, weakness, shivering. Peripheral oxygen saturation in room air 87 %, respiratory
rate 15/min. SARS-CoV-2 RT-PCR from nasal swab performed the same day was positive.
CT shows discreet, patchy and geographic, peripheral and perifissural ground-glass
opacities bilaterally in all lobes – typical image of mild COVID-19 pneumonia.
Fig. 2 Moderate COVID-19 pneumonia. 36-year-old male with laboratory-proven SARS-CoV-2 infection,
5 days after symptom onset: progressive cough and intermittent fever. Peripheral oxygen
saturation in room air 94 %, respiratory rate 22/min. CT shows extensive, multifocal,
bilateral, rounded and geographic ground-glass opacities predominantly in lower lung
zones. Note immediate subpleural sparing in both lower lobes.
Fig. 3 Severe COVID-19 pneumonia. a Critically ill 80-year-old male receiving high-flow nasal oxygen, 13 days after onset
of symptoms. Combination of confluent multifocal, bilateral, peripheral ground-glass
opacities with subtle crazy paving and consolidations, predominantly affecting posterior
zones of both lower lobes. Bronchiectasis in both lower lobes and minimal pleural
effusion on the left as secondary findings. b Critically ill 33-year-old male receiving high-flow nasal oxygen, 10 days after onset
of symptoms. Peripheral oxygen saturation on 10 l O2/min 83 %, respiratory rate 28
/min. Extensive peripheral and central ground-glass opacities with crazy paving in
all lobes bilaterally, most pronounced in lower lung zones. In addition, moderate
consolidations in both lower lobes. Pneumomediastinum.
Fig. 4 Residual changes following COVID-19 pneumonia. 65-year-old male, 3 weeks after recovering
from moderate COVID-19 pneumonia without hospitalization. Multifocal bilateral curvilinear
parenchymal bands and irregular consolidations, predominantly in posterior lung zones.
Solitary lesions, exclusively peribronchovascular distribution of changes, and nodules
or cavitations are not typical for COVID-19 pneumonia [11]
[12]
[13]. Pleural effusions accompanied by lymphadenopathy are rare. However, in the case
of protracted severe courses, they are slightly more common and may indicate a possible
concomitant pathology or complication (see below) [11]
[12]
[13].
Disease severity correlates to a certain degree with the extent of the pulmonary changes
on CT [23]. In 10.6 % of symptomatic COVID-19 patients, however, chest CT imaging findings
are normal, particularly in the first days of the disease [11]
[15]. On the other hand, typical pulmonary changes can be seen on CT in 54 % of asymptomatic
SARS-CoV-2-positive patients [24].
Concomitant pulmonary pathologies like pulmonary emphysema, interstitial lung diseases,
fibrotic changes, or pulmonary edema make it difficult to detect typical COVID-19
changes and to discriminate between these and other (e. g., bacterial or viral) forms
of pneumonia [11]
[25]
[26]. Complications of COVID-19 pneumonia like bacterial superinfection (in 10 % of hospitalized
patients), acute respiratory distress syndrome (ARDS), pulmonary infarction (due to
pulmonary embolism, see below), or cardiac decompensation due to COVID-19 are sometimes
difficult to differentiate from pulmonary changes caused directly by SARS-CoV-2 [11]
[25]
[26].
COVID-19 pneumonia on chest X-ray
The described morphological changes seen on CT can also be identified on chest X-ray
[12]
[27]. In the early stages of the disease, the sensitivity is lower (55 % in the first
two days after symptom onset) than that of CT (88 %, performed on average on day 4
after symptom onset) but improves as the disease progresses to 79 % (more than 11
days after symptom onset) while the specificity decreases (from 83 % to 70 %, p = 0.02).
Repeating chest X-ray also increases the sensitivity from 73 % to 83 % but reduces
the specificity from 80 % to 73 % [28]
[29]. Multifocal (bilateral), primarily peripheral infiltrates should always be considered
possible manifestations of COVID-19 pneumonia and a corresponding workup should be
initiated, whereas pleural effusions, cavitations, or a pneumothorax make COVID-19
pneumonia less probable. The latter changes in patients with confirmed COVID-19 pneumonia
indicate complications [30]
[31]
[32].
COVID-19 pneumonia on thoracic ultrasound
Ultrasound primarily plays a role as a bedside examination of intensive care patients
[12]
[33]
[34]. Based on B-line artifacts, irregular pleural thickening, and subpleural consolidations,
conclusions about the presence and extent of pneumonia can be made [33]
[35]. B-line artifacts are hyperechoic artifacts that are vertical to the surface of
the lung and change dynamically as the lung moves, arise from the pleura or consolidated
areas of the lung, and resemble a “beam of light” or a “comet tail” [35]
[36]. They correspond to the accumulation of fluid in the pulmonary interstitium and
the alveoles and are therefore suitable for identifying even early forms of COVID-19
pneumonia [33]
[35]. However, the specificity of these signs is limited [34]
[37].
Indications for thoracic imaging
The indications for thoracic imaging (chest X-ray or CT) in COVID-19 continue to be
the object of scientific discussion. The gain of diagnostic information with potential
therapeutic consequences comes at the cost of radiation exposure for patients, risk
of pathogen transmission to medical personnel and other patients during the examination,
and the utilization of personnel, space, and diagnostic and material resources (e. g.,
personal protective equipment) [38]. The knowledge that is gained relates to multiple areas:
-
Diagnosis: Early publications on the diagnostic performance of chest CT show a pooled
sensitivity of 94.6 % (95 % CI: 91.9 %, 96.4 %) and a pooled specificity of 46.0 %
(95 % CI: 31.9 %, 60.7 %) in the detection of COVID-19. Subsequent studies with up
to 4824 patients achieved higher specificities (between 73 % and 94 %) with an approximately
equivalent sensitivity (between 86 % and 90 %) in relation to the results of reverse
transcriptase-polymerase chain reaction (RT-PCR) as the diagnostic reference standard,
usually using structured reporting (see below) [13]
[39]
[40]
[41]
[42]
[43]. When using a reference standard composed of RT-PCR results and clinical evaluation,
the sensitivity of chest CT was 94.7 % and the specificity was 91.4 % [44]. A suggestive appearance on CT often results in RT-PCR testing being repeated in
initially (false) SARS-CoV-2-negative patients who are ultimately positive [39]
[43]
[45]
[46]. COVID-19 cannot be reliably ruled out – particularly in asymptomatic patients –
based on chest CT which makes it unsuitable for screening [11]
[41]
[47].
-
Differentiation from alternative diagnoses and detection of concomitant pathologies:
Thoracic imaging allows quick detection of additional or alternative pulmonary pathologies
like bacterial pneumonias, decompensated cardiac insufficiency, pulmonary embolisms,
or tuberculosis. These diseases require specific treatment and their swift diagnosis
(prior to a negative RT-PCR result) not only accelerates improvement of the patient
but also shortens the patient's stay at an emergency department, hospital, or intensive
care unit [38]
[39].
-
Detecting complications: Thoracic imaging, particularly CT imaging, enables the detection
of pulmonary complications (bacterial superinfection, ARDS, pulmonary infarction,
cardiac decompensation, see above) as well as vascular and extrapulmonary manifestations
of COVID-19, primarily pulmonary embolisms (see below) [25]
[38].
-
Evaluation of severity, baseline for follow-up examinations, and prognostic information:
Imaging data regarding preexisting and concomitant pulmonary diseases as well as the
extent of COVID-19-associated pulmonary changes is useful for the evaluation of COVID-19
severity, facilitates the evaluation of follow-up examinations, and can be used for
prognostic classification [25]
[38]
[48]. Standardized scores make it possible to objectively evaluate disease severity based
on imaging but have not yet become established in practice [23]
[48]
[49]. The use of automated prediction algorithms for diagnosing and determining the prognosis
of COVID-19 is currently not recommended in the clinical routine [23]
[49]
[50].
National and international societies including the Thoracic Imaging Working Group
of the German Radiological Society and the Fleischner Society do not recommend thoracic
imaging either as a screening test for asymptomatic persons or as routine imaging
for patients with minimal COVID-19-typical symptoms (except in the case of an increased
risk for rapid disease progression): Given sufficient and quick availability, RT-PCR
should be given preference here [34]
[38]
[51]
[52]
[53]. However, this was not always the case in different phases of the pandemic, and
it often took multiple days to obtain RT-PCR results. A typical CT examination in
such situations provides an almost immediate preliminary diagnosis and makes it possible
to rule out other differential diagnoses with corresponding implications including
patient isolation [38]
[53].
Thoracic imaging is recommended in the case of moderate to severe disease with typical
COVID-19 symptoms (regardless of the availability of an RT-PCR test result), in the
case of worsening of the respiratory situation of SARS-CoV-2-positive patients, and
in the case of a discrepancy between a negative RT-PCT test and high clinical suspicion
of COVID-19 [38]
[51]
[52]
[53].
While the afore-mentioned recommendations of the national societies primarily relate
to the use of chest CT, the consensus declaration of the Fleischner Society and the
recommendations of the WHO do not specify which modality is to be selected for thoracic
imaging [34]
[38]
[51]
[52]
[53]. Particularly in early stages of the disease, CT has higher sensitivity regarding
the detection of characteristic pulmonary changes. It is also superior with respect
to the detection of alternative diagnoses and complications. As a result of earlier
and more precise diagnosis, the length of stay of patients in the corresponding functional
areas, the emergency department, and in the hospital can potentially be shortened,
thereby reducing the risk of transmission of the virus [38]. However, chest X-ray is more quickly available in most cases and is associated
with less radiation exposure. Moreover, the use of mobile X-ray units makes it possible
to avoid transporting the patient, thereby lowering the infection risk [38]. In the case of repeated examinations and advanced disease stages, the sensitivity
of chest X-ray is close to that of CT (see above) [28]
[29]. The decision between X-ray and CT as the primary imaging method for COVID-19 patients
ultimately depends on the local situation and expertise, individual patient-related
factors, and the epidemiological situation [38]
[54]
[55]. The authors have had success with the early use of chest CT when indicated.
CT examination technique
Non-contrast, low-dose chest CT examinations should be used for diagnosing COVID-19
unless contrast agent is required for differential diagnoses (e. g., pulmonary embolism)
[51]
[53].
Structured reporting
Structured reporting allows simple and concise communication of findings, thereby
facilitating clear diagnosis and treatment planning [56]
[57].
The Radiological Society of North America (RSNA) recommends the use of a four-category
system (typical, indifferent, atypical, no pneumonia) for interpreting chest CT examinations
with respect to COVID-19. The German Radiological Society has adopted a similar system
[51]
[58]. In two studies, the system showed moderate to significant agreement between different
observers. However, a not negligible number of SARS-CoV-2-positive patients were classified
as “atypical” and “no pneumonia” [59]
[60].
Another system is the CO-RADS (COVID-19 Reporting and Data System), which was developed
by the Dutch Radiological Society (Nederlandse Vereniging voor Radiologie). On a 5-point
scale based on existing “RADS” like BI-RADS, the probability of COVID-19 pneumonia
is rated on a scale of 1 (highly unlikely) to 5 (highly likely). CO-RADS category
6 indicates a SARS-CoV-2 infection already confirmed by RT-PCR, and CO-RADS category
0 is assigned in the case of incomplete or insufficient image quality [13]
[61]. Using CO-RADS for the diagnosis of COVID-19, various groups achieved a sensitivity
between 86 % and 95 % and a specificity between 73 % and 94 % [13]
[39]
[40]
[41]
[44].
Based on the authors' experience, CO-RADS is extremely useful in the clinical routine
since it uses a clear and intuitive scale with increasing probability for COVID-19
pneumonia and has a high level of acceptance among referring colleagues.
Extrapulmonary manifestations
Extrapulmonary manifestations
Vascular (thromboembolic)
COVID-19 patients have a greater risk of thromboembolic complications like deep vein
thrombosis (DVT) and pulmonary embolism (PE) as well as arterial events like ischemic
stroke, myocardial infarction, and systemic arterial embolism [9]
[12]
[62].
Data regarding the frequency of DVT and PE are relatively heterogeneous and at times
contradictory with respect to whether intensive care patients are affected to a greater
degree [62]. In 16 507 COVID-19 patients, a current meta-analysis shows a prevalence of venous
thromboembolism of 14.7 % (95 % CI: 12.1–17.6 %): PE occurred in 7.8 % (95 % CI: 6.2–9.4 %)
and DVT in 11.2 % (95 % CI: 8.4–14.3 %) of patients [62]. Venous thromboembolisms were significantly more common in patients requiring intensive
care compared to those not requiring intensive care (23.2 %, 95 % CI 17.5–29.6 %,
versus 9.0 %, 95 % CI 6.9–11.4 %; p < 0.0001) and in studies with systematic screening
compared to studies in which only symptomatic patients were examined (25.2 % versus
12.7 %, p = 0.04) [62].
According to current meta-analyses, ischemic stroke occurred in 1.1–1.6 % of SARS-CoV-2-positive
patients. The risk is elevated compared to non-infected control patients [62]
[63]. In most cases, these strokes were classified as cryptogenic. However, it must be
added as a limitation that a complete diagnostic workup was often not performed [63]
[64]. In particular, the possibility of paradoxical embolisms due to a persistent foramen
ovale has often not been sufficiently clarified but is of particular interest in light
of the increase in venous thromboembolisms seen in COVID-19 [65]. In addition to hypercoagulation, vasculitic processes and SARS-CoV-2-induced cardiomyopathy
are also involved in the pathogenesis of COVID-19-associated ischemic stroke [66].
According to a current meta-analysis, acute myocardial infarction or an acute coronary
syndrome occurs in 1.1 % of patients with COVID-19 [62]. The risk seems elevated during the disease [67]. An (at least partial) specific pathogenetic relationship with the SARS-CoV-2 infection
can be presumed based on experience with other viral diseases like SARS and influenza
and based on the systemic prothrombotic and hyperinflammatory changes [67]
[68].
There are a number of case reports regarding acute mesenteric ischemia in COVID-19
[69]. In a study including 412 SARS-CoV-2-positive patients, bowel wall changes (usually
bowel wall thickening) were seen in 31 % of performed CTs and pneumatosis intestinalis
or gas inclusions in the portal venous system were seen in 20 % of CTs in intensive
care patients [70]. Although an arterial occlusion could not be detected on imaging in any of these
patients, an ischemic cause was confirmed intraoperatively or histologically in the
majority of cases. Occlusions of small vessels, non-occlusive ischemia, and additional
direct toxic effects of the virus may have pathophysiological effects [70]. In a further study including 141 SARS-CoV-2-positive patients, abnormalities were
seen on abdominal CT in 80 (57 %) patients, including 14 (18 % of the abnormal CT
examinations) organ infarctions and vascular occlusions but no clear cases of mesenteric
ischemia [71].
Multiple publications report acute limb ischemia in patients with laboratory-confirmed
COVID-19 [72]. It is noteworthy that many of these patients did not have preexisting peripheral
arterial occlusive disease and limb ischemia occurred in spite of thrombosis prophylaxis
[72]. Some authors additionally report a higher incidence or greater severity of acute
limb ischemia during the COVID-19 pandemic compared to the corresponding period in
the previous year [73]
[74].
Extrapulmonary organ manifestations
SARS-CoV-2 can affect a wide range of additional organs and result in changes that
are usually nonspecific on imaging. Abnormalities were seen in 34 % to 56 % of patients
with acute or subacute COVID-19 who underwent neuroimaging [75]
[76]. Ischemic stroke was most common (see above) [76]
[77]. Further common imaging findings were 1) signal alterations in the medial temporal
lobe as a result of encephalitis; 2) multifocal, non-confluent, hyperintense white
matter lesions on fluid-attenuated inversion recovery (FLAIR) images and diffusion-weighted
sequences with variable enhancement and possible associated hemorrhagic lesions (similar
to acute disseminated encephalomyelitis ([Fig. 5a]) and 3) extensive and isolated white matter microhemorrhages ([Fig. 5b]) [78]. Moreover, leptomeningeal contrast enhancement and extensive and confluent white
matter FLAIR hyperintensities without associated hemorrhagic lesions have been described
[75]
[76]
[78].
Fig. 5 Cerebral manifestations of COVID-19. a Transverse FLAIR (Fluid Attenuated Inversion Recovery). Patchy, non-confluent, T2-hyperintense
white matter lesions, corresponding to inflammatory demyelinating changes (similar
to acute disseminated encephalomyelitis – ADEM). b Transversal SWI (Susceptibility-Weighted Imaging). Pronounced disseminated white
matter microhemorrhages involving the corpus callosum. Both figures (a, b): courtesy of Prof. Dr. H. Rolf Jäger, Neuroradiological Academic Unit, UCL Queen
Square Institute of Neurology, London, UK.
Myocardial manifestations are seen in severe cases of COVID-19 and contribute to the
mortality of the disease, particularly in patients with preexisting cardiac diseases
[9]
[79]
[80]. Ischemic (see above) as well as inflammatory processes seem to play a decisive
role [9]
[68]
[81]. In a meta-analysis including 26 studies with a total of 11 685 patients, the weighted
pooled prevalence of myocardial damage was 20 % (95 % CI: 17–23 %). In the individual
studies, the prevalence fluctuated between 5 % and 38 % [82]. Multiple case reports show acute myocarditis in patients with active COVID-19 [82]. In the case of hospitalized COVID-19 patients with elevated troponin levels and
no other identifiable cause, myocardial damage could be detected on cardiac MRI in
69 % of these patients one month after discharge [83]. In a further study, even unselected patients who had recovered from COVID-19 still
showed signs of cardiac involvement (78 %) or active myocardial inflammation (60 %)
on MRI approximately 70 days after recovery – regardless of preexisting conditions,
disease severity, and time to initial diagnosis [84].
Apart from the lung, the liver is the organ most commonly affected by COVID-19 [85]. However, the changes visible on imaging are usually only subtle and nonspecific.
Among other things, periportal edema and heterogeneity of the liver parenchyma indicate
SARS-CoV-2-induced hepatitis [70]
[71]
[85]. A distended gallbladder filled with sludge and enlarged intrahepatic bile ducts
are also often observed and indicate impaired bile drainage without a mechanical obstruction.
This can result in cholecystitis [70]
[71]
[85]. Hepatic steatosis is considered an independent risk factor for severe COVID-19
[85].
If not of an ischemic origin (see above), involvement of the gastrointestinal tract
is the result of viral gastroenteritis and is seen in the form of typically hypodense
thickening of the intestinal wall [70]
[85]. It can mostly be attributed to submucosal edema and is sometimes accompanied by
hyperenhancement of the mucosa, moderate distension and fluid filling of the affected
bowel loops, and inflammatory changes in the surrounding fat tissue [70]
[85].
Moreover, in addition to the already mentioned organ infarctions (see above), COVID-19-associated
changes have been described in the pancreas (pancreatitis), the kidney (heterogeneity,
loss of corticomedullary differentiation), and urinary system (diffuse irregularity
and thickening of the wall of the bladder due to interstitial or hemorrhagic cystitis),
the spleen (splenomegaly), the musculoskeletal system, the eyes, and the skin [85]. Since providing a detailed description of these changes exceeds the scope of this
overview, please refer to the relevant specialized literature.
COVID-19 in children
Children contract COVID-19 significantly less frequently and generally experience
a milder disease course compared to adults [85]
[86]. Nevertheless, approximately one third of children hospitalized with COVID-19 require
intensive care and individual cases have been fatal, particularly in children with
preexisting conditions [85]
[86]. In addition, pediatric multisystem inflammatory syndrome (PIMS), a presumably autoimmune-mediated
hyperinflammatory response with parallels to atypical Kawasaki disease, occurs in
rare cases in children after acute COVID-19 disease [85]
[87]. Since providing a detailed description of the pediatric aspects of COVID-19 is
beyond the scope of this study, please refer to the specialized literature for more
information.
Long-term effects of COVID-19 (long COVID)
Long-term effects of COVID-19 (long COVID)
To date, only minimal data regarding the long-term effects of COVID-19 is available.
Abnormalities, usually ground-glass opacities followed by irregular lines, were seen
on chest CT 6 months after discharge in approximately half of 353 patients hospitalized
due to COVID-19 [88]. Another publication describes fibrosis-like changes in 35 % of cases and residual
ground glass opacity or interstitial consolidations in 27 % of 114 patients 6 months
after severe COVID-19 pneumonia [89]. Further studies with larger patient numbers and longer observation periods are
needed to better evaluate the possible long-term effects of COVID-19.
Risk of COVID-19 for personnel in radiology
Risk of COVID-19 for personnel in radiology
Employees in radiology departments are at an increased risk of SARS-CoV-2 infection,
similar to those working in intensive care units and dedicated COVID-19 units [90]. Due to the limited scope of this overview, please refer to the relevant specialized
literature for more detailed information regarding these risks and possible protective
measures.
Conclusion
COVID-19 results in typical findings in the lung that can be visualized most effectively
with CT. In the case of quickly available RT-PCR test results, the purpose of radiological
imaging is not primary diagnosis but rather differentiation from other diseases, investigation
of unclear cases with discrepancies between clinical suspicion and RT-PCR test results,
evaluation of severity, and detection of comorbidities and complications. Thromboembolic
events, particularly venous thromboembolisms as well as arterial vascular occlusions
with resulting infarctions in the corresponding target organs, are the most common
extrapulmonary complications of COVID-19. Knowledge of additional extrapulmonary organ
manifestations is helpful for management particularly of critically ill patients with
a protracted course who require intensive care. The possible long-term effects of
COVID-19 are only known to a minimal extent and require longer and more detailed observation.
