Nama Dosen: Drh R Harry Soehartano, MAppSC, Ph.

D
Date: 16 February 2020
Group: 2

INTERSTITIAL AND THORAX REGION

RADIOGRAM INTERPRETATIONS

BY.
1. Darryl Yee Zhi Heng B04178009
2. Vinieysha Loganathan B04178011
3. Karen Lee Mei Fong B04178012
4. Mogambigai Uthayachanthiran B04178013
5. Chai Wen Ni B04178017
6. Chow Yong Jun B04178018
7. Natasha Anne Binti Mohammed Noor Azam B04178034

FACULTY OF VETERINARY MEDICINE

BOGOR AGRICULTURAL UNIVERSITY
EVEN SEMESTER 2019/2020
BOGOR
 DEFINITION
The lung interstitium consists of the space sandwiched between the alveolar
lining epithelium which are made up of connective tissue where fibroblasts and
macrophages resides. Besides, it also contains the lung capillaries and lymphatics
without including the lining epithelium of the alveoli. When lung interstitium is
diseased, chances are it will involve adjacent structures and once the process has
spread to the alveoli, pneumonia is present (Corcoran 2008). Interstitial lung diseases
(ILDs), also known as diffuse parenchymal lung diseases, are a large heterogenous
group of non-infectious, non-neoplastic disorders characterized by varied patterns of
inflammation and fibrosis (Reinero 2019). It represents a diffuse subset of pulmonary
disease that includes abnormalities in the microscopic interstitium (the anatomic space
between the basement membranes of the epithelial and endothelial cells) as well as
the inflammatory and/or fibrotic processes that extend into the alveolar space, as well
as the bronchioles and bronchiolar lumen (Reinero et al. 2019). Radiographic findings
consistent with interstitial lung disease include bilateral diffuse infiltrate, without
consolidation or mass. Interstitial lung disease (ILD) is uncommonly recognized in
veterinary medicine in contrast with human medicine. A proposed classification
scheme of canine and feline ILDs, modified from a human classification scheme,
consists of three major groups: idiopathic interstitial pneumonias (IIPs), ILDs
secondary to known causes, and miscellaneous ILDs (Reinero 2019).

Pathogenesis of Interstitial Pattern of Lung Disease

The proposed pathogenesis of interstitial lung disease is irritation of the

alveolar epithelial lining, specifically type I alveolar epithelial cells (inhaled or
hematogenous), triggering a host inflammatory response (profibrocyte and pro-
inflammatory cytokine release) with subsequent deposition of extracellular matrix and
fibrosis.3 Fibrin formation is critical in the pathogenesis of these diseases, and
abnormal fibrinolysis could play a role as does an imbalance of matrix
metalloproteinases and tissue metalloproteinase inhibitors (Koster and Kirberger
2016).
Besides that, a variety of pathological process will affect the lung interstitium
and the most convincing ILD disease entities in the dog are pulmonary infiltration
with eosinophilia PIE (also known as eosinophilic bronchopneumopathy) and
idiopathic pulmonary fibrosis. PIE is characterised by large numbers of eosinophils
being present in the lung. The involvement of the interstitium alone or additional
involvement of the alveoli and bronchi can be seen. It is hard to identify a pure PIE
ILD, but the initial process of eosinophil migration into the lung will involve the
interstitium, and in many of these cases a distinct interstitial pattern can be identified
on radiography. Meanwhile there is often a circulating eosinophilia suggesting the
stimulation of bone marrow to satisfy a lung demand for eosinophils (Cocoran 2008).
As for idiopathic pulmonary fibrosis (IPF), despite the comprehensive
understanding of IPF pathogenesis remains elusive, research efforts in the last few
years have reached important milestones. The fibrotic process development is
supported by individual genetic and epigenetic. However, their interaction with
putative external factors has yet to be clarified although the contribution of variants is
so far identified (Sgalla et al. 2018).
Canine idiopathic pulmonary fibrosis (CIPF) is a progressive fibrotic lung
disease which is most commonly reported in aged dogs. CIPF share clinical,
tomodensitometric and histopathological characteristics of both human IPF and other
human interstitial lung diseases displaying non-specific interstitial pneumonia pattern.
An imbalance between thrombosis and fibrinolysis has been demonstrated in favour
of a local and systemic pro-thrombotic state associated with disease severity and
outcome has been identified in human idiopathic pulmonary fibrosis (IPF).
Extravascular coagulation involving fibrin formation in the intra-alveolar
compartment has been proposed as a provisional matrix for migrating fibroblast
contributing to pulmonary fibrosis (Roels et al. 2019).

CASE STUDIES OF INTERSTITIAL

CASE 1
Case study: Radiographic and Histopathologic Characteristics of Pulmonary Fibrosis
In Nine Cats

Introduction
Pulmonary Fibrosis is a progressive, fatal, interstitial lung disease with
varying clinical, radiographic, and histopathologic signs. The disease is described in
both human and veterinary medicine, and often leads to severe hypoxia and ultimately
death. In humans, pulmonary hypertension has been well documented in patients with
idiopathic pulmonary fibrosis. The disease is described in both human and veterinary
medicine, and often leads to severe hypoxia and ultimately death. In humans,
pulmonary hypertension has been well documented in patients with idiopathic
pulmonary fibrosis (Evola et al. 2013).

Methods
An email was sent to American College of Veterinary Radiology Diplomates
to recruit cases of feline patients with at least one lateral and one orthogonal view
thoracic radiographs and a histopathological diagnosis of pulmonary fibrosis.
Diplomates were also asked to send the slides or paraffin blocks of lung tissue that
were the basis for histopathologic diagnosis. Medical records for all cats were
reviewed and clinical findings were recorded. Survival times were calculated based on
the initial day of presentation to a specialty hospital for respiratory problems until the
date of death or the date of necropsy for all patients, and in patients who were seen at
a general practitioner for respiratory problems prior to referral, additional calculations
of survival time based on initial presentation at a veterinarian until time of death or
necropsy were also calculated. Episodes of respiratory problems that occurred
previously, had a separate diagnosis that was not pulmonary fibrosis and resolved,
were excluded from the study (Evola et al. 2013).

Imaging findings
None of the thoracic radiographs were normal. Six cats had moderate to severe,
multifocal to diffuse, bilaterally dis- tributed mixed interstitial, and bronchial
infiltrates (Figs. 1, 2, and 3). Five were bilaterally symmetrical (Figs. 1 and 2), two
also showed alveolar patterns (Fig. 3), one had small bullae (Fig. 2) and one had
mineralized pulmonary tissue (Fig. 3). Two patients had asymmetrical multifo- cal
indistinctly marginated areas of pulmonary infiltrates that were most severe in the
caudal lung lobes (Fig. 3), and one had bronchointerstitial infiltrates that initially ap-
peared miliary, but on closer inspection showed central air lucencies surrounded by
circular opacities, indicating thick- ened bronchial walls surrounding air filled lumens
(Fig. 1A and B) rather than nodules. Two other patients had focal soft tissue masses
seen on radiographs. One patient with pulmonary masses had ovoid but irregularly
marginated pulmonary masses in the right middle and right and left cranial lung lobes
measuring 1–2 cm in dimension (Fig. 4). The second patient diagnosed with a
pulmonary mass had an irregularly shaped soft tissue opacity measuring 2.6 cm in
length and 1.4 cm in width in the caudal left lung lobe (Fig. 5A). Three patients had
pleural effusion; one patient had mild pleural effusion as well as mixed pulmonary
infil- trates (Fig. 3), one had mild pleural effusion and pulmonary masses (Fig. 4), and
one patient had severe pleural effu- sion without evidence of abnormal pulmonary
infiltrates or bronchiolar disease (Fig. 6). Two cats had radiographic ev- idence of
cardiomegaly (Figs. 2 and 6). No lymphadenopa- thy or mediastinal abnormalities
were recognized in any patient. The visible abdomen of some patients showed gas
within the gastrointestinal tract suggesting aeropha- gia. Although pulmonary
hypertension was diagnosed via echocardiography in three patients, the pulmonary
arter- ies did not show radiographic signs of enlargement in any patient (Evola et al.
2013).
CT was performed on the two patients with radiograph- ically diagnosed
pulmonary masses. One of these patients had focally increased soft tissue attenuation
creating a mass in the left caudodorsal lung that did not invade the bronchus (Fig. 5B).
Additional areas of soft tissue atten- uation were seen in the right ventro-lateral thorax
at the junction of the right cranial and right middle lung lobes. In the second patient
with radiographically identified lung masses (Fig. 4), CT showed a well-defined mass
occupying the entire right middle lung lobe and ventral consolidation with normal
lung shape maintained in the cranial lung lobes (this did not improve with dorsal
versus ventral recumbency of the patient). At the time the CT study was performed on
this patient, pneumothorax was also present; however this was most likely secondary
to prior thoracocentesis. Masses from both patients that were diagnosed histologically
as fibrosis showed contrast-medium enhancement on CT. Echocardiography was
performed in three patients (patients in Figs. 2, 3 , and 6), though the
echocardiographic exam was limited in two of these patients due to respi- ratory
distress. All three of these patients demonstrated pulmonary hypertension, and two
patients (those in Figs. 3 and 6) also showed right ventricular dilation and right
ventricular hypertrophy. All of these changes were determined to be secondary to
primary pulmonary disease (cor pulmonale). Pulmonary arterial hypertension was
quantified in only one patient based on severely elevated right ventricular systolic
pressure measuring 80–90 mmHg (patient in Fig. 6), and in this patient, necropsy
findings supported the echocardiographic findings of cor pulmonale, including right
atrial dilation and hypertrophy, as well as dilation of the pulmonary artery (Evola et al.
2013).
Radiography results

FIG. 1. (A and B) Ventrodorsal (VD) projection and close-up of the thorax of case number 1
showing a severe, diffuse, bilaterally symmetrical bronchial pattern (arrows), and
unstructured interstitial pulmonary infiltrates.

FIG. 2. (A and B) Lateral projection and close-up of the thorax of case number 2 showing
cardiomegaly with the cardiac silhouette spanning three intercostal spaces and elevating the
trachea dorsally. A diffuse, symmetrical bronchointerstitial pattern is present with small
bullae (arrows) that were histopathologically confirmed.

FIG. 3. Ventral dorsal projection of thorax of case number 3 shows retraction of the lung
lobes indicating mild pleural effusion (black arrowheads), patchy, multifocal to diffuse
bronchiolar and unstructured interstitial pattern with an alveolar component most severe in
the left caudal lung lobe (white arrow- heads indicating air bronchograms) and pulmonary
mineralizations (black arrow).
FIG. 4. Ventral dorsal projection of thorax of case number shows lung masses(arrows) in the
cranial lung lobes bilaterally and retraction of the lung lobes and pleural fissure lines
indicating mild pleural effusion.

FIG. 5. (A) VD projection of the thorax of case number 5 showing a left caudal lung lobe
mass. (B) Axial CT image of case number 5 showing increased soft tissue attenuation in the
left caudal lung lobe surrounding, but not invading the airways. This mass showed
enhancement after intravenous administration of iodinated contrast medium.

FIG. 6. VD projection of the thorax of case number 6 showing cardiomegaly and severe
pleural effusion.
Conclusion
In conclusion, findings from the current study indicated that cats with pulmonary
fibrosis may have a wide variety of radiographic characteristics including severe,
bilaterally symmetrical bronchointerstitial disease; pulmonary masses; bullae;
alveolar patterns; right ventricular hypertrophy and pulmonary hypertension; and
pleural effusion. Radiographic and CT characteristics in cats may also mimic other
diseases such as asthma and neoplasia. Cats with idiopathic and induced forms of the
disease may have similar histopathologic characteristics (Evola et al. 2013).

CASE 2
Case Study: Presumptive Development of Fibrotic Lung Disease From Bordetella
bronchiseptica and Post-infectious Bronchiolitis Obliterans in Dog

Case Presentation
A 7-month old male Miniature Poodle that was bought from a pet store by its
owner has developed acute respiratory distress and was reported at the University of
Misouri Veterinary Health Center. Medication such as antibiotics were first given for
2 weeks period by primary care veterinarians, but no improvements were observed.
Further diagnosis was made with auscultation. After proper physical examinations, it
was found that the dog developed crackle murmurs in all lung fields. This was further
diagnosed and concluded that the dog was suffering from Bordetella bronchiseptica.
A respiratory polymerase chain reaction assay was also conducted on the dog and
Bordetella bronchiseptica, Influenza A virus, adenovirus-2, distemper, herpesvirus,
parainfluenza, respiratory coronavirus, and Streptococcus equi subsp. zooepidemicus.
In light of these results and sensitivity testing, the dog was treated with
sulfamethoxazole/trimethoprim (12.5 mg/kg PO q12 h); additionally, fenbendazole
(23.4 mg/kg PO q24 h) for 5 days was administered (Sgalla et al. 2018).
Ten days later, the dog was re-presented with respiratory decompensation despite
antimicrobial therapy guided by susceptibility testing. Cervical tracheal palpation
elicited a hacking cough. Cardiothoracic auscultation revealed crackles and soft
wheezes in all lung fields. Pulse oximetry yielded a hemoglobin saturation of 84%,
(reference range, 95–100%) while breathing room air. Supplemental oxygen via
intranasal prongs was provided (Sgalla et al. 2018).
Thoracic radiographs indicated diffuse changes consistent with pneumonia
including consolidation of multiple lung lobes and atelectasis of the left cranial lobe
(Figure 7). Repeat BAL revealed predominantly degenerate neutrophils and numerous
extracellular/intracellular bacteria. Culture of BAL showed heavy growth of only
Bordetella bronchiseptica. Enrofloxacin (10 mg/kg IV q24 h) was administered based
on antimicrobial susceptibility. Hypoxemia and pyrexia resolved but tachypnea and
cough persisted. After 4 weeks, the dog showed no improvements. Thoracic computed
tomography (CT, single slice CT scanner, Picker PQ 6000, Phillips Medical Systems,
North America, Bothell, WA, USA) was performed to investigate an underlying cause
for chronic cough and intermittent labored respiration (Figures 8A,C,E,G). Severe
reduction in left lung volume was compensated by hyperinflation of the right lung,
leading to medial displacement of right cranial and accessory lung lobes. Several end
on gas-filled structures were seen in left lung lobes. Tracheal bifurcation and left
principal bronchus were slightly collapsed. No additional diagnostics were performed
to look for evidence of an underlying immune defect (Sgalla et al. 2018).
Histopathology of the left cranial lung lobe demonstrated small airway
disease consisting of intraluminal plugging of bronchioles with downstream
honeycombing, air trapping and subpleural fibrosis (Figure 9A); the upstream
bronchiolar lesions strongly supported small airways disease as the cause of the
fibrosis. Larger airways (bronchi) were similarly narrowed with epithelial and goblet
cell hyperplasia, intraluminal mucus and mucosal and submucosal inflammatory cell
infiltration. Special stains failed to identify bacteria/microbes. Interestingly, culture of
lung tissue showed heavy growth of Bordetella bronchiseptica. The absence of
histologic evidence of infectious bronchopneumonia or bacterial organisms would
strongly argue against Bordetella as a pathogen at the time of biopsy. positively
staining. However, as small airway disease was not recognized as a clinical syndrome
in dogs at that time, the positive culture of Bordetella bronchiseptica was treated with
marbofloxacin (5.2 mg/kg PO q24 h) for 28 days in accordance with antimicrobial
susceptibility. Dog was administered with antimicrobials over the next five years and
yet complete resolution sighn were not achieved (Sgalla et al. 2018).

FIGURE 7. Marked mixed pulmonary pattern with diffuse radiographic lesions in a 7-month-
old Miniature Poodle presented with respiratory decompensation while receiving appropriate
antimicrobials. (A) Right and (B) left lateral radiographic projections showing bilateral
diffuse lesions characterized by marked diffuse small airway thickening (white arrow),
peribronchial cuffing and multifocal alveolar pattern (*) with air bronchograms (arrowheads).
Incidentally, intra-thoracic tracheal luminal diameter (doubleheaded arrows) varied on
average 28% between both lateral projections suggesting dynamic tracheal collapse (7). The
tracheal bifurcation and principal bronchus were narrowed on the left lateral projection. (C) On
the ventrodorsal projection, the left cranial lung lobe is completely opacified (*) and the cardiac
silhouette is shifted to the left (long horizontal arrow). The lesions are centered around the lobar
and segmental bronchi (short arrows) and decrease in severity toward the periphery. The left
caudal lung lobe (LCd; flared arrows) is the second most severely affected lobe after the left
cranial lobe.
FIGURE 8. Transverse (3 mm-thick) computed tomographic (CT) images of a Miniature
Poodle obtained at 9 months (A,C,E,G; using a single slice CT) and 8 years (B,D,F,H; using a
64-detector row CT) of age displayed from the same level side by side. On the first study, the
left cranial lung lobe (single opened arrow) is completely collapsed with almost complete
absence of air in the airways. The caudal branch of the left cranial lobar bronchus is narrowed
but filled with air (ventral to opened arrow on C). The left caudal lung lobe is also severely
reduced in volume and thus, increased in attenuation with several air-filled end on airways
(double arrows). The right lung is hyperinflated with the right cranial (RCr) and accessory
(RAcc) lobes extending to the left of midline. Mosaic pattern characterized by a well
circumscribed hypoattenuating area is seen in the accessory lobe (arrowhead). The
parenchyma is otherwise relatively normal. By 8 years of age and after undergoing left cranial
lobectomy as a puppy, the entire hyperinflated right lung has developed severe patchy
parenchymal lesions consisting of ground-glass opacification (black arrows) and
consolidation (*). This latter is most severe surrounding medium- to large-caliber dilated
airways. Traction bronchiectasis (black arrowheads) in areas of architectural distortion is seen
at the periphery of several of these airways, a common feature seen with pulmonary fibrosis.
The mosaic pattern previously recognized in the accessory lobe (white arrowheads) is
accentuated. Several cystic air-filled structures (white arrows) of varying size occupy the left
caudal lobe.

After 5 years, thoracic radiographs revealed an alveolar pattern and air

bronchograms, bronchial thickening and unstructured interstitial pattern caudodorsally
and occasionally in the dependent lung field (Figure 4). In lieu of a definitive
diagnosis the dog was treated with sildenafil (1.3 mg/kg PO q12 h) and enrofloxacin
(5.8 mg/kg PO q 12 h) for pulmonary hypertension and possible bronchopneumonia,
respectively. The dog clinically improved and was discharged 4 days later. The dog
was treated with sildenafil indefinitely. Approximately 2 years later the dog returned
for evaluation of respiratory distress. In the intervening 2 years the dog’s cough and
exercise intolerance worsened substantially. The dog was treated with 40%
inhalational oxygen, furosemide (2 mg/kg IV once), pimobendan (0.32 mg/kg PO
once), and butorphanol (0.1 mg/kg IV once). The following day, the dog was
breathing at 108 breaths/min in an orthopneic posture. Because of progressively
worsening respiratory distress and grave prognosis, euthanasia was elected (Sgalla et
al. 2018).
In this study it can be concluded that, Bordetella bronchiseptica is the most
common bacterial pathogen in CIRDC, an umbrella term encompassing multiple
bacterial and viral pathogens leading to acute respiratory tract infection. Most cases
are self-limiting and confined to the trachea and bronchi, but when there is extension
to the terminal bronchioles and alveoli, bronchopneumonia results. Bordetella
bronchiseptica is the most common cause of community-acquired pneumonia in
puppies. Results of thoracic radiography may be normal and are non-specific in
bronchiolar diseases. Thoracic radiography in children with PIBO classically
demonstrate hyperinflation/hyperlucency, atelectasis, patchy consolidation, airway
wall thickening and bronchiectasis. As a puppy, radiographic changes reflected some
changes reported in children (Sgalla et al. 2018).
Pulmonary fibrosis (fibrotic interstitial lung disease), represents a
heterogeneous group of syndromes originating from diverse injuries culminating in
scar tissue and an endstage lung. Fibrosis attempts to repair tissue and protect against
subsequent injury by increasing tissue strength; however, repetitive injury may lead to
dysregulated fibrosis that is maladaptive and detrimental. In dogs, fibrosis may
originate secondary to genetic contributors (e.g., West Highland White terrier) or
drugs/toxins, with most cases failing to have an identified trigger he dog in this report
strongly suggests PIBO can progress to widespread airway-centered interstitial
fibrosis. It is unknown if targeted therapy (e.g., glucocorticoids) could have prevented
or slowed fibrosis by diminishing inflammation leading to aberrant repair. In dogs,
PIBO should be a differential diagnosis for otherwise healthy young dogs developing
CIRDC pneumonia and respiratory signs persisting despite appropriate antimicrobials
and with compatible thoracic imaging or histologic changes (Sgalla et al. 2018).

FIGURE 9. Dog lung at 9 months of age (A) and again at the time of post-mortem
examination 7 years later (B,C). (A) Two bronchial profiles are dilated and contain mucus
and inflammatory cells within their lumens and the mucosa is thickened. There is
compression and collapse of the surrounding alveolar parenchyma.
Pulmonary arterial walls are markedly thickened.
(B) Dog lung at the time of post-mortem examination. A markedly dilated airway contains
eosinophilic proteinaceous fluid and cellular debris. There is compression and collapse of the
surrounding alveolar parenchyma. The mucosa is irregular and the lamina propria contains
myxomatous material and chronic inflammation. Inset: High magnification of the airway
mucosa. There is squamous metaplasia of the mucosal epithelium and abundant myxomatous
matrix is within the lamina propria. (Hematoxylin and eosin.) (C) Away from the dilated
airways regions of subpleural fibrosis with metaplastic epithelium (arrow) as well as fibrosis
in the deeper parenchyma is present. Inset: A well-organized plug of fibrous connective tissue
(polypoid bronchiolitis obliterans) extends into the lumen of a respiratory bronchiole.

FIGURE 10. Five years post left cranial lobectomy, radiographic lesions were still present
especially in the left caudal lung lobe of a 6-year-old Miniature poodle. (A) Left lateral
projection showing several areas of increased opacity in the cranioventral, caudoventral and
caudodorsal lung field (arrows). In the caudodorsal lung field, a large bronchus (arrowhead) is
dilated and does not taper as it extends toward the periphery indicating bronchiectasis. In the
more severe opacified areas, small air bronchograms are seen (white arrow). (B) Right lateral
projection revealing radiographic lesions (black and white arrows) similar to those on the left
and most prominent in the caudodorsal lung field. They are less extensive in the ventral aspect
of the thorax in comparison to the left lateral view. Note that some lesions maybe less distinct
due to motion artifact. (C) As expected following left cranial lobectomy, leftward mediastinal
shift remains visible (black arrow) on the ventrodorsal projection. The borders of the left
caudal lobe appear retracted (arrowhead) and the lung lobe is increased in opacity. Lesions are
most severe centrally and less extensive toward the periphery. Similarly, radiographic opacity is
increased (white arrows) surrounding major lobar structures (vessels and bronchus) of the right
lung and gradually diminish in periphery of the lung

CASE 3
Case presentation
Steroid-responsive idiopathic interstitial lung disease in dog.

An 11-year-old, spayed, female, cocker spaniel, with a body mass of 17.8 kg,
that had lived in Hong Kong its entire life, was referred with a three-week history of
chronic cough, reduced exercise tolerance, weight loss and persistent pyrexia. The
clinical signs had failed to respond to antibiotic treatment at appropriate dosages,
including multiple courses of enrofloxacin and doxycycline, which had been
discontinued three days before presentation. The dog was housed exclusively indoors
and fed a commercial veterinary diet for the prevention of uroliths. There was no
history of tick exposure, and vaccination and parasite prophylaxis, including
heartworm (Dirofilaria immitis) prevention, were current. Clinical examination
revealed a pyrexia, mild submandibular lymphadenopathy, mild tachypnoea with mild
expiratory effort and adventitious lung sounds (harsh crackles) on auscultation (Liza
and Robert 2014).

Investigations
Thoracic radiographs, made using direct digital, showed a patchy interstitial
lung pattern throughout with some focal areas of poorly defined nodular consolidation
(Fig 11). A complete blood count (CBC). A Dirofilaria immitis antigen test was
negative. Urinalysis was normal. The dog was placed on intravenous Ringer’s lactate
solution at 10 ml/kg/hour in preparation for general anaesthesia for special procedures.
The dog was premedicated with butorphanol at 0.4 mg/kg intravenously and induction
achieved with propofol at 4.4 mg/kg intravenously to effect and maintained on 2 per
cent. A thoracic CT using a helical dual slice scanner was performed in sternal
recumbancy. Survey and postcontrast, manually injected iohexol at 600 mg iodine/kg,
made immediately after injection, CT images were acquired. Slices 2 mm thick were
examined in transverse and multiplanar reformatted dorsal and sagittal planes in
mediastinal and lung windows. Abnormal pulmonary findings included several
parenchymal bands, multifocal patchy ground-glass opacities and multifocal
subpleural and peribronchial hyperattenuating poorly defined nodular opacities
bilaterally throughout the lungs (Fig 12). There was no evidence of intrathoracic
lymphadenopathy. Bronchoscopy, using a 2.8 mm flexible bronchoscope, and
bronchoalveolar lavage (BAL) were performed under the same anaesthetic. No
abnormalities were seen during tracheobronchoscopy. The lavage fluid was submitted
for cytology, aerobic and fungal culture and sensitivity. Both the culture and cytology
were negative for micro-organisms, but cytology revealed chronic active
inflammation with 60 per cent neutrophils, 35 per cent monocytes, 5 per cent small
lymphocytes and scattered eosinophils within a background of mildly basophilic
mucous strands. A presumptive diagnosis of COP was made based on the exclusion of
bacterial or fungal infections, cytology that was not consistent with EBP and the
typical history including vaccination status and clinical abnormalities. Mycoplasma
infections were considered unlikely due to the lack of response to doxycycline therapy
(Liza and Robert 2014).

Figure 11. Right lateral recumbent (a) and dorsoventral (b) thoracic radiograph of an 11 years
old female, spayed, cocker spanial that presented with persistent pyrexia and coughing.
Treatment
An immunosuppressive dose of prednisolone was started at 1 mg/ kg, every
12hours and clinical signs resolved within 48hours. Follow-up radiographs at this
time showed a marked improvement.

Outcome and follow-up

The dog was re-examined five days and 21 days later, during which time the
corticosteroid therapy was gradually tapered off. The owner reported no coughing
since discharge; return to normal exercise tolerance and the rectal temperature, which
was monitored on a daily basis, remained normal. Follow-up thoracic radiographs at
these examinations showed continuing improvement. Radiographs made two months
after the initial examination showed complete resolution of radiological changes (Fig
3). By three months after discharge, the dog was completely tapered off the steroid
therapy and had remained free of clinical signs. A telephonic update three weeks and
one year later confirmed that, despite discontinuation of the prednisolone, there was
no recurrence of clinical signs (Liza and Robert 2014).

Figure 12. Right lateral recumbent (a) and dorsoventral (b) thoracic radiograph follow-up
radiograph made two months later of Case 1.
 REFERENCES
Cocoran BM. 2008. Interstitial Lung Disease (ILD) in the Dog. World Small Animal
Veterinary Association World Congress Proceedings. Scotland (UK):The University
of Scotland Press.
Evola M, Edmondson E, Reichle J, Biller D, Mitchell C, Valdés-Martínez A. 2013.
Radiographic and histopathologic characteristics of pulmonary fibrosis in nine
cats. Veterinary Radiology & Ultrasound. 55(2):133-140.
Jared A, Jaffey, Mark H , Isabelle M, Kurt J. Williams, Carol Reinero. 2019. Case Study
Presumptive Development of Fibrotic Lung Disease From Bordetella
bronchiseptica ]and Post- infectious Bronchiolitis Obliterans in Dog. Front. Vet. Sci.
10(2): 78-86.
Köster LS, Kirberger RM. 2016. A syndrome of severe idiopathic pulmonary parenchymal
disease with pulmonary hypertension in Pekingese. Veterinary Medicine: Research
and Reports. 5(7):19.
Liza K and Robert K. 2014. Steroid-responsive idiopathic interstitial lung disease in dog.
Veterinarian record case reports. South Africa (ZAF): Department of Companion
Animal Clinical Studies, University of Pretoria
Reinero CR. 2019. Interstitial lung diseases in dogs and cats part I: The idiopathic interstitial
pneumonias. Vet J. 243(1):48-54.
Roels E, Bauer N, Lecut C, Moritz A, Gothot A, Clercx C. 2019. Haemostatic, fibrinolytic
and inflammatory profiles in West Highland white terriers with canine idiopathic
pulmonary fibrosis and controls. BMC veterinary research. 15(1):379.
Rozanski CR et al. 2019. Perspectives in veterinary medicine: Description and classification
of bronchiolar disorders in cats. J Vet Intern Med. 33(3):1201–1221.
Sgalla G, Iovene B, Calvello M, Ori M, Varone F, Richeldi L. 2018. Idiopathic pulmonary
fibrosis: pathogenesis and management. Respiratory research. 19(1):32.
 Thorax
Interpretation
CAT THORAX (LATERO-LATERAL

Animal type : 10-year-old female neutered Siamese cat

Orientation : Latero-lateral
Radiogram quality : Good
Shape : Normal
Size : Increased (dilated nasopharynx and trachea - severe inflammatory
airway disease)
: Increased (dilated stomach – hyperinflation)
Position : Normal (diaphragm flattened – maximum inspiration)
Number : Normal
Location : Normal
Marginalisation : Abnormal (Heart margins are unclear)
Opacity : Increased (Greyish area in lungs – pneumonitis/infiltrative neoplasia)
: Decreased (Black area in stomach indicating gas – aerophagia or
fasting)
: Increased (White spot in kidney – calculus)

NAMING OF ORGANS

1. Trachea
2. Heart
3. Vena cava cranialis
1
4. Aorta
4
7
5. Pulmonary artery and vein
56
3 (branches)
5 2 6. Vena cava caudalis
7. Diaphragm
CLOCK ANALOGY
12
11 1

10 2 Clock Chamber/Structure
12-2 Left atrium
9 3 3-5 Left ventricle
5-7 Right ventricle
7-9 Main pulmonary artery, Right
8 4
auricle
9-10 Aorta
7 5
6

CARDIAC MENSURATION

3.5 intercostal space

Heart width = ≥ 3.5 intercostal space

 A

A = 1/3 - ¼ of A+B
B = 2/3 - ¾ of A+B

T10
T9
T8
T7

VHS = 4.2 (long) + 3.2 (short) = 7.4

DOG THORAX (DORSO-VENTRAL

Animal type : 11 year old Golden Retriever

Orientation : Dorsal- ventral
Radiogram quality : Good
Size : The heart size is enlarged
Shape : No changes
Position : No changes
Number : Normal
Location : Normal
Marginalisation : The margination of the heart is irregular
Opacity : No changes
NAMING OF ORGAN

8. Trachea
1 9. Carina
10. Right and left caudal lobe
11. Heart
2 12. Pulmonary artey and
vein (caudal lobe)
13. Caudal vena cava
4
3 3 14. Diaphragm

6 7
5

Clock Chamber/Structure
11-1 Aortic arch
1-2 Main pulmonary artery
1-3 Left atrium
2-6 Left ventricle
6-9 Right ventricle
9-11 Right atrium

CLOCK ANALOGY
CARDIAC MENSURATION

L>R
B > 2/3 of A