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\begin{document}

\title{Hemoptysis secondary to Anomalous Origin of Right Pulmonary Artery from
ascending aorta in a young male: A case report}



\author[1]{Simran Nimal}%
\author[2]{Gowrishankar Palaniswamy}%
\author[3]{Navya Doddareddy}%
\author[4]{Sahithi Talacheru}%
\author[5]{Shraddha Jadhav}%
\author[6]{Tanmayee Mareedu}%
\author[7]{Mihirkumar Parmar}%
\author[8]{Anup Banur}%
\affil[1]{B.J Medical College}%
\affil[2]{SIMATS Deemed University Saveetha Medical College and Hospital}%
\affil[3]{Bangalore Medical College and Research Institute}%
\affil[4]{MediCiti Institute of Medical Sciences}%
\affil[5]{Teaching University Geomedi LLC}%
\affil[6]{Mamata Academy of Medical Sciences}%
\affil[7]{Gujarat Medical Education and Research Society}%
\affil[8]{SS Institute of Medical Sciences \& Research Center}%


\vspace{-1em}



  
  \date{June 14, 2024}


\begingroup
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\textbf{Title:} Hemoptysis Secondary to Anomalous Origin of Right
Pulmonary Artery from Ascending Aorta in a Young Male: A Case Report

\textbf{Abstract}

We report a rare case of a 24-year-old male with a rare anatomic variant
of patent ductus arteriosus (PDA). The patient presented with symptoms
of productive cough with recurrent and severe bouts of hemoptysis and
grade I dyspnea. There were no prior episodes reported. The patient was
vitally stable with bilateral clubbing. On cardiopulmonary auscultation,
a prominent parasternal heave, loud P2, and right lung crepitus were
noted. A complete blood count revealed an elevated hemoglobin and RBC
count. An electrocardiogram (ECG) revealed sinus tachycardia and RV
strain. ECHO confirmed these findings as dilated right atrium (RA) and
right ventricle (RV), mild tricuspid valve regurgitation (TR), and
severe pulmonary hypertension were noted. Computerized tomography (CT)
of the chest demonstrated multiple ground glass opacities, right lung
consolidation, and volume loss suggestive of right-sided pneumonia with
atelectasis. CT also proved the presence of patent ductus arteriosus and
an anomalous origin of the right pulmonary artery from the right
ascending aorta, causing compression of the right main bronchus. We show
the clinical and radiological findings and discuss the implications and
approach to this rare congenital cardiovascular malformation, as well as
how a patient-centered approach is necessary for its management.

\textbf{Correspondence}

Mihirkumar P. Parmar, Department of internal medicine,

Gujarat Medical Education and Research Society, Vadnagar, India

\emph{mmihir981@gmail.com}, 0000-0002-5110-1544

\textbf{INTRODUCTION}

Adults with congenital heart disease represent an expanding patient
population requiring life-long tertiary medical care. Approximately 5\%
to 10\% of them develop pulmonary arterial hypertension (PAH) of
variable severity {[}1{]}. In the anomalous origin of the pulmonary
artery, the pathological branch originates from the ascending aorta,
with an incidence of about 0.12\% {[}2{]}, hence often being a
misdiagnosis or a missed diagnosis. Left-to-right shunting caused by
patent ductus arteriosus is more pronounced in the presence of an
additional shunt-like anomalous origin of the pulmonary artery (AOPA).
AOPA coupled with PDA could present with lethal complications like
hemoptysis in the clinical course of disabling pulmonary hypertension
{[}3{]}. The incidence of hemoptysis is estimated at 3.1\% to 5.5\%
{[}4{]} in PAH-congenital heart disease (CHD) patients and is thus a
rare clinical picture. Follow-up is key for these patients to promptly
detect new or misdiagnosed pathologic findings {[}3{]}. CHD-PAH patients
have been found to have a survival advantage compared to those with
other types of PAH presenting with hemoptysis and hence require prompt
recognition and multi-centered treatment strategies {[}5{]}. Numerous
strategies employed in the past include supportive care, surgical
resection, and lung transplants. Presently, the most commonly used
strategy is bronchial artery embolization (BAE) {[}5{]}. BAE is
minimally invasive and has proved to be an immense success, resulting in
rapid cessation of hemoptysis with low complication rates {[}4{]}.
Recent studies have shown the effectiveness of tranexamic acid in
reducing the volume and duration of hemoptysis {[}6{]}. Despite
milestone advances in PAH-targeted treatment strategies and techniques,
the morbidity burden of hemoptysis remains high, causing impaired
quality of life with a global impact on healthcare systems, hence
requiring a case-specific approach and close interdisciplinary
management. This includes collaboration among adult CHD experts,
pulmonologists, radiologists, and thoracic surgeons in tertiary centers
{[}3, 4{]}.

\textbf{CASE REPORT}

A 24-year-old male patient presented to the Outpatient Department with
chief complaints of cough with expectorations associated with recurrent
and severe bouts of hemoptysis for 5 days. The patient also experienced
Grade 1 dyspnea on the\emph{mMRC (Modified Medical Research Council
Dyspnea Scale}). The patient denied having any chest pain or
palpitations. The patient had neither a fever nor any similar complaints
in the past and also denied having a history of pulmonary tuberculosis
contact. A COVID (coronavirus disease 2019) rapid antigen test was done
and was also negative. The patient also denied having a history of any
bleeding disorder or anticoagulation use.

\textbf{Physical examination}

On admission, the patient looked unwell but had normal vital signs
(temperature, 36.3 C; blood pressure, 133/81 mmHg; pulse, 96
beats/minute; respiratory rate, 22 breaths/minute; oxygen saturation
Spo2: 97\% room air). The patient had bilateral pan-digital clubbing
(\textbf{Figure 1)} . A cardio-pulmonary examination yielded findings
such as a prominent parasternal heave. Chest wall auscultation revealed
a loud P2 in the left parasternal space, as well as crepts in the right
lung fields.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1.} Bilateral pan-digital clubbing.

\textbf{Laboratory findings}

Initial blood tests, including a complete blood count and metabolic
panel, were done and are provided in Table 1. The patient was noted to
have elevated hemoglobin levels and an elevated RBC count.\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
\textbf{CBC} & &\tabularnewline
\textbf{1) Hemoglobin} & \textbf{20.3} & 13-18 g/dl\tabularnewline
\textbf{2) RBC count} & \textbf{7.8 million/cumm} & 4.5-6.5
million/cumm\tabularnewline
3) Total count & 7440 cells/cumm & 4000-11,000 cells/cumm\tabularnewline
\textbf{Differential leukocyte count} & &\tabularnewline
1) Neutrophils & 67\% & 40-75\%\tabularnewline
2) Lymphocytes & 25\% & 20-45\%\tabularnewline
3) Eosinophils & 2\% & 1-6\%\tabularnewline
4) Monocytes & 6\% & 2-10\%\tabularnewline
\textbf{Packed Cell Volume (hematocrit)} & \textbf{63.2\%} &
\textbf{47-77\%}\tabularnewline
MCV & 81 fl & 76-96 fl\tabularnewline
MCH & 26 pg & 27-32 pg\tabularnewline
MCHC & 31.1\% & 30-35\%\tabularnewline
\textbf{RDW-CV} & \textbf{19.4} & \textbf{12-15}\tabularnewline
\textbf{Platelet count} & \textbf{1.30 lakhs/cumm} & \textbf{1.5-4.5
lakhs/cumm}\tabularnewline
\textbf{TABLE 1:- Results of complete blood count} \textbf{MCV -- Mean
Corpuscular Volume} \textbf{MCH -- Mean Corpuscular Hemoglobin}
\textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation} \textbf{TABLE 1:- Results of complete blood count}
\textbf{MCV -- Mean Corpuscular Volume} \textbf{MCH -- Mean Corpuscular
Hemoglobin} \textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation} \textbf{TABLE 1:- Results of complete blood count}
\textbf{MCV -- Mean Corpuscular Volume} \textbf{MCH -- Mean Corpuscular
Hemoglobin} \textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation} & &\tabularnewline
\bottomrule
\end{longtable}

\&\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
\textbf{TABLE 1:- Results of complete blood count} \textbf{MCV -- Mean
Corpuscular Volume} \textbf{MCH -- Mean Corpuscular Hemoglobin}
\textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation} & \textbf{TABLE 1:- Results of complete blood count}
\textbf{MCV -- Mean Corpuscular Volume} \textbf{MCH -- Mean Corpuscular
Hemoglobin} \textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation} & \textbf{TABLE 1:- Results of complete blood count}
\textbf{MCV -- Mean Corpuscular Volume} \textbf{MCH -- Mean Corpuscular
Hemoglobin} \textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation}\tabularnewline
\bottomrule
\end{longtable}

\&\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
\textbf{TABLE 1:- Results of complete blood count} \textbf{MCV -- Mean
Corpuscular Volume} \textbf{MCH -- Mean Corpuscular Hemoglobin}
\textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation} & \textbf{TABLE 1:- Results of complete blood count}
\textbf{MCV -- Mean Corpuscular Volume} \textbf{MCH -- Mean Corpuscular
Hemoglobin} \textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation} & \textbf{TABLE 1:- Results of complete blood count}
\textbf{MCV -- Mean Corpuscular Volume} \textbf{MCH -- Mean Corpuscular
Hemoglobin} \textbf{MCHC -- Mean Corpuscular Hemoglobin Concentration}
\textbf{RDW-CV -- Red cell Distribution Width -- Coefficient of
Variation}\tabularnewline
\bottomrule
\end{longtable}



\textbf{Clinical course}

This prompted further investigations. A chest X-ray revealed an enlarged
cardiac silhouette with prominent pulmonary trunk and pulmonary arteries
proximally (\textbf{Figure 2)} , and the ECG revealed sinus tachycardia
with right ventricular strain. An ECHO was done to confirm these
findings, it revealed a dilated RA, RV and mild TR. The most notable
finding was severe pulmonary artery hypertension (62 mmHg).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

\textbf{Figure 2.} Enlarged cardiac silhouette with prominent pulmonary
trunk and pulmonary arteries proximally.

A chest CT was done to find out what was causing the high blood pressure
in the pulmonary arteries. The scan showed volume loss in the right
hemithorax. The CT scan also showed a patent ductus arteriosus and an
abnormal origin of the right pulmonary artery from the right ascending
aorta, which has compressed the right main bronchus \textbf{Figure 3.} A
spirometry analysis was avoided due to ongoing hemoptysis and infection.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

\textbf{Figure 3.} Patent ductus arteriosus and an abnormal origin of
the right pulmonary artery from the right ascending aorta, which has
compressed the right main bronchus.

The final diagnosis was hemoptysis with atelectasis because of Patent
Ductus Arteriosus and an abnormal origin of the right pulmonary artery
from the ascending aorta, which caused compression of the right main
bronchus. The patient was managed conservatively for the hemoptysis. The
patient was given supplementary oxygen and IV antibiotics for 3 days to
manage his pneumonia.

However, the patient returned a year later, in 2022, with similar
complaints. During this episode, the patient was again managed
conservatively with antifibrinolytics and cough suppressants and was
advised to rest for the next 10 days. However, Tab. Tadalafil 20 mg was
added to control pulmonary hypertension\emph{.} The patient was also
administered the pneumococcal and annual flu vaccines to avoid any
further infectious complications\emph{.} The patient was advised to make
follow-up visits in 3 months for close monitoring and improving
pulmonary hypertension.

\textbf{DISCUSSION}

Congenital heart defects like patent ductus arteriosus cause
left-to-right shunts. This shunt causes the pulmonary vasculature to
undergo pathological changes such as hypertrophy and fibrosis,
consequently causing PAH. Initially, most patients are asymptomatic
until a significant rise in pulmonary arterial pressure occurs and is
thus present in adulthood, as seen in this patient {[}7{]}. Exercise
intolerance, palpitations, and arrhythmias are all different
presentations of PAH. Hemoptysis is a rare presentation and is seen in
only 12\% of adult survivors, as seen in this case {[}8{]}. These
presentations are more pronounced in the presence of an additional
shunt. As noted in this patient, there is another shunt between the
right pulmonary artery and the aorta. To the best of our knowledge, this
is the first anatomic variant of PDA reported and thus warrants a very
patient-centered approach concerning its management.

The workup for hemoptysis invariably depends on the past medical
history, which in our case was not significant despite the excessive
pulmonary hypertension (68 mmHg on echocardiography) seen in this
patient and is a rather rare clinical picture {[}9{]}. Chest X-ray (CXR)
remains the best initial test of choice {[}10{]}. It determines the site
of bleeding in 45 to 65\% of the cases and the cause in 25 to 35\%
{[}11{]}. The next step has been a subject of debate as to whether
bronchoscopy is better than CT in determining the cause of hemoptysis;
however, recent studies demonstrate the superiority of CT {[}9{]}. In a
case of active hemoptysis, such as ours, bronchoscopy can stimulate
coughing and therefore increase the risk of bleeding. For this reason,
it is often safer to delay the bronchoscopy until a definitive diagnosis
is made {[}9{]}. A radiologic definition based on CT states that
pulmonary artery hypertension is diagnosed when the pulmonary artery
diameter is more than 28mm {[}11{]}. In our case, this is conclusively
proven by a pulmonary artery diameter of 38mm {[}14{]}. The utilization
of computed tomography (CT) in the assessment of patients with pulmonary
hypertension can be advantageous in several ways by providing valuable
insights into the potential underlying causes of the condition, such as
lung parenchymal disease or primary cardiac processes, as well as
chronic thromboembolic disease, and can effectively depict the current
condition of the right ventricle, which is a crucial aspect of patient
care in pulmonary hypertension cases. Echocardiography is used to
consider the probability of PAH, and its parameters help to determine
survival outcomes {[}13{]}.

Embolotherapy is a widely accepted treatment modality for patients with
severe recurrent hemoptysis {[}8{]}. Embolotherapy has been proven to
show immediate control of bleeding in up to 90\% of patients; however,
it is associated with a significant risk of re-bleeding in approximately
50\% of patients in long-term follow-up {[}12{]}. Recent studies have
shown that acute presentations, like in this case if treated surgically,
present with more complications in the long term {[}11{]}. Studies have
shown that a surgical approach is also associated with high operative
mortality (\textgreater{} 15\%) {[}8{]}. On the contrary, conservative
management has shown better patient outcomes in some patients {[}11{]}.
This includes, a combination of cough suppressants, anti-fibrinolyitcs
like tranexemic acid and antibiotics. Studies have shown a significant
reduction in volume and duration of hemoptysis with the use of
antifibrinolytic agents, thus reducing morbitdity{[}6{]}. The other
spectrum of management is to control and adequately monitor PAH, which
is the major cause of mortality in patients with multiple left to right
shunts.

As one of the highest concentrations of PDE5 is found in the lungs, the
PDE-5 inhibitor tadalafil was shown to effectively control PAH when
given once a day {[}15{]} {[}16{]}. Furthermore, it is regarded as the
most economical choice when compared to alternative treatment methods
{[}17{]}. Hence conclusively we state that, due to the rare anatomic
variant, as well as pronounced symptoms present in this patient, it
might prove counter-intuitive to plan a surgical approach and have
preferentially selected the aforementioned conservative approach.

\textbf{CONCLUSION}

In instances of this nature, the individual is required to undergo a
series of procedures and investigations. The evaluation process relies
on the individual's medical history, which, in this instance, is not
significant. The rarity of this case is attributed to the presence of
significant pulmonary hypertension characterized by a pulmonary artery
diameter measuring 38mm and the additional active hemoptysis, which
necessitated a delay in performing bronchoscopy due to the potential
risk of bleeding. Despite being a well-acknowledged therapeutic
technique for patients experiencing severe recurrent hemoptysis and
providing prompt control of bleeding, embolotherapy still carries a
notable risk of re-bleeding. In the current context, the heightened
severity of the illness may lead to exacerbated long-term complications
when surgical intervention is employed, due to the patient's atypical
anatomical variation of the PDA in relation to the aorta as well as the
severity of the symptoms presented. Furthermore, this particular
instance serves as a cautionary tale for medical professionals to
exercise vigilant monitoring of patients presenting with identical
symptoms and displaying signs of pulmonary hypertension.

\textbf{AUTHOR CONTRIBUTIONS}

Simran Nimal: Conceptualization; method-ology; writing - original draft.
Gowrishankar Palaniswamy: Conceptualization; writing - original draft.
Navya Pillikunte Doddareddy: Conceptualization; software. Mandip
Dhungel: Investigation; method-ology. Sahithi Talacheru: Writing -
original draft. Shraddha Jadhav: Investigation; methodology. Tanmayee
Mareedu: Investigation; methodology. Mihirkumar P. Parmar:
Conceptualization; methodology; super-vision; writing - original draft;
writing - review and editing. Anup Banur: Super-vision;
conceptualization; resources.

\textbf{FUNDING INFORMATION}

None.

\textbf{CONFLICT OF INTEREST STATEMENT}

The author does not possess any conflict of interest.

\textbf{DATA AVAILABILITY STATEMENT}

Available from the corresponding author on reasonable request.

\textbf{CONSENT}

Written informed consent was obtained from the patient to publish this
report in accordance with the journal's patient consent policy.

\textbf{ORCID}

Mihirkumar P. Parmar,\emph{https://orcid.org/0000-0002-5110-1544}

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