In a masquerade ball, everyone wears a mask. Unknown. Anonymous. Mysterious.

Deceiving. We have been given a case like this. Like a mask. Concealing it's true nature. Thus,
we are here today to uncover the identity of this case. We are here to make the unknown, known.

Ladies and gentlemen, join us as we enter the thrilling masquerade event this afternoon.

Hagámoslo as they say in Spanish, friends, let’s do this.

Welcome to the Masquerade: A Trail of Deceit.

We now enter the ball.

We present a case of Spontaneous Splenic Rupture in a 21 year old, Male from Sara, Iloilo.
He had a chief complaint of cough. To get a clear picture of what happened, let’s travel back in
time with the Clinical Course.
Six (6) days prior to admission, he had productive cough, difficulty of breathing and
undocumented fever.
Three (3) days before the actual hospitalisation the following interventions were done
(flash). However, cough and difficulty of breathing were persistent.
The following pertinent physical and clinical findings lead us to an initial impression of:
Community Acquired Pneumonia- Moderate Risk.
On the day of admission, patient was started with the following treatment regimen.
On the second day of admission prolonged INR, and the following CT scan and Chest
Ultrasound findings, Splenic involvement noted.
On the 7th day of admission, fine rales were persistent and a prolonged INR was still
present. Light growth of Candida famata was seen on sputum culture and immune status was
unremarkable. Ultrasound reevaluation was done, still with Splenomegaly with Hypoechoic
lesion and retroperitoneal lymphadenopathies.
He was diagnosed with Childhood Bronchial Asthma but with no maintenance
medication. Furthermore, there was family history of pulmonary tuberculosis on the maternal
grandfather’s side.
The sound of music is inviting us to dance our way on the floor. Let’s gather up and find
our partners as we waltz to the rhythm of the differentials.
Having the background of the case in hand and collating the important information
available, we came up with the following pertinent findings and were group as follows. Four key
findings were taken (Flash).

With these three general categories (flash)

Hematologic causes specifically the Autoimmune Blood Diseases present with the
following triad (flash) However, it was highly unlikely since the patient did not manifest with
Jaundice.
We remain with Malignancy and Infectious.

For the Neoplasms we tackle first Primary Lung Cancer with Splenic Metastasis. We
considered it because of the following manifestations (flash symptoms). However, 80% of lung
cancers occur in active smokers, which is not present in our patient. Furthermore, site of
metastasis are as follows (flash) Thus, primary lung cancer with splenic metastasis is highly
unlikely.

For the next differential diagnosis, we have lymphoma.

 Lymphoma was ruled in because of the following pertinent findings. Most importantly, it
is more common in males with a bimodal incidence peak at age 15-34 and more than 60 years
old. Also, according to this study, lymphoma was ranked 8th among the most common
malignancy in males.

However, 60-70% presents with cervical and supraclavicular lymph node enlargement
which was not seen in our patient. Likewise, it was emphasized that it should present with
leukocytosis, in contast, our patient has normal WBC. Therefore, the diagnosis, highly unlikely.

The culprit has nowhere to hide. We are almost near.

We focus on the INFECTIOUS CAUSES. Under it, 4 areas were considered (flash)

First, the VIRAL causes.

We considered HIV given the following presentations (flash). Most worthy to mention is
that Iloilo has the highest statistics in Western Visayas and males having the highest percentage
of acquiring the disease.

However, HIV was highly unlikely due to unremarkable immune status screening and
absence of pertinent sexual history, overall makes HIV highly unlikely.

Infectious Mononucleosis was ruled in due to presence of (flash). However, absence of

these findings (flash) makes it highly unlikely.

CMV was also considered (flash). However, the absence of a prolonged high grade fever
makes CMV highly unlikely.

Collectively, a Viral Cause is unlikely.

Let’s explore the Fungal Causes.

Histoplasmosis was considered given the following. However the disease is rare in the
Philippines. The disease is more endemic in the following areas (flash). The lack of exposure to
bat/bird droppings and the epidemiological distribution of the disease makes it unlikely.

Next stop, the Parasitic Causes.

Schistosomiasis was considered with the aforementioned symptomatology. The absence

of these associated pertinent manifestations (flash) makes it highly unlikely.

Also, Paragonamiasis was considered because of the following (flash). However this is
highly unlikely because P. westermani is not endemic in Iloilo City, had no history of
consumption of inadequately cooked crustaceans and Hemoptysis the most common
manifestation was not present.

Thus, we are left with the a Bacterial Cause, specifically Tuberculosis.

Tuberculosis (TB) is well known for its ability to masquerade as other infectious
and disease processes. It has been proven through time and clinical practice that TB is a
great mimicker.
 True to this, the following manifestations, varied as they are, can be found in
Tuberculosis (flash).

Early in the course of disease, symptoms and signs are often nonspecific and insidiou
(flash)
Anemia has many etiologies, but a particular focus is given to Anemia of chronic
disease which can explain the cause of anemia in this case.

There was also a finding of an irregular border nodule in the right upper lung. In this
study, a solitary pulmonary nodule in a Tuberculosis-endemic area has benign and
malignant etiologies. Tuberculoma has the highest frequency under the benign form.

In general, most frequent infections that give rise to intrathoracic adenopathy are
caused by Mycobacterial disease. It is in fact the most common presentation of
extrapulmonary TB.

Virtually all organ systems may be affected in TB giving rise to extrapulmonary

manifestations. For our patient, there was splenomegaly and a possible splenic abscess.

The following journals present a similar ultrasound and CT findings in the spleen of
patients with splenic tuberculosis along with other similar clinical manifestations in this
case.

This last journal took the liberty of constructing a clinical profile of patients having
splenic involvement in Tuberculosis. The results mirror that of our patient with the
following manifestations (flash) These ultrasonographic findings were present (flash)
Thus, this diagnosis was highly considered.

The following were identified to be important risk factors associated with Tuberculosis,
three of which are present in our patient, namely (flash). AGE was also noted as an important
determinant of disease, highest during late adolescence and early childhood, our patient is 21
years old. Lastly, investigation of the disease according to _identified that Sara, Iloilo has _ of
cases for the year.

Given the above mentioned risk factors, disease process ensues with the inhalation of
droplets containing Mycobacterium tuberculosis. Invasion of the alveoli in the apices of the lung
happens thereafter. With this, the bacilli is ingested by alveolar macrophages. Inhibition of
intracellular increase in Calcium by bacterial cell wall Lipoarabinomannan impairs the Calcium-
Calmodulin pathway with resulting failure of phagosome-lysosome fusion rendering the survival
of the microorganism, thus the PRIMARY TUBERCULOSIS infection.

Further recruitment of unaffected alveolar macrophage lead to tuberculoma formation,

causing necrotic degeneration. Bronchial walls are invaded and destroyed. Cavities are formed
resulting to scarring and calcification, thus the presence of IRREGULAR BORDER NODULE,
in the right upper lobe on imaging studies was seen.

We know focus our attention into these two important risk factors (flash). A case of
asthma can lead to increase release of lung matrix degrading proteases resulting to chronic airway
inflammation. The BMI of 15.6 kg/m2 classified as underweight culminates to decreased
vitamin, mineral and protein synthesis as sequelae. This can result to failure to mount an
appropriate T-helper 1 cell mediated response. All these ultimately lead to the REACTIVATION
of foci.

According to this study, 55% of primary tuberculosis cases presents as POSTPRIMARY

TUBERCULOSIS. In this 55%, the bacilli is spread by the following routes (flash)

Lymphatic spread results to lymphadenopathies which in the case presented as Subcarinal,

Left Hilar, Paraaortic and Retroperitoneal. Such spread is supported by this Journal (show
Journal).

Hematological alterations and changes in coagulation profile would increase prothrombin

destruction in the lungs. This journal likewise reported that cytokines and mediators from a
tuberculosis lesion are considered to prolong prothrombin time.

Such a mystery that we dig for more clues. We enter the deepest secrets of the culprit’s
whereabouts. Take a deep breathe, light our candles as we enter into the dark.

The red pulp of the spleen is relatively devoid of phagocytic activity, helping the
entrapped, slow-growing mycobacteria to escape from the reticuloendothelial system of the
spleen. Increased demand for splenic function results to immune hyperplasia, thus the
SPLENOMEGALY. Tuberculous foci formation and necrosis with release of bacilli leads to new
lesion formation thereby evidence of COMPLEX HYPOECHOIC FOCI in parenchyma and
upper aspect of spleen seen on ultrasound (flash Surgical Pathology).

We are near to solving the case we have in hand. The culprit is near. Tighten your grip, as
we go up the stairs in silence, Shhhhhhhhh…….

Correlating the case of Splenomegaly, three pathologic processes can occur. First stop,
increased splenic sequestration of formed elements. 67% of patients with pulmonary tuberculosis
have generally normal WBC count in a background of infection.

Increased levels of hepcidin in combination with the release of several cytokines results
to iron trapping and suppression of hematopoiesis thus, the ANEMIA .

Splenomegaly can cause obstruction of the normal physiologic lymphatic flow in the
affected lung, in this case, the left. Obstructive pneumonia occurs resulting to an inflammatory
response. Release of specific cytokines and chemokines occur with the following effects:
a. MINIMAL PLEURAL EFFUSION on the left lung
b. The case of undocumented fever
c. Difficulty of Breathing with fine rales and productive cough with whitish phlegm.

It was emphasized from this source, the indirect role of antibacterials on decreasing
microbial competition, therefore the LIGHT GROWTH of Candida fomata on sputum culture.

On the other side of the spectrum, these pro inflammatory cytokines resulted to the
containment of bacteria within the lung segments, thereby, INFILTRATES with BASAL
CONSOLIDATION on the left mid to base lung was visible on imaging.

Remember the clues given by the culprit? The involvement of the spleen? Let’s culminate
the search and solve the mystery, folks.
 With the result of necrosis and Bacilli release, chemical factors from persistent injurious
stimuli activated the fibroblasts thus, SPLENIC FIBROSIS.

The tuberculous foci gave rise to the formation of granulomatous TB infiltrates in the red
pulp, resulting to a hemorrhagic focus and eventual splenic capsule tear. Consequent SPLENIC
RUPTURE as the endpoint.

Raise your glasses and let’s drink to this culmination.

Splenic Rupture is the most common indication of Splenectomy. Life threatening

infection in an asplenic patient from loss of splenic macrophages makes our patient susceptible
to infection from encapsulated bacteria, thus the following vaccines were given (flash vaccines).

Ladies and gentlemen, we present to you the culprit of this trail of deceit! Let’s remove our masks
and shout, Viva!

Our final diagnosis is:

Community Acquired Pneumonia- Moderate Risk; Presumptive Pulmonary TB ? Case:

Clinically Diagnosed with Extrapulmonary TB (Lymph Nodes and Spleen); Splenic abscess vs
Caseation Necrosis; Bronchial Asthma not in Acute Exacerabation; Anemia of Chronic Disease

S/P 2 units PRBC and 1 unit FFP transfusion

S/P Splenectomy