Good afternoon everyone. I am _______ of section K, the discussant of this week’s CPC case.

Patient overview:
Patient XX is a 55-year-old female, filipino, widowed, Roamn Catholic, non smoker, non
alcoholic drinker, with sedentary lifestyle, and menopausal, presently residing at Binangonan,
Rizal, admitted for the first time on June 4, 2021 with a chief complaint of continuation of her
medical care

Salient Features:
Here are the salient features in the History of Present Illness of the patient
● Vague pain on both feet
● Body weakness
● Headache
● Sudden onset of palpitations
● Anemia
● Hyponatremia
● UTI
● Intermittent fever 38.1C
● Bipedal edema
● Increased creatinine and BUN
● BP elevations
● Difficulty of breathing
On the Review of Systems of the patient the followings were noted
● Estimated weight loss of 12%
● Fatigue
On the Physical exam the findings were
● Bilateral crackles on both lung base
● Tachycardia
● ⅗ motor function

Differential diagnoses:
ONLY READ RULE IN RULE OUT IF ASKED.

> FIRST DIFFERENTIAL: CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY

> NEXT IS, SYSTEMIC LUPUS ERYTHEMATOSUS
> LAST DIFFERENTIAL IS INCLUSION BODY MYOSITIS.

The class decided to rule in Chronic Inflammatory Demyelinating Polyneuropathy due to the
following reasons:
○ CIPD does not occur within a particular age group and it may affect any age at
any decade in life.She also presented with throbbing pain on the right foot,
sudden difficulty in ambulation, numbness of both upper and lower extremities,
and reduced deep tendon reflexes which are all common symptoms of CIPD.
However, we ruled this out due to:
 ○ The prevalence of the disease because men are more likely to develop CIPD, as
compared to women. The symptoms of this disease also occur during a course of
8 weeks, while the disease of our patient has occurred for greater than 8 weeks.
The patient was also diagnosed to have anemia and hyponatremia which is
uncommon in this disease. Her urinary tract infection, fever, weight loss, bipedal
edema, changes in blood pressure, and difficulty in breathing does not also fit the
disease manifestations.

Siz, nakahide to sa PPT ha.

We are also considering Idiopathic Necrotizing Autoimmune Myopathy for reasons such
as:
● The patient’s throbbing pain on her right right foot, severe proximal weakness, lower
extremity weakness, easy fatiguability, difficulty in ambulation, weight loss, positive
creatine kinase-MB, positive antinuclear antibodies as well as respiratory weakness.

However we ruled it out due to:

● Lack of muscle biopsy showing inflammatory myopathies characterized pathologically
by necrotic muscle fibers with absent or minimal inflammation to confirm diagnosis.
There was also no MRI done to reveal diffuse or patchy edema and no mention of
anti-SRP and anti-HMGCoAR autoantibodies that are associated with this condition.

We also considered Systemic Lupus Erythematosus as a differential diagnosis.

We ruled it in because:
● Of the patient’s positive antinuclear antibody titer, her systemic symptoms such as easy
fatigability, body weakness and 12% weight loss over the past 2 months, the presence of
anemia, the presence of renal symptoms. The patient also showed neurologic symptoms
such as a reduction in her upper and lower extremity motor function as well as a single
seizure episode.
Systemic Lupus Erythematosus may be ruled out because of the following reasons
● The absence of photosensitivity, the characteristic malar rash, positive anti-DsDNA test,
splenomegaly and joint pains..

We also ruled in Inclusion Body Myositis because of the following reasons:

● Inclusion Body Myositis is sometimes misdiagnosed as polymyositis, and the patient has
been mentioned to have an impression of polymyositis. The patient also falls within the
age group of its occurrence as it occurs for those beyond the age of 50. Other reasons
include the pain on patient’s right foot, accompanied by swelling, redness, weakness of
right lower extremity, numbness of both her upper and lower extremities, difficulty in
ambulation, reduction in her deep tendon reflexes, decreased motor function on all
extremities, elevated serum creatinine kinase, positive antinuclear antibody test, and the
presence of renal injury.
Inclusion Body myositis may be ruled out because of its prevalence. It affects more men
than women. It also usually involves inflammation, weakness and atrophy of not only the legs
and arms but also the fingers and the wrist. However, we cannot totally rule it out because
there was a lack of testing done because there was no mention of a muscle biopsy, or imaging
tests to differentiate it from polymyositis, which the patient was diagnosed with based on the
HPI. Pain, cardiac, renal and pulmonary may also occur with inclusion body myositis.

This is why after thorough study of the case, our main diagnosis is Polymyositis secondary to
SLE.

Flowchart:
Moving on to the flow chart, We begin again with our index patient who is a 55 year old female,
non-smoker, non-alcoholic beverage drinker, leads a sedentary lifestyle and is menopausal who
came into the institution for continuation of her care.

Polymyositis to Congestive Heart Failure

Polymyositis is an inflammatory muscle disease that causes muscle weakness that is proximal
to the trunk of the body. In our case, our patient has decreased sensory in her T10 area which
means that her hips, thighs and upper arms are affected. The patient only have 70% of sensory
in all extremities, below T10, and a motor function of 3 /5. Polymyositis commonly occurs in
women that age from 31-60 years. Cardiac manifestation that is common to polymyositis is
myocarditis. This affects the muscular walls of the heart that leads to Acute Coronary
Syndrome, this inflammation causes the heart to enlarge due to hypertrophy and then weakens
its walls. This can present with elevated troponins and ischemic changes. Our patient exhibited
positive troponin I, increase in CKMB, her ECG also showed sinus tachycardia with diffuse
ischemia. This ischemia comes from the plaque formation due to the complication of
atherosclerosis formation in polymyositis. Which then predisposes the patient to develop
congestive heart failure. CHF is evident in this case due to the presentation of difficulty in
breathing, o2 saturation of 86%, bipedal edema and tachycardia.

Polymyositis to ARI d/t Rhabdomyolysis

Before we dwell further on this, I would like to discuss another complication of polymyositis if we
can please focus on the left side of the flowchart, that is acute renalinjury due to
rhabdomyolysis. Rhabdomyolysis from the breakdown of muscle cells causes increased risk for
developing kidney injury that affects the patient’s glomerular filtration rate that causes her to
have decreased urine output, increases BUN, creatinine and potassium and decreases in
sodium levels. It is evident in the patient’s labs that there is electrolyte imbalance. With this
kidney injury the patient had to undergo hemodialysis that caused her to lose 2L of body fluids

Polymyositis to SLE to Lupus Nephritis to Acute Renal Injury

This time let us focus on the right side of the screen where we can see another connective
tissue complication of polyomyositis which is Systemic Lupus Erythematosus. SLE
predominantly affects women. It is an autoimmune disease that involves multiple organs,
characterized by a vast array of autoantibodies particularly antinuclear antibodies or ANA in
which injury is caused mainly by the deposition of immune complexes and binding of antibodies
to various cells and tissues. SLE can present before or after, or simultaneously with the onset of
polymyositis. Even though SLE typically presents with mucocutaneous lesions, 50-70% of SLE
cases have significant, renal involvement or renal impairment as the most common
symptomatology of SLE. This is evident in the patient’s elevated BUN and creatinine by 1.5
times, bipedal edema, and with her declining kidney function, and the protenuiria. This condition
is called Lupus Nephritis. Lupus nephritis occurs when immune complexes accumulate within
the kidneys, followed by infiltration of the kidney by T cells and macrophages. This can progress
to acute kidney injury because of consistent renal inflammation that induces kidney injury, and
acute renal injury happens which is evident in the patient’s elevated creatinine and BUN.
Another important function of the kidney is to produces erythropoietin that promotes proliferation
and differentiation of erythrocyte precursors, so if it continues to deteriorate, a low erythropoietin
level can cause the RBC count to drop and anemia to develop, this caused the patient’s
frequent anemic episodes with a decrease hemoglobin count..

SLE to Neuro
Among the neurologic manifestations of systemic lupus erythematosus, organic
encephalopathies are the most common. This comprises all potential variations from acute
confusion, lethargy, coma, chronic and subacute dementias. This can also manifest as
psychiatric symptoms including depression, mania or psychosis. I’d like to focus on organic
encephalopathy. This is evident in our case since her eyes open only to pain, with 2mm in
diameter of pupil size and are sluggishly reactive to light. Seizures of any type may be caused
by lupus. Seizures can happen if there is electrolyte imbalance and again, kidneys help to
maintain electrolyte concentrations. Also an increase in the BUN of the patient, this can
stimulate a seizure in our patient. This is evident in our case as our patient had experienced one
seizure episode with tonic clonic movement and upward rolling of the eyeballs and experienced
motor weakness of all extremities.

SLE to Cardio
Cardiac involvement in patients with SLE has been described since the early 20th century. This
can involve all components of the heart, including the pericardium, valves, myocardium and
conduction system of the heart. Pericarditis is the most common manifestation however our
patient did not present with any manifestation of pericarditis but asymptomatic pericardial
involvement with SLE occurs more frequently than clinical pericarditis. And knowing that this is a
part of autoimmune disease, CAD from SLE can result from several pathophysiologic
mechanisms including atherosclerosis as the most common type, thrombosis, embolization or
abnormal coronary flow reserve. The development of CAD in patients with SLE is high however,
only a minority of patients show clinical manifestations. The reason why coronary artery disease
develops in patients with SLE is unknown, but a leading theory is that immune complex
deposition causes initial damage, that is followed by accelerated development of atherosclerosis
in patients. With the myocardial dysfunction from chronic inflammation, as well as a combination
of the coronary disease, the heart is vulnerable to function. Even with the absence of risk factors
primarily present, the patient was also medicated with glucocorticoids which could also be a
factor that leads her to develop CHF.

SLE to Anemia of Chronic Disease to Death

Another complication from SLE is anemia of chronic disease. ACD coexists usually with anemia
with other anemia that is caused by other mechanisms. We have found peptic ulcer disease as
an incidental finding in this case because of the unintentional weight loss and a positive FOB,
and iron deficiency is common with Peptic Ulcer disease, as a result of increased
gastrointestinal blood loss with the use of NSAIDS, aspirin and oral anticoagulants. As we have
known from the HPI, our patient has been hospitalized for 3 months and was diagnosed
previously with anemia of chronic disease. Due to the low level of hemoglobin, our patient also
had to get a blood transfusion twice. Because of the low hemoglobin, the heart needs to
compensate by pumping more blood to compensate for the hypoxia brought about by the
anemia. The anemia can also worsen the cardiac function because it causes cardiac stress by
increasing the rate and increase in stroke volume, causing reduced renal blood flow and fluid
retention, adding further stress to the heart. Long standing anemia of any cause can cause left
ventricular hypertrophy as a means of compensating, which can lead to cell death through
apoptosis and can worsen congestive heart failure. Therefore, a vicious circle is set up wherein
CHF causes anemia, and the anemia causes more CHF, and both damage the kidneys
worsening the anemia and CHF further. This is coined as the cardiorenal anemia syndrome. Let
us not forget that there is also dysfunction in the erythropoietin production of the kidneys that
contributed also to the anemia. And as a consequence of inadequate compensatory responses,
this leads the heart not able to pump enough blood towards the body, and starts to back up to
the lungs, pulmonary veins and capillary beds that increases the pressure in the pulmonary
artery wall and in the interstitial space causing pulmonary congestion therefore causing
dyspnea. Heart failure, heart cells get irritated that can lead to heart arrhythmias. The ventricles
don’t contract in sync making them less able to pump blood efficiently and worsening the
cardiorenal syndrome, causing the patient to undergo cardiogenic shock before her demise.

Cause of death
● For this case the underlying cause of death is Polymyositis. And the antecedent is
anemia of chronic disease. Lastly, for the immediate cause of death is cardiogenic shock