Section 3D Script:

PATIENT OVERVIEW

For our case, we have XX who is a 55-year-old female, Filipino currently residing in
Binangonan, Rizal. She is a non-smoker, non-alcoholic beverage drinker with no known
exposure to deleterious chemical. She has a sedentary lifestyle and a family history of
hypertension and acute stroke.

Next slide - CLINICAL HISTORY

For the clinical history:

3 months prior to admission (PTA), the patient started to have throbbing pain on her right foot
over the dorsal area which was followed by swelling, redness, and weakness of the right lower
extremity.

2 months PTA
● The patient experienced sudden difficulty in ambulation and numbness of both upper
and lower extremities with associated easy fatigability and body weakness. The patient
was then admitted. Lung findings revealed the presence of bibasal crackles. Her
neurologic examination showed motor function of 3/5 in all extremities, decreased
sensory in 70% of the right lower extremity. Her deep tendon reflex was +1 in all
extremities and Babinski is present bilaterally.
● The lab results revealed that she had hyponatremia with a serum sodium of 125.8
mmol/L, and anemia with a hemoglobin level of 8.6 g/dL. To address her electrolyte
imbalance, she was given NaCl tab 3 times a day and for her anemia, was transfused
with 2 units of properly typed and crossed packed RBCs. She was also diagnosed with
Pneumonia where her chest x-ray showed bibasal pneumonia.
● Discharge diagnosis then was to consider Cervical Spinal Cord lesion, Anemia,
corrected Electrolyte Imbalance, Hyponatremia and Pneumonia - improving. Several
home medications were given, one of which is an NSAID (Meloxicam) and antibiotic
Moxifloxacin.

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2 weeks PTA

● The patient was doing better until 2 weeks prior to her 2nd admission when she
experienced vague pain on both feet, body weakness, headache and sudden onset of
palpitation. She was brought back to the same hospital and was subsequently admitted.
(So this would be her 2nd admission)

1st hospital day

 ● Laboratory work ups showed hyponatremia (although her serum Na was unrecalled),
and still with anemia which was attributed to her hemoglobin level of 9.8g/dL. The same
interventions were done to address the hyponatremia and anemia of the patient.
Urinalysis revealed that she has proteinuria, pyuria and UTI.
● On the 2nd day, the patient developed intermittent fever of 38.1C. Bone marrow
aspiration biopsy was done which revealed reactive normocellular marrow with noted
plasma cells; no tumor clusters.
● On the 5th day, she developed bipedal edema and her creatinine and BUN was 1.5
times elevated. Clinical impression during this time was Acute Renal Injury, etiology
multifactorial, drugs and frequent anemia episode. NSAIDS and amikacin were
discontinued.

● Hyponatremia is a common complication associated with acute kidney injury. In

the setting of reduced glomerular filtration rate, the ability of the kidney to excrete
electrolyte free water is diminished. To the extent that water intake exceeds this
decreased maximal free water excretion, hyponatremia will ensure.
● UTI through an ascending mechanism manifested as pyuria, and bacterial toxin
now causing renal damage. Proteinuria may be due to tubulointerstitial cause of
AKI.
● The result of the bone marrow biopsy may be due to a normal reaction to
infection because the patient has pneumonia.
● Bipedal edema and increased BUN and creatinine is attributed to AKI.

● During the 16th hospital day, the patient suddenly developed difficulty of breathing and
oxygen desaturation of 86%. ECG showed sinus tachycardia with diffuse ischemia and a
positive Troponin I.

Drop in blood oxygen level was caused by the patient’s pneumonia. The result of the ECG and a
positive Troponin I suggests a recent myocardial infarction.

ROS

For the Review of System, the patient experienced fatigue, as well as weight loss of 12% for the
past 2 months which is due to hypercatabolic state caused by the patient’s current condition
such as pneumonia, acute renal injury, and myocardial infarction.

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PHYSICAL EXAMINATION

Moving on to the PE of the patient,

the patient appeared to be tachycardic, hypertensive, and assisted breathing which may be a
compensatory mechanism of the body to Acute kidney injury increasing circulating volume,
elevating blood pressure which will also increase the heart rate of the patient

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Upon the PE of HEENT, the patient had a pale palpebral conjunctiva which is a sign of anemia

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Upon the auscultation of the lungs, bilateral crackles on both lung bases were heard, this is due
to the patient’s pneumonia. The movement of fluid in the tiny air sacs of the lungs

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The patient also had a bipedal edema, the accumulation of fluid is usually caused by an
increased pressure inside the veins pushing the fluid in the surrounding tissue

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For the neurological examination of the patient, the patient seemed to have a weak gag reflex
and a diminished deep tendon reflex specifically at the right achilles tendon. Probable cause
may be due to polymyositis that damaged the lower motor neuron of the spinal cord.

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COURSE IN THE WARD

At the ER, the patient came in with assisted ventilation and presented with hypertension and
tachycardia. ECG also revealed the presence of diffuse ischemia. 3 hours after the admission,
the patient experienced hypertension, hence Nicardipine drip 2mg/min was initiated. Later that
day, the patient’s vital signs went back to normal. On the 2nd hospital day, she once again
presented with hypertension.

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During the 4th hospital day, the patient’s BP was still elevated. This is most likely due to the
presence of O2 desaturation which will be discussed in the next few slides. On the same day,
the patient was referred to Rheumatology because of a history of (+) ANA titer from previous
hospitalization.

On the 5th hospital day, the patient was status quo but had one seizure episode for a few
seconds, hence Phenobarbital was given thru IV. Her vital signs went back to normal on the 7th
day and since then, no change was noted until the patient suddenly experienced bradycardia
and asystole on the 12th day.

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For neurological examination, the patient was found to present with declining eye response and
motor function. Results showed eye opening to voice on the 3rd day and eye opening only to
pain on the 4th day. The motor function declined from full range of motion against gravity to
insufficient muscle contraction to produce joint motion even with elimination of gravity. This will
be further correlated with our diagnosis later.

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Laboratory Interpretations

Upon admission to the hospital emergency room, ABG, Electrolyte (mainly sodium and
potassium), BUN and creatinine, CBC, Chest xray in anteroposterior view, ECG and capillary
blood glucose were requested.

as we can see there is a gross decrease in cellular components in the blood test of the patient,
there is a decrease of wbc indicating that our patient is in a state of leukopenia, Patient also has
anemia with a classification of macrocytic normochromic anemia which may indicate that the
patient has nutritional deficiency related anemia despite taking ferrous sulfate and folic acid 3
times a day as stated in the interval history. We also have an increase in platelets which can
correlate also to nutritional deficiency anemia where the patient also has iron deficiency
supported by the decreased hemoglobin of the patient.

(Additional notes: presence of macroovalocytes can confirm the type of anemia - pbs not
requested, ELISA can confirm serum B12 and folate deficiency but was not requested)

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Next, for chemistry results. Patient's creatinine and blood urea nitrogen are progressively
increasing with decreasing eGFR denoting that the patient is already experiencing acute kidney
injury. Patient's sodium and potassium levels were within normal range on the first day however
only her potassium was monitored and continually increased. In the history of present illness it
was stated that her Troponin I tested positive and had ECG showing sinus tachycardia with
diffused ischemia indicating patient had a heart attack prior to getting transferred to this hospital
and is further confirmed with patient's CK total, LDH and CK MB upon admission.

Highlighting the 4th day where in the patient's eGFR is 5.3, potassium at 6.9 and BUN and
creatinine were high the patient was suggested to undergo hemodialysis.
On the 7th day, patient CPK total registered at 129 noting some form of tissue damage in the
system. It's important to note that the patient was already experiencing acute kidney injury and
may have been one of the contributing factors for it's increase. We also requested an fecal
occult blood test which yielded positive results.

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For arterial blood gas results, we can see that the patient was undergoing Respiratory Acidosis.

1 hour after reintubation at the ICU, the patient showed normal abg and then 3 hours after
reverted to respiratory alkalosis.

On the 3rd day abg was once again requested and the patient already manifested compensated
metabolic acidosis.

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For radiology readings, chest x-rays were requested on admission, on the 4th day and on the
5th day while a skull radiography was requested on the 2nd day. For the chest x ray readings
the first day yielded linear and reticulo hazed densities in the left lung which might indicate an
on going pneumonic process and on the 4th and 5th day it confirms that the patient has pleural
effusion due to the presence of bilateral pneumonia and congestion with blunting of left
costophrenic sulcus and left sided effusion was seen.

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DIFFERENTIAL DIAGNOSIS

For the differentials, We considered multiple myeloma since our patient presented with
anemia,fatigue, leukopenia, dilutional hyponatremia, and renal insufficiency. However, in the
absence of joint pain, a negative punched out skull x-ray scan, a reactive normocellular with no
tumor clusters bone marrow aspirate ruled out MM.

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Another differential diagnosis that we’ve considered is Systemic Lupus Erythematosus because
our patient is positive for antinuclear antibodies which may indicate an autoimmune disease,
there is also weight loss, renal insufficiency, hypertension, Leukopenia, anemia and
hypercoagulable state which is common to this illness. However, the patient did not experience
muscle and joint pain,as well as dermatological manifestations such as malar rash or butterfly
rash.

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Lastly we’ve considered STEMI Acute coronary syndrome since the patient had a shortness of
breath, and elevation in troponin I as well as CKMb. On the other hand, our patient did not
experience any chest pain, dizziness, nausea, ruling out STEMI acute coronary syndrome.

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MAIN CLINICAL DIAGNOSIS

The patient, a 55 year-old-female, had several predisposing factors to Deep Vein Thrombosis,
like having a sedentary lifestyle, old age, and infection. Three months prior to her admission,
she experienced throbbing pain on her right foot, swelling, redness, and weakness on her right
lower extremities. She was treated in her previous hospital and was sent home.

Two months prior to her admission, she was again admitted to the previous hospital due to
numbness of her upper and lower extremities, her motor functions were 3/5 (movement against
gravity without any resistance), a score of +1 on her deep tendon reflexes, and a bilaterally
positive Babinski reflex. These findings show that the patient had an acute stroke. However a
neurologic exam finding of DTR +1 that will include his lower extremity is perplexing due to the
fact that an upper motor abnormality is involved when modulating the lower motor neuron
activity of the lower extremities at the lower vertebra, which is the reason for the positive
babinsky. We conjecture that there may be probably a superimposing event that can relate to
low DTR’s at the level of the peripheral nervous system that may involve any of the
neuromuscular unit. And ruling in polymyositis especially if chronic and progressive can lead to
weak Deep Tendon Reflexes which may have probably occurred before the event of stroke. It
was later expressed during her 3rd admission that she had positive ANA. These findings
confirm the presence of polymyositis. Polymyositis can also be contributory to the patient having
nonresolving aspiration pneumonia because it causes weakness to the neck muscles.

During the patient’s second admission to the first hospital, it was also noted that she had bibasal
crackles which was later confirmed when reticulohazed densities were found on her chest x-ray.
These findings point to pneumonia which further complicated to pleural effusion due to
extension of inflammatory infiltrates and increased permeability. Because of the persistent
pneumonia, the lungs required more blood supply thus the patient developed pulmonary
hypertension that presented as an increase in her blood pressure.

Another finding during her 2nd admission was anemia which was seen in her CBC as
decreased hemoglobin, and was later supported by findings in her 3rd admission with
decreased hematocrit and RBC. Due to her persistent anemia and numerous drugs during her
hospital admissions, she eventually developed acute kidney injury. This presented as
hyponatremia, increased BUN and creatinine, proteinuria, bipedal edema, and decreased urine
output. She also had a urinary tract infection that presented as pyuria which contributed to her
acute kidney injury.
Because of increased workload to the heart brought upon by the patient’s acute kidney injury
(fluid overload and hyperkalemia), anemia of chronic disease, and pulmonary hypertension, her
heart developed diffuse ischemic heart disease. Diffuse ischemic heart disease is
characterized by inadequate blood supply to the heart.

During transfer to the 3rd hospital admission, her heart can no longer meet the oxygen demand
of the body, that is why she had a Non-ST elevation myocardial infarction. Her NSTEMI was
Type 2 because it was ischemic in origin. NSTEMI presented as sinus tachycardia, positive
troponin I, increased CKMB and CK total, and a predisposing factor of elevated LDH.

The patient’s NSTEMI progressed even further during her 12-day admission to the 2nd hospital.
In her course in the ward, we can see that she is slowly deteriorating with decreasing O2
saturation, decreasing GFR, decreasing motor response, decreasing blood pressure, and
decreasing urine output. The patient then developed decompensated heart failure where her
heart can no longer compensate for the heavy workload brought upon by her numerous
illnesses. The patient’s decompensated heart failure is evident when she went into bradycardia
at asystole which eventually led to her death.