Leila Marie A.
Mancera Jan 29, 2025
2022-0164
MEDICINE II
BI Case 6
I. History and PE
A. Demographic Data
Patient Adney Abrams (AA) is a 64-year old African-American woman.
B. Chief Complaint
The patient is complaining of nausea, back pain associated with
paresthesia in her upper limbs, fatigue, weakness in the lower limbs, and weight
loss.
C. History of Present Illness
Aside from her back pain and bilateral arm paresthesia that started 1
month PTC, the patient experienced a fall while walking on the street just before
PTC. She fell onto the left side of her chest and passed out for a few seconds
before getting up.
Upon arrival in the Emergency room, it was elicited that she has pleuritic
chest pain which she attributed to her fall.
D. Past Medical History
She is a known hypertensive and dyslipidemic patient. She was also
recently diagnosed with anemia 1 week ago. She had repeated renal colic a few
years ago that prompted visits to the emergency room.
Her maintenance medications include metoprolol and pravastatin. And
she has been taking iron for 1 week and diclofenac for 2 weeks. She has no
known allergies and did not have recent surgeries.
E. Personal and Social History
Patient AA has not been exercising due to fatigue that she started feeling
4 months ago. She has also noted weight loss in the past 4 months, but
especially in the last month. She does not smoke tobacco or drink alcoholic
beverages.
F. Family History
She has no knowledge of severe illness in the family.
II. Review of Systems
General: No recent fever but is feeling nauseous
Skin: No complaints of skin lesions, discoloration, or other changes
HEENT Head: No complaints
Eyes: No complaints
Ears: No complaints
Nose: No complaints
Throat: No complaints
Neck: No complaints
Respiratory: No recent cough, dyspnea
Cardiovascular: No complaints
Gastrointestinal: No recent vomiting, diarrhea
Urinary: No complaints
Genital: No complaints
Peripheral No complaints
vascular:
Musculoskeletal: Paresthesia in upper limbs and weakness in lower limbs
Neurologic: No complaints
Hematologic: No complaints
Endocrine: Fatigue (started 4 months ago)
Psychiatric No complaints
III. Physical Exam
Patient BE’s vital signs were as follows:
● Weight: 55 kg
● Height: 165 cm
● BMI: 20.2 kg/m2 (Normal based on American standards)
● BP: 171/77 mmHg
● HR: 122 bpm
● RR: 32 cycles/min
● O2 Sat.: 98% at room air
● Temp.: 36℃
● Glucose level: 142 mg/dL
The patient was conscious and coherent. Her skin was dry and warm to the
touch. No rashes were observed on inspection. Her hair is white and evenly distributed
on her head. She has brown eyes with anicteric sclerae. No conjunctival suffusion,
redness, or discharge was noted. Her nose is midline with no redness, lesions, or
discharge noted. On oral examination, she had reddish lips, moist buccal mucosa with
no lesions, ulcers, foreign bodies, or blockages noted.
She had no clubbing or central or peripheral cyanosis. On chest examination,
she had no chest deformities and had symmetrical chest expansion. No use of
accessory muscles during breathing, resonant on percussion, and normal lung sounds
on auscultation. However, her left chest was painful on palpation due to a suspected
rib fracture.
She had a normal capillary refill time of 2 seconds.On cardiac examination, she
had no cardiac murmurs on auscultation and had strong and rhythmic pulses on her
upper and lower limbs.
On abdominal examination, she had no abdominal scars and skin markings
suggestive of disease. Her abdomen was tympanic in all four quadrants and no
organomegaly, masses, peritoneal irritation, guarding, or tenderness was noted on
palpation. On auscultation, she had hyperactive bowel sounds in all four quadrants.
She had a Glasgow coma scale score of 15, and both of her pupils were round
and equally reactive to light. Genitourinary exam was normal.
IV. Salient Features
Patient AA is a 64 year old woman who presented with nausea, back pain, upper
limb paresthesia, weakness in the lower limbs, fatigue, and weight loss. She just had a
fall where she fell unconscious for a few seconds, but was able to walk to the ER. She
has a history of repeated renal colic and is a known hypertensive, dyslipidemic, and
anemic patient who is maintained on metoprolol, pravastatin, iron (1 week), and
diclofenac (2 weeks). On physical examination, she had elevated SBP (171/77 mmHg),
slightly elevated glucose levels (142 mg/dL), tachypneic (32 cpm), and tachycardic (122
bpm). She had pleuritic chest pain and pain on palpation of her left chest. She also had
hyperactive bowel sounds. All other physical exam findings were unremarkable.
V. Clinical Schema
The patient had non-specific symptoms, but her main complaints were nausea
and upper limb paresthesia. She also had weakness of the lower limbs, anemia, back
pain, fatigue, and weight loss that started four months ago. Different organ systems
were considered for her condition’s etiology as there was no specific organ system
directly involved. A renal injury was considered at first due to her recent use of
Diclofenac and comorbidity of hypertension that could induce renal injury and cause
systemic-wide symptoms. A systemic infection such as tuberculosis was also
considered due to her symptoms of fatigue and weight loss. And finally, a cardiac
etiology such as coronary artery disease was considered due to her hypertension and
dyslipidemia that predisposes her to developing heart disease that can manifest as
chest pain and fatigue.
VI. Illness Script
DDX 1: Tuberculosis (TB)
Tuberculosis is caused by mycobacterium tuberculosis and remains to be a
significant cause of concern worldwide as 7.1 million new cases of TB were reported
last 2019 (Loscalzo, et al., 2022). It is transmitted via droplet nuclei aerosolized by
coughing, sneezing, or speaking. The immunologic status of an individual is important in
calculating the risk of tuberculosis infection, namely their HIV status, history of cancer
therapy, or use of immunosuppressive drugs. Primary TB is described as clinical illness
directly following infection, but secondary TB or reactivation of TB much later after initial
infection can occur due to storage of latent TB bacilli in deep tissues of the body. Once
TB enters the alveoli after inhalation, they are phagocytosed by macrophages and
opsonization is activated with subsequent cytokine production. The bacterium prevent
phagosome-lysosome fusion via its cell wall that contains lipoglycan
lipoarabinomannan. This interferes with the destruction of the mycobacterium and
allows it to migrate to deeper tissues while avoiding immunologic responses. Primary
TB can be asymptomatic or can present with symptoms such as fever, cough, or
pleuritic chest pain. Other non-specific symptoms early in the disease include: night
sweats, weight loss, anorexia, general malaise, and weakness (Stuck, et al., 2024).
Although these are classic symptoms of TB, new research has questioned the validity of
persistent cough as a classic symptom of TB, as there have been studies on TB (+)
individuals not presenting with cough or respiratory signs (Dall, 2024). Nevertheless,
aside from clinical signs, other diagnostic tests used for TB include chest x-ray (to look
for Ghon focus that develops after initial infection), Xpert MTB/RIF assay, AFB
microscopy, and culture. In the patient’s case, her age was a factor that could explain
atypical non-respiratory symptoms of TB infection. Her symptoms of fatigue and weight
loss are also red flags for TB and coincide with symptoms of the condition.
DDX 2: Coronary Artery Disease
Coronary artery disease is essentially an imbalance of cardiac demand with
oxygen supply which can lead to ischemia of the myocardium. The most common cause
of coronary artery disease is atherosclerosis which induces structural changes in
epicardial coronary arteries that limits effective cardiac perfusion. Atherosclerotic
plaques develop due to changes in the vascular endothelium such as loss of vascular
tone and antithrombotic surface. The loss of these defenses cause inappropriate arterial
constriction, luminal thrombus formation, and abnormal interactions of monocytes and
platelets with the vascular endothelium (Loscalzo, et al., 2022). Risk factors for
developing atherosclerosis include high levels of plasma LDL, smoking, hypertension,
and diabetes. The intraluminal narrowing of coronary arteries disrupts normal blood flow
to the heart and causes undue stress that can manifest as chest pain (angina pectoris),
diminished pulses to extremities, bruits, and murmurs in the case of a damaged
myocardium. This was considered in the patient due to her comorbidities of
hypertension and dyslipidemia. Although her fall may be the primary reason for her
chest pain, the fall would not have been able to explain her recent fatigue, weakness,
and paresthesia. If the patient does have coronary artery disease, perfusion to her
extremities may have been compromised and contributed to her lower limb weakness
and upper limb paresthesia, while decreased blood flow to her abdominal system could
have contributed to nausea.
DDX 3: Renal Failure
Acute kidney injuries (AKIs) that can lead to renal failure can be caused by
pre-renal, intrinsic, or post-renal causes. In the case of the patient, she has non-specific
symptoms that makes it difficult to directly diagnose without additional lab tests to check
her metabolic state. In the community, common causes of AKIs include volume
depletion, heart failure, adverse effects of medications, urinary tract obstruction, or
malignancy. Prerenal azotemia is the rise in serum creatinine or BUM concentration due
to inadequate renal plasma flow. This is commonly associated with conditions such as
hypovolemia, decreased cardiac output, and NSAID or angiotensin II inhibitors. This
type of kidney injury seems to be the most relevant to our patient as she is taking
NSAIDs and has hypertension that can amplify the effects of NSAIDs on nephrotoxicity.
However, prerenal azotemia may develop into intrinsic kidney injury and damage to
renal parenchyma if left untreated. Normal renal blood flow is maintained by
constrictions of afferent and efferent renal arterioles. Homeostatic responses in
controlling salt and water reabsorption, are controlled by multiple blood pressure
mechanisms in the body. In the context of NSAIDs, prostaglandins are mediators in
renal vasodilation when renal autoregulation detects low renal perfusion pressures.
Prerenal azotemia or acute kidney injury that can lead to renal failure was considered
due to her age, recent use of NSAIDs, hypertension, and past history of renal colic that
increase the patient’s risk of renal injury. She was also recently diagnosed with anemia,
and her symptoms of fatigue and weight loss can also be explained by failure of her
kidney to effectively filter out waste products, leading to uremia in her blood.
VII. Lead Diagnosis/Impression
Acute Drug-induced Exacerbation of Chronic Kidney Disease leading to Acute Renal
Failure (with Suspected Traumatic Rib Fracture on Left Chest)
Tuberculosis is not likely the cause of her chief complaints as the patient did not
manifest other common symptoms of tuberculosis such as fever and night sweats. A
recent history of persistent cough was also not in the history of the patient and upon
respiratory auscultation, no signs of crackles or rubs were heard. Fatigue and weight
loss are indeed red flags for latent tuberculosis, but her blood tests and chest x-ray
revealed no leukocytosis and no cavitations or Ghon focus that supports TB. It would
have been appropriate to do a PCR assay for TB if she lived in a country where TB is
endemic, but assuming that she lives in the United States that has a low-burden for this
disease, it would be more appropriate to search for other causes for her condition. The
patient has risk factors for coronary artery disease such as hypertension and
dyslipidemia, and some of her symptoms such as fatigue and weakness of lower limbs
may be explained by this condition. But, she did not manifest with chest pain until after
her fall and even the patient herself suspects that this pleuritic comes from her fall. The
character of the chest pain is also not in line with angina as angina pectoris (if stable) is
felt during periods of physical exertion, and should disappear after rest. This could not
be completely ruled out as it is possible that the patient has coronary artery disease, but
the acute presentation of nausea that is strong enough to cause a fall and subsequent
syncope is not inline with its common manifestation. The development of coronary
artery disease should also have had a more chronic, progressive course instead of
resulting in an acute incident such as this.
A renal etiology for the patient’s condition is most likely as her age reduces
kidney function, and her past history of renal colic could have induced renal injury that
developed subclinically as chronic kidney disease. Her fatigue and weight loss that
developed four months ago, and her recent diagnosis of anemia also support the
diagnosis of CKD as the kidney is the main producer of erythropoietin that induces
production of red blood cells. She may have already had anemia for a longer period of
time and just did not notice as she was only diagnosed formally one week ago. Her
back pain also started four months ago and could have been a sign of advanced renal
injury as her kidneys become inflamed. Her (assumedly) long-standing hypertension
could also induce kidney injury by damaging afferent renal arterioles and decreasing
GFR, and her dyslipidemia could have damaged glomeruli as it accumulates in her
kidneys. Her recent use of diclofenac (NSAID) could have induced an acute renal injury
that exacerbated her CKD. In a sense, it could have been the “straw that broke the
camel’s back” as her other comorbidities contributed to the development of her CKD.
The reduced GFR caused by inhibition of prostaglandins by diclofenac may have
induced ischemic injury and subsequent renal failure in the patient that manifested as
nausea (via accumulation of waste products such as creatinine and urea) and caused
her to fall. The fall, in turn, caused her fractured ribs as she landed on them hard.
This diagnosis is supported by her lab results that showed elevated serum
creatinine, very low GFR, and multiple metabolic abnormalities that should have been
managed by healthy, functioning kidneys. The most glaring concern for the patient is her
hyperkalemia that must be controlled to prevent cardiac injury. She also has multiple
electrolyte abnormalities that could explain her non-specific symptoms of fatigue. Her
upper limb paresthesia and weakness of lower limbs may be due to accumulation of
uremic toxins in serum, or her multiple electrolyte abnormalities such as hyperkalemia
that could cause neuromuscular dysfunction. Her GFR of 7 mL/min places her CKD at
Stage 5 which makes it reasonable that renal failure occurred in the patient. Her lack of
leukocytosis also helped rule out an infectious etiology. Her renal ultrasound showed
poorly differentiated, atrophic kidneys that suggest significant loss of renal tissue and
supports the diagnosis of CKD. Her urinalysis results showed proteinuria which is also
indicative of renal damage. And her chest x-ray was able to identify rib fractures that
could explain her pleuritic pain after the fall. In essence, the patient’s use of diclofenac
exacerbated her chronic kidney disease and caused acute renal failure that is supported
by her blood tests and renal ultrasound.
VIII. Diagnostic Plan
Diagnostic Method with Rationale Expected Findings
1. History, Physical Examination, and The patient has significant history that must be
Vitals Monitoring explored as this may correlate to her current
● A detailed history and physical condition. Namely, her past episodes of renal
exam must be done to assess colic, her fatigue and weight loss that started 4
damage to other organs and months ago, her hypertension, dyslipidemia, and
risk of multiorgan failure. recent diagnosis of anemia.
2. Chest X-ray Her chest x-ray revealed 2nd and 3rd costal
● An X-ray will allow the arches fracture. But aside from that, no pleural
physician to address her most leakage, hilar reinforcement, or other findings
recent incident (the fall on her were significant. This rules out pneumothorax
left chest) and would provide and hemothorax as a reason for her pleuritic
insight into the painful palpation pain.
of her left chest and pleuritic
pain.
3. 12-lead ECG Her 12-lead ECG had the following result:
● This allows the physician to Sinusal tachycardia, peaked T waves, P-wave is
detect abnormalities with heart flattened, and prolonged PR interval. This
rhythm that should be indicates hyperkalemia, a medical emergency
monitored and corrected if that must be immediately remedied.
needed.
● Her complaint of nausea and
paresthesia of the upper limbs
were non-specific symptoms
that could benefit from a
12-lead ECG that could bring
some insight into her heart’s
condition
4. Renal Ultrasound Her renal ultrasound revealed poorly
● Due to the ECG result of the differentiated and atrophic kidneys
patient, her kidneys must also
be investigated for
abnormalities. She is also
taking an NSAID that could
have contributed to renal injury.
3. Abdominal Ultrasound No alterations or abnormalities were seen on her
● An ultrasound allows abdominal ultrasound.
visualization of the chosen body
field.
● Considering the patient’s age
and her recent fall, it would be
apt to examine her abdominal
area that could have also been
impacted in her fall.
4. Arterial Blood Gas The patient was acidemic (pH 7.22), had low
● An ABG can assess the hemoglobin (8.2 g/dL), had low PaCO2 (31
patient’s oxygenation status mmHg) and HCO3- (16 mEq/L), and a highly
and guide the physician on how negative base excess (-10.28).
to correct oxygenation
abnormalities. It can also She also had multiple electrolyte abnormalities
assess lactate levels that could such as: hyponatremia (129 mEq/L),
be suggestive of infection hyperkalemia (6.5 mEq/L), hyperchloremia (115
mEq/L), and hypercalcemia (13 mg/dL).
5. Biochemistry Test Biochemistry results were similar to her ABG,
● The biochemistry panel test but it gave more insights into her renal status
searches for hepatic or renal and liver status. She had an abnormally low
involvement. It can also help creatinine clearance (7 mL/min) and a
assess electrolyte significantly high serum creatinine (627.6
abnormalities. umol/L) and CRP (6.5 mg/L). She also had high
AST (114 IU/L) and ALT levels (72 IU/L).
6. Complete Blood Count No leukocytosis was seen in herCBC. The only
● A CBC can assess the levels of significant findings were her low erythrocyte
erythrocytes, leukocytes, and (2.7x106/uL), hemoglobin (8.2 g/dL), and
thrombocytes. This can help hematocrit (24%) levels. These are all congruent
distinguish between a bacterial with her anemia diagnosis 1 week ago.
or viral infection depending on
what is elevated.
7. Urinalysis His urinalysis showed an acidic urine, and was
● This can help assess renal (+) for WBC, protein, and leukocytes. These can
abnormalities such as indicate renal abnormalities and inflammation.
proteinuria, pyuria, and
hematuria.
8. Lipid Profile Her results showed elevated total cholesterol
● As the patient is a known (207 mg/dL), triglycerides (156 mg/dL), LDL
dyslipidemic, this may be a levels (145 mg/dL), and cholesterol ratio (6.7).
routine bloodwork to assess her She also had low HDL levels (31 mg/dL) which
maintenance medication’s all confirms her diagnosis of dyslipidemia.
effectiveness and to check the
need for more intensive
support.
9. Cardiac Biomarkers Due to the hyperkalemic and hypercalcemic
● To assess for myocardial status of the patient, it is important to assess if
damage there is myocardial damage for more intensivec
cardiac support
IX. Management Script
For Admission:
● The patient should be admitted to the nephrology unit of a hospital for close
monitoring and assessment for dialysis need as her kidney disease is at an
advanced state.
For Acute Treatment:
● IV peripheral catheter
○ For administration of IV drugs
● Urinary Catheter
○ To help monitor urine output in tandem with GFR monitoring
● Furosemide (IV, 2.5 mg/min)
○ To manage fluid overload and electrolyte imbalances such as excretion of
potassium
● Calcium gluconate (IV, 10% solution: 10-20 mL bolus)
○ Due to the patient’s hyperkalemic state, calcium gluconate is administered
to protect the cardiac membrane and prevent cardiac overexcitability.
● Insulin + Glucose (IV, 10% solution, 10 mL over 2 minutes)
○ The mechanism of action of insulin helps glucose enter cells with
potassium, reducing serum potassium levels. Glucose is given as an
adjunct to prevent acute hypoglycemia.
● Sodium Bicarbonate
○ To correct acid-base state of the patient
For Secondary/ContinuingTreatment:
● Assess need for dialysis and candidacy for kidney transplant
● Continued monitoring of cardiac health
● Continued monitoring of electrolytes
X. Prevention and Health Maintenance
As the patient is already at an advanced state of kidney disease, her only
definitive treatment is a kidney transplant. However, she may control her symptoms via
dialysis and supplementation of EPO to address her fatigue and anemia. She would
have to be monitored closely as her kidneys are no longer able to correct electrolyte
imbalances and flush out waste products in her blood. More generic lifestyle
modifications such as ample exercise, a controlled, salt-restricted diet, sleep, and social
support are all important as they improve the quality of life for the patient.
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