A 55 years old Man Came In With Severe Shortness of Breath Since 1 Day

Before Admission
Luthfy Uly M. Sihite*, Nelvin Raesandra Jauhari*, Eddy M. Salim**
ABSTRACT
smoker, since 15 years ago with daily of 2-3 box.
History of drinking a cup of coffee every morning
until now. History of drinking alcohol when hes
still young, 1 bottle every 2-3 days. Family history
was free from hypertension, diabetic, kidney
disease and heart disease. Based on physical
examination, high blood pressure 150/100mmHg,
patient swelling at his eyelid, conjunctiva palpebral
was pale, ronkhi present, convex abdomen, shifting
dullness (+), scrotum edema (+), pretibia edema
(+). From the laboratory findings Hb: 8 mg/dl,
erythrocyte: 3.01x106, leucocyte: 12.000/mm3,
hematocrite: 24%, MCV: 79.4fL, MCH: 27pg,
LED: 108mm/hour, pH: 7.302, pCO2: 24.4, HCO3:
12.2, ureum: 237mg/dL, creatinine: 14.14mg/dL,
BSPP: 286. Urinalysis showed protein +++,
glucose ++, keton +, blood ++, cylinder +, bactery
++. Hence, patient was diagnosed with Chronic
Kidney Disease stage V ec DM type II and
Hypertension stage II.

It was reported a case with shortness of

breath and Chronic Kidney Disease at RSMH. A 55
years old man was admitted with a chief complain
of shortness of breath since 1 day before admission.
Two years before admitted, patient started to feel
thirsty and hungry abnormally (increased in
frequency). The patients urination frequency was
also started to increase. Because of that, patient like
to wake up at night during his sleep. Then, patients
went to general practitioner to check his blood
sugar and blood pressure. He was told that he got
hypertension and diabetes mellitus. He was given
anti-hypertension and anti-diabetes drugs. One
month prior to admission, patient complained about
swelling on foot in the morning after awakening.
Shortness of breath that relieve with rest and
oxygen. Decreased in urination than usually, 3-4
x/day. Two weeks prior to admission, patient
complained about swelling spread to thigh. The
patient was difficult to walk. Shortness of breath
more severe but still relieve with rest and oxygen.
Nausea (+). Decreased of appetite (+). Frequency
of urination still like before. One week prior to
admission, patient complained that he was often
shortness of breath but still relieve with rest and
oxygen, nausea, and decreased of appetite. But, his
stomach was getting bigger and tight. Patient just
stay in bed because he was difficult to walk.
Frequency of urination less than before, 2-3 x/day.
One day prior to admission, patient complained of
severe shortness of breath, not relieve with rest and
oxygen. Swelling of whole body. Frequency of
urination was 1 x/day. Patient came to Emergency
Instalation of Mohammad Hoesin Hospital and was
hospitalized. Patient has medical history of
hospitalized in Charitas hospital 4 month ago
because shortness of breath, doctor said that he has
enlarged heart. Hypertension since 2 years ago,
there was medication with amlodipine but he was
not routine consume the medication and controlled
to doctor. Diabetes Mellitus since 2 years ago, there
was medication with glibenclamide and glimepiride
but he was not routine consume the medication and
controlled to doctor medication. Patient was also a

Keywords : Chronic Kidney Disease, Diabetes

Mellitus type II, Hypertension stage II

* Medical Student of Sriwijaya University, Clerkship Program

Moh.Hoesin General Hospital
** Staff of Allergy-Immunology Division of Internal Medicine
Department of Dr. Moh. Hoesin General Hospital

INTRODUCTION
The thalassemia syndromes are inherited
disorders of - or -globin biosynthesis. The
reduced supply of globin diminishes production
of hemoglobin tetramers, causing hypochromia and
microcytosis. Unbalanced accumulation of and
subunits occurs because the synthesis of the
unaffected globins proceeds at a normal rate.
Unbalanced chain accumulation dominates the
clinical phenotype. Clinical severity varies widely,
depending on the degree to which the synthesis of
the affected globin is impaired, altered synthesis of
other globin chains, and coinheritance of other
abnormal globin alleles.1

Kalo bisa sih tabel klasifikasi thalassemia

Beta thalassemia syndromes are a group of
hereditary disorders characterized by a genetic
deficiency in the synthesis of beta-globin chains. In
the homozygous state, beta thalassemia (ie,
thalassemia major) causes severe, transfusiondependent anemia. In the heterozygous state, the
beta thalassemia trait (ie, thalassemia minor) causes
mild to moderate microcytic anemia.2
Beta thalassemia is inherited as an
autosomal recessive disorder. The defect can be a
complete absence of the beta-globin protein (ie,
beta-zero thalassemia) or a severely reduced
synthesis of the beta-globin protein (ie, beta-plus
thalassemia).3
Two major consequences of the genetic
defect of thalassemia are severe anemia and
expansion of the bone marrow in the bodys effort
to produce more red blood cells.1 This leads to poor
growth, impaired physical activities, facial and
other bone deformities, fragile bones and
enlargement of the liver and spleen. If left
untreated, it will lead to death within the first
decade of life. The only treatment to combat severe
anemia is regular blood transfusions and iron
chelation therapy.1
Thalassemia major occurs when a child
inherits two mutated genes, one from each parent.
Children born with thalassemia major usually
develop the symptoms of severe anemia within the
first year of life. They lack the ability to produce
normal, adult hemoglobin and experience chronic
fatigue. They may also fail to thrive.4
Mutations causing -thalassemia can
affect any step in the pathway of globin gene
expression: transcription, processing of the mRNA
precursor, translation, and posttranslational
metabolism of the -globin polypeptide chain.
posttranslational metabolism of the -globin
polypeptide chain. The most common forms arise
from mutations that derange splicing of the mRNA
precursor or prematurely terminate translation of
the mRNA. Hypochromia and microcytosis
characterize all forms of thalassemia because of
the reduced amounts of hemoglobin tetramers.1
The frequency of beta thalassemia varies
widely, depending on the ethnic population. The
disease is reported most commonly in
Mediterranean, African, and Southeast Asian
populations, presumably as an adaptive association
to endemic malaria. The incidence may be as high
as 10% in these areas. The manifestations of the
disease may not be apparent until a complete

switch from fetal to adult Hb synthesis occurs. This

switch typically is completed by the sixth month
after birth.2
The diagnosis of -thalassemia major is
readily made during childhood on the basis of
severe anemia accompanied by the characteristic
signs of massive ineffective erythropoiesis:
hepatosplenomegaly, profound microcytosis, a
characteristic blood smear, and elevated levels of
HbF, HbA2, or both. Many patients require chronic
hypertransfusion therapy designed to maintain a
hematocrit of at least 2730% so that
erythropoiesis is suppressed.1

CASE ILLUSTRATION
A 55 years old man who lives at Ratu
Sianum Street, Ilir Barat II, Palembang, was
admitted in Moh.Hoesin General Hospital on 16th
June 2016 with chief complaint of shortness of
breath since 1 day before admission. Two years
before admitted, patient started to feel thirsty and
hungry abnormally (increased in frequency). The
patients urination frequency was also started to
increase. Because of that, patient like to wake up at
night during his sleep. Then, patients went to
general practitioner to check his blood sugar and
blood pressure. He was told that he got
hypertension and diabetes mellitus. He was given
anti-hypertension and anti-diabetes drugs. One
month prior to admission, patient complained about
swelling on foot in the morning after awakening.
Shortness of breath that relieve with rest and
oxygen, wheezing (-), influenced by weather (-),
influenced by emotional (-), influenced by activity
(-). Wake up in the night because shortness of
breath (-). Patient can sleep with one pillow. Cough
(-), sniffles (-). Chest pain (-). Decreased in
urination than usually, 3-4 x/day, bubbles in urine
(-), red urine (-), cloudy urine (-), fever (-). Two
weeks prior to admission, patient complained about
swelling spread to thigh. The patient was difficult
to walk. Shortness of breath more severe but still
relieve with rest and oxygen. wheezing (-),
influenced by weather (-), influenced by emotional
(-), influenced by activity (-). Wake up in the night
because shortness of breath (-). Patient can sleep
with one pillow. Nausea (+). Decreased of appetite
(+). Frequency of urination still like before. One
week prior to admission, patient complained that he
was often shortness of breath but still relieve with
rest and oxygen, nausea, and decreased of appetite.

But, his stomach was getting bigger and tight.

Patient just stay in bed because he was difficult to
walk. Frequency of urination less than before, 2-3
x/day. One day prior to admission, patient
complained of severe shortness of breath, not
relieve with rest and oxygen, wheezing (-),
influenced by weather (-), influenced by emotional
(-), influenced by activity (-). Wake up in the night
because shortness of breath (-). Night sweating (-).
Swelling over whole body (+). Frequency of
urination was 1 x/day. Patient came to Emergency
Instalation of Mohammad Hoesin Hospital and was
hospitalized.

abnormalities. In abdominal percussion there was

positive shifting dullness. On the palpation liver
and lien showed no abnormalities and normal
bowel sound was detected during auscultation. On
the upper extremities showed swelling and lower
extremities showed pretibial edema.
From the laboratory findings Hb: 8 mg/dl,
erythrocyte: 3.01x106, leucocyte: 12.000/mm3,
hematocrite: 24%, MCV: 79.4fL, MCH: 27pg,
LED: 108mm/hour, pH: 7.302, pCO2: 24.4, HCO3:
12.2, ureum: 237mg/dL, creatinine: 14.14mg/dL,
BSPP: 286. Urinalysis showed protein +++,
glucose ++,keton +, blood ++, cylinder +, bactery +
+.

Patient has medical history of hospitalized

in Charitas hospital 4 month ago because shortness
of breath, doctor said that he has enlarged heart.
Hypertension since 2 years ago, there was
medication with amlodipine but he was not routine
consume the medication and controlled to doctor.
Diabetes Mellitus since 2 years ago, there was
medication with glibenclamide and glimepiride but
he was not routine consume the medication and
controlled to doctor medication. Patient was also a
smoker for approximately 25 years with daily of 23 box. History of drinking a cup of coffee every
morning until now. History of drinking alcohol
when hes still young, 1 bottle every 2-3 days.
Family history was free from hypertension,
diabetic, kidney disease and heart disease.

From chest x-ray it showed an enlarged

heart. Differential diagnosis of this patient could be
renal failure e.c. nephropathy diabetic, renal failure
e.c. nephrosclerosis, and renal failure e.c. chronic
glomerulonephritis
The patient and the family were informed
about from the aspect of non- pharmacology patient
was given diet protein 50 gram, fluid consumption
was controlled by maintenance, bed rest.
Pharmacology includes furosemide 2x20 mg IV,
amlodipine 1x5 mg tablet per oral, ceftriaxone 2x1
gram IV, folic acid 3x1 mg tablet per oral, CaCO3
3x500 mg tablet per oral, and routine
haemodialysis. The patient showed a bad functional
prognosis but a good vital outcome.

Based on the condition of the patient he

was fully conscious, general appearance was
moderately sick with body weight 88 kg and height
170 cm, blood pressure 150/100 mmHg, pulse rate
94x/minute regular, respiration rate 30x/minute
regular and body temperature 36.5oC. Physical
examination of the head, mouth, ears, throat,
showed no abnormalities, eyes
physical
examination showed swelling at his eyelid and pale
conjungtiva palpebra. Physical examination of the
neck showed there are no enlargement of lymph
nodes and jugular venous pressure (5-2) cm H2O.
The chest was symmetric, tactile fremitus was
symmetric upon both lungs,vesicular sound was
normal, rales present upon both of lungs. For heart
examination, ictus cordis was not visible and
palpable, upon percussion it appeared slide
enlargement of the left heart boundary shifting
towards the left axial line on 5th ICS. On
auscultation, heart sound AI-AII, PI-PII, MI-MII,
TI-TII normal, no murmur and no gallop heard.
Inspection on the abdominal region showed no

Further examinations, such as laboratory

finding of globulin and albumin, Hb after
transfusion are needed to accurately sum up the
prognosis of the disease including the therapy.
DISCUSSION
Beta thalassemia are a group of hereditery
disorders characterized by a genetic deficiency in
synthesis of beta-globin chain in formation of
hemoglobin. Beta thalassemia is inherited as an
autosomal recessive disorder. Clinical severity of
beta thalassemia patient is widely depending on the
degree to which the synthesis of the affected beta
chain of globin is impaired. This patient experience
severe fatigue as a chief complain. It was a sign of
severe anemia in major thalassemia. Thalassemia
major can occurs when a child inherits two mutated
genes, one from each parent. It means that patients
parents are carrier of thalassemia gene. Children
born with thalassemia major usually develop the
symptoms of severe anemia, lack the ability to

produce normal adult hemoglobin and experience

chronic fatigue.1
Beta thalassemia induced inbalanced and -globin accumulation causes accumulation of
highly insoluble unpaired chains. They form toxic
inclusion bodies that kill developing erythroblasts
in the marrow. Few of the proerythroblasts
beginning erythroid maturation survive. The
surviving RBCs bear a burden of inclusion bodies
that are detected in the spleen, shortening the RBC
life span and producing severe hemolytic anemia.
The resulting profound anemia stimulates
erythropoietin release and compensatory erythroid
hyperplasia, but the marrow response is sabotaged
by the ineffective erythropoiesis. Anemia persists.
Erythroid hyperplasia can become exuberant and
produce masses of extramedullary erythropoietic
tissue in the liver and spleen. 1 On this patient, there
are signs of anemia, such as: pale conjungtiva
palpebra, fatigue, dizziness, and pale palmar.
This patient has developed a charasteristic
face due to chronic anemia. Massive bone marrow
expansion deranges growth and development.
Children develop characteristic chipmunk facies
(facies Cooley) due to maxillary marrow
hyperplasia and frontal bossing. Thinning and
pathologic fracture of long bones and vertebrae
may occur due to cortical invasion by erythroid
elements and profound growth retardation.1
Besides that, diabetes is the number one
cause of kidney failure in United States.4 Diabetes
can harm the kidneys by causing damage to blood
vessel inside our kidneys, nerves in our body, and
urinary tract. The filtering units of the kidney are
filled with tiny blood vessels. Over time, high sugar
levels in the blood can cause these vessels to
become narrow and clogged. Diabetic nephropathy
consist of 5 different stages depending on
glomerular damage. On this patient, there is a
possibility of renal failure because of the low GFR
(<15 mL/min per 1.73 m2), and sign of uremic
syndrome.
Hypertension also the one of the leading
causes of CKD due to the deleterious effects that
increased BP has on kidney vasculature. Longterm, uncontrolled, high BP leads to high
intraglomerular pressure, impairing glomerular
filtration.5 Evaluation of target organ damage, on
this case kidney, can be done with checking
whether there is proteinuria or albuminuria and also
calculating the GFR estimation. This patient
already has proteinuria/albuminuria and also

decreasing GFR. So we can suggest that CKD on

this patient is caused by the hypertension.
In this case report, patient came with
shortness of breath, as known it is an abnormal
breathing or distress symptom. Dyspnea could
occur due to various conditions such as COPD,
asthma, pleura effusion, pulmonal edema, etc.
Based on the anamnesis, shortness of breath in this
patient was not influenced by activity, was not
triggered by any change of weather. In physical
findings there was no barrel chest, no wheezing,
there was decreased in stem fremitus, vesicular
sound decreased with the presents of rales.
Therefore, shortness of breath on this patient was
not caused by COPD or asthma. Percussion of the
heart showed that the left boundary was shifted
towards to the left axial line and based on the x-ray
it shown presents of cardiomegaly. Patient had a
history of hypertension since 2 years ago but was
not well controlled. So, cardiomegaly on this
patient
maybe
caused
by
uncontrolled
hypertension. Uncontrolled hypertension also
contributed to cause CKD on this patient.
Abdominal examination showed a positive shifting
dullness in this patient and in extremities, pretibial
edema was found. Ascites and pretibial edema on
this patient caused by overloaded fluids due to
renal failure.
From the laboratory findings Hb: 8 mg/dl,
erythrocyte: 3.01x106, leucocyte: 12.000/mm3,
hematocrite: 24%, MCV: 79.4fL, MCH: 27pg,
LED: 108mm/hour, pH: 7.302, pCO2: 24.4, HCO3:
12.2, ureum: 237mg/dL, creatinine: 14.14mg/dL,
BSPP: 286. Physical examination, high blood
pressure 150/100mmHg, patient swelling at his
eyelid, conjunctiva palpebral was pale, rales
present, convex abdomen, shifting dullness (+),
scrotum edema (+), pretibia edema (+). Patients
laboratory results showed positive chronic kidney
disease. The management of patient with chronic
kidney disease and chronic disease anemia consists
of non pharmacology and pharmacology. Non
pharmacology is to explain about patients illness
to the family also including the therapy and
outcome, bed rest is required, diet protein. In
addition, fluid balance must be monitored strictly.
Pharmacology therapy for this patient
include furosemid 2x20 mg IV, amlodipine 1x5 mg
tablet per oral, ceftriaxone 2x1 gram IV, folic acid
3x1 mg tablet per oral, CaCO3 3x500 mg tablet per
oral, and routine haemodialysis. Diuretic in this
matter is used to reduce ascites and bilateral
pretibial edema.

CONCLUSION
We have discussed a case of chronic
kidney disease in a 55 year old, male patient who
also had shortness as breath, swelling over whole
the body, pulmonal edema including rales.
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