Translated from Indonesian to English - www.onlinedoctranslator.

com

Effusion Pleura dextra et causa

Congestive Heart Failure +
Chronic Kidney Disease
By
HanaSulistia(712021065)

Advisor
Prof. dr. Eddy Mart Salim, Sp. PD., KAI
Preface
01
Disease pleura is something disturbancewhich
influence more from3,000 peoplein1million
population every the year.

Reason main morbidity&mortality

lungs.Reason most common malignancy,
TB and pneumonia
Fail heart is gathering symptom which complex form:
symptom typical fail heart:congested breath moment rest/activity,fatigue,oedema limbs
sign typical fail heart:tachycardia,tachypnea,rhonchi lungs,effusion pleura, JVP↑,oedema
peripheral, hepatomegaly
sign objective disturbance structure or functional heart:cardiomegaly, murmurs heart,abnormality
echocardiography and ↑peptide natriuretic
 02
Case Report
 IDENTIFICATION
Full name :Mrs. Y
Gender :Woman
Date of birth :01-01-1943/80Year
Address :JL. H. Faqih Usman, Palembang
Profession :Mother Home Ladder
Islam
No.reg.RS :35-07-62
Examination date :13January2023
Room :Ahmad Dahlan 10
MRS :12January2023
 Anamnesis 01
Patient come to the IGD Muhammadiyah
Palembang Hospital withcomplaint dyspnea which
has gotten worse since± 4 hours SMRS.
 Disease history
Shortness of breath is felt Keep going continuously since ± 1 year ago. Shortness of
breath occurs when the patient performs pekerja activitycurrently and does not
decrease when the patient rests. The patient said that at night the patient often wakes
up because of shortness of breathAt what hour1-2 nights. The patient admits that he
has difficulty sleeping because of tightness when lying down, and is more
comfortable sleeping in a sleeping position using 2 pillows. Shortness of breath is
not affected by weather, dust or animal hair. The patient admits that sometimes he
feels his chest feels tight when he is active or resting.
 Disease history

Complaint also accompanied exists swollenon second that legfelt 3day

SMRS.Patient say complaint swollen increase critical if patient stand uplongso
Becomes hard asstone andpatient sayonmomentworshiponly capable in
circumstancessit.In addition, patients also complain that the body often feels weak
and easily tired. The patient complained of abdominal pain that felt like it was being
stabbed on the left side which radiated to the back of the waist. The patient says
pain in the stomach only when the stomach is pressed.
 Disease history

The patient complained of blurred vision (-), decreased consciousness (-), dizziness
(-), coughingphlegm (+) but only occurs if the patient wakes up at night and takes
deep breaths, hearing loss (-), cold sweat (+), long cough (-), nausea (+), vomiting
(-), decreased appetite (+), history of drug use (-), head trauma (-), bowel
movements (+) normal, urination (+) normal.
 Disease history
The patient said there was a history of the same complaint before. The patient has
been treated for the same complaint. The patient also said there was a history of
high blood pressure since ±20years ago and routinely treated. The patient alsoataka
if during this timeroutine taking high blood pressure medication. Patient own
history disease heartand diabetesmellitus since10year final.in the patient's familyno
anyone suffering from the same complaintwith patient. The patient had no history of
asthma and no one in his family had asthma. Patient no own history disease kidney.
 ANAMNESIS
Past medical history
Historyhypertension:there is
Historydisease DM:there is
Historydisease kidney:denied
Historydisease lungs:denied
Historydisease stomach:denied
Historydisease asthma:denied
Historydisease heart:there is
Historydisease thyroid:denied
Disease HistoryFamily
Historyhypertension:denied
History disease DM:denied
History disease kidney:denied
History disease lungs:denied
History disease stomach:denied
History disease asthma:denied
History disease heart:denied
History disease thyroid:denied
Habit History
Smoke :-
Herb :-
Sport :-
Coffee :3 glass coffee in a week
Liquor :-
Recreation :-
Tea :-
Drugs :-
Etc :-
 Inspection Physical

circumstances umum:Looks Sick Currently

Awareness: Compos mentis
Pressure blood: 160/80 mm Hg
Pulse : 98x/minute,regular, content voltage enough
Breathing :24x/minute,type thoracoabdominal
Temperature : 36,8oC
Heavy Body: 55 kg
Tall Body: 150 cm
Status nutrition:BMI : 24,44(Ideal BB)
 SPECIFIC EXAMINATION
Inspection Head: InspectionEye:
Shape head:Normocephaly Exophthalmos:Not there is

Hair :Qno fall out,no easy revoked Endophthalmus:Not there is

Mlike:Symmetrical Palpebra :Efever (-/-)

Conjunctiva :Anemis(-/-)
Sclera :Iicteric(-/-)
Inspection Ear:
pupils :Rreflex light(+/+),isokor
Liangear:Nnormal
Lens : Clear (+/+)
Serumen :(-/-)
Vision:Not conducted inspection
Sdischarge :(-/-)
Movement:Well to all direction
Nscream press :(-/-)
RoomyView :Luas
Gg hearing :(-//)
 SPECIFIC EXAMINATION

Inspection Nose: Inspection Mouth and Tthroat:

deformity :(-) Mouth coot: (-)
Nafas lobe nose :(-) Lips :cyanosis(-),
Sdischarge: (-) Gold :Bleeding (-) Hiperemi(-)
Epistaxis :(-) Lbeautiful :dirty(-),atrophy papillae(-)
Mukosa hyperemic :(-) Qonsil:T1-Q1Calm
septumdeviation: (-) Fdry:hyperemic(-)
SPECIFIC EXAMINATION
Inspection Mouth andThroat:
Mouth coot: (-)
Lips:cyanosis(-)
Gum:Hiperemi(-)
Tongue:dirty(-),atrophy papillae(-)
Tonsils : T1-T1Calm
pharynx :hyperemic(-)
 SPECIFIC EXAMINATION
Inspection Neck
Inspection: Symmetrical, no visible lumps, lesions on the skin (-)
Palpation: Enlargementthyandroid (-),KGB enlargement (-)
JVP : 5+2 cm H2O

Inspection Skin
hyperpigmentation:(-)
Iicteric:(-)
Petichie:(-)
Sianosis:(-)
Pulcers on the palms and feet:(-)
Qurgor: CRT < 2second.
 SPECIFIC EXAMINATION
Lungs Front
Lungs Bevade
Inspection :Static,Dynamic,Symmetrical, Spider nevi (-)
Inspecti :Symmetrical
Static Kanan same with left
Palpation : Stem fremitusright decrease
Ddynamic Qno there iswhichleft behind
thanwhichleft
Sell ribs widened(-),retraction intercostal(-).
Percussion:Sonoron all roomy lungs rightandleft.
Palpation : Stem fremitusright decrease thanwhichleft
Percussion:Sonor on all roomy lungs right and left. Auscultation:Vesicular(+/+),ronkhi(+/+) in

Auscultation:Vesicular (+/+),ronkhi wet fine(+/+), wheezing basallungs,wheezing (-/-)

(-/-)
 SPECIFIC EXAMINATION
Heart
Inspection :Ict cordis no seen
Palpation :Ict cordis no palpable
Percussion :
On :ICSII linea parasternalis dextraetleft
Right Bwow:ICSV linea parasternalist dextra
Left lower :ICS VI linea axillaris anteriorleft
Auscultation :Sound heart1and2normal,regular,Murmur (-), gallop (-)
 SPECIFIC EXAMINATION
InspectionAbdomen
Inspection:flat,venectation(-), caput medusa (-),spider nevi (-),lump(-).
Palpation:weak,painful pressepigastrium (+),liverand lienno palpable,mass(-),ballotement(-),painful press
(-),knockCVA (-)
Percussion: Tympany (+),undulation(-),shifting dullness (-)
Auscultation:Noisyintestinal (+) normal
.

Inspectiongenitalia :Notindo check

InspectionEextreme: Pucat, warm acral, CRT <2,
 SPECIFIC EXAMINATION
Extremity:
Arm Left Right
TonusEutony Eutony
MovementEnough Enough
Strength 55
Muscle Eutrophy Eutrophy
Hand Left Right
Color palm Nnormal Normal
Nail Normal Normal
Abnormalities finger Normal Normal
Flapping Tremor (-) (-)
 SPECIFIC EXAMINATION

limbs andfootLeft Right

TonusEutony Eutony
Movement Enough Enough
Strength 55
Muscle Eutrophy Eutrophy
Edema - -
 SPECIFIC EXAMINATION
reflex Physiological Left Right
Biceps NormalNormal
Triceps NormalNormal
Patella NormalNormal
Achilles NormalNormal
reflex pathological Left Right
Babynski Negative Negative
Oppenheim Negative Negative
Gordon Negative Negative
Schaeffer Negative Negative
Rossolimo Negative Negative
LABORATORY EXAMINATION
Date12January2023

Parameter Results Normal Value Interpretation

Hematology
Hemoglobin 10,0g/dl 14- 18g/dl Anemia
Hematocrit 28,3 % 42-52% Decrease
Platelets 233.103/ul 150-440thousand/ul Normal
Leukocytes 8,13/ul 5-10thousand/ul Normal
Count Type
Eosinophils 2,7 % 1-3% Normal
Basophils 0,6% 0-1% Increase
Neutrophils 64,2 % 40-60% Increase
Lymphocytes 22,0 % 20-40% Normal
Monocytes 10,6% 2-8% Normal
Ratio N/L 2,9 <3,13 Normal
LABORATORY EXAMINATION
Date12January2023

Parameter Results Normal Value Interpretation

ChemicalClinic
Urea 60mg/dL 10-50mg/dL Increase
Creatinine 3.8mg/dl 0.6-1.5mg/dl Increase
Sodium 142mEq/l 135-155mg/dl Normal
Potassium 4,6mEq/l 3.5-6.5 Normal
Immunology
Testing for SARS Negative Negative Normal
CoV-2 antigen
 ECG EXAMINATION
1) Irama Sinus Rhytm
2) HR : 75 x/menit reguler
3) Axis normal
4) Gelombang P normal
5) R/S di V1 < 1, SV1 + RV5 >
35 atau ditemukan LV
strain
6) PR interval: Normal
7) Gelombang Q: Normal
8) Kompleks QRS: Normal
9) Gelombang T: Normal
Kesan : Hipertrofi ventrikel kiri
 X-ray examination
Corgrow
patterns bronchovascularnormal
Not looked infitlrat
Diaphragm right and left slippery
The right and left costophrenic sinuses are sharp
Intact bones
Soft tissue baik
Impression:
Cardiomegaly,effusion pleura right,PulmoNormal
 RESUME
Name :Mrs. Y
Age: 80year
Type Sex:Woman

The patient came to the IGD Muhammadiyah Palembang Hospital with complaints of shortness of
breath which had been getting worse since ±4SMRS hours. Shortness of breath felt intermittent
since ± 1 year ago. Shortness of breath occurs when the patient performs pekerja activitycurrently
and does not decrease when the patient rests. The patient said that at night the patient often wakes
up because of shortness of breathAt what hour1-2 nights. The patient admits that he has difficulty
sleeping because of tightness when lying down, and is more comfortable sleeping in a sleeping
position using 2 pillows. Shortness of breath is not affected by weather, dust or animal hair.
 RESUME
The patient admits that sometimes he feels his chest feels tight when he is active or resting. In
addition, patients also complain that the body often feels weak and easily tired. The patient
complained of abdominal pain that felt like it was being stabbed on the left side which radiated to the
back of the waist. The patient says pain in the stomach only when the stomach is pressed.
The patient said there was a history of the same complaint before. The patient has been treated for the
same complaint. The patient also said there was a history of high blood pressure since ±20years ago
and routinely treated. The patient alsoataka if during this timeroutine taking high blood pressure
medication. Patient own history disease heartand diabetesmellitus since10year final.in the patient's
familyno anyone suffering from the same complaintwith patient. The patient had no history of asthma
and no one in his family had asthma. Patient no own history disease kidney.
 RESUME
On examination of vital signs, blood pressure was found to be 160/80 mm Hg, pulse98x/m, respiration
24x/m.Lung examination revealed fine moist raleson basallungs rightanand left. Cardiac examination
revealed enlargement of the lower left heart border at ICS VI linea axillaris anterior leftand limitsheart
right lowerat ICS V Parasternaldextra.

On laboratory examination it was foundanemia,hematocrit decrease,increased levels of neutrophils

(64.2%),ureaandcreatinine increase. On ECG examination, there was suspicion of an enlarged left
atrium and atrial fibrillation, on chest X-ray examination, the impression of cardiomegaly was found.
obtained effusionpleuraright.
 DIFFERENTIAL
DIAGNOSIS

1. effusionpleuradextra ecCongestive
Heart Failure + Chronic Kidney
Disease
2. CHF Heart Failureec caD
3. CHFecThyroid heart disease
 WORKING
DIAGNOSIS
Pleural effusion dextraecCongestive
Heart Failure + Chronic Kidney Disease
 MANAGEMENT
NonPharmacological Pharmacological
• restlay down • IVFDasering gtt20x /minute
• Education about • Injectionfurosemide 1 x 20 mg IV
disease(definition,reason,manifestation • Spironolactone1 x 25 mg P
clinical,governance,andprognosis)to • NitrocafRetarded 2 x 2.5 mg PO
patient and family • Carvedilol 2 x 3.125 mg PO
• Diet • Clopidogrel 1 x 75 mg PO
• Reduce activity physical • Kidmininfusion 1 x 200 mL IV.
• Therapy nutrition(reduce foodhigh salt,
greasy,coconut milk)
• Oxygen2 Lwithnasalcannula
• Position sleep “semi fowler's position”
 RECOMMENDED EXAMINATION

 Echocardiography
 PROGNOSIS

-Quo advitamins :Dubia adBonam

-Quo adfunctionam :Dubia adBonam
- Quo adSanationam:Dubia adBonam
ature review
03
Aanatomy and physiology
Cavitypleurais cavity potential,have size
thick10-20mm,containing around10 ccfluid
clearwhichno colored

Cell fluidpleuradominated
monocytes,lymphocytes,macrophagesandcell
mesothelium.Cell polymorphonuclearandcell
blood red found in totalwhich is verysmall in
the fluidpleura
effusionPleura
Acumulation fluidinAmongparietal pleura
andvisceral(cavitypleura).circumstances this could
happen with itself or could Becomes consequence
from disease parenchyma

increasing reduction
production absorption
 Eepidemiology

Estimation prevalence
effusionpleurais320caseper 100,000
people in the countryindustry,with
distribution etiologywhichrelated with
prevalence diseasewhichunderlying

• Type sex?
• Age?

influence1.5million patientperyearin
AmericaUnion.
Etiology Etiology
Classification
Pathophysiology
 Anamnesis Diagnosis Inspection Support

• There is symptoms • Photothorax

disease reason • Thoracentesis
• Fever • Cytology
• Cough • Bacteriology
• Chest pain

Governance
Inspection Physical
• Therapy disease base
• Dthere islooked asymmetric • Thoracentesis
• Stem • WSD
fremitusweakenedonside • Pleurodesis
sick
• Dimonsidewhichsick
• Voice vesicular
weakenedonside sick
Fail Heart

Abnormalities in heart structure or heart

function that cause the heart to fail to
DEFINITION distribute oxygen throughout the body
Epidemiology?
• in America and Europe around 1-2%.
• In 2003, heart disease in Indonesia was in eighth
place (2.8%) in the top 10 causes of death

increased from 3 at the The incidence of heart

age of 50 - 59 years to 27 failure is relatively
at the age of 80 - 89 years lower than in men
 Kclassification of congestive heart
failureAmerican Heart Association)

01 Stage A Stage C
03
02 Stage B Stage D
04
 Classification of heart
failureThe NewYork
Heart Association)
4th grade
Grade 2 unable to do physical
activity
Physical activity is
slightly restricted
04
03
02
01
Grade 3
Physical activity is
Class !
strictly limited
Physical activity is
not limited
Etiology
● Coronary artery disease
● Hypertension
● Valvular heart disease
● Heart disease due to malnutrition
 Your Picture Here Your Picture Here

Pathophysiolo
gy
Your Picture Here Your Picture Here
 Your Picture Here Your Picture Here

Clinical
Manifestations

Your Picture Here Your Picture Here

 Diagnosis
CriteriaMajor CriteriaMinor

- Paroxysmal nocturnal dyspnea - Edemaextremity

- distentionveinneck - Cough night day
- Ronchi lungs - dyspnea d'effort
- Cardiomegaly - Hepatomegaly
- Edemalungs I - effusionpleura
- Gallop S3 - Decline capacityvitals 1.3fromnormal
- exaltation pressureveinjugular - Tachycardia(>120/minute)
- reflux hepatojugular
 Supporting investigation

• X-rayThorax Electrocardiography(
• Peptidenatriuretic
EKG)
• TroponinI orQ

Pem. Laboratory
Echocardiograph
y
 Your Picture Here Your Picture Here

SchemeDiagnostic
Fail Heart

Your Picture Here Your Picture Here

 Management
Nonpharmacology ● Angiotensin-Converting
● Self weight monitoring Enzyme Inhibitors(ACE-
● Fluid intake I)
● Weight reduction ● Receptor blockerB
● Aldosterone antagonists
● Angiotensin Receptor
Blockers(ARB)
● Digoxin
● diuretic
Pharmacology
 Chronic Kidney Disease

Definiti
DEFINITION
on

Damage kidney more

from3month,form abnormality GFRnot enough
structural or functional with/without from60ml/minute/1.73m2Duri
declineGFRwith manifestation ng3month with or without
abnormality pathological or there is damage kidney.
sign abnormality kidney,including
abnormality in composition
bloodandurine,or abnormality in
imaging
 EPIDEMIOLOGY

CKDmore many
CKDown prevalenceglobaltall with
foundonman(0.3%)compared
estimate prevalence in a
with woman(0.2%).
mannerglobalAmong11until13%wit
h majority level3.

Pprevalence highestoncategory age

on75year(0.6%),where start happen
enhancementonage35year to on.
Etiology

Hypertension

DM
glomerulonephritis Idiopathic
Manifestation ClinicalCKD
Anemia
defiron
Production
erythropoieti Hyperkalemia
If kidney function
n &
continues to Hyperphosphate
decrease mia
TD
Uremia
&hypolakse
Acidosis mia
metabolic
Classification Based onGFR
1. Stage 1
2. Stage 2
3. Stage 3
4. Stage 4
5. Stage 5

Based on Diagnosis and Etiology

1. Diabetic kidney disease
2. Non-diabetic kidney disease
3. Diseases of transplants
 pathophysiolo
gisti rateurea
Be marked with
enhancement
At the most stageearly happen lost power spare kidney
andcreatinineserum.
GFR 60%,patient not yet feel
complaint(asymptomatic).
hypertrophy structuralandfunctional nephronwhichstill remaining as effort
GFR 30%,start happen
compensation
complaint.
GFR inlower30%,patient show
symptomandsign
uremiawhichreal. Hyperfiltration
GFR inlower15%patient already
need therapy replacement kidney
that is dialysis or transplant Enhancement pressure capillary as well as Genre bloodglomerulus
kidney. Oncircumstances this
Decline function nephronwhichprogressive.
patient said untilat the
stadiumfail kidney.
 Inspection support

 Albumin
 Urea nitrogenblood
 Hemoglobin  CystacinC  MRIskidney
 Creatinine  CT scanskidney  Radionecleotides
 clearance  Cystometogram  Angiogramskidney
 ultrasoundkidney  GFRmeasurable  Biopsy kidney
 IVP  Photoplain abdomen
 Scanskidney  Retrograde
Differential diagnosis
1. Acute kidney injury (AKI)
2. glomerulonephritis chronic
3. nephropathy diabetic
4. Nephrolithiasis
5. Nephrosclerosis
6. Renal artery stenosis
 Diagnosis
Inspection Support DescriptionClinical
 In accordance with the underlying disease
(DM, infection and urinary tract stones,
ology hypertension).
 Uremia syndrome (fatigue, lethargy,
crazy
anorexia, nausea, vomiting, nocturia, fluid
volume excess, seizures)
 Symptoms of complications (anemia,
failure cardiac arrest, metabolic acidosis,
electrolyte disturbances)
 According to KDGI (2012)
Criteria CKD (> 3 month)

Sign damage kidney albuminuria (AER ³30 mg/24 o'clock,

(1 or more) ACR ³30 mg/g [³3 mg/mmol])

Abnormality sediment urine

Abnormality electrolyte and tubular
Abnormalities detected from

Radiology
History transplant kidney
 Governance

 Kidney transplant
 Hemodialysis  Treatment of anemia
 Transplant kidney  Blood transfusion
 Therapy transplant kidney
extra corporeal
orperitonealdialysis

 ControlTD  Supplement iron

(election agent  Nutrition
hypertensionandelectionstatins,
antiplatelets)
 Plan governanceCKDbased on degree

Level GFR Plan Governance

Therapy disease base, condition comorbid

1 ≥ 90 evaluation make it worse function kidney, zoom
out risk
cardiovascular.
2 60-89 Hinder make it worse function kidney

3 Evaluation and therapy complications

30-59
4 15-29 Preparation therapy replacement kidney

5 < 15 Renal replacement therapy

 Complications
SyndromeUremia Anemia

Hypoalbuminea CKD-MBD

Fail Heart Congestive

 Prognosis
CKD has no cure, so the long-term prognosis
is poor unless a kidney transplant is
performed.
CHAPTER II LITERATURE
Management carried out aims to prevent the
REVIEWof chronic kidney disease.
progression
Chronic kidney disease often goes unnoticed
until it reaches an advanced stage and causes
symptoms, so that treatment is often delayed.
 04
ACase analysis
 Based on the results of the anamnesis, physical examination and
supporting examinations, the possible diagnosis of this patient
is:Congestive Heart Failureec HypertensionHeart
disease.Congestive Heart Failureor heart failure is an abnormality
of heart structure or heart function that causes the heart to fail to
distribute oxygen throughout the body.
There are several Framingham criteria in this patient, namely the major
criteria found in this patient are cardiomegaly, paroxysmal nocturnal
dyspnea, crackles in the lungs. While the minor criteria found were
shortness of breath during activity,right pleural effusion, edema
onextremity,and cough at night. The Framingham criteria found were 3
major criteria and4minor criteria so that a diagnosis of Congestive Heart
Failure (CHF) can be established. Based on NYHA, CHF suffered by
patients is classified as class IV, that is, unable to carry out any physical
activity, even in a state of rest can cause symptoms..
Clinically, heart failure is a complex collection of symptoms in which a person
has typical symptoms of heart failure (shortness of breath at rest or exertion,
fatigue, leg edema), typical signs of heart failure (tachycardia, tachypnea,
pulmonary crackles, pleural effusion, increased jugular venous pressure). ,
peripheral edema, hepatomegaly) and objective signs of structural or functional
disturbance of the heart at rest, cardiomegaly, triple heart sounds, heart
murmurs, abnormalities in echocardiography.Thingthis corresponding
withwhichobtainedonpatientdiagnosedCHFwith complaint shortness of breath
during activity, there are crackles, cardiomegaly and pleural effusion.
Dyspnea, or the feeling of having difficulty breathing is the most common
manifestation of heart failure.

Dyspnea is caused by an increase in the work of breathing due

to pulmonary vascular congestion which reduces lung
flexibility. The increased resistance to airflow also causes
dyspnea. Dyspnea on exertion is an early symptom of left heart
failure.
 Complaints of shortness of breath on exertiondyspnea d'effort) in patients
with heart failure will get worse as the disease progresses, this will
interfere with the functions and activities of daily life.

Intolerance to activity in people with heart failure is caused by the heart's inability to pump
blood rich in oxygen and nutrients throughout the body to meet metabolic needs, for example
for muscle movement, causing fatigue. Shortness of breath in patients with heart failure is
caused by pulmonary congestion or accumulation of fluid in the interstitial spaces and alveoli
of the lungs. This fluid will inhibit the development of the lungs so that you experience
difficulty breathing.
 The patient has a history of hypertension since ±20years ago and routinely
treated.

The etiology of heart failure can be congenital heart disease, rheumatic heart
disease, hypertensive heart disease, coronary heart disease, thyroid heart disease,
cardiomyopathy, cor-pulmonale and pregnancy.PHypertensive heart disease (HHD)
is a disease associated with an impact on the heart due to long and prolonged
systemic hypertension. HHD Refers to a condition caused by increased blood
pressure (hypertension). Prolonged and uncontrolled hypertension can change the
structure of the myocardium, blood vessels and cardiac conduction system.
 The patient had a right pleural effusion.

The results of the physical examination of the lungs showed decreased right stem
fremitus and dull percussion of the right lung field. This is related to the state of the
pleural effusion experienced. Where the affected part will move less in breathing,
fremitus is weak (touch and vocal), on percussion there is a deaf area, in a sitting
state the surface of the liquid forms a curved line (Ellis Damoiseu line).
Congestive heart failure (CHF) is perhaps the most common cause of pleural
effusion. Pleural effusion in CHF is a transudative pleural effusion caused by an
increase in systemic venous pressure and pulmonary capillary pressure.
The pathogenesis of pleural effusion in CHF is due to an increase in
systemic venous pressure and pulmonary capillary pressure. When the
pressure in the pulmonary capillaries increases, an increasing amount of
fluid enters the interstitial spaces of the lungs. The increased fluid in the
interstitial space causes an increase in interstitial pressure in the
subpleural interstitial space.
Fluid then moves from the pulmonary interstitial
space across the visceral pleura into the pleural space

In addition, an increase in pulmonary capillary pressure will reduce the

reabsorption capacity of the subpleural blood vessels and lymph flow
will also decrease (obstructed) so that the filtration of fluid into the
pleural cavity and lungs increases.
 In addition, patients also complain that the
body often feels weak and easily tired.

This is consistent with the theory that complaints of clinical symptoms that arise in
CKD affect almost the entire system, namely weakness, malaise, growth
disturbances and debility, edema, pale, brittle, itching, bruising, fetor uremia,
fundus hypertension, red eyes, hypertension, syndrome overload, heart failure,
uremic pericarditis, tamponade, pleural effusion.
 Increased urea (60mg/dL), increased creatinine
(3,8mg/dL) this indicates that the patient has stage V
CKD.

according to theory,Chronic Kidney Disease(CKD) is an abnormality in the

structure or function of the kidneys, which lasts > 3 months, which has an impact
on health. CKD is classified by cause, GFR category (G1-G5) and albuminuria
category (A1-A3). Chronic Kidney Disease (CKD) is defined as kidney damage
with decreased Glomerular Filtration Rate (GFR) of less than 60 ml/min/1.73 m 2for
at least 3 months. GFR 11ml/min/1.73m2included in the stages5.
Management of this patient is divided into 2,
namely, non-pharmacological and
pharmacological therapy. Non-pharmacological
therapy in the form of education about the
disease, bed rest, reduced physical activity,
nutritional therapy (reduce foods high in oily
salt, coconut milk), oxygen with a 2 L nasal
cannula. Meanwhile, the pharmacological
therapy given in this case is IVFDaseringgtt20x
/ minute, injection of furosemide1x 20 mg IV,
Spironolactone 1 x 25 mg PO,NitrocafRetard 2
x 2.5 mg PO, Carvedilol 2 x 3.125 mg PO,
Clopidogrel 1 x 75 mg PO,Kidmininfusion 1 x
200 mL IV.
Infusionasering is a solutionelekfull trolyte,
contains 140 mmol/l Na. Acetate is an isotonic
fluid. KBoth fluids (hypotonic and hypertonic)
can irritate blood vessels. So that it can be
concluded that patients should use less astringent
fluid, this is because astringent is an isotonic
fluid that is suitable for the human body.

Nitrocafretardedis drug
classvasodilatorsnitrate. ObatThis (nitrate
compound) is used because nitrate is a
vasodilator (blood vessel widen) which relaxes
the walls of blood vessels when the coronary
arteries improve blood flow to the heart
muscle..
Clopidogrelasantiplateletclopidogrel for
penInhibits platelet aggregation by inhibiting
platelet ADH pathway.

Carvedilolis drug classthe beta blockersused for the

treatment of cardiovascular and non-cardiovascular diseases.
Benefits of beta-blockersin patients with myocardial
infarction including reducing the short-term risk of
reinfarction and the long-term risk of death.

Furosemide is a diuretic class of drugs that is

useful for removing excess fluids from the body
through urine. This drug is often used to treat
edema (buildup of fluid in the body) or
hypertension (high blood pressure).
Spironolactone is a drug that can be used to
treat hypertension and heart failure. This drug
is a potassium-sparing diuretic whose main
function is to increase urine production
(diuresis). Spironolactone is a potassium-
sparing diuretic drug for the treatment of
hypertension and heart failure.

Kidmin indicated for gift souramino

onpatient with fail kidney I or
chronic.Kidmin is fluid infusion with
content souramino 7.2% which ininside
there is souraminochain branch asvaline,
leucine,as well asisoleucine.
Conclusion

Hasexposed case
withdiagnosiseffusionPleuradextraet
causaCongestive Heart Failure +
Chronic Kidney Disease. Diagnosis in
patients is carried out by history,
physical examination, and laboratory
investigations in the form of complete
blood counts and clinical chemistry, x-
rays,andEKG.
Conclusion

Management of this patient is divided into 2, namely, non-

pharmacological and pharmacological therapy. Non-
pharmacological therapy in the form of education about the
disease, bed rest, reduced physical activity, nutritional
therapy, oxygen with a 2 L nasal cannula. As for the
pharmacological therapy given in this
case,hIVFDaseringgtt20x / minute, injection of
furosemide1x 20 mg IV, Spironolactone 1 x 25 mg
PO,NitrocafRetard 2 x 2.5 mg PO, Carvedilol 2 x 3.125 mg
PO, Clopidogrel 1 x 75 mg PO,Kidmininfusion 1 x 200 mL
IV.
THANK YOU