MORNING REPORT dr.

Yeni
Monday, November 28th 2016

PHYSICIAN INCHARGE:
I : dr. Yeni, dr. Handy, dr. Ari
II CVCU : dr. Rifal
II HCU : dr. Rahmad
II ER : dr. Ami, dr. Meli
Chief : dr. Hesti
Consultan : dr. Atma Gunawan, Sp.PD-KGH
Moderator MR : dr. Sri Sunarti, Sp.PD-KGer
 SUMMARY OF DATA BASE
Mrs. L/ 40 yo/Ward 28
HISTORY TAKING : autoanamnesis and alloanamnesis with her husband
CHIEF COMPLAINT : shortness of breath
HISTORY OF PRESENT ILLNESS :
Patient presented in ER with chief complaint shortness of breath. She complained about
shortness of breath since a week before admission and getting worse since 3 days.
Shortness of breath is mainly triggered by mild activities, such as sweeping or taking a
bath. She felt shortness of breath especially while she was walking about 10 meters and
relieved by rest. She cannot sleep in a flat position. She said that she often awakened at
night because of shortness of breath.
In this 2-3 days, she complained about heartburn. Heartburn appeared constantly.
Heartburn was not subsided by taking meal. It made her stomach feel bloating sensation,
nausea without vomitting .
Patient also feels fatigue and only bed rest ion the bed since two days
Patient has undergone hemodialysis 1 time on September and not routinly hemodialysis
after that until now. She also has hypertension since 15 years old. The higher tension that
she has ever had 200/... She does not routinly seek for medication for hypertension.
SUMMARY OF DATA BASE
Patient knew that she was getting diabetes since 4 years ago, she often had passing urine at night , felt often more
thristy and she examined to the general practisioner, and the random blood sugar was 400. and she gave
glibenclamide. She didnt control the GP nor primary helath center until the last 1 year because the complain that she
felt getting better.

PAST MEDICAL HISTORY :

She had been hospitalized 2 times, the last times in RSSA 2 months ago with the same complain shorthness of breath

SOCIAL HISTORY : Patient is a housewife who has two children . Her husband worked as a farmer

FAMILY HISTORY :

She has sisters who has diagnosed with hypertension. Unkown history of her parents
 Physical Examination
Looked normoweight
General Appearance: looked moderately ill

HR : 72 bpm regular
GCS: 456 110/80 mmHg RR : 24 tpm Tax : 36.3 C
strong
Head Anemic conjunctiva (+) icteric sclerae (-).
Neck JVP: R + 5 cm H2O in 30 position Lymphonode enlargement -
Wall Chest expansion symmetric

Chest Ictus invisible, palpable ICS VI 1 cm lateral MCL S Trill: - Heaves: -

Heart RHM ~ SL D LHM ~ ictus
S1 and S2 single, no murmur
Stem Fremitus D=S S S v v Rh - - Wh - -
SS v v + - - -
Lung
SS v v + + - -
Percussion : dullness at basal lung dextra and sinistra
flat, bowel sound normal, epigastrial tenderness (-), liver span 8 cm, Traubes space
tympani

Extremities Warm, pitting edema minimal

 LABORATORY FINDING (November, 27th 2016) Ny. Lilik
Lab Value (Normal) Lab Value (Normal)
Hemoglobin 7,5 4.700 11.300 /L Natrium 135 136-145 mmol/L
leukocyte 7,360 11,4 - 15,1 g/dl Kalium 4,57 3,5-5,0 mmol/L
PCV 23,5% 38 - 42% Chlorida 122 98-106 mmol/L
Trombocyte 280.000 142.000 424.000 /L HbsAg Non
reactives
MCV 83 80-93 fl Anti HCV Negative
MCH 26,5 27-31 pg Calsium 8,2 7,6 11,0 mg/dl
Eo/Bas/Neu/ 2,7/0,5/65/27,6/ 4,1 0-4/0-1/51-67/25-33/2-5 Phospor 5,8 2,7-4,5 mg/dl
limf/Mon
SGOT 12 0-32 mU/dL

SGPT 7 0-33 mU/dL

Alb 2,74 3,5-4,5 g/dl

GDS 96 < 200 mg/dl

Ureum 167,1 16,6 - 42,5mg/dl

Creatinine 7,7 < 1,2 mg/dl

E-GFR 5,9 > 90/ Mil/min

BGA Result (November 27 th 2016)

Temp 37,0 C Nasal canule 4 lpm

pH 7,26 7.35-7.45
pCO2 21,0 35 45 mmHg
pO2 70,3 80 100 mmHg
HCO3 9,6 21 28 m mol/L
O2 saturation 92,5 > 95 %
True 02 65,90
BE -17,6 (-3) - (+3) m mol/L
Hb 7,9
Conclusion : Acidosis metabolic partially compensated with alcalosis respiratory
Moderate hypoxemia
ECG (November, 27 th 2016) Ny. Lilik
ECG (27/11/2016)
Sinus tachycardia, heart rate 72 bpm
Frontal Axis : normal
Horizontal Axis : normal
PR interval : 0. 012
QRS complex : 0. 04
QT interval : 0. 36
Conclusion : Rythmwith heart rate 72 bpm
CXR (27/11/2016)
CXR: 27-11-2016

Interpretation :

AP position, Asymetric, enough KV, less inspiration

Soft tissue normal, bone normal
Trachea in the middle
Right and left hemidiaphragm : Difficult to evaluate
Left and right phrenicocostalis angle : blunt
Lung : bronchovascular pattern was increase, bat wing sign (+),
hilus D/S were normal
Heart : site normal, CTR 60%, shape normal, cardiac waist (-), apex
embeded
Conclusion : cardiomegaly, acute lung edema
 CUE AND CLUE Problem List Initial Diagnosis Planning Diagnosis Planning Therapy Planning Monitoring
Mrs.L/40 yo/w.28 1. Acute lung 1. Non cardiogenic Echocardiography O2 4 lpm (NC) Subjective
AX : oedema 1.1.1 Bilateral lung Bed rest Vital Sign
Shortness of Breath 1 w effusion semifowler Urine production
Dyspnea the effort
1.1.2 Overload position Fluid Balance
PND
Drop out HD 2 month syndrome Renal diet 1700 Ureum
Hypertension 15 years 1.1.3. Uremic Lung kcal/day, low salt Creatinine
PE : < 2 gram/day, SE
BP : 110/80 mmHg 2.Cardiogenic protein 0,6-08
RR : 24 tpm 2.1 HF st C fc III gr/kgBW/ day PEdu:
PR : 72 tpm Disease
Anemic conjungtiva : Iv plug Underlying disease
(+/+)
Inj Furosemide 3x Treatment Prognosis
Ronkhi + mediobasal /+
basal , dullness at basal 40 mg (iv)
lung dextra/ sinistra
Cor : ictus ICS VI 1 cm Elective
lateral MCL S Hemodyalized
Ronkhi
LF :
Hb :7.50 g/dL
Ur : 167 mg/dL
Cr : 7,78 mg/dL
 CUE AND CLUE Problem List Initial Diagnosis Planning Diagnosis Planning Therapy Planning Monitoring

Mrs.L/44 yo/w.28 2. CKD stage 5 2.1HT Bedrest Subjective

AX :
Shortness of Breath 1
drop out HD nephrosclerosis O2 4 lpm via Vital Sign
week 2.2 Diabetic nasal canule CBC
HD drop out 2 months kidney disease Renal diet 1700
Hypertension 15 years
DM 4 years kcal/day, low PEdu:
PE : sodium Disease
BP : 110/80 mmHg
RR : 24 tpm <2gram/day, Underlying disease
PR : 72 tpm protein 0,6-0,8 Treatment
Anemic conjungtiva :
(+/+)
gr/kgBW/ day Prognosis
Ronkhi + mediobasal/ +
basal, dullness basal Negative fluid
+/+
Edema +/+ balance 500
LF : cc/day
Hb :7.50 g/dL
Ur : 167 mg/dL
Cr : 7,78 mg/dL Elective HD
eGFR : 5.9 ml/mnt
BGA :
Acidosis metabolic
partially compensated
with alcalosis
respiratory, moderate
hypoxemia
 CUE AND CLUE Problem List Initial Diagnosis Planning Diagnosis Planning Therapy Planning Monitoring

Mrs.L/40 yo/w.28 3. HT on treatment 3.1 Secondary Telmisartan 0-0- Subjective

AX : Hypertension 80 mg Vital Sign, defisit
She has HT since 3.1.1 neurology
15 years ago Renoparenchymal
poorly controlled hypertencion PEdu:
3.1.2 Renovascular Disease
PE : hypertension Underlying disease
TD : 110/80 mmHg 3..2 Primary Treatment Prognosis
( After given clonidin
3x0,15 mg and
telmisartan 1x80 mg)
Mrs.L/40 yo/w.28 4. Anemia 5.1 EPO deficiency SI, TIBC, Fe Plan to EPO Subjective
AX :
Shortness of Breath
Normochromic 5.2 Decrease RBC therapy Vital Sign
Weakness, Fatigue normocyter survival PEdu:
Looked pale Disease
Underlying disease
PE :
Pale conjuctiva Treatment Prognosis

LF :
Hb : 7,5 g/dL
MCV : 83 fl
MCH : 26,50 pg
 CUE AND CLUE Problem List Initial Diagnosis Planning Diagnosis Planning Therapy Planning Monitoring

Mrs.L/40yo/w.28 5. Dyspepsia 5.1 urenic Inj. Subjective

AX :
syndrom gastropathy Lansoprazole 1 Vital Sign
Epigastric pain
Nausea, fatigue 5.2 diabetic x 30 mg iv
gastropharese Inj.
PE : Metochlorpra
Epigastric
mide 3x10 mg
tenderness (+)
iv
LF :
Ur : 167 mg/dL
Cr : 7,78 mg/dL

Mrs.L/40yo/w.28 6. 5.1 urinary loss Diet protein Subjective

AX :
Hypoalbuminemi 5.2 0,8 Vital Sign.
Leg swelling since 2
months a Hypercatabolic gr/kgBW/day Albumin / 3 days
state
PE :
Pulmo: dullness
basal +/+
Edema +/+ grade 2
LF :
Albumin: 2,75
 CUE AND CLUE Problem List Initial Diagnosis Planning Diagnosis Planning Therapy Planning Monitoring

Mrs.L/40yo/w.28 5. DM type II FBG Waiting for Subjective

AX : 2hppBG FBG/2hppBG Vital sign
Diagnosed DM since
4 years, not routinly resluts Blood glucose level
controlled ,
Sometimes consume
glibenclamide

PE :
-
LF :
RBG : 96 gr/dl

Mrs.L/40yo/w.28 6. Billateral 6.1 dt Proof pleural Pleural fluid RR

AX : hypoalbuminemia effusion evacuation CXR
pleural effusion
SOB since 1 weeks 6.2 Lung primary Pleural fluid
get worse 3 days
analysis
PE :
Pulmo: dullness
basal +/+
LF :
Albumin: 2,75
Problem Analysis Family history

Hypertension Diabetes Mellitus type II

Poorly control
Bad compliance

Heart failure st C fc IV Chronic Kidney Disease

Anemia Dyspepsia Uremic gastropathy

ALO Diabetic gastrparese
Risk Factor Analysis
PROBLEM THEORY FACTUAL
CKD st V Risk Factor of CKD that
undergone HD Hypertension
Glomerulonefritis Diabetes melitus
Diabetes Melitus
Obstruction and infection
Hypertension
Other Causes

PAPDI
RISK FACTOR ANALYSIS
PROBLEM THEORY FACTUAL
Hypertension - Age - Age
- Race - Lifesyle
- Family history - Family history
- Being overweight/obese
- Sedentary life style :
High salt diet
Alcohol
Not physically active
 RISK FACTOR ANALYSIS
PROBLEM THEORY FACTUAL

Risk Factor of Heart Failure

Coronary artery disease

Past heart attack (myocardial infarction)
High blood pressure (hypertension or HBP)
Abnormal heart valves
Heart muscle disease (dilated cardiomyopathy, hypertrophic
cardiomyopathy) or inflammation (myocarditis)
Heart defects present at birth (congenital heart disease)
On This Patient
Severe lung disease
HF st. C fc. III High Blood Pressure
Diabetes
Diabetese Melitus
Obesity
Sleep Apnea

Other conditions
Low red blood cell count (severe anemia)
An overactive thyroid gland (hyperthyroidism)
Abnormal heart rhythm (arrhythmia or dysrhythmia)

American Heart Association

 Management Analysis
Problem Theory Factual
Chronic Kidney
Disease Slow down the disease progression
Treatment of Chronic Kidney Disease Negative fluid balance
Renal diet, low salt < 2G/day, protein 0.8
Based on Stages (PAPDI) gram/kgBW/day
Stages GFR Treatment
1 90 Treat undelying disease, comorbid condition, evaluation of worsening renal Prevent and treatment of cardiovascular
function, reduced cardiovascular risks.
disease
2 60-89 Menghambat perburukan fungsi ginjal HT st II
3 30-59 Evaluasi dan terapi komplikasi Telmisartan 1x 80 mg
4 15-29 Persiapan untuk terapi pengganti ginjal HF st. C fc. III
5 15 Terapi pengganti ginjal Inj. Furosemide 40-40-40 mg

Renal Replacement Therapy

Specific treatment for underlying disease HD elective
Prevent and treatment of comorbid condition
Slow down the disease progression
Prevent and treatment for cardiovascular diseases
Renal replacement therapy including dialysis and renal transplantation
MANAGEMENT ANALYSIS
PROBLEM THEORY FACTUAL

Hypertension Management of HT st. II Low salt diet, <2g/day

- Lifestyle modification Telmisartan 1x 80 mg
- Two drugs combination of antihypertensive drugs
Thiazide diuretics
Beta blocker
ACE inhibitors
ARBs
Calcium Channel blockers
Renin inhibitors
Additional
Alpha blockers
Alpha-beta blockers
Central-Acting agents
Vasodilators
Aldosterone antagonists
 MANAGEMENT ANALYSIS
PROBLEM THEORY FACTUAL

Management of Heart Failure

The need to perform thorax rontgent, echocardiography, and BNP

Oral Diuretic or Parenteral Diuretic is the main treatment in patient On this patient :
with heart failure
Low dose ACE inhibitor or ARB may begun when the patient - Bed rest, semifowler position
Heart Failure
euvolemic - Low salt diet < 2 gram/ day
Low dose beta blocker until optimal dose of beta blocker can - Inj. Furosemide 40 mg-40-40
begun after diuretic and ACEi or ARB given to the patient
Digitalis could be given if there is any supraventricular aritmia (AF
or SVT) or the 3 drugs above cant give the satisfied result.

PAPDI
Key message Pathophysiology
The uremic syndrome is characterized by a deterioration of
biochemical and physiological functions in parallel with the
progression of renal failure. This results in a variable number of
symptoms.
Key message management
Recommendations for the optimal time for initiation of renal replacement
therapy have been established by the National Kidney Foundation in their KDOQI
Guidelines and are based on recent evidence demonstrating that delaying
initiation of renal replacement therapy until patients are malnourished or have
severe uremic complications leads to a worse prognosis on dialysis or with
transplantation.
Because of the interindividual variability in the severity of uremic symptoms and
renal function, it is ill-advised to assign an arbitrary urea nitrogen or creatinine
level to the need to start dialysis. Moreover, patients may become accustomed to
chronic uremia and deny symptoms, only to find that they feel better with dialysis
and realize in retrospect how poorly they were feeling before its initiation.
Key message Social
Educate patient to consume the nutrition food not in large portion but in mach
time, educate patient to recognise the sign and symptoms hypoglicemia
Patients who are provided with educational programs are more likely to choose
home-based dialysis therapy. This approach is of societal benefit because home-
based therapy is less expensive and is associated with improved quality of life.
Condition this morning
GCS 456
BP 150/90 mmHg
HR 80 bpm
RR 20 tpm
Tax 36,7 0C
Urin output 120cc/8 hour
Thank You
Anemia of Chronic Kidney Disease (CKD)
Progressive CKD is usually associated with a moderate to severe hypoproliferative anemia; the level of the
anemia correlates with the stage of CKD. Red cells are typically normocytic and normochromic, and
reticulocytes are decreased. The anemia is primarily due to a failure of EPO production by the diseased kidney
and a reduction in red cell survival. In certain forms of acute renal failure, the correlation between the anemia
and renal function is weaker. Patients with the hemolytic-uremic syndrome increase erythropoiesis in response
to the hemolysis, despite renal failure requiring dialysis. Polycystic kidney disease also shows a smaller degree
of EPO deficiency for a given level of renal failure. By contrast, patients with diabetes or myeloma have more
severe EPO deficiency for a given level of renal failure.
Assessment of iron status provides information to distinguish the anemia of CKD from the other forms of
hypoproliferative anemia (Table 103-6) and to guide management. Patients with the anemia of CKD usually
present with normal serum iron, TIBC, and ferritin levels. However, those maintained on chronic hemodialysis
may develop iron deficiency from blood loss through the dialysis procedure. Iron must be replenished in these
patients to ensure an adequate response to EPO therapy (see below).
Anemia CKD

Schematic representation of the mechanisms

underlying anemia of CKD. Iron and EPO are crucial
for red blood cell production in the bone marrow.
Iron availability is controlled by the liver hormone
hepcidin, which regulates dietary iron absorption
and macrophage iron recycling from senescent red
blood cells. There are several feedback loops that
control hepcidin levels, including iron and EPO. In
CKD patients (particularly in end stage kidney
disease patients on hemodialysis), hepcidin levels
have been found to be highly elevated, presumably
due to reduced renal clearance and induction by
inflammation, leading to iron-restricted
erythropoiesis. CKD also inhibits EPO production by
the kidney, and may also lead to circulating uremic-
induced inhibitors of erythropoiesis, shortened red
blood cell lifespan, and increased blood loss. Black
and gray arrows represent normal physiology (black
for iron and hormonal fluxes, gray for regulatory
processes). Colored arrows represent the additional
effects of CKD (blue for activation, red for
inhibition). RBC, red blood cell.
 Recent data suggest that hepcidin excess may account for the impaired
dietary iron absorption and reticuloendothelial cell iron blockade present
in many CKD patients. Discovered independently by three groups in 2000
2001, hepcidin is the main hormone responsible for maintaining systemic
iron homeostasis. Produced by the liver and secreted into circulation,
hepcidin binds and induces degradation of the iron exporter, ferroportin,
on duodenal enterocytes, reticuloendothelial macrophages, and
hepatocytes to inhibit iron entry into the plasma. Inflammatory cytokines
directly induce hepcidin transcription, presumably as a mechanism to
sequester iron from invading pathogens, leading to the iron sequestration,
hypoferremia, and anemia that are hallmarks of many chronic diseases
including CKD. (JASN, 2012)
 Recognition of a key role for hepcidin excess in causing the functional iron
deficiency and anemia of CKD has ignited interestin targeting the hepcidin-
ferroportin axis as a new treatment strategy for this disease. By blocking hepcidin
and/or increasing ferroportin activity, these agents could improve dietary iron
absorption and iron mobilization from the patients own body stores, thereby
minimizing the need for supraphysiologic doses of intravenous iron and ESAs with
their potential adverse effects. Importantly, in CKD patients with hepcidin excess,
large intravenous boluses of iron would be predicted to have limited effectiveness
because much of the iron is rapidly taken up by the liver and sequestered, and
the remainder that is incorporated into red blood cells would be recycled
ineffectively. In addition, intravenous iron itself would further increase in
hepcidin level and worsen this phenomenon. Several strategies under
investigation include antagonizing hepcidin directly, inhibiting hepcidin
production, interfering with the hepcidin/ferroportin interaction, or stabilizing
ferroportin