Case Report

ARRANGED BY:

Anugrah Dwi Riski

2013730011

PRECEPTOR :

dr. Ihsanil Husna, Sp.PD

Clinical Internship Internal Medicine

Cempaka Putih Jakarta Islamic Hospital

2017

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 FOREWORD
AssalamualaikumWr. Wb.

Alhamdulillah, Praise be to gratitude for the compilation of the presence of ALLAH SWT for the
completion of the task of "CHF" Case Report.
This paper is structured in order to be able to deepen and understand about "CHF". The specific
purpose is to fulfill the task of the Registrar's Stake of Internal Medicine.
Hopefully with the existence of this case report can add knowledge and useful for the compilers
and other learners.
The authors are aware that this case report is far from perfection, therefore the authors
desperately need advice and criticism to build better case reports in the future.
Thanks.

Wassalamualaikum Wr. Wb

Jakarta, June 2017

Author

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 BAB I

PATIENT STATUS

A. Patient’s identity
Name : Mr. M
Age : 54 Year, 1 month, 30 days
Sex : Male
Place/DoB : Jakarta, April 7th 1963
Marital status : Married
Occupation : Driver
Religion : Moslem
Date of admission :June, 5th 2017
MR number : 007319xx

B. Anamnesis
1. Chief complaint :
Dispneu since 1 days ago
Another complaint :
Feel burn in the chest area since 1 days ago
2. History of present illness
Patient came to RSIJ with Dispneu since 1 day before hospital admission.
Dispneu getting worse if he go up stairs, getting better if patient take a rest. vomiting
one time. Before vomiting patient feel nausea. weakness from 1 day before entering
the hospital. Headache with dizzy, feel burn in the chest area and spreading
backwards. and cough since 2 days ago. patients loss the appetite since three days
before entering the hospital. Denied fever, but cold sweat. There’s no complain about
urinary track and defecation.

3. History of past illness

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 a. There is a history of DM for 10 years
b. Gangrene in his right foot
c. History of trauma was denied
d. History of surgery
e. Asma (-)
f. Hypertension (-)

4. History of family
a. His father had CHF and
b. mother had DM

5. History of allergy
Patient has no allergy to food, drugs and weather.

6. History of treatment

Patient said he’s consuming metformin and glibenclamid but stop 1 month
ago and now he is consuming insulin

.
7. History of social economi
Patient difficult to eat, no appetite,eat 1-2x a day, small portions, he stop smoked for
7 months ago
Alcohol: Denied

C. Physical Examination
- Generalis status : Moderate ill
- Conciusness: composmentis
- Vital sign
o Blood pressure : 120/70 mmHg
o Heart rate : 80x/minute
o Respiratory rate : 20x/minute

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 o Temperature : 36° C

D. General physical examination

 Head : normocephal, black hair, deformity (-)
Eyes : anemic conjungtiva (-/-), icteric sclera (-/-),pupil isokor diameter
3mm/3mm, light reflex (+/+)
Mouth : the oral mucosa moist
Neck : not palpable mass, suprasternal retracion (-)
 Thorax
a. Inspection : The movement of the chest symmetrical, intercosta
retraction (-)
b. Palpation : Same vocal fremitus in dextra and sinistra
c. Percussion : Sonor
d. Auscultacion : Vesicular breath sounds + / +, ronkhi - / -, wheezing - / -
 Heart
e. Inspection : Ictus cordis does not seen
f. Palpation : Ictus cordis have not palpable
g. Percussion
i. Right Heart : ICS 4 linea parasternal dextra
ii. Upper Heart : ICS 3 linea parasternal dextra
iii. Left Heart : ICS 5 linea mid clavicula sinistra
h. Auscultation : Heart sound I-II regularly pure, noisy (-),
 Abdomen
i. Inspection : Disetended
j. Auscultation : Bowel sounds (+)
k. Palpation : pressure epigastric pain (+), hepatomegali (+)
l. Percussion : Timphani (+)

 Extremities

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 a. Left Ext and Right Ext: Superior: Edema (- / -), warm akral(+ / +), RCT <2
seconds (+ / +), Gangrene (-/+)
b. Left Ext and Right Ext: Inferior: Edema (- / -), warm akral (+ / +), RCT <2
seconds (+ / +), Gangrene (-/+)
E. Laboratorium

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F. Resume :
Patient came to RSIJ with Dispneu since 1 day before hospital admission.
Dispneu de effort (+). vomiting one time. Before vomiting patient feel nausea.
weakness from 1 day before entering the hospital. Headache with dizzy, feel burn in
the chest area and spreading backwards. and cough since 2 days ago. patients loss the
appetite since three days before entering the hospital. Denied fever, but cold sweat.
There’s no complain about urinary track and defecation. Blood pressure 120/70
mmHg, Heart rate: 80 times/minute, Respiratory rate : 20 times/minute, Temperature
: 36° C. There is not abnormalities at physical examination. At laboratory
examination decrease haemoglobin, hematocrit, eritrosit. And increased ureum,
creatinin, leukosit

G. Problem List:
CHF
DM
Leukositosis
Anemia

H. Assesment
1. CHF
S: Patient’s complain about Dispneu and feel burn in the chest area. Nausea and
vomiting one time, headache with dizzy and weakness.
O:
Blood pressure : 120/70 mmHg
Pulse : 80 times/ minute
Temperature : 36°c
Respiratory rate : 20 times/ minute
Physical Examination
Thorax

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 I: normochest
P: vocal fremitus +/+
P: sonor +/+
A: vesicular sound. breathing sounds ronki - / -, wheezing - / -
Heart :
I: ictus cordis is not visible
P: ictus cordis is not palpable
P: Upper line  ICS 3 linea parasternal dextra
Right Line  ICS 4 linea parasternal dextra
Left line  ICS 5 linea mid clavicula sinistra
A: Regular heart sounds I & II, gallops (-), murmur (-)

A: Congestive Heart Failure (CHF)

P : Treatment plan: Lasic 2x2

Letonal 25 mg 1x1
Valsartan 80 mg 1x1
Aspilet 1x1
Ranitidin 1x1
Omz 1x1

2. Diabetic Mellitus
S: Patient had DM for 10 years, uncontrolled, and his mother died because
diabetic mellitus. History of insulin use (+)
O: Blood pressure : 120/70 mmHg
Heart rate : 80 times/minute
Respiratory rate : 20 times/minute
Temperature : 36° C
Amputation foot because diabetic complication. 05/06/17 Glucose : 330 mg/dL
07/06/2017 Glucose : 338 mg/dL
A: Diabetic mellitus

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P: HbA1c, GDS, G2PP
Injeksi insulin

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 BAB II
LITERATURE REVIEW

I. Congestive Heart Failure

A. Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is a complex clinical syndrome that can result
from any functional or structural cardiac disorder that impairs the ventricle’s ability to fill
with or eject blood. Since there is no definitive diagnostic test for heart failure, it remains
a clinical diagnosis that is largely based on a careful history and physical examination
and supported by ancillary tests such as chest radiograph, electrocardiogram, and
echocardiography. Heart failure is a common disease, affecting approximately 5 million
people in the United States, and it occurs predominately in the elderly, with almost 80%
of cases occurring in patients over the age of 65.1 The magnitude of the problem cannot
be precisely assessed, because reliable population-based data on the prevalence,
incidence, and prognosis are lacking. Nevertheless, several studies have found that CHF
is associated with a 2-year mortality rate of approximately 45–50%, which approaches
that of many malignancies.2 Moreover, from a societal perspective, caring for patients
with CHF accounts for 2–3% of the federal health-care budget. The estimated direct and
indirect cost of CHF in the United States in 2005 was $27.9 billion.1 There are 2
mechanisms of reduced cardiac output and heart failure: systolic dysfunction and
diastolic dysfunction. The most common causes of systolic dysfunction (defined by a
left-ventricular ejection fraction of 50%) are ischemic heart disease, idiopathic dilated
cardiomyopathy, hypertension, and valvular heart disease. Diastolic dysfunction (defined
as dysfunction of left-ventricular filling with preserved systolic function) may occur in up
to 40–50% of patients with heart failure, it is more prevalent in women, and it increases
in frequency with each decade of life. Diastolic dysfunction can occur in many of the
same conditions that lead to systolic dysfunction. The most common causes are
hypertension, ischemic heart disease, hypertrophic cardiomyopathy, and restrictive
cardiomyopathy. Many patients who have symptoms suggestive of heart failure
(shortness of breath, peripheral edema, paroxysmal nocturnal dyspnea) but also have
preserved leftventricular function may not have diastolic dysfunction; instead, their

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symptoms are caused by other etiologies, such as lung disease, obesity, or occult
coronary ischemia.3 This article will review the pathophysiology, diagnosis, and
treatment of CHF, with specific discussion of the pulmonary manifestations and their
treatment, including noninvasive positive-pressure ventilation (NPPV) strategies.

B. Epidemiology
Applying these new criteria, McKee and colleagues characterized the
epidemiology of CHF in the Framingham cohort. They followed 5,209 men and women
from the Framingham cohort for up to sixteen years. Eliminated from the analysis were
17 subjects who had a diagnosis of CHF at the time of Framingham recruitment. Subjects
were assessed every two years with vital signs, ECG, chest x-ray, urinalysis, vital
capacity on pulmonary function testing, and blood work. Only 2% of subjects were
completely lost to follow up. A total of 142 individuals developed ‘definite’ CHF
according to the Framingham criteria. The rate of CHF per person-year rose more than 10
times between the age of 29–39 years (0.6–0.8 cases/1000 years) and 70–74 years (8.7
cases/1000 years).
The longitudinal design of the cohort facilitated the characterization of antecedent
comorbidities in the 142 individuals with CHF. Definite hypertension, defined using
criteria employed at the time (systolic blood pressure ≥ 160 mm Hg or diastolic blood
pressure ≥ 95 mm Hg), was present in 75% of cases. This was typically accompanied by
evidence of cardiomegaly on chest X-ray or ECG. Coronary heart disease was present in
approximately half of the individuals with hypertension. Conversely, coronary heart
disease without hypertension was present in only 10% of individuals with CHF.
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C. Etiology
a. Weakened heart muscle (cardiomyopathy)
b. Damaged heart valves.
c. Blocked blood vessels supplying the heart muscle (coronary arteries), which
may lead to a heart attack (This is known as ischemic cardiomyopathy. ...
d. Toxic exposures, such as alcohol or cocaine
D. Patophysiology

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E. Clinical Manifestations

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F. Treatment Pharmacology and Non Pharmacology
 ACE-1 (Angiotensin – Converting enzym inhibitor)
Digitalis, 3x0,25 mg 3 days, and then maintenance dose 1x0,25 mg
Diuretik: Furosemide (1-2)x40 mg
Decreased afterload:
-Captopril 2-3x6,25 – 12,5 mg/day
-Calsium Antagonis
Increase contractility heart : Digoksin: loading dose 3x0,25 mg, 3 days
Decreased preload
-Furosemide: 20-40 mg/day (minor case), 40-80 mg/day (mayor case)
 Decreased wok hard and rest

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 II. Diabetic Mellitus
A. Diabetic Mellitus
Diabetes is a group of metabolic diseases characterized by hyperglycemia
resulting from defects in insulin secretion, insulin action, or both. The chronic
hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure
of differentorgans, especially the eyes, kidneys, nerves, heart, and blood vessels.

B. Epidemiology

Globally, an estimated 422 millions adults are living with diabetes mellitus,
according to the latest 2016 data from WHO. Diabetes prevalence is increasin rapidly,
previous 2013 estimates from the international Diabetes federation put the number at 381
million people having diabetes. The number is projected to almost double by 2030. type 2
diabetes makes up about 85-90% of all cases. Increases in the overall diabetes prevalence
rate largely reflect an increase in risk factors for type 2, notably greater longevity and
being overweight or obese.

C. Etiology

. The etiology of type 2 diabetes mellitus appears to involve complex interactions

between environmental and genetic factors. Presumably, the disease develops when a
diabetogenic lifestyle (ie, excessive caloric intake, inadequate caloric expenditure,
obesity) is superimposed on a susceptible genotype.
The body mass index (BMI) at which excess weight increases risk for diabetes varies
with different racial groups. For example, compared with persons of European ancestry,
persons of Asian ancestry are at increased risk for diabetes at lower levels of
overweight. Hypertension and prehypertension are associated with a greater risk of
developing diabetes in whites than in African Americans.
In addition, an in utero environment resulting in low birth weight may predispose some
individuals to develop type 2 diabetes mellitus. Infant weight velocity has a small,
indirect effect on adult insulin resistance, and this is primarily mediated through its effect
on BMI and waist circumference.

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 About 90% of patients who develop type 2 diabetes mellitus are obese. However, a large,
population-based, prospective study has shown that an energy-dense diet may be a risk
factor for the development of diabetes that is independent of baseline obesity.
Some studies suggest that environmental pollutants may play a role in the development
and progression of type 2 diabetes mellitus. A structured and planned platform is needed
to fully explore the diabetes-inducing potential of environmental pollutants.
Secondary diabetes may occur in patients taking glucocorticoids or when patients have
conditions that antagonize the actions of insulin (eg, Cushing syndrome, acromegaly,
pheochromocytoma).

D. Clinical symptoms

Increased thirst and frequent urination

Increased hunger

Weight loss. .

Blurred vision.

Slow-healing sores or frequent infections.

Areas of darkened skin.

E. Risk Factor

Weight. Being overweight is a primary risk factor for type 2 diabetes. The more
fatty tissue you have, the more resistant your cells become to insulin. However, you don't
have to be overweight to develop type 2 diabetes.

Fat distribution. If your body stores fat primarily in your abdomen, your risk of
type 2 diabetes is greater than if your body stores fat elsewhere, such as your hips and
thighs.

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 Inactivity. The less active you are, the greater your risk of type 2 diabetes.
Physical activity helps you control your weight, uses up glucose as energy and makes
your cells more sensitive to insulin.

Family history. The risk of type 2 diabetes increases if your parent or sibling has
type 2 diabetes.

Race. Although it's unclear why, people of certain races — including blacks,
Hispanics, American Indians and Asian-Americans — are more likely to develop type
2 diabetes than whites are.

Age. The risk of type 2 diabetes increases as you get older, especially after age
45. That's probably because people tend to exercise less, lose muscle mass and gain
weight as they age. But type 2 diabetes is also increasing dramatically among children,
adolescents and younger adults.

Prediabetes. Prediabetes is a condition in which your blood sugar level is higher

than normal, but not high enough to be classified as diabetes. Left untreated, prediabetes
often progresses to type 2 diabetes.

Gestational diabetes. If you developed gestational diabetes when you were

pregnant, your risk of developing type 2 diabetes increases. If you gave birth to a baby
weighing more than 9 pounds (4 kilograms), you're also at risk of type 2 diabetes.

Polycystic ovarian syndrome. For women, having polycystic ovarian syndrome

— a common condition characterized by irregular menstrual periods, excess hair growth
and obesity — increases the risk of diabetes.

F. Management

The management of type 2 diabetes diseases will include different parts:

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 Changing lifestyle This will include proper diet which will leads to weight loss
and a significant improvement in blood sugar level, and aerobic exercise which will lead
to reduction in the HbA1C and improved insulin sensitivity.

Medications:

Biguanide

Sulfonylureas

Non Sulfonylureas and other types.

Insulin injection may either be add to oral treatment or used alone.

REFERENCES

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797383/
2. American Diabetes Association, Standards of Medical Care in Diabetes 2017
3. http://emedicine.medscape.com/article/117853-overview#a4
4. World Health Organization, Global Report on Diabetes. Geneva, 2016. Accessed 30
August 2016.
5. Braunwald E. The war against heart failure; the Lancet lecture. Lancet 2014;385:812–
824.

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6. Bartunek J, Vanderheyden M, Hill J, Terzic A. Cells as biologics for cardiac repair in
ischaemic heart failure. Heart 2010;96:792–800.
7. Sanganalmath SK, Bolli R. Cell therapy for heart failure: a comprehensive overview of
experimental and clinical studies, current challenges, and future directions. Circ Res
2013;113:810–834.

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