Case report

syok sepsis
Preseptor : dr Ihsanil Husna, Sp.PD
Arranged by : shela maulida / 2009730035

Patients identity
Name

: Mr. Amr

Age

: 43nd years old

Education

: Senior High school

Marital

status

Occupation
Religion
Date

: Married
: Shopkeeper

: Moslem

of admission

: Juli 2016

Anamnesis

Chief complaint :
Patient come to hospital with synope condition 30 minutes
before

Another complaint :

Body fever, weakness, loss of appetite, dizziness, low energy,

fatigue and cough with little mucus and out of breath
sometime

History of present illness

History of past illness

Have history of same problem 3 months ago.

Having history of Hypertension

Having Nefrotic syndrome since 3 years

before

No history of DM

No history of urinary or kidney disease

No history of asthma

No history of allergic

No history of hematologic disease

History of family
None

of his family has same

problem

Has

history of hypertension

No

history of DM

No

history of allergic

No

history of hematologic disease

History of allergy

Patient has no allergy to food,

drugs and weather.

History of illness
This patients has nefrotic syndrome for
3 years ago, and get routine medication
at hospital. Uncontroled Hypertention
medication

Habits
Smoking

habits

Drinking

alcohol

Taking

: Denied
: Denied

any medication : Denide

Physical examination

Laboratory examination
Examination

Value

Units

Normal

CHEMICAL CLINIC

Hemeoglobin

14.4

g/dL

13,2-17,3

H 11 .15

10/UL

3.80

41

40 52

Trombosit

186

10/ul

150-440

Eritrosit

4.78

10/ul

4.40-5.90

Leukosit
Hematokrit

MCV/VER

86

Fl

80-100

MCHC/HER

30

pg

26-34

MCHC/KHER

35

gdl

32-36

FAAL HATI

SGOT (AST)

H 358

U/L

10-34

SGPT (ALT)

H 528

U/L

9-43

FAAL GINJAL

Ureum Blood

H 62

Creatinin Blood

1.3

Mg/dl

Mg/dl

10-50

<1.4

ELECTROLIT

Natrium (na)

L 131

Meq/L

135-147

Kalium (k)

L 3.4

Meq/L

3.5-5.0

Clorida (cl)

96

Meq/L

94-111

Calcium (c)

L 7.9

Meq/L

70-200

GDS

126

Mg/dl

70-200

Resume
Patients come to the hospital with fainting
condition 30minutes before, after consume
nifedipin 5mg . patients felt his body fever come
and go since 6 days ago, feel better after consume
paracetamol. Patients also complained of body felt
loss of appetitle,low energy and fatigue . Also
cough with little yellow mucussometimes he feels
out of breath .Undefecated for 3days.History of
past illness : have history of same problem 3
months ago. Physical examination Blood pressure:
70/50 mmHg, Heart rate: 120x/minute, Respiratory
rate: 17x/minute, Temperature : 39 C. Laboratory
examination: Lukosite 11.15 10/UL, Hematokrit
41%, SGOT 358, SGPT 528, Natrium 131, Kalium
3,4 ,kalsium 7,9.

Problem list

Syok

Septic

Gangguan
Nefrotik

fungsi hati

Syindrome

Assesment

1. Syok Sepsis e.c Pneumonia

dd/ hepatitis

S : Patient complaints of swelling in both legs since three weeks ago,

Patients also complained of decreased appetite, body felt weak and
a little nauseous. urination 3 times a day, a little frothy.

O: Blood pressure: 110/90 mmHg, Heart rate: 86x/minute,

Respiratory rate: 20x/minute, Temperature : 36.6 C, Extremities
Inferior : Edema (+/ +).

Lab examination :
11th Maret 2016

12th Desember 2015

Total Cholesterol : 696 mg/dL
(H), Total Protein : 3.9 g/dL
(L), Albumin : 1.3 d/dL (L).
Urinalisis
Protein

;
:

BJ

1,047,

Positive

(150mg/dl), Keton : Positive 1

(5mg/dl), blood : Positive 1
(50/uL).

Sediment

Eritrosit : 3-5, Lekosit : 5-7,

Bakteri Positive

Cholesterol : 734 mg/dL,

Triglisrida : 381 mg/dL, LDL :
549 mg/dL. Urinalisis ;
protein : Positive 3
(500mg/dl),

A: Nephrotik Syndrome
P: Laboratory :
Full

peripheral blood

Total

Protein

Ureum

and creatinine blood

Urinalisis
USG

Abdomen

Renal

Biopsy

Therapy :
Bedrest
Protein
Diet

until until the swelling disappears

intake is restricted from 0.8 to 1 g / kg / day

low in salt 2 grams / day and low-fat

Prednisone
Furosemid

5 mg full dose 3 x 8 tab

40 mg/day

Prognosis

Quo ad vitam

: bonam

Quo ad functionam

: dubia ad bonam

Quo ad sanationam

: dubia ad bonam

LITERATURE
REVIEW

Definition of Nephrotic Syndrome

Nephrotic syndrome is a set of clinical manifestations
characterized by
massive

proteinuria (greater than 3.5 g / 1.73 m2

body surface area per day),
hypoalbuminemia

(less than 3.5 g / dl),

edema,
hyperlipidemia

( >200) and lipiduria.

Anatomy of Renal
Renal parenchyma
composed of two
special areas: the
renal cortex which is
located on the outside
and looks granular, as
well as the inner
regions that form a
triangle striped (renal
pyramids), which are
collectively referred to
Renalkidney
is bean-shaped
organ
locatedone
on million
both sides
of the units
vertebral
Each
is composed
of about
functional
(the
as the renal medulla.
column. In
general,
thanofthe
right kidney
kidney because
smallest
unit
that islower
capable
forming
urine) left
microscopic
called
of the liver Each
and isnephron
closer to consists
the midline
theBowman's
body. It is as
high asand
XII
nephrons.
of of
the
capsule
thoracic vertebra,
while
the upper
pole of the
left kidney
capillary
glomerolus,
proximal
convoluted
tubule,
loop is
of located
Henle,
as high
as thoracictubules
vertebra
XI. empties into the collecting tubules.
distal
convoluted
which
Each kidney obtain blood supply from the renal artery.

The glomerulus is a dominant

part in the vascular
component of the nephron.
The most important function
of glomerolus
is formed
Under
normal circumstances,
ultrafiltrate
can
fit into
about
20% ofwhich
plasma
that
went
theglomerolus
tubules due
to capillary
into
filtrated
with a
hydrostatic
pressure
greater
net filtration
pressure
10
than the
hydrostatic
pressure
mmHg,
produces
filtration
rate
intrakapiler
and colloid
glomerolus
average
(GFR) of
osmotic
125 mL
/ min.pressure.
As the filtrate

Physiology of
Glomerulus

flows
through
The
layersthe
of tubules,
the membrane to function as molecular sieves
added
or taken
variousred blood cells and plasma proteins, but skip
glomerolus
holding
substances
from other
the filtrate,
H2O and
solutesomolecular size is quite small. Although
that eventually
only about
1.5not
L be filtered because it can not pass
plasma proteins
can
/ day
is excreted
as urine.
through
the pores
from above, the pore itself is large enough to
pass the plasma protein albumin which is the smallest.

Epidemiology

Incidence may affect all ages but most (74%) was found at
the age of 2-7 years. The ratio of male: female = 2: 1,
whereas in adolescence and adulthood this ratio ranges
from 1: 1. Usually 1 of 4 patients with nephrotic syndrome
are patients with age> 60 years. But in exact incidence
and prevalence of nephrotic syndrome in geriatrics is not
known because often misdiagnosed.

Etiology
Primary glomerulonephritis
with an unknown cause
(idiopathic) with a wide variety
of histopathological
abnormalities, include:
minimal lesion
glomerulonephritis
focal glomerulosclerosis
membranous
glomerulonephritis
glomerulonephritis
membranoproliferative
the other proliferative
glomerulonephritis

Glomerulonephritis secondary to:

infections, such as HIV infection, hapatitis
virus B and C, syphilis, malaria, Schistosomal,
tuberculosis, and leprosy.
Malignancy, such as adenocarcinoma of the
lung, breast, colon, Hodgkin's lymphoma,
multiple myeloma, and renal carcinoma.
connective tissue diseases, such as systemic
lupus erythematosus, rheumatoid arthritis,
MCTD (mixed connective tissue disease)
The effects of drugs and toxins, such as nonsteroidal anti-inflammatory drugs, gold
preparations, penicillamine, probenecid,
mercury, captopril, and heroin.
Other, including diabetes mellitus,
amyloidosis, pre-eclampsia, chronic allograft
rejection, vesicoureteric reflux, or a bee sting.

Clinical Manifestations

Clinical Manifestations
Hyperlipidemia

EDEMA
Edema
in nephrotic
can beincreased,
explained while
Cholesterol
levelssyndrome
generally
with the
theory
ofnormal
underfill
overfill.
Underfill
triglycerides
varies
from
toand
slightly
elevated.
Increased
explains
hypoalbuminemia
causes
a
due to theory
increased
LDLthat
cholesterol
levels. High
triglyceride
decrease
in plasma
oncotic pressure
so that
theincrease
levels are
associated
with increased
VLDL. Also
found
fluid shift fromdensity
the intravascular
thelipoprotein
interstitial (Lp) a,
in IDL (intermediate
lipoprotein)toand
and to
edema.
As a result
whereastissue
HDL tend
be normal
or low of
. a decrease in
plasma oncotic pressure and plasma fluid shifts
occur
hypovolemia.
Kidneys
compensate
by
This
situation
is due to
increased
lipid synthesis
in the
sodium
and water
The(decrease
liver andincreasing
decreased
catabolism
in retention.
peripheral
mechanism
will improve
lipoprotein, compensation
VLDL, intermediate
density
lipoproteins and
intravascular
volume,
but also
exacerbates
the
chylomicrons
from the
blood).
Increased
lipoprotein
lipid
of hypoalbuminemia
so edema
synthesis occurrence
is stimulated
by a decrease in serum
albumin and
increasingly continue.
decrease in oncotic pressure.

DIAGNOSIS
Anamnesis
Supporting
investigation

It Examination
should be ofnoted
the problem
of drugurinalysis,
use, the
urine, including
urine protein,
possibility
of various
andand
thesediment
history of
hamaturia,
dipstick urine
specific infections,
gravity of urine
other
systemic
diseases.
examination.
Volume
is usually
less than 400 ml / 24 hours.
Blood tests, including serum albumin, serum cholesterol,
Physical
triglycerides,
hemoglobin,
hematocrit, erythrocyte sedimentation
examination
rate (ESR), and serum electrolytes.

There anasarca edema. Not infrequently eyes closed

due to edema
ofbiopsy
the eyelids.
Serology
and renal
is often needed to confirm the

diagnosis and rule out possible causes of nephrotic syndrome

secondary. Serology is often not a lot of information and it is
expensive because it should only be done by a strong indication.

Treatment
Some definitions / limitations used in SN :

Remission: negative or trace proteinuria (proteinuria <4 mg /

m2 LPB / h) 3 consecutive days in one week

Relapse: 2+ proteinuria (proteinuria 40 mg / m2 LPB / h) 3

consecutive days in the first week 3

Relapse rare: relapses occurred less than two times in the first
6 months after the initial response to or less than 4 times per
year of observation

Relapses often (frequent relapses): relapses occurred 2 times

in the first 6 months after the initial response or 4 times in a
period of 1 year

Dependent steroids relapses occurred during steroid doses

lowered or within 14 days after treatment was stopped, and
this occurs two times in a row

Steroid Resistant: no remission in the treatment of full-dose

prednisone (full dose) 2 mg / kg / day for 4 weeks.

Non Pharmacology
Diet for patients with nephrotic syndrome is 35 cal / kg /
day, consisting mostly of carbohydrates. Proteinuria may
improve hypoalbuminemia control and reduce the risk of
complications caused. Normal protein diet recommended 0.81.0 g / kg / day. In patients with dietary protein 0.6 g / kg / day
plus the number of grams of protein according to the number
Proteinuri result Proteinuri reduced, increased blood levels of
albumin and fibrinogen levels decreased. To reduce edema
given a low salt diet (1-2 grams of sodium / day) along with
diuretics and bedrest.

Pharmacology
CORTICOSTEROIDS
Minimal lesion nephropathy and membranous
nephropathy are two disorders that respond well to
steroid therapy. Other researchers have found that
focal segmental glomerulosclerosis up to 40% of
patients respond well to steroids with a complete
remission. In most patients with idiopathic
membranous nephropathy, symptomatic therapy
with better kidney function for a longer period and
can heal spontaneously.

Figure 1. The initial treatment with

corticosteroids

Information:
The full dose prednisone (full dose)
60 mg / mLPB / day (2mg / kg /
day) divided into 3 doses given
daily for 4 weeks, followed by
prednisone 40 mg / mLPB / day
(2/3
full
dose),
can
given
intermittently (3 consecutive days
in the first week) or alternating
(every other day) for 4 weeks.

When remission occurs within

the first 4 weeks, then
intermittent
prednisone
/
alternating 40 mg / mLPB /
day administered for 4 weeks.
When remission does not occur
in the first 4 weeks, then the
patient is diagnosed as a
steroid-resistant
nephrotic
syndrome.

Figure 2. Treatment of nephrotic syndrome relapse

Information:
Prednisone full dose every day until remission (maximum of 4
weeks) followed by intermittent prednisone / alternating 40 mg /
mLPB / day for 4 weeks.
When you get a full dose treatment for 4 weeks did not also
occur revision, the patient was diagnosed as a steroid-resistant
SN and should be given other immunosuppressive therapy

Figure 3.
Treatment of
nephrotic syndrome
relapsed frequently

Information:
Full dose prednisone daily until remission (maximum of 4 weeks)
followed by intermittent prednisone / alternating 40 mg / mLPB / day
and immunosuppressive / oral cytostatic (cyclophosphamide 2-3 mg /
kg / day) dose for 8 weeks


Information:

Prednisone full Monitoring

dose everyofday
until
remission (maximum 4 weeks),
Hb,
leukocytes,
Or, Prednisone full dose every
day
until remission (maximum of 4
followed by cyclophosphamide
puls with a dose of 500-750 mg /
platelets
week
weeks) , followed
by oralevery
cyclophosphamide
2-3 mg / kg / day dose for
mLPB given byLeukocytes
infusion once
a
month
for
6
months and
<3000 / ml40
mg
CPA/consecutive
12 weeks and alternating prednisone
mLPB.hari for 12 weeks.
intermittent prednisone
/ alternating 40 mg / mLPB for 12 Sunday.
stopped
first
Then tapering off
prednisone
at a dose of 1 mg / kg / day for 1 month,
Then tapering off
prednisone
at
a dose
of CPA
1 mg / kg / day for 1 month,
ml
followed by 0.5Leukocytes>
mg / kg / day5000
for 1/ month
(long tapering off: 2 months)
followed by 0.5awarded
mg / kg
/ day for 1 month (long tapering off: 2
again
months)
Figure 4. The treatment of steroid dependent nephrotic
syndrome

Figure 5.
Treatment
of steroidresistant
nephrotic
syndrome.

Information:
Or, Cyclophosphamide puls with a dose of 500-750 mg / mLPB
oral cytostatic: cyclophosphamide 2-3 mg / kg / day dose for 3-6 months
dibertikan via intravenous infusion once a month for six months,
Prednisone dose of 40 mg / mLPB / alternating days during
may be continued depending on the patient's condition.
administration of oral cyclophosphamide.
Prednisone alternating doses of 40 mg / mLPB / day during
Then prednison in tapering-off with a dose of 1 mg / kg / day for 1
administration of cyclophosphamide puls (5 months). Then tapering
month, followed by 0.5 mg / kg / day for 1 month (long tapering off 2
off prednisone at a dose of 1 mg / kg / day for 1 month, followed by
months).
0.5 mg / kg / day for 1 month (long tapering off 2 months).

Pharmacology
ACE inhibitors and
angiotensin receptor blockers
In patients who are not responsive to corticosteroids, to reduce
Proteinuri used symptomatic therapy with angiotensin converting
enzyme inhibitors (ACEI), for example, captopril or enalapril low doses,
and the dose is increased after 2 weeks, or anti-inflammatory drugs
non-steroidal (NSAIDs), such as indomethacin.
Antiproteinurik effect of this drug lasts longer (approximately two
months after the drug is stopped). Angiotensin receptor blockers (ARBs)
were also able to improve Proteinuri because it inhibits inflammation
and interstitial fibrosis, inhibiting the release of cytokines, growth
factors, adhesion molecules occupational local angiotensin II in the
kidneys.

Pharmacology
Non-steroidal anti-inflammatory
drugs (NSAIDs)

may be used in patients with membranous nephropathy and

focal segmental glomerulosclerosis to decrease the
synthesis of prostaglandins. It causes renal vasoconstriction,
decreased glomerular capillary pressure, filtration surface
area and reduces proteinuria to 75%. Besides NSAIDs can
reduce the levels of fibrinogen, fibrin-related antigenic and
prevent platelet aggregation. However, please note that
NSAIDs cause a progressive decline in kidney function in
some patients. This drug should not be given if creatinine
clearance <50 ml / min.

Pharmacology
Cyclophosphamide and Chlorambucil

In patients with frequent relapses with corticosteroids or

corticosteroid resistant to other therapies may be used with
cyclophosphamide or chlorambucil. Cyclophosphamide give
remission longer than corticosteroids (75% over 2 years) at
a dose of 2-3 mg / kg / day for 8 weeks. The side effects of
cyclophosphamide is bone marrow depression, infections,
alopecia, hemorrhagic cystitis and infertility when given
over 6 months. Chlorambucil given at a dose of 0.1-0.2 mg /
kg / day for 8 weeks.

Pharmacology
Cyclosporine

Cyclosporine A may be tried in patients who

relapsed after being given cyclophosphamide or
to extend the period of remission after
corticosteroid administration. A dose of 3-5 mg /
kg / day for 6 months to 1 year (after 6 months
the dose reduced by 25% every 2 months).
Cyclosporine A may also be used in combination
with prednisolone at the failed cases of nephrotic
syndrome in combination with other therapies.

Pharmacology
DIURETICS

To reduce edema diuretics (furosemide 40 mg / day or class

thiazides) with or without combination with potassiumsparing diuretics (spironolactone).

In patients with nephrotic syndrome can occur resistance to

diuretics (furosemide 500 mg and 200 mg spironolactone).
Resistance to this diuretic is multifactorial. Suspected
hipoalbuminemi cause a reduction in drug transport to the
workplace, while binding by urinary protein is not the main
mechanism of this resistance.
This therapy may increase plasma volume, increases in
glomerular filtration rate, urine flow, and sodium excretion.
However, albumin infusion is still doubt its effectiveness because
albumin rapidly excreted through urine, but it can increase blood
pressure and even pulmonary edema in patients hypervolemi.

Pharmacology
Anticoagulants

Risk of thromboembolism is increased in nephrotic syndrome

and the need to get treatment. Although the long-term
administration is still controversial, but in one study proved
beneficial. To prevent complications hypercoagulable namely
thromboembolism occurring in approximately 20% of cases of
nephrotic syndrome (most often in membranous nephropathy),
used dipyridamole (3 x 75 mg) or aspirin (100 mg / day) as an
anti-platelet aggregation and deposition of fibrin / thrombus.

Complication

Infection

Hipogamaglobulinemi, particularly immunoglobulin G (IgG), together

with factors B causes nephrotic syndrome sufferers are highly
susceptible to infection. Much more use of corticosteroids which
we know as immunosuppression, susceptibility to infection is
greater.

Thrombosis

Thrombosis can occur in veins and arteries, especially the large vein
in the liver, pelvis, renal, mesenteric and pulmonary.

Acute Renal Failure

The cause of ARF is not known for sure, but there is evidence
involving hypovolemia and renal ischemia resulting in acute
tubular necrosis, interstitial edema and elevation of pressure
occurs in proximal tubules with consequent reduction in filtration
rate glomelurus.

Prognosis

Mortality and the prognosis of patients with nephrotic

syndrome varies by etiology, severe, extensive
damage to the kidneys, the child's age, the underlying
condition, and response to treatment

REFERENCES

Sherwood, L. 2014. Fisiologi Manusia dari Sel ke Sistem. Edisi 2, Alih

Bahasa: Brahm U. Pendit. Jakarta, Penerbit Buku Kedokteran EGC.
pp: 463-475.
Wilson, L. M. 2006. Anatomi dan Fisiologi Ginjal dan Saluran Kemih.
Dalam: Patofisiologi Konsep Klinis Proses-Proses Penyakit. Volume 2.
Ed: Sylvia A. Price dan Lorraine M. Wilson. Alih Bahasa: Brahm U.
Pendit, dkk. Jakarta, Penerbit Buku Kedokteran EGC. pp: 867-875.
Kidney
Disease:
Improving
Global
Outcomes
(KDIGO)
Glomerulonephritis Work Group. KDIGO Clinical Practice Guideline
for Glomerulonephritis. Kidney inter. 2012;Suppl.2: 139 274
National Kidney and Urologic Disease Information Clearinghouse.
Nephrotic Syndrome in adults. National Institute of Health; 2010.
Hull RP., Goldsmith DJ., Nephrotic syndrome in adults. BMJ,
2011;336:1185-9
Siddall EC, Radhakrishnan J. The pathophysiology of edema
formation in the nephrotic syndrome. Kidney Int. 2012. 82:635642
Prodjosudjadi W., SindromNefrotik.Buku Ajar Ilmu Penyakit Dalam
Ed VII. 2015; 2082 2088.