BLOK 24

K E G AWAT DA R U R ATA N
MEDIK
PRE TEST

1.Contoh mikrorganisme penyebab watery

diarrhea adalah ...
2. Contoh mikroorganisme penyebab
inflammatory diarrhea adalah ...
3. Komplikasi dari watery diarrhea adalah ....
DIARE DAN
KOMPLIKASI
H I L D E B R A N D H A N O C H V I C T O R W AT U P O N G O H
D E P A R T E M E N I L M U P E N YA K I T D A L A M F K U K I
2016
PENDAHULUAN
• Diare akut pada orang dewasa merupakan tanda dan gejala penyakit
yang umum dijumpai dan bila terjadi tanpa komplikasi, secara umum
dapat diobati sendiri oleh penderita
• Komplikasi akibat dehidrasi atau toksik menyebabkan morbiditas dan
mortalitas
• Terapi kausal tentunya diperlukan pada diare akibat infeksi, dan
rehidrasi oral maupun parenteral secara simultan dengan kausal
memberikan hasil yang baik terutama pada diare akut yang
menimbulkan dehidrasi sedang sampai berat
DEFINISI
• Diare atau mencret didefinisikan sebagai buang air besar dengan
feses yang tidak berbentuk (unformed stools) atau cair dengan
frekuensi lebih dari 3 kali dalam 24 jam.
• Bila diare berlangsung kurang dari 2 minggu, disebut sebagai
Diare Akut.
• Apabila diare berlangsung 2 minggu atau lebih, maka
digolongkan pada Diare Kronik
• Pada feses dapat dengan atau tanpa lendir, darah, atau pus.
• Gejala ikutan dapat berupa mual, muntah, nyeri abdominal, mulas,
tenesmus, demam dan tanda-tanda dehidrasi
KLASIFIKASI
Inflammatory diarrhea
• Akibat proses invasion dan cytotoxin di kolon dengan manifestasi sindroma
disentri dengan diare yang disertai lendir dan darah (disebut juga Bloody
diarrhea).
• Biasanya gejala klinis yang menyertai adalah keluhan abdominal seperti mulas
sampai nyeri seperti kolik, mual, muntah, demam, tenesmus, serta gejala dan
tanda dehidrasi.
• Pada pemeriksaan tinja rutin secara makroskopis ditemukan lendir dan/atau
darah, secara mikroskopis didapati leukosit polimorfonuklear.
• Mikroorganisme penyebab seperti : E.histolytica, Shigella, Entero Invasive E.coli
(EIEC),V.parahaemolitycus, C.difficile, dan C.jejuni.
KLASIFIKASI
Non Inflammatory diarrhea
• kelainan yang ditemukan di usus halus bagian proksimal, proses
diare adalah akibat adanya enterotoksin yang mengakibatkan
diare cair dengan volume yang besar tanpa lendir dan darah, yang
disebut dengan Watery diarrhea.
• Keluhan abdominal biasanya minimal atau tidak ada sama sekali,
namun gejala dan tanda dehidrasi cepat timbul, terutama pada kasus
yang tidak segera mendapat cairan pengganti.
• Pada pemeriksaan tinja secara rutin tidak ditemukan leukosit.
• Mikroorganisme penyebab : V.cholerae, Enterotoxigenic E.coli (ETEC),
Salmonella
KLASIFIKASI
Penetrating diarrhea
• Lokasi pada bagian distal usus halus.
• Penyakit ini disebut juga Enteric fever, Chronic Septicemia,
dengan gejala klinis demam disertai diare.
• Pada pemeriksaan tinja secara rutin didapati leukosit
mononuclear.
• Mikrooragnisme penyebab : S.thypi, S.parathypi A,B,
S.enteritidis, S.cholerasuis,Y.enterocolitidea, dan C.fetus.
KARAKTERISTIK DIARE AKUT
Tabel 2 :Tipe Diare Yang Ditimbulkan Oleh Enteropatogen
TERAPI
PRINSIP TERAPI
• Prinsip pengobatan :
– menghilangkan kausa diare dengan memberikan antimikroba yang sesuai dengan etiologi,
– terapi supportive atau fluid replacement dengan intake cairan yang cukup atau dengan Oral
Rehidration Solution (ORS) yang dikenal sebagai oralit
– tidak jarang diperlukan obat simtomatik untuk menyetop atau mengurangi frekwensi diare.
• Untuk mengetahui mikroorganisme penyebab diare akut dilakukan pemeriksaan
feses rutin dan pada keadaan dimana feses rutin tidak menunjukkan adanya
miroorganisme atau ova, maka diperlukan pemeriksaan kultur feses dengan
medium tertentu sesuai dengan mikroorganisme yang dicurigai secara klinis
dan pemeriksaan laboratorium rutin.
• Indikasi pemeriksaan kultur feses antara lain, diare berat, suhu tubuh > 38,50C,
adanya darah dan/atau lender pada feses, ditemukan leukosit pada feses,
laktoferin, dan diare persisten yang belum mendapat antibiotik
 Indikasi Pemberian Antibiotik Pilihan Antibiotik
Demam (suhu oral >38,50C), bloody Kuinolon 3 – 5 hari
stools,leukosit, laktoferin, hemoccult, sindroma Kotrimoksazole 3 – 5 hari
disentri
Traveler’s diarrhea Kuinolon 1 – 5 hari
Diare persisten (kemungkinan Giardiasis) Metronidazole 3x500 mg selama 7 hari
Shigellosis Kotrimoksazole selama 3 hari Kuinolon selama 3 hari
Intestinal Salmonellosis Kloramfenikol/Kotrimoksazole/Kuinolon selama 7 hari
Campylobacteriosis Eritromisin selama 5 hari
EPEC Terapi sebagai Febrile Dysentry
ETEC Terapi sebagai Traveler’s diarrhea
EIEC Terapi sebagai Shigellosis
EHEC Peranan antibiotik belum jelas
Vibrio non kolera Terapi sebagai febrile dysentery
Aeromonas diarrhea Terapi sebagai febrile dysentery
Yersiniosis Umumnya dapat di terapi sebagai febrile dysentri.Pada kasus berat : Ceftriaxon IV 1 g/6
jam selama 5 hari
Giardiasis Metronidazole 4 x 250 mg selama 7 hari. Atau Tinidazole 2 g single dose atau Quinacine
3 x 100 mg selama 7 hari
Intestinal Amebiasis Metronidazole 3 x 750 mg 5 – 10 hari + pengobatan kista untuk mencegah relaps:
Dihiodohydroxyquin 3 x 650 mg 10 hari
atau Paramomycin 3 x 500 mg 10 hari atau
Diloxanide furoate 3 x 500 mg 10 hari
Cryptosporidiosis Untuk kasus berat atau immunocompromised :
Paromomycin 3 x 500 selama 7 hari
KOMPLIKASI DIARE
Gangguan Keseimbangan Cairan (Dehidrasi)

Syok hipovolemik

Asidosis metabolik
GANGGUAN
KESEIMBANGAN
CAIRAN
KESEIMBANGAN CAIRAN

• 50 - 70 % dari berat badan terdiri dari cairan.

• Jaringan lemak lebih kurang mengandung air dibanding otot
• Sumber :
• Air yang diminum
• Bersama makanan
• Hasil metabolisme
Total Body Water 49 L 70 % X BB
1. Ekstra sel 14 L 16-23 % X BB
2. Intravaskuler 3L 4 – 5 % X BB
3. Ekstravaskuler 11 L 12 –18% X BB
4. Intra sel 35 L 50 % X BB
Fungsi :
• Kehidupan sel
• Melarutkan makanan, ion ( Na – K )
• Metabolisme

Distribusi cairan tubuh dipengaruhi oleh :

• Sistem saluran limfe
• Tekanan darah
• Permeabilitas kapiler
• Protein plasma
• Retensi air dan garam
Eksresi cairan dalam tubuh melalui :
a. Urin
b. Keringat
c. Paru
d. Feces

Rata kehilangan cairan / hari :

• Kulit/paru
(insensible water loss) : 800 cc - 1200 cc
• Urine : 1500 cc
• Feces : 100 cc – 1200 cc
PENGATURAN CAIRAN TUBUH

• Terdapat keseimbangan ( input & output ) yang diatur

hipotalamus melalui osmoreseptor

• Pada dehidrasi  me↑ haus dan ADH me↑ sehingga

intake me↑ dan eksresi me↓
 DEHIDRASI
(volume sirkulasi efektif ↓)

Osmolality plasma ↑

Thirst ↑ ADH ↑
Water ingestion ↑ Water excretion ↓

Water retention

Osmolalitas plasma ↓

Volume sirkulasi ↑
DEHIDRASI
• Tubuh kekurangan cairan
• Etiologi kekurangan cairan :
– Melalui saluran cerna
• Muntah
• Diare
• Perdarahan
– Melalui saluran kencing
• Pemakaian diuretik
• Penyakit ginjal
• diabetes
– Melalui kulit
• Luka bakar
• Keringat ↑↑
– Perpindahan ke ruang dalam badan
• Peritonitis
• Pankreatitis
Tanda dan Gejala dehidrasi :
Lesu Akral dingin
Tekanan darah menurun Mukosa kering
Nadi halus cepat Turgor menurun
Urin output menurun

Pengobatan :
• Sesuai penyakit dasar
• Pemberian cairan oral - parenteral
FLUID LOSS AND SHOCK
% Dehydration Examination Findings
<5 History of fluid loss, but no findings on
physical examination
5 Dry oral mucous membranes, but no
panting or pathological tachycardia
7 Mild to moderate decreased skin turgor,
dry oral mucous membranes, slight
tachycardia, and normal pulse pressure
10 Moderate to marked degree of decreased
skin turgor, dry oral mucous membranes,
tachycardia, and decreased pulse pressure.
12 Marked loss of skin turgor, dry oral mucous FLUID AND ELECTROLYTE THERAPY
(http://www.cvmbs.colostate.edu/clinsci/

membranes, and significant signs of shock

wing/fluids/fluids.htm)
Wayne E. Wingfield, MS, DVM
PERKIRAAN JUMLAH CAIRAN
YANG HILANG (DEFISIT)
1. Sistem skor ( dehidrasi akut, misalnya GE akut )

2. Pemasangan CVP (Central Venous Pressure)

3. Ukur Kadar Na Plasma

defisit cairan = 0,6 X BB {Na plasma / 140 - 1}

4. Ukur Hematokrit
defisit cairan = 0,2 X BB {Ht / Ht normal - 1}

5. Ukur BJ plasma
SISTEM SKOR (DALDIYONO SCORE)
SIGNS & SYMPTOMS SKOR

1. Muntah 1
2. Vox cholerica 2
3. Apatis 1
4. Somnolen/sopor/koma 2
5. TDS ≤ 90 1
6. TDD ≤ 60 2 Defisit Cairan :
7. Nadi ≥ 120 mm/Hg 1 Skor / 15 x BB x 100
8. Nafas Kussmaul 1
9. Turgor ↓ 1
10. Facies Cholerica 2
11. Ekstremitas dingin 1
12. Jari tangan keriput 1
13. Sianosis 2
14. Umur > 50 tahun -1
15. Umur > 60 tahun -2
HYPOVOLEMIC
SHOCK
HYPOVOLEMIC SHOCK
DEFINITION
syndrom characterized by decreased circulating blood
volume (hypovolemia), which results in reduction of
effective tissue perfusion pressure and generalized cellular
dysfunctions.

Forms:
• Hemorrhagic shock
• Non-hemorrhagic hypovolemic shock
 HYPOVOLEMIC SHOCK
CAUSES:
• Hemorrhagic:
 External blood loss (wounds)
 Exteriorization of internal bleeding (hematemesis, melena, epistaxis,
hemoptysis,etc.)
 Internal bleeding (hemothorax, hemoperitoneum,etc. )
 Traumatic shock
• Non-hemorrahagic:
 Digestive losses (vomiting, diarrhea, nasogastric suction, billiary, digestive
fistula, etc )
 Renal losses (diabetes mellitus, polyuria caused by diuretics overdose, osmotic
substances, polyuric phase of acute renal failure, etc.)
 Skin losses (intense physical effort, overheated enviroment, burns, etc.)
 Third space losses (peritonites, intestinal oclussion, pancreatits, ascitis pleural
effusions, etc.)
PATHOPHYSIOLOGY
Hypodynamic shock:
 Macrocirculatory reaction:
• sympatho-adrenergic + humoral reaction (ADH, cortizol, SRAA)
o EFFECTS: centralisation of the circulation (compensatory effect)
worsening of tissular hypoperfusion (decompensatory effect)
 Microcirculatory reaction:
• Alterations of capillary exchanges
o EFFECTS: transcapillary filling (compensatory effect)
capillary leak (decompensatory effect)
• Maldistribution of blood flow
o EFFECTS: preferential renal blood flow towards medular region (cortical
vasoconstriction)
• Abnormal peripheral oxygen extraction
o EFFECTS: early - increased (compensatory effect)
late - decreased (decompensatory effect)
• Rheologic changes
o EFFECTS: ↑ blood viscosity,  blood flow, CID
• Endhotelial modifications
o EFFECTS: morpho-functional modifications
proinflamatory and procoagulatory status,
altered permeability
HYPOVOLEMIC SHOCK
CLINICAL SIGNS:
 Intense thirst
 Tachycardia
 Tachypnea
 Positive orthostatic test
 Small pulse wave
 hTA (blood hypotension)
 Agitation, anxiety , confusion, coma
 Oliguria
 Cold extremities
 Profuse sweating
 Collapsed peripheral veins
 Delayed return of color to the nail bed
+ History of hemorrhagic or non-hemorrhagic losses
CLASSIFICATION OF HYPOVOLEMIC SHOCK

Class I Class II Class III Class IV

Blood loss- ml < 750ml 750-1500ml 1500-2000ml >2000ml

Blood loss-% <15% 15-30% 30-40% >40%

Pulse rate <100/min < 100/min 120-140/min >140/min

BP N N  

Pulse wave N   

amplitude
Capillary refill N + + +

Respiratory rate 14-20/min 20-30/min 30-40/min >40/min

Urinary output >30ml/oră Oliguria Oligoanuria Anuria

Mental status Mild anxiety Anxiety Confused Lethargy

DIFFERENTIAL DIAGNOSIS
WITH OTHER FORMS OF SHOCK

HR BP CO CVP PAOP SVR Da-vO2 SvO2

Hypovolemic
shock
↑     ↑ ↑ 

Cardiogenic
shock
↑   ↑ ↑ ↑ ↑ 

Septic shock
↑  ↑N N N   ↑
ABBREVIATIONS:
• HR – heart rate
• BP – arterial blood pressure
• CO – cardiac output
• CVP –central venous pressure
• PAOP – pulmonary artery occlusion pressure
• SVR – systemic vascular resistance
• Da-v O2 – oxygen arterial-venous difference
• SvO2 – mixed venous blood oxygen saturation
HYPOVOLEMIC SHOCK
TREATMENT PRINCIPLES
• Initial treatment of shock states
• Causative treatment – STOP losses
• Volume repletion
• Inotropic therapy
• Vasomotor therapy
TREATMENT OF HYPOVOLEMIC SHOCK
• Causative treatment – STOP losses
– essential role
– surgical treatment (when appropriate)
– emergency surgery for ongoing hemorrhage
• Volume replacement
– Vascular access site
– Solutions for volume replacement
– Rhythm of administration
TREATMENT OF HYPOVOLEMIC SHOCK
• Volume replacement – SITE of VASCULAR ACCESS
– Peripheral vascular access
• Multiple access (2-4 veins)
• Large peripheral catheters
• External jugular vein
Advantages:
– Short time of instalation
– Requires basic knowledge and simple matherials
– Minor complications (hematomas, cutaneous seroma, etc.)
Disadvantages:
– The diameter of peripheral catheter must be adapted for peripheral veins dimensions
– Vascular access can be lost (restless patient, during transportation); must be changed at 24-48
hours;
– no catecholamines administration (except in emergency for a short time period,until a central
venous access is available)
– Central venous access
• After peripheral vascular access is established and volume replacement is initiated
Advantages:
– Reliable and long lasting venous access (7-10 days)
– Allows CVP measuring and guiding of treatment
– Allows the administration of catecholamines and hypertonic substances
Disadvantages:
– Risk of complication (at instalation – pneumothorax, cervical or mediastinal hematoma, cardiac
dysrhytmias; during utilization – infection, gas embolism)
TREATMENT OF HYPOVOLEMIC SHOCK

• Volume replacement - Solutions for volume

replacement

– Isotonic crystalloid solutions

– Hypertonic crystalloid solutions
– Colloid solutions

– Whole blood and red blood cells

– Fresh-frozen plasma
– Platelets
 TREATMENT OF HYPOVOLEMIC SHOCK
Solutions for volume replacement
-Isotonic crystalloid solutions
• Normal saline (NaCl 0,9 %), Ringer solution, lactated Ringer solutions
• Advantages:
– easy available
– cheap
– reduced risks
• Disadvantages:
– Small volume effect (out of 1000ml infused solution – 250-300ml remains
intravascullarly, the rest is distributed to the interstitial space)
– short duration of volume effect
– risk of interstitial edema, metabolic hyperchloremic acidosis
-Hypertonic crystalloid solutions
• Hypertonic saline (NaCl 7,4%)
• Advantages:
– Efficient blood volume resuscitation with small solution volume (water is atracted
from interstitial space )
– Avoidance of fluid overload and peripheral edema
• Disadvantages:
– may result in acute pulmonary edema
TREATMENT OF HYPOVOLEMIC SHOCK
Solutions for volume replacement
Colloid sollutions
• Dextrans: Dextran 70, Dextran 40
• Gelatines: Gelofusin, Haemacel, Eufusin
• Hetastarch: Haes, Voluven, Refortan
• Human albumin 5%, 20%

– Advantages:
• Good volume effect
• Long duration of volume effect

– Disadvantages:
• expensive
• risk for anaphylactic reactions
• interfere with blood groups determination
• can induce/ aggravate coagulation disorders
TREATMENT OF HYPOVOLEMIC SHOCK

Solution for volume replacement

Blood and blood products are not volume solutions
• Only isogroup isoRh blood
• Only after restauration of intravascular volume with cristalloid /colloid
solutions;
• For correction of oxygen transport
• In case of posthemorragic anemia (after volume replacement) or ongoing
hemorrhage
• In case of massive blood transfusion – add fresh-frozen plasma and
platelet concentrate
TREATMENT OF HYPOVOLEMIC SHOCK

Volume replacement
RHYTHM OF ADMINISTRATION
– Rhytm of administration depends on:
• Ongoing losses / stopped losses
• Rhytm of losses – rapid (minutes, hours) or slow (days) instalation
– For the patient with hypotension – normal saline (2000 ml in the first 15-30
minutes)
– after the first 15-30 minutes - volume replacement continues depending on
the clinical and hymodinamic parameters (BP, HR, etc..)
TREATMENT OF HYPOVOLEMIC SHOCK

Volume replacement –
MONITORING THE TREATMENT EFFICIENCY
– Clinical parameters
• normalisation of BP, HR, pulse amplitude, skin colour and
temperature, mental status, urinary output
– Hemodynamic parameters
• Normalization of CVP, PCPB, DC, RVS, so
– Laboratory parameters
• Normalization of acid-base balance, liver, renal tests, Hb, Ht
TREATMENT OF HYPOVOLEMIC SHOCK

• Inotropic support
– Only after volume replacement
– Used to improve cardiac output
– Dobutamine
• inotropic positive support
• peripheral arterial vasodilatation
TREATMENT OF HYPOVOLEMIC SHOCK
Vasopressor therapy
• NOT RECOMMENDED (may aggravate peripheral hypoperfusion and
metabolic acidosis)

EXCEPTIONS
• Only temporary
• In case of ongoing hemorrhage, which outruns the possibilities of
volume replacement
• Only until surgical procedure stops the hemorrhage (emergency surgical
treatment)
• Noradrenaline, dopamine, adrenaline
GANGGUAN
KESEIMBANGAN
ASAM BASA
CLİNİCAL EVALUATİON
• Patient history
• Clinical presentation
• Acidemia  Hyperventilation
• Alkalemia  Paresthesias and Tetany
• Laboratory: Blood acid-base status:
• Blood pH (4 º C, with anticoagulant, promptly),
• Urine pH
• Plasma and urine electrolyte concentration
• Lactate concentration
ACİDOSİS
• Clinical effects of severe acidosis: pH <7.2
• Cardiovascular system effects:
– Decreased myocardial contractility
– Decreased cardiac output
– Cardiac failure
– Hypotension
– Decreased hepatic and renal blood flow
– Centralization of effective blood volume
– Tissue hypoxia
– Pulmonary edema
 METABOLİC ACİDOSİS
Hallmark is [HCO3-]

1. Acid production  net acid intake  above net renal excretion

(ketoacidosis, lactic acidosis, ammonium chloride loading)

2. failure of renal net excretion

(chronic renal failure, renal tubular acidosis)

3. Bicarbonate loss via the gastroinestinal tract

(diarrhea, gastrointestinal fistula)

4. Nonbicarbonate solutions added to ECF

(dilutional acidosis)
STEPS OF EVALUATİON
1. Examine pH= Reduction ( 7.2)  Acidosis
Increase (7.5) Alkalosis
2. Examine directional change of PCO2 , [HCO3-] ,
pH acid, HCO3- low  Metabolic acidosis
pH alkal., HCO3- high  Metabolic alkalosis
3. Assess degree of compensation : Mixed acid-base disorder?
– Metabolic acidosis  PCO2 
– Metabolic alkalosis  PCO2
– Failure of respiratory compenstion= primary respiratory acid-base
disorder
– Never to initial pH through compensation !!
4. Calculate the serum anion gap
– Is the acid-base disorder organic or mineral in origin??
– We use venous sample blood electrolytes
– Electroneutrality demands:
Serum anion gap, that means:
[Na+] + [UC]= [Cl-] +[Total CO2] + [UA]
(U means: unmeasured)
Normally the serum anion gap is about 9 (6-12 mEq/l), a major increase in
Anion gap > 26 mEq/l always implies existence of an organic acidosis
DİFFERENTİAL DİAGNOSİS OF
METABOLİC ACİDOSİS
Normal anion gap Increased anion gap
• (hyperchloemic) (organic)
• GI loss of HCO3-  acid production
• Diarrhea Lactic acidosis
• Renal tub. Acidosis Diab. Ketoacidosis
• Parenteral alimentation Toxic alcohol,salicy.
• Carbonic anhydr. İnh. Acute renal failure
• K-sparing diuretics Chronic renal failure
INCREASED ANİON GAP
METABOLİC ACİDOSİS

• Ketoacidosis (diabetic)
• Uremia (renal failure)
• Salicylate intoxication
• Starvation
• Methanol intoxication
• Alcohol ketoacidosis
• Unmeasured osmoles (intoxication)
• Lactic acidosis
SİMPLE DECOMPENSATED ACİD-BASE DİSORDERS

Acid Base Disorder: pH pCO2 HCO3-

• Metabolic acidosis   
• Respiratory acidosis   
• Metabolic alkalosis   
• Respiratory alkalosis   
T H A N K YO U
TERIMA KASIH