Blok 23

HYPOVOLEMIC SHOCK
Penyaji :

dr. Patiyus Agustiansyah, SpOG(K)

BAGIAN/DEPARTEMEN OBSTETRI DAN GINEKOLOGI FK UNSRI / RSMH PALEMBANG

Introduction to Hemorrhage and Shock

Hemorrhage
Abnormal internal or external loss of blood

Homeostasis
Tendency of the body to maintain a steady and normal internal environment

Shock
INADEQUATE TISSUE PERFUSION Transition between homeostasis and death

Stages of Shock Cellular Level

Four Stages
Stage 1: Vasoconstriction Stage 2: Capillary and venule opening Stage 3: Disseminated intravascular coagulation Stage 4: Multiple organ failure

Stage 1: Vasoconstriction (1 of 4)
Vasoconstriction begins as minimal perfusion to capillaries continues.
Oxygen and substrate delivery to the cells supplied by these capillaries decreases. Anaerobic metabolism replaces aerobic metabolism.

Stage 1: Vasoconstriction (2 of 4)
Production of lactate and hydrogen ions increases.
The lining of the capillaries may begin to lose the ability to retain large molecular structures within its walls. Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).

Stage 1: Vasoconstriction (3 of 4)
Sympathetic stimulation produces:
Pale, sweaty skin Rapid, thready pulse Elevated blood glucose levels

The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles.
Blood is shunted to the heart, brain, skeletal muscle, and capillary flow to the kidneys and abdominal viscera decreases.

Stage 1: Vasoconstriction (4 of 4)
If this stage of shock is not treated by prompt restoration of circulatory volume, shock progresses to the next stage.

Stage 2: Capillary and Venule Opening

(1 of 5)

Stage 2 occurs with a 15% to 25% decrease in intravascular blood volume. Heart rate, respiratory rate, and capillary refill are increased, and pulse pressure is decreased at this stage. Blood pressure may still be normal.

Stage 2: Capillary and Venule Opening

(2 of 5)

As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space. Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.

Stage 2: Capillary and Venule Opening

(3 of 5)

As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly.
Even normal blood volume may be inadequate to fill the container.

The capillary and venule capacity may become great enough to reduce the volume of available blood for the great veins and vena cava.
Resulting in decreased venous return and a fall in cardiac output.

Stage 2: Capillary and Venule Opening

(4 of 5)

Low arterial blood pressure and many open capillaries result in stagnant capillary flow. Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid.
The respiratory system attempts to compensate for the acidosis by increasing ventilation to blow off carbon dioxide.

Stage 2: Capillary and Venule Opening

(5 of 5)

As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation).
Halts perfusion Affects nutritional flow and prevents removal of cellular metabolites

Clotting mechanisms are also affected, leading to hypercoagulability. This stage of shock often progresses to the third stage if fluid resuscitation is inadequate or delayed, or if the shock state is complicated by trauma or sepsis.

Stage 3: Disseminated Intravascular Coagulation (DIC) (1 of 4)

Time of onset will depend on degree of shock, patient age, and pre-existing medical conditions. Stage 3 occurs with 25% to 35% decrease in intravascular blood volume. At this stage, hypotension occurs. This stage of shock usually requires blood replacement.

Stage 3: Disseminated Intravascular Coagulation (DIC) (2 of 4)

Stage 3 is resistant to treatment (refractory shock), but is still reversible. Blood begins to coagulate in the microcirculation, clogging capillaries.
Capillaries become occluded by clumps of RBCs.
Decreases capillary perfusion and prevents removal of metabolites

Distal tissue cells use anaerobic metabolism, and lactic acid production increases.

Stage 3: Disseminated Intravascular Coagulation (DIC) (3 of 4)

Lactic acid accumulates around the cell.
Cell membranes no longer have the energy needed to maintain homeostasis. Water and sodium leak in, potassium leaks out, and the cells swell and die.

Stage 3: Disseminated Intravascular Coagulation (DIC) (4 of 4)

Pulmonary capillaries become permeable, leading to pulmonary edema.
Decreases the absorption of oxygen and results in possible alterations in carbon dioxide elimination May lead to acute respiratory failure or adult respiratory distress syndrome (ARDS)

If shock and disseminated intravascular coagulation (DIC) continue, the patient progresses to multiple organ failure.

Stage 4: Multiple Organ Failure (1 of 2)

The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ.
Usually hepatic failure occurs, followed by renal failure, and then heart failure. If capillary occlusion persists for more than 1 to 2 hours, the cells nourished by that capillary undergo changes that rapidly become irreversible.

In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less).
Cells can no longer use oxygen, and metabolism stops.

Stage 4: Multiple Organ Failure (2 of 2)

If a critical amount of the vital organ is damaged by cellular necrosis, the organ soon fails.
Failure of the liver is common and often presents early. Capillary blockage may cause heart failure. GI bleeding and sepsis may result from GI mucosal necrosis. Pancreatic necrosis may lead to further clotting disorders and severe pancreatitis.

Pulmonary thrombosis may produce hemorrhage and fluid loss into the alveoli.
Leading to death from respiratory failure.

Shock and Hemorrhage

Defining Shock (1 of 2)
Shock is best defined as inadequate tissue perfusion.
Can result from a variety of disease states and injuries. Can affect the entire organism, or it can occur at a tissue or cellular level.
The rude unhinging of the machinery of Life
Gross, 1877

Defining Shock (2 of 2)
Shock is not adequately defined by:
Pulse rate Blood pressure Cardiac function Hypovolemia Loss of systemic vascular resistance

Physiological Response to Hemorrhage

The bodys initial response to hemorrhage is to stop bleeding by chemical means (hemostasis).
This vascular reaction involves:
Local vasoconstriction Formation of a platelet plug Coagulation Growth of tissue into the blood clot that permanently closes and seals the injured vessel

Stages of Hemorrhage
60% of body weight is fluid.
7% circulating blood volume (CBV) in men
5 L (10 units)

6.5% CBV in women

4.6 L (910 units)

Stages of Hemorrhage Stage 1

15% loss of CBV
70 kg pt = 500750 mL

Compensation
Vasoconstriction Normal BP, pulse pressure, respirations Slight elevation of pulse Release of catecholamines
Epinephrine Norepinephrine
Anxiety, slightly pale and clammy skin

Stages of Hemorrhage Stage 2 (1 of 2)

1525% loss of CBV
7501250 mL

Early decompensation
Unable to maintain BP Tachycardia and tachypnea

Stages of Hemorrhage Stage 2 (2 of 2)

Decreased pulse strength Narrowing pulse pressure Significant catecholamine release
Increase PVR Cool, clammy skin and thirst Increased anxiety and agitation Normal renal output

Stages of Hemorrhage Stage 3 (1 of 2)

2535% loss of CBV
12501750 mL

Late decompensation (early irreversible)

Compensatory mechanisms unable to cope with loss of blood volume

Stages of Hemorrhage Stage 3 (2 of 2)

Classic Shock
Weak, thready, rapid pulse
Narrowing pulse pressure

Tachypnea Anxiety, restlessness Decreased LOC and AMS Pale, cool, and clammy skin

Stages of Hemorrhage Stage 4

>35% CBV loss
>1750 mL

Irreversible
Pulse: Barely palpable Respiration: Rapid, shallow, and ineffective LOC: Lethargic, confused, unresponsive GU: Ceases Skin: Cool, clammy, and very pale Unlikely survival

Intravenous Fluid Therapy and Blood Component

Fluid Compartments
Total body consists of 60% water by

weight in adults
Body fluids divided into:

Intracellular compartment Extracellular compartment, further divided into: Interstitial compartment Intravascular compartment

Fluid Compartments
Intracellular Fluid 2/3
Extracellular Fluid 1/3

Interstitial Fluid=75% IntracellularFluid

Intravascular Fluid=25%

Intravascular compartement
Consists of:

Cellular components of blood

Proteins Ions mainly sodium, chloride and bicarbonates Potassium only a small portion in plasma Normal blood volume is about 72 mL/kg of body weight

Interstitial compartement
Larger than intravascular compartment Water and electrolytes pass freely between blood

and interstitial spaces, which have similar ionic composition Plasma proteins are not free to pass out of the intravascular space unless there is damage to capillaries, e.g., septic shock or burns With fluid loss or fall in blood pressure, water and electrolytes pass from interstitial compartment into blood (intravascular) to maintain volume (physiologic priority)

Intracellular Compartement
Water within cells: Largest reservoir of body water Ionic composition different from extracellular fluid Contains high concentration of potassium ions and low sodium and chloride ions Normal saline given IV: Tends to remain in extracellular compartment Glucose solution gets distributed throughout all body compartments Pure water given IV: Causes massive hemolysis (dangerous)

Principles of Fluid Therapy

Fluid replacement should be as close as possible

in volume and composition to those fluids lost

Acute losses should be replaced quickly
Chronic lossesreplace with caution; rapid

infusion may cause fluid overload and heart failure Better replaced by oral or rectal rehydration Mostly deficient in water: Do not overload with sodium

Fluid Therapy During Operation

Use salt solution Normal saline or Ringer s

lactate Preload 1 L before spinal anesthesia Ketamine anesthesia does not need preloading Maintenance fluid 4mL/kg/hour

Fluid Therapy During Operation

Replacement for the loss of fluid Blood loss replace with crystalloid 3 times the

volume of blood loss Blood loss more than 1 L consider giving blood Desirable to have a hemoglobin minimum 89 mg after surgery

Intravenous Fluid Therapy

Estimation of Blood Loss

Subjective Fully soaked and dripping mop approximately

100 mL Monitor heart rate, blood pressure throughout the operation Urine output 0.5 mL/kg/hr considered adequate fluid replacement

Types of IV Fluids
Crystolloids

5% dextrose in aqua

5% dextrose in NaCl Normal saline (NaCl) Hartman s solution Ringer s lactate solution Cholera saline Colloids Dextran 40, 70 Gelatin preparations e.g., Haemacel Hetastarch, Pentastarch
Intravenous Fluid Therapy

TRANSFUSI DARAH

Pemberian Transfusi Darah Pada Pasien

Nilai ulang: - check list pelaksanaan transfusi darah - golongan darah pasien = donor ? (tanyakan/peneng) - identitas pasien tepat ? - identitas donor dan golongan darah donor - awasi selama dan setelah transfusi (tanggung jawab dokter) - awasi reaksi transfusi darah

Table 1. Blood Components and Plasma Derivatives (1)

Component/Product Whole Blood Composition Volume Indications

RBCs (approx. Hct 40%); plasma; 500 ml Increase both cell mass & plasma WBCs; platelets volume (WBCs & platelets not functional; plasma deficient in labile clotting Factors V and VIII) RBC (approx. Hct 75%); reduced plasma, WBCs, and platelets 250 ml Increase red cell mass in symptom atic anemia (WBCs & platelets not functional) Increased red cell mass; < 5 x 106WBCs to decrease the likelihood of febrile reactions, immunization to leukocytes (HLA) antigens) of CMV transmission Increase red cell mass; reduced risk of allergic reactions to plasma proteins

Red Blood Cells

RBCs Leukocytes Reduced (prepared by filtration)

> 85% original volume of RBC; < 5 x 106WBC; few platelets; minimal plasma

225 ml

RBCs Washed

RBCs (approx, Hct 75%); < 5 x 108 WBCs; no plasma

180 ml

(Continued)

Component/Product Composition

Volume

Indications

Platelets

Platelets (> 5.5 x 1010/unit); RBC; WBCs; plasma Platelets (> 3 x 1011); RBCs; WBCs; plasma

300 ml

Bleeding due to thrombocytopenia or thrombocytopathy Same as platelets;l sometimes HLA matched

Platelets Pheresis

300 ml

FFP; FFP Donor Retested plasma; Solvent/detergentTreated plasma

Plasma; anticoagulation factors; complement (no platelets)

220 ml

Treatment of some coagulation

Cryoprecipitated AHF

Fibrinogen; Factors VIII and XIII;15 ml von Willebrand factor

Deficiency of fibrinogen; Factor XIII; second choice in treatment of hemophilia A, von Willebrand s disease

(Continued)

Transfusi Trombosit
Trombosit disimpan dalam kondisi digoyang terus (Reciprocal agitator), pada suhu kamar (20C) Harus segera diberikan (tidak boleh disimpan di kulkas/ di ruangan) Kecepatan cepat Gunakan infus set khusus (jangan menggunakan set transfusi darah merah)

Kebutuhan Trombosit
Trombosit: - dosis umumnya: 1 unit per 10 kg BB (5-7 unit untuk orang dewasa) - 1 unit meningkatkan 5000/mm3 (dewasa 70 kg)

- ABO-Rh typing saja, tak perlu cross match, kecuali pada keadaan tertentu

Transfusi Plasma KEBUTUHAN PLASMA/FFP

Dosis bergantung kondisi klinis dan penyakit dasarnya Coagulation factor replacement: 10 20 ml/kg BB (= 4-6 unit pd dewasa) Dosis ini diharapkan dapat meningkatkan faktor koagulasi 20 % segera setelah transfusi Plasma yang dicairkan (suhu 30 - 37 C) harus segera ditransfusikan ABO-Rh typing saja (tak perlu cross match)

KEBUTUHAN KRIOPRESIPITAT Transfusi Kriopresipitat

Diencerkan pada suhu 30 37 C 1 unit akan meningkatkan fibrinogen 5 mg/dl pada dewasa Target hemostasis level: fibrinogen > 100 mg % Segera transfusikan dalam 4 jam

REAKSI REAKSI Reaksi Transfusi Darah TRANSFUSI DARAH

Bila dilaksanakan pemeriksaan laboratorium sebelum pemberian transfusi darah, mayoritas transfusi darah tidak memberikan efek samping kepada pasien
Namun, kadang-kadang timbul reaksi pada pasien, walaupun pemeriksaan laboratorium pratransfusi darah telah dilaksanakan dan hasilnya COMPATIBLE (= cocok antara darah resipien dan donor) Reaksi: reaksi RINGAN (suhu meningkat, sakit kepala) s/d BERAT (reaksi hemolisis), bahkan dapat meninggal

KOMPLIKASI TRANSFUSI Komplikasi Transfusi Darah DARAH

Komplikasi LOKAL: - kegagalan memperoleh akses vena - fiksasi vena tidak baik - masalah ditempat tusukan - vena pecah saat ditusuk, dll
Komplikasi UMUM: - reaksi reaksi transfusi - penularan/transmisi penyakit infeksi - sensitisasi imunologis - kemokromatosis

REAKSI TRANSFUSI DARAH

Reaksi Tranfusi Darah AKUT: hemolitik, panas, alergi, hipervolume, sepsis bakteria, lung injury, dll Reaksi Transfusi Darah LAMBAT

REAKSI REAKSI REAKSI TRANSFUSI DARAH TRANSFUSI DARAH

Yang paling sering timbul:

- reaksi febris - reaksi alergi - reaksi hemolitik

REAKSI FEBRIS
Nyeri kepala menggigil dan gemetar tiba tiba suhu meningkat Reaksi jarang berat Berespon terhadap pengobatan

REAKSI ALERGI
Reaksi alergi berat (anafilaksis): jarang

Urtikaria kulit, bronkospasme moderat, edema larings: respon cepat terhadap pengobatan

REAKSI HEMOLITIK
REAKSI YANG PALING BERAT Diawali oleh reaksi: - antibodi dalam serum pasien >< antigen corresponding pada eritrosit donor - antibodi dalam plasma donor >< antigen corresponding pada eritrosit pasien Reaksi hemolitik: - intravaskular - ekstravaskular

REAKSI HEMOLITIK
REAKSI INTRAVASKULAR: - hemolisis dalam sirkulasi darah - jaundice dan hemogolobinemia - antibodi IgM - paling bahaya anti-A dan anti-B spesifik dari sistem ABO - fatal akibat perdarahan tidak terkontrol dan gagal ginjal

REAKSI HEMOLITIK
REAKSI EKSTRAVASKULAR: - jarang sehebat reaksi intravaskular - reaksi fatal jarang - disebabkan antibodi IgG destruksi eritrosit via makrofag - menimbulkan penurunan tiba triba kadar Hb s/d 10 hari pasca transfusi