BTCLS: BASIC TRAUMA, CARDIAC AND LIFE SUPPORT: May 2018

WOUNDS AND BLEEDING

A. Wounds

The wound is the loss / partial damage of body tissues.

Various sores:

• Vulnus scissum (wound cut)

• Vulnus punctum (stab wound)

• Vulnus laseratum (tear wound)

• Excoriation (blisters / friction)

• Combostio (burns) Ethylogy:

• Sharp / dull object trauma

• Temperature changes

• Chemicals

• Explosion

• Electric shock

• Animal bites

The next phase is tissue damage, then healing. Phase of healing:

• Phase of Inflammation

It lasts from the wound until about the 5th day. PD that breaks in the wound will cause bleeding and the body will try to stop it with vasoconstriction, PD shrinking disconnected, and hemostatic reactions. Hemostatis occurs because the platelets that come out of the PD stick together and together fibrin net formed freeze blood coming out of the PD, while an inflammatory reaction occurs.

Mast cells in connective tissue produce serotonin and histamine which increase capillary permeability resulting in fluid exudation. Inflammation of the inflammatory cell with local vasodilation resulting in edema and swelling.

• Proliferative phase

It lasts from the end of the inflammatory phase until approximately the end of week 3. This phase of the fibers is formed and destroyed again for adjustment to the tension wound which tend to shrink. This property is along with the fibroblast's contractive properties. This phase of the wound is filled with inflammatory cells, fibroblasts, collagen forming a reddish tissue with a smooth surface called granulation tissue. The epithelial wound comprising a basal cell is detached from its base and displaces the surface of the wound. The place is then filled by new cells formed from the process of mitosis. The process of migration can only occur towards the lower / flat, because the epithelial can not migrate to the higher direction. This process only stops after epithelial cells touch each other and cover the entire surface of the wound. With the closed surface of the wound, the fibroplasia process with the formation of granulation tissue will also stop and begin the process of maturation in the phase of the end

• End of phase

There is a maturation process consisting of excessive tissue absorption, shrinkage in accordance with the force of gravity and ultimately resurfacing of newly formed tissue, this phase may last for months and is declared ended if all signs of inflammation have disappeared.

NO PHASE PROCESS SYMPTOMS AND SIGNS

1. Inflammation Reaction of Dolor, rubor, calor, tumor

2. Prolefiration Regeneration / fibroplasia Network granulation / bone callus. Epithelial closure / endotel / mesotel

3. termination Maturation and re-closure of scar tissue / fibrosis

Classification of healing:

• Secondary healing (sanatio persecundam intentioem) wound healing without external help

• Primary cure (sanatio perprimam intentioem) wounds are linked.

B. Bleeding

Bleeding is the discharge of blood from the blood vessels

Type of bleeding

1. Artery (blood looks out spray, fresh red)

2. Veins (blood flow out, blackish)

3. Capillaries (blood out seeps, fresh red)

Action on bleeding

Stop the bleeding

• Pressing on one point from 6 points on one side of the body

• Direct emphasis on wounds (with clean sterile fabrics)

• Coat press

• Torniquet only on amputation / as life saving

Replace the lost blood

Blood component

1. Complete Blood

2. Packed red blood cells

3. Washed red cells

4. Fresh plasma

5. Fresh frozen plasma

6. Platelet rich plasma

7. Platelet concentrat

8. Cryoprecipitate

Non Clotting Class

• Packed red blood cells (which contain red and 1/3 plasma blood grains, so they are not pure components).

• Washed red cells (which contain red blood grains and electrolytes) are cleaner than packed red cells.

• Frozen red cells (which are cleanest and can be stored long and also red blood remained like frozen time, should be worn within 24 hours after being heated, expensive).

• Plasma protein fraction (plasma reduced gamma globulin, with pasteurization hazard hepatitis absent).

• Albumin (this component is in isoosmotic and hypercotic forms). • leukocytes (only made at complete transfusion centers).

• Immunoglobulins (tetanus immunoglobulin germs) are known by the name of hypertet trade.

Clotting Group

• Fresh frozen plasma (contains all blood clotting factors, except thrombocyte).

• Cryoprecipitate (factor i and viii only)

• Platelet rich plasma (containing all clotting factors coupled with platelets).

• Platelet concentrate (containing platelets and factor ii, v, vii, ix, x).

C. Complications

• Overload volume

• Plebitis

• Air Emboli

• Disease transmission

• Bacterial contamination

• Allergy

• Hyperpyrexia

• Metabolic

Signs of Hemolytic Complications

• Incompatibility of class A, B, O from donors and recipients.

• Rapid reactions that should be watched first 30 minutes / 50cc first with signs: fever, pruritis, chills, headache, chest and hip pain, breathlessness, nausea, vomiting, diarrhea, hypotension, hemoglobinuri and diffuse bleeding.

• Slow reaction after several hours / weeks is anemia, jemas, jaudice

• Best prevention o Stop transfusion o Overcome hypotension o Overcome bleeding

o Prevent anuria

Causes of allergy

• Patients who have often received transfusions become allergic to serum proteins.

• Leucocytes and platelets of donors have other antigens from red blood.

• Maybe donor blood contains allergic antibodies.

Hyperpyrexis

The causes are not clear, can be by pyrogens, the reaction of some components of blood and leukocytes and platelets. Long lasting blood changes

• The affinity of hb to o2 increases. Because in the blood more 5 days occurred 2.2 dpg depletion.

• The presence of citric acid and the formation of lactic acid the blood becomes acidic.

• K concentration ranges from 30 mlgr / l more than normal, K out of red blood into plasma.

• Old blood transfusion can cause cardiac arrhythmias and arestia. Higher hb affinity and lower ph can damage the kidney causing hyper K to be great. The image in the blood of the donor will bind calcium recipients and this hypocalcemia state will intensify hyperkalemia against the heart.

• Old blood may appear bad ammonia if it is given to a circulatory patient.

• The platelet count after 1 day is zero and at week 3 the v and vi factor is only 10%.

The wrong habit

• Transfusion of 1 bottle to pursue anesthesia requirements with hb ≥ 10gr%.

• Fresh blood use in patients without hemostatic disturbance.

• High temperatures are not contra-indicative transfusions

• Blood need not be heated first, except on massive transfusion.

BIOMEKANICA TRAUMA

Understanding

Traumatic biomechanics is the study of the incidence of injury to a particular type of violence or accident. For example, people falling from a motorcycle will cause different injuries compared with people who were hit by a car.

Traumatic biomesias are important to know because they will help in:

- The consequences will be generated

- Be aware of the type of injury caused by trauma.

While the type of injury can be divided into visible surface (visible) for example, wounds on the outside. And injuries that cannot be seen directly, eg internal organ injuries. The organs in the body can be divided into:

- Hollow organs (solid, solid), eg: liver, spleen, lung, brain - Hollow organs such as intestines

Treat the organs in the event of an injury mechanism:

a. Direct injury

For example, the head beaten hammer. The scalp may tear and cause external bleeding, the bone of the head may be cracked or broken, or may result in bleeding in the brain

b. Injury due to retarding force (deceleration)

For example, a motorcyclist had a traffic accident that hit a tree. After the body stops in the tree, the internal organs will still move forward in their respective cavities. The heart will be detached from its bond (aorta) and aortic rupture occurs. The intestines will tear apart from the mesentery and so on.

c. Injury due to acceleration force (acceleration)

For example: motorists hit from behind.

d. Compression injury (paper bag effect)

For example: children's toy is a blowing paper bag, then closed, then hit to get explosive effect. This can also occur in cavity organs that can be ruptured by pressure

Car Crashes

Collisions can occur by:

a. From front (frontal)

In a frontal collision with a patient without a seat belt will be impacted by several phases:

- Phase 1

The bottom of the patient is shifted forward, usually the knee will hit the dashboard. Thigh bone will hold the bebab too heavy consequence if not strong hold can cause broken.

The hip joint is pushed backward, if it is not strong enough to withstand the burden, the hip joint may escape from its bowl.

- Phase 2

The top of the patient also shifts forward, in this phase the chest or stomach will hit the steering wheel. Under these circumstances chances are that the injury may be chest or abdomen, depending on the steering wheel of the vehicle there where (the type of car).

If a small car may be exposed to the chest, if the car is likely to affect its stomach, may also be chest and abdominal injury, in this case the helper should be careful in doing the examination.

- Phase 3

The body of the patient will go up, then to hit the windshield. In this phase that should be suspected is the injury in the head or neck of the patient

- Phase 4

Patients bounce back to the seat. In this phase the possibility of injury resulting from a vertebral fracture (from the cervical bone to the sacrum). In the type of vehicle that does not wear headbands (head rest) should be careful possible injury whips (whiplash injury) on the neck bone. While the most severe possibility in this phase of the patient can bounce off the vehicle, and more serious injuries (multi trauma)

b. From behind

A rear-end collision may occur on a stop vehicle or on a slower-speed vehicle. Common injuries are usually due to whiplash injury and injuries to watch out for are injuries in the neck area, let alone the vehicle does not wear headrest.

c. From the side (lateral)

Frequent side collisions at crossroads with no traffic signs. Injuries that can occur on the side of the vehicle hit, which can be from head to toe depending on the type of vehicle that crashed and who was hit.

d. Reversed

A slowly reversed vehicle and the driver or passenger on a seat belt rarely suffer serious injuries, as with a roll over vehicle, especially if the passenger does not wear a seat belt, can result in injury in all parts (multi trauma). In handling such cases should be more careful because all parts can be injured both visible and invisible. On the incident

with the vehicle upside down to watch out for are spinal cord injuries and internal organ injuries.

Vehicle Protection Tool

1. Seat belts

This seat belt has been proven to be very helpful to the passengers, seat belts can reduce injury, disability or death caused by accidents in the vehicle. Although wearing a belt does not mean to avoid injury, the possibility of injury still exists, but wearing a seat belt can reduce the injury caused by collisions or accidents especially in the use of the seat belt is wrong or not in place.

Use of seat belts on a car vehicle

commonly used are three points ie one point in the shoulder area, two points in the left and right pelvic region. If there is a four-point, two dots on the left and two on the right, on the right, while on an airplane the seat belt is usually worn with two dots attached to the pelvis, and also the four points commonly used by pilots fighter. The use of a proper seat belt can still cause injury, especially if pemakainnya wrong.

For example, if the use is wrong, the seat belt is installed in the stomach, then the stomach of soft organ can be ruptured, due to the pressure of the safety belt (seat belt). Removing the seat belt should also be careful, do not let go immediately, because the seat belt itself can be a tampon in the event of bleeding caused by the impact with the coir. If you open it suddenly the seat belt that has been as a tampon and bleeding already hooked up can be open again and there will be re-bleeding.

Vehicles traveling at 60 km / h, if the frontal collision and rider do not use seat belts, then a rider will hit the front of the vehicle, tantamount to the person feel free from the 3rd floor of the building.

2. Head rest (headrests)

The headrest is now standard equipment in the car. The use of the backrest is as a support / holding the head so that the neck is not injured. The use of the headrests should also be correct in position, if not true headrests could hurt the neck passengers. For example, headrests mounted not exactly on the back of the head but mounted under the head just at the back of the neck, in the event of a head collision nobody hold, while the neck stuck by the back, consequently the neck to be injured.

3. Air bag (airbag)

Air bag is currently only in luxury cars, in the form of an airbag placed at the centre of the wheel and will expand if there is a frontal collision. In some types of vehicles there are currently airbags located on the side that will expand during impact from the side.

The front air bag develops when it is frontal, can cause injuries such as fracture of the arm, injury to the face, injury to the eyes for wearing glasses and so on, while the air bag on the side will expand when the impact from the side. Possible injuries to the side from head to toe, depending on which direction the impact and what part of the body is affected.

Must be careful to help the patient whose water bag is not open yet, not to inflate at an unwanted moment. To avoid this the way is to turn off the electric current on the vehicle (the engine is turned off). In the water bag itself there is a powder that melaluri water bag, which functions to make the water bag does not occur adhesive, the powder is very irritative, especially in people who are sensitive to powder, if untouched rinse with clean water.

Trauma Biomechanics in Motor Beam

There are 3 ways that often occur at the time of accident:

1. Frontal collision

At the frontal collision, the driver will hit the front. Both limbs will hit the handlebars, which may cause the fracture of one or both thighs or lower leg bones. After that the driver will experience a "free fall", with injuries that cannot be predicted.

2. Collision from the side

Usually what happens here will knock is the foot first, after which the driver will bounce with the type of injury that cannot predict / prediction.

3. Sliding down the bike (shifted)

In the event of a collision, the driver deliberately (professional) or accidentally pressed his bike down, so the bike will speed and the driver behind him. This causes the slightest injury, but injuries to soft tissue can be very heavy if the biker does not wear a thick jacket and pants. This traumatic wound does not cause death.

Vehicle Protection Tool

1. Seat belts

Use of seat belts on a car vehicle

commonly used are three points ie one point in the shoulder area, two points in the left and right pelvic region. If there is a four-point, two dots on the left and two on the right, on the right, while on an airplane the seat belt is usually worn with two dots attached to the pelvis, and also the four points commonly used by pilot’s fighter. The use of a proper seat belt can still cause injury, especially if pemakainnya wrong.

2. Head rest (headrests)

3. Air bag (airbag)

Air bag is currently only in luxury cars, in the form of an airbag placed at the center of the wheel and will expand if there is a frontal collision. In some types of vehicles there are currently airbags located on the side that will expand during impact from the side.

Protective equipment on motor vehicles

a. Helmets

- The type of helmet should be correct

- Usage must be correct

- Be careful when removing

b. Water jacket bag

SHOCK AND LIQUIDS THERAPY (ELECTROLYTE)

A. SHOCK

Shock is a condition in which the blood supply is insufficient for the needs of organs in the body. Shock is also defined as a circulatory disorder that results in a critical decrease in the perfusion of vital tissue or a decreased circulating blood volume effectively. In animals with shock, there is a decrease in tissue perfusion, delayed delivery of oxygen, and cell metabolic disorders resulting in insufficient energy production by cells. If the cells can not produce energy adequately, then the cell will not function properly so that in turn will lead to dysfunction and failure of various organs, eventually can cause death.

In less severe shock, body compensation may include increased heart rate and peripheral vascular constriction (both reflexes), so that it can maintain peripheral resistance and blood flow to vital organs. When shock gets worse, this compensation will fail.

Shock type

Shock is classically divided into three categories, namely cardiogenic, hypovolemic, and distributive shock. Cardiogenic shock occurs when the heart fails to function as a pump to maintain adequate cardiac output. Dysfunction can occur at the time of sistole or diastole or may be the result of obstruction. Sistole failure or blood drainage may be caused by a dilated cardiomyopathy that causes poor contractility, or toxins / drugs that cause depression or myocardial damage. Diastole failure or cardiac filling may be due to hypertrophic cardiomyopathy resulting in poor preload, regurgitation such as valve defect, tamponad or pericardial fibrosis resulting in poor preload, or severe arrhythmias resulting in poor preload and takeficient contractility.

1. Hypovolemic shock

occurs when there is a blood volume deficit of ≥15%, resulting in insufficient oxygen delivery and nutrients to the tissues and buildup of cell metabolism remnants. Reduced intravascular volume may result from acute or chronic body fluid loss, eg oligemia, haemorrhage, or fire.

2. Distributive Shock

caused by maldistribution of blood flow due to peripheral vasodilation so that circulating blood volume is effectively inadequate for tissue perfusion. Peripheral vasodilation results in relative hypovelemia. The classic example of distributive shock is septic shock. However, the state of vasodilation due to other factors can also lead to distributive shock, such as heat stroke, anaphylaxis, neurogenic shock, and systemic inflammatory response syndrome (SIRS). Septic shock is a common complication found in small animal practices and is reported to be the most common cause of death in non-cardiac intensive care units.

3. Cardiogenic shock

is the inability of the heart to drain enough blood to the tissues to meet the needs of basal membolism due to impaired heart pump function.

4. Obstructive shock

is the shock caused by filling disorders in the right and left ventricle which in severe bias condition leads to decreased Cardiaac Output. This can occur in cava vein obstruction, pulmonary embolism, pneumothorax, pericardium disorders (eg cardiac tamponade) or atrial myxoma.

Etiology

The specific etiology of shock is unknown, but shock may occur due to serious stress, such as severe trauma, heart failure, bleeding, burning, anesthesia, severe infection, intestinal obstruction, anemia, dehydration, anaphylaxis, and intoxication.

Clinical Sign

Clinical signs of shock vary depending on the cause. In general, clinical signs may include apathy, weakness, pale mucous membrane, poor pulsus quality, rapid respiration, low body temperature, low blood pressure, slow capillary refill time, tachycardia or bradycardia, oliguria and hemoconcentration (except in hemorrhage ).

Low arterial pressure, pale mucous membrane, slow capiilarity refill time (CRT) (> 2 seconds), low or normal rectal temperature, tachypnea, and cold extremities are the hallmarks of cardiogenic and hypovolemic shock. To distinguish cardiogenic shock with hypovolemic shock requires complete anamnesis and heart evaluation.

Patients with initial septic shock, mucous membranes may still be red, CRT rapid (<1 sec), tachycardia, fever, and feel warm to the touch. In subsequent development, the mucous membrane appears "cloudy," the CRT progresses slowly (> 2 s), the pulsus becomes weak, and the extremities become cold. A unique picture occurs in distributive shock in cats that often show bradycardia rather than tekicardia.

Handling

The goal of early shock handling is to restore tissue perfusion and oxygenation by restoring blood volume and blood pressure. In a further stage of shock, the return of tissue perfusion alone is usually not enough to stop the development of inflammation, so it is necessary to eliminate toxic factors that are primarily caused by bacteria.

Giving oxygen is a very common treatment, regardless of the cause of shock. Other therapies depend on the cause of shock. Liquid therapy is the most important therapy for patients with hypovolemic and distributive shock. Intravenous fluid administration improves circulating blood volume, decreases blood viscosity, and increases venous blood flow, thus helping to improve cardiac output.

The next result is to increase tissue perfusion and provide oxygen supply to the cells. Initial therapy may be either crystalloid or colloidal administration. In hypovolemic animals with normal heart function, Ringer's lactate or Ringer acetate fluids are rapidly administered. The recommended dose for shock is 90 ml / kg IV for dogs and 60 ml / kg IV for cats. A quarter of this amount is given for the first 5-15 minutes and at the same time an evaluation of the cardiovascular response (heart rate, mucous membrane color, pulsus quality, and CRT) is evaluated.

Colloids or plasma at a dose of 22 ml / kg in dogs and 10-15 ml / kg in cats are used for shock resuscitation. The speed and volume of fluid therapy should be tolerable by the individual patient. The speed and amount of fluid administration is monitored at central venous pressure and urinary expenditure.

If tissue perfusion is reduced due to loss of blood, ideally a blood transfusion should be done at a rate not exceeding 22 ml / kg in IV and bleeding control should be performed well. If PCV decreases acutely to below 20%, red packed red blood cell transfusion or total blood significantly improves blood pressure and oxygen delivery to the tissues.

In cardiogenic shock, fluid therapy that is too fast can be fatal because it will increase the workload of the heart and further endanger the circulation. Cardiogenic shock therapy depends on the cause. If shock is caused by poor myocardial contractility, a beta-agonist is recommended. Dobutamine is a betaagonist capable of increasing cardiac output and oxygen delivery, without causing vasoconstriction, the most commonly used drug to improve cardiac function. If an animal is being given a drug that suppresses myocardium (eg anesthesia), then the administration of the drug should be stopped. Pericardiocentesis should be performed if pericardial effusion is sufficient and causes tamponad.

In distributive shock if hypotension persists despite adequate fluid therapy, vasopressor administration is required. Since cardiac output and systemic vascular resistance affect oxygen delivery to the tissues, hypotensive patients should be used to maximize heart function with fluid and inotropic therapy, and / or modify vascular tone with vasopressor agents.

The use of glucocorticoids to treat shock is controversial. However, when used, glucocorticoids should be used in treatment and not repeated. Prednisolone is recommended at a dose of 22-24 mg / kg in IV. Other rapid-acting glucocorticoid available in parenteral form is dexamethasone sodium phosphate, recommended at a dose of 2-4 mg / kg in IV.

Septic shock is often associated with gram-negative bacteria, and antibiotics suitable for it such as sepalosporin or aminoglycosides and penicillins. When using aminoglycosides, the animal must be in a good hydration state, because aminoglycosides can cause nephrotoxicity. Animals that are getting shock handling should continue to be monitored. Two very important factors to monitor are blood pressure and volume. As a guide to therapy, cardiovascular parameters may be used (heart rate, mucous membrane color, pulsus quality, CRT, central venous pressure), respiratory rate, temperature, hematocrit, and urinary expenditure. To evaluate fluid therapy in shock due to hemorrhage it is important to measure PCV (packed cell volume) and TS (total solid). Blood pressure in the blood is very important in the determination and monitoring of acid-base balance.

B. LIQUID THERAPY (ELECTROLITE)

Management of patients with electrolyte and fluid disorders requires an understanding of the composition of fluids in the body, compartments and metabolism of water and electrolytes. Most of the body composition is water, almost 60% in men and 50% in the female body is water. The total amount of water is referred to as total body water (TBW). TBW is divided into two parts of volume, namely extracellular fluid volume (ECF) and intracellular fluid volume (ICF).

The ECF is defined as all the fluids in the body that are outside the cell. ECF is divided into plasma fluids and interstitial fluids. Normally ECF is 40% of TBW. Intracellular fluid (ICF) is defined as the volume of fluid present in the cell. ICF reaches 60% of TBW. The water balance is maintained by altering the intake and water expression. Intake is controlled by thirst, while the water excretion is controlled by the kidney through the hormone ADH (anti diuretic hormone). The fluid requirement is determined by weight. On average it takes 25-30 cc / kg body weight per day.

In principle fluid therapy includes resuscitation and maintenance therapy.

TERAPI CAIRAN

RESUSITASI

PERAWATAN

Kristaloid

Koloid

Elektrolit

Nutrisi

Penggantian cairan yang hilang secara akut (perdarahan, diare dll

1. Penggantian normal loss (IWL, urine, faecal)

2. Support Nutrisi

Liquid Resuscitation

Liquid management is a fault and management error can be fatal. To maintain fluid balance, the fluid input should be the same to replace the lost fluid. Iru fluids include water and electrolytes. The purpose of fluid therapy is not to perfect balance, but to save lives by reducing mortality.

Bleeding a lot (hemorrhagic shock) will cause interference with cardiovascular function. Hypovolemic shock because bleeding is a further result. In such circumstances, improving the general state by overcoming the shock that occurs can be done by giving fluids electrolytes, plasma or blood.

For improved circulation, the main step is to seek adequate venous flow. Start by giving a saline infusion or isotonic lactate ringer. Previously, take ± 20 ml of blood for routine laboratory examination, blood type, and if necessary cross test. Severe haemorrhage is a life-threatening emergency. If the hemoglobin is low then the best replacement fluid is infusion.

Rapid fluid resuscitation is the foundation for hypovolemic shock therapy. The source of blood or fluid loss must be immediately known in order to take action immediately. Intravenous fluids should be given at sufficient speed to quickly overcome the deficit or fluid loss from shock. Common causes of hypovelemia are bleeding, loss of plasma or other body fluids such as burns, peritonitis, prolonged gastroenteritis or emesis and acute pancreatitis.

Intravenous Fluid Maintenance

Crystalloids are a balanced salt solution that is free to pass through the endothelial capillaries and will experience a quick balance with extravascular fluids, for example NaCl, RL, Asering, and others.

Colloid is a liquid solution containing larger molecules that will provide oncotic pressure so that it will last in the intravascular longer if compared with crystalloid.

The choice of fluid should be based on the patient's hydration status, electrolyte concentrations, and existing metabolic abnormalities. Various parental solutions have been developed according to the physiological needs of various medical conditions. But intravenous fluids or infusions are one of the most crucial aspects of patient handling and care. The initial therapy of the hypotensive patient is resuscitation fluid by using 2 liters of Ringer's Lactate isotonic solution. However, Ringer's Lactate is not always the best fluid for resuscitation. Adequate fluid Resuscitation can normalize blood pressure in kombustio patients 18-24 hours after burn injury.

Parental solutions in hypovolemic shock are classified as crystalloid, colloid and blood. The crystalloid fluid is good enough for hypovolemic shock therapy. The advantages of crystalloid fluids are, among others, readily available, cheap, easy to use, does not cause allergic reactions, and few side effects. Excess crystalloid fluid in administration may continue with edema throughout the body so overuse should be prevented. A isotonic NaCL solution is recommended for early treatment of hypovolemic shock with hyponatremic, hypochlorine or metabolic alkalosis. The RL solution is the isotonic solution most closely resembling the extracellular fluid. RL can be safely administered in large amounts to patients with conditions such as Hypovolaemia with metabolic acidosis, kombustio, and shock syndrome. 0.45% NaCl in 5% Dextrose solution is used as a temporary liquid to replace insensible fluid loss.

Ringer acetate has a similar profile to Ringer's Lactate. Place lactate metabolism mainly is the liver and a small part of the kidney, while acetate in the metabolism in almost all body tissues with muscles as the most important place. The use of Ringer Acetate as a resuscitation fluid should be given to patients with severe liver dysfunction such as liver cirrhosis and lactic acidosis. The presence of lactate in the solution of Ringer Lactate endanger the severely ill patients as converted in the liver to bicarbonate. Simply stated, the purpose of the fluid therapy is divided into resuscitation to replace acute fluid loss and maintenance to replace daily requirements.

Electrolyte

1. Hyponatremia

Hyponatremia is an electrolyte disorder (interference in the salt in the blood) where the plasma concentration of sodium is lower than normal, especially below 135 mmol / L. Most cases of hyponatremia occur in adult outcomes of excess amount or the effects of water retention hormone known as the usual ADH antidiuretic hormone abbreviated.

Hyponatremia most often is a complication of other medical illnesses in which either a sodium-rich liquid is lost (eg due to diarrhea or vomiting), or excess water accumulates in the body to a higher level than can be excreted (eg in polydipsia (rare) or hormon syndrome inappropriate antidiuretic, SIADH). Regarding the loss of sodium as the cause of hyponatremia, it is important to note that these losses promote hyponatremia only in an indirect way. In particular, hyponatremia occurring in association with sodium loss does not reflect adequate sodium availability as a result of the loss. In contrast, loss of sodium causes a volume depletion state, with volume depletion serving as a signal for ADH release. As a result of ADH-stimulated water retention, blood sodium becomes the result of diluted and hyponatremia.

There may also be false hyponatremia (pseudohyponatremia or artificial hyponatremia) if other substances expand serum and dilute sodium (eg, high blood sugar (hyperglycemia) or if blood constituents lead to the creation of a sodium-free phase in the blood causing excessive blood plasma volume

(eg extreme hypertriglyceridemia).

Hyponatremia can also affect athletes who consume too much fluid during endurance events, fasting people in juice or water for long periods and people who diet sodium intake is chronic enough.

The diagnosis of hyponatremia depends primarily on examination, clinical and blood medical history and urine testing. Treatment may be directed to the cause (eg, corticosteroids in Addison's disease) or involves limiting intake of water, intravenous salts or drugs such as diuretics, demeclocycline, urea or vaptans (antidiuretic hormone receptor antagonists). Improving the salt and fluid balance needs to be done in a controlled manner, as too rapid correction may lead to severe complications such as heart failure or sometimes irreversible brain lesions known as central pontine mielinolysis.

2. Hypernatremia

Hypernatremia (high blood sodium levels) is a condition where the sodium content in the blood is more than 145 mmol / L of blood. Hyponatremia is caused by excess fluid and sodium depletion. Sodium depletion may result from inadequate intake or excessive loss. Hypernatremia is an increase in sodium concentration almost always caused by water depletion and the loss of extracellular fluid can also be caused by a rarely excessive sodium intake.

Hypernatremia is treated with fluid administration. In all cases, especially mild cases, fluids are administered intravenously (via an IV). To help determine whether fluid purchases are sufficient, blood tests are performed every few hours. Blood sodium concentration is slowly lowered, because over-rapid repair can cause damage to permanent brain damage.

Blood tests or additional urine are done to determine the cause of high sodium concentration. If the cause has been found, it can be treated more specifically. For example for diabetes insipidus given antidiuretic hormone (vasopresin).

3. Hypokalemia

Defined as serum potassium levels of less than 3.5 mmol / l, resulting from a lack of fluid intake, increased fluid loss from the kidneys or gastrointestinal tract. Clinical symptoms that arise: body weakness, depression, constipation, ileus, respiratory failure, ventricular tachycardia, atrial tachycardia. Therapy, among others, with KCL scrambled or IV. Intravenous administration of KCL does not exceed 40 mmol / l.

4. Hyperkalemia

It is potassium levels greater than 5 mmol / l, resulting from excessive potassium intake, severe tissue damage such as burns, or reduced excretion.

Clinical manifestations are: weakness, paresthesias, flacyd paralysis, hypotension and brachardia. ECG picture is obtained T wave elevation.

Treatment includes causes and hemodialysis. Management of life-threatening hyperkalemia namely:

a. IV dextrose, 50 g with 20 U insulin

b. IV calcium chloride 10% 5 - 10 ml

c. IV sodium bicarbonate 50 - 100 ml

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HYPERNATREMIA

AIR DEFICIT → (water entry << & water expenditure >> many)

Correction: Normal TBW x 140 = TBW now X Na + plasma now

TBW = Total Bpody Water

Male = 60%

Women = 50%

Normal Na + = 135-145 meg / lt

Sample case:

Suppose a male patient, weight 70 Kg, Na Plasma is now 160 meg.

TBW = 60% X 70

(60% x 70) X 40 = TBW skg X 160

TBWskg (42 X 140) / 160 = 36.75

Water deficit = TBW normal - TWB skg

42 lt - 36.75 lt = 5.25 lt.

HYPOTERMIA

Excess water from Na

Water >> Na

Correction: TBW X (Na + desired - Na + actual)

Sample case:

Eg A female patient, 60 kg body weight, Na + now 110meg / lt, Na + desired 130 meg / lt

TBW = 50% X 60

Correction = (50% X 60) X (130-110) = 600 meg / lt

If; 1 liter NaCl 0.95 contains 154 meg / lt, it is required 600/154 lt NaCl 0.9% = 3.8 lt NaCl 0.9%

If; 1 liter NaCl 0.3% contains 500 meg / lt, it is required 600/500 lt NaCl 3% = 1,2 Lt NaCl 3%

If the correction density is 0.5 meg / lt / hr, then ((130-110)) / 0.5 X 1 hour = 40 h

HYPOKALEMIA

K + <3.5 meg / lt

Giving per oral (K> 3 meg / lt)

Dose 75 mg / KgBB

Administration = 0.3 X KgBB X desisit K

Given within 24 hours

K +> 5.3 meg / lt

KgBB= Kg Body Wight

Treatment:

K serum> 7 meg / lt

EKG = DBN

Therapy= Kayexalate oral or rectal / gr / KgBB.

ECG = Normal

It is recommended bicnat 1-2 meg / KgBB

Intravenous à 5-10 minutes.

Or continue glucose 0.5 -1 g / KgBB à intravenously à 15-30 min + insulin 0.1 IU / KgBB à subcutaneous or intravenous à monitor blood sugar

ECG = Arrhythmias

Add Ca Gluconas 10% à 0.5 - 1ml / KgBB / intravenous à 2-5 minutes

Monitor ECG

Prepare for Dialysis

TERAPI CAIRAN



	RESUSITASI			PERAWATAN



Kristaloid		Koloid	Elektrolit		Nutrisi



Penggantian cairan yang hilang secara akut (perdarahan, diare dll			1. Penggantian normal loss (IWL, urine, faecal) 2. Support Nutrisi