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INTRODUCTION Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure

due to inadequate circulating volume and subsequent inadequate perfusion .1 The main cause of hypovolemic shock is hemorrhage, however, understanding other cause of hypovolemic shock, in this case burn trauma, is essential in clinical setting. Fire-related deaths still rank fifth in the leading causes of unintentional injury-related deaths. But, improvements in burn care, i.e., quality of burn centers, recognition and effective management of burn shock, has reduced the number of deaths from fires and burns since the 1960s.2 The treatment of hypovolemic shock in burn trauma not only given by emergency doctor, but also rescue personnel at accident of fire scene. They have to own the capability to do initial treatment include immobilization of cervical spine, lifting the legs 12 inchess off the ground, giving oxygen, and cold water treatment to the victims. Advanced life support is also important in case of prolonged refered time (i.e., more than 30 minutes).2 Rescue personnel have to give fluid resuscitation before referal. Those interventions might seem less important than hospital care, but they can prevent the irreversible stage of hypovolemic shock which lead to death.1

HYPOVOLEMIC SHOCK IN PATIENT WITH BURN TRAUMA DEFINITION AND ETIOLOGY Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion.1 Hypovolemic shock can be caused by any disorder that causes volume depletion of the intravascular space. Typical causes are hemorrhage, acute volume losses (e.g., diarrhea, vomiting), capillary leak and burns. Patients with hypovolemic shock initially are able to compensate for the decreased stroke volume with compensatory increases in heart rate and systemic vascular resistance. This leads to the characteristic clammy extremities, and oligouria. Another findings on physical examination and basic laboratory testing are diminished skin turgor, dry skin and mucosa, hypotension, low urine sodium levels and high urine osmolarity, and a high serum urea nitrogencreatinine ratio (20:1).3 In patient with burn trauma, because vessels in burned tissue exhibit increased vascular permeability, an extravasation of fluids into the burned tissue occurs. Hypovolemia is the immediate consequence of this fluid loss, which accounts for decreased perfusion and oxygen delivery. This leads to hypovolemic shock.4 EPIDEMIOLOGY Shock accounts for more morbidity and mortality worldwide. Morbidity may be widespread and can include renal failure, brain damage, gut ischemia, hepatic failure, metabolic derangements, diffuse intravascular coagulation, acute respiratory distress syndrome, cardiac failure, and death. Hypovolemic million deaths annually worldwide.5 For burn injuries, its incidence varies from country to country, typically peaking during the country's holiday period. In the 1940's, hypovolemic shock or shockinduced renal failure was the leading cause of death after burn injury. In 2007, the World Fire Statistics Centre released fire-related death data by country (from lowest to highest number of deaths per 100,000 person) from 2002-2004. The countries with shock alone result in 6-20

the lowest incidences include Singapore (0.08) and Switzerland (0.51). Those with the highest include Finland (2.08) and Hungary (2.10).2 Although fire-related deaths still rank fifth in the leading causes of unintentional injury-related deaths, the number of deaths from fires and burns has declined since the 1960s. Improvements in burn care (ie, quality burn centers, recognition, and effective management of burn shock) have reduced the number of deaths in the early postburn period.2

PATHOPHYSIOLOGY Hypovolemic shock results from an absolute deficiency of intravascular blood volume. Physiologycally, rapid loss of intravascular volume reduces ventricular preload, resulting in decreased stroke volume and cardiac output and, thus, decreased oxygen and substrate delivery.1 As cells are starved of oxygen and substrate, they can no longer sustain efficient aerobic oxygen production. Aerobic metabolism generates 36 ATP molecules per glucose molecule. As oxygen delivery (DO2) is impaired, the cell must switch to the much less efficient anaerobic metabolic pathway, which generates only 2 ATP molecules per molecule of glucose, with resulting production and accumulation of lactic acid. Eventually, cellular metabolism is no longer able to generate enough energy to power the components of cellular homeostasis, leading to the disruption of cell membrane ionic pumps, accumulation of intracelllular sodium with an efflux of potassium, and accumulation of cytosolic calcium. The cell swells, the cell membrane breaks down, and cell death ensues. Widespread cellular death results in multiple system organ failure and if irreversible, death.5 Physiologycally, three stages of hypovolemic shock are recognised, i.e., compensated, progressive or uncompensated, and irreversible. Compensated shock is when baroreceptor reflex result in increase in myocardial contractility, tachycardia and vasoconstriction. They maintain cardiac output and blood pressure and lead to the release of vasopressin, aldosterone, and renin. Progressive or uncompensated shock occurs with myocardial depression, failure of vasomotor reflexes and failure of the microcirculation, with increase in capillary permeability, sludging and

thrombosis, resulting in cellular dysfunction and lactic acidosis. Irreversible shock means failure of vital organs with inability to recover.6 In patient with burn trauma,whose burns exceed 30% of total body surface area, hypovolemic shock results from systemic inflammatory response which caused by the release of cytokines and other mediators into the systemic circulation. Vascular permeability in the site of burned tissue increases, an extravasation of fluids into the burned tissues occurs. Inordinate amounts of fluid are also lost by evaporation from the damaged surface that is no longer able to retain water. Hypovolemia which is the immediate consequence of these fluid loss, accounts for decreased perfusion and oxygen delivery. In patients with serious burns, release of catecholamines, vasopressin, and angiotensin causes peripheral and splanchnic bed vasoconstriction that can compromise in-organ perfusion. Myocardial contractility also may be reduced by the release of inflammatory cytokine tumor necrosis factor-alpha.4 The most common type of burns are thermal burns. Soft tissue is burned when it is exposed to temperatures above 1150F (460C). The extend of damage depends on surface temperature and contact duration. Direct thermal injury results in marked changes in the microcirculation. Most of the changes occur locally at the burn site, when maximal edema formation occurs at about 8-12 hours post-injury in smaller burns and 12-24 hours post-injury in major thermal injuries. The rate of progression of tissue edema is dependent upon the adequacy of resuscitation.7

SIGNS AND SYMPTOMS The symptoms may include the feeling of cold, unwell, anxious, faint and shortness of breath. There may be faintness on standing or even on sitting up, due to postural hypotension. There may be symptoms related to the cause of the hypovolemia, in this case burn wound.1 The signs that may presence are pale and sweaty appearance, tachypnoea, cold periphery due to poor perfusion, capillary refill time will be prolonged, however, this may be a poor indicator of hypovolemia. There will be tachycardia and a fall in blood pressure. Late features include confusion or even coma.1

Pulse rate, blood pressure, and core temperature should be recorded. Heat exhaustion may be associated with a rise in core temperature, requiring active cooling, and extensive burns are associated with loss of thermoregulatory ability. This means both excessive heat loss and reduced response of sweating when temperature rises.6 DIAGNOSES AND DIFFERENTIAL DIAGNOSES There are some tests that can be done in order to confirm the diagnoses of hypovolemic shock in general, i.e. through history, physical examination, and laboratory studies. The clinical history can determine the etiology of hypovolemic shock. In patient with burn trauma, if later, hypovolemia occurs during the course of management, it is caused by extravasation of fluids from intravascular to interstitial tissues adjacent to the burn wound. Patients may appear puffy and total-body fluid overloaded; however, they are actually significantly intravascularly depleted, with inadequate preload, and are in significant shock. Despite their overall edmatous appearance, such patients need even more fluid administration, in order to improve oxygen delivery and prevent or correct a state of shock.5 Shock, in this case hypovolemic shock, is a clinical physiologic diagnosis. The diagnosis of hypovolemic shock involves the clinical recognition that the body's tissues and cells are not receiving adequate delivery of oxygen and metabolic substrate. Symptoms and clinical findings are an extension of organs not getting what they need to function. A lack of kidney perfusion results in decreased urine output. If the brain's needs are not met, mental status changes occur. The lack of delivery of metabolic needs results in changes to gut and liver function.5 From laboratory studies, after the history is taken and the physical examination is performed, further workup depends on the probable cause of the hypovolemia, as well as on the stability of the patients condition. Initial laboratory studies should include analysis of the CBC, electrolyte levels (e.g., Na, K, Cl, HCO3, BUN, creatinine, glucose levels), prothrombin time, activated partial thromboplastin time, urinalysis (in patient with trauma), and a urine pregnancy test. Blood should be typed and cross-matched.1

In patient with burn trauma, laboratory tests is essential in confirming the presence of hypovolemia because they may serve as a baseline as the patient is likely to experience fluid shifts and electrolyte derangements shortly after the burn takes place. The tests are CBC count, chemistry profile (especially BUN and creatinine to determine renal function), liver function test, arterial blood gases with carboxyhemoglobin levels, coagulation profile, urine analysis, type and screen, creatine phosphokinase (CPK) and urine myoglobin levels; the presence of myoglobin can signify muscle breakdown as well as impending kidney impairment.2 Differential diagnoses of hypovolemic shock including other type of shock, i.e., anaphylactic shock, cardiogenic shock, neurogenic shock, or other disorders like cardiac tamponade and tension pneumothorax.1 TREATMENT The treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field. In patient with hypovolemic shock due to burn injury, the treatment in the prehospital setting should consist of immobilization of cervical spine, elevating the patients legs 12 inches off the ground and administering humidified oxygen. If rescue personnel have advenced life support capability and transport time may be prolonged, these treatments are complemented by intravenous (IV) fluid administration. Fluid resuscitation need not be initiated if patient is transported to the hospital in less than 30 minutes. When transport time is longer than 30 minutes, the indications for fluid resuscitation are thermal injuries involving greater than 20% of total body surface or evidence of burn shock.8 Cold water treatment also can be given to the patient. The beneficial effect of immediate cold water treatment of burned skin appear to be related to several factors. First, cold inhibits lactate production and acidosis, thereby promoting catecholamine function and cardiovascular homeostasis. Cold also inhibits burn wound histamine release, which in turn blocks local and remote histamine-mediated increases in vascular permeability. This minimizes edema formation and intravascular volume losses.4

In emergency department, the goals of treatment of the patient hypovolemic shock are maximize oxygen delivery-completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow and fluid resuscitation.1 After the airway is stabilized, establish intravenous access and begin fluid resuscitation. Begin 2 large-bore peripheral lines and administer crystalloids. With the loss of the vapor barrieer provided by intact skin, burn victims have large insensible fluid losses.

(2-4 cm3 of crystalloid) X (% body surface area burn) X (body weight in kg) Example: A man who weighs 70 kg and has a 30% BSA burn would require (30) X (70 kg) X (4 cm3/kg) = 8400 cm3 in the first 24 hours. One half of the calculated fluid requirement is administered in the first 8 hours, and the balance is given over the remaining 16 hours. Thus, fluids would be given at 525 cm3/h for the first 8 hours, then at 262.5 cm3/h for the remaining 16 hours.

Monitor typical markers of fluid status (eg, urine output) and adjust fluids accordingly. Placement of a Foley catheter simplifies monitoring of hourly urine output. Urine output should be maintained at 0.5 cm3/kg/h.

If the need is expected to exceed 6 mL/kg of the percentage of total body surface area burned per 24 hours, then the need arises to evaluate the intravascular volume with placement of a pulmonary artery catheter. If the volume is found to be adequate but urine output remains diminished, then dopamine (5 mcg/kg/min) may be used to increase renal perfusion.2

Another treatment that can be given is pharmacotherapy. The goals are to reduce morbidity and prevent complications. The agent that can be administered is antisecretory agents which have vasoconstrictive properties and can reduce blood flow to portal system, e.g., somatostatin (zecnil) and octreotide (sandostatin).1 PROGNOSIS AND COMPLICATION The prognosis is dependent on the degree of volume loss. Prognosis is worse in the elderly than in the young. Physical fitness improves outcome. Rapid and adequate

replacement of the circulating volume will prevent the complications of hypoperfusion, including renal failure, ischemic damage to the gut, brain damage and cardiac arrest. However, advanced stages of hypovolemic shock with a fluid loss of more than 25% of total body fluid are considered irreversible shock and are usually associated with a poor outcome or death.1

SUMMARY
1) Hypovolemic shock refers to a medical or surgical condition in which rapid

fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion.1 Hypovolemic shock can caused by hemorrhage, acute volume losses (e.g., diarrhea, vomiting), capillary leak and burns.3
2) Hypovolemic shock alone result in 6-2- million deaths annually worldwide.5

For burn injuries, from the date released by world Fire Statistics Centre in 2007, the fire-related death is the lowest in Singapore and Switzerland, the highest include Finland and Hungary.2
3) Pathologic condition in hypovolemic shock results from diminished

peripheral oxygen and substrate delivery. As oxygen delivery is impaired, the cell switch the aerobic metabolism into the much less efficient metabolism, anaerobic metabolic pathway, which generates only 2 ATP molecules per molecule glucose, with resulting production and accumulation of lactic acid. There will be no enough energy to power the components of cellular homeostasis, and cell death ensues, which in turn leads to multiple system organ failure and if irreversible, death.5 In patient with burn trauma, hypovolemic shock results from extravasation of fluid from intravascular into the adjacent interstitial tissues which caused by increased vascular permeability in burn tissues which exhibit systemic inflammatory response by the release of cytokines and other mediators into the systemic circulation.4 4) The signs of hypovolemic shock may include pale and sweaty appearance, tachypnoea, cold periphery, prolonged capillary refill time, tachycardia, and a fall in blood pressure. The symptoms that may presence are the feeling of cold, unwell, anxious, faint, and shortness of breath, faintness on standing, and symptoms related to the cause of the hypovolemia, in this case burn wound.
5) Tests to confirm hypovolemic shock in general are history, physical

examination, and laboratory studies. In patient with burn trauma, laboratory

tests which is essential in confirming the presence of hypovolemia are CBC count, chemistry profile (especially BUN and creatinine to determine renal function), liver function test, arterial blood gases, coagulation profile, urine analysis, creatinine phosphokinase and urine myoglobin levels.2
6) Treatment of hypovolemic shock in patient with burn trauma include

prehospital and hospital care. The prehospital setting should consist of immobilization of cervical spine, elevating the patients legs 12 inches off the ground and administering humidified oxygen. Cold water treatment is preferable. Fluid resuscitation need not be initiated if patient is transported to the hospital in less than 30 minutes.2 In emergency department, the goals of treatment of the patient with hypovolemic shock are maximize oxygen delivery, increasing oxygen saturation of the blood, and restoring blood flow and fluid resuscitation. The fluid given based on the formula of 2-4 cm3 of crystalloid per % body surface area burn times body weight. Pharmacotherapy agents which can be administered is antisecretory agents which have vasoconstrictive properties, e.g., somatostatin (zecnil) and octreotide (sandostatin).1
7) The prognosis is dependent on the degree of volume loss. Prognosis is worse

in elderly than in young. Rapid and adequate replacement of the circulating volume will prevent the complications.1

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BIBLIOGRAPHY
1

Paul Kolecki, Carl R Menckhoff. Shock, Hypovolemic. eMedicine. [cited

2010 July]. Available from: http://emedicine.medscape.com/article/760145overview.


2

Jamie Goodis, Erik D Schraga. Burns, Thermal, Emergency Medicine.

eMedicine. [cited 2009 December]. Available from: http://emedicine.medscape. com/article/769193-overview. 3 Stefan Herget-Rosenthal, Fuat Saner, and Lakhmir S. Chawla. Approach to Hemodynamic Shock and Vasopressors. Clin J Am Soc Nephrol. 2008;3:546553.
4

Richard F Edlich, David B Drake. Burns, Thermal, Plastic Surgery. [cited 2010 March]. Available from:

eMedicine.
5

http://emedicine.medscape.com/article/ 1278244-overview. Adam J Schwarz. Shock. eMedicine. [cited 2010 March]. Available from: 6 Gurvinder Rull. Resuscitation in Hypovolemic Shock. EMIS. [cited http://emedicine.medscape.com/article/1833578-overview.
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2010 February]. Available from: http://www.patient.co.uk/doctor/Resuscitationin-Hypovolaemic-Shock.htm. 7 Glenn D Warden. Total Burn Care. Elsevier Science. [cited 2001]. Available from: http://www.totalburncare.com/tbcbookpage8.htm. 8 Prem C Shukla, Robert L Sheridan. Initial Evaluation and Management of the Burn Patient. eMedicine. [cited 2008 February]. Available from: http://emedicine.medscape.com/article/435402-overview.

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