Advanced Trauma Life Support_Journal@2011

Hemorrhagic Shock

Hemorrhagic Shock
Author : John Udeani, MD, FAAEM Assistant Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science, University of California, Los Angeles, David Geffen School of Medicine ,
Chief Editor : John Geibel, MD, DSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital

Background
Hemorrhagic shock is a condition of reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function. Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock. On a multicellular level, the definition of shock becomes more difficult because not all tissues and organs will experience the same amount of oxygen imbalance for a given clinical disturbance. Clinicians struggle daily to adequately define and monitor oxygen utilization on the cellular level and to correlate this physiology to useful clinical parameters and diagnostic tests. The 4 classes of shock, as proposed by Alfred Blalock, are as follows:[1] Hypovolemic Vasogenic (septic) Cardiogenic Neurogenic

Hypovolemic shock, the most common type, results from a loss of circulating blood volume from clinical etiologies, such as penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding. Humans are able to compensate for a significant hemorrhage through various neural and hormonal mechanisms. Modern advances in trauma care allow patients to survive when these adaptive compensatory mechanisms become overwhelmed.

Pathophysiology
Well-described responses to acute loss of circulating volume exist. Teleologically, these responses act to systematically divert circulating volume away from nonvital organ systems so that blood volume may be conserved for vital organ function. Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure. These changes are sensed by baroreceptors in the aortic arch and atrium. With a decrease in the circulating volume, neural reflexes 1

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cause an increased sympathetic outflow to the heart and other organs. The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain nonvital organs, such as the skin, gastrointestinal tract, and kidneys. Concurrently, a multisystem hormonal response to acute hemorrhage occurs. Corticotropin-releasing hormone is stimulated directly. This eventually leads to glucocorticoid and beta-endorphin release. Vasopressin from the posterior pituitary is released, causing water retention at the distal tubules. Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption. Hyperglycemia commonly is associated with acute hemorrhage. This is due to a glucagon and growth hormoneinduced increase in gluconeogenesis and glycogenolysis. Circulating catecholamines relatively inhibit insulin release and activity, leading to increased plasma glucose. In addition to these global changes, many organ-specific responses occur. The brain has remarkable autoregulation that keeps cerebral blood flow constant over a wide range of systemic mean arterial blood pressures. The kidneys can tolerate a 90% decrease in total blood flow for short periods of time. With significant decreases in circulatory volume, intestinal blood flow is dramatically reduced by splanchnic vasoconstriction. Early and appropriate resuscitation may avert damage to individual organs as adaptive mechanisms act to preserve the organism.

Epidemiology
Age Hemorrhagic shock is tolerated differently, depending on the preexisting physiologic state and, to some extent, the age of the patient. Very young and very old people are more prone to early decompensation after loss of circulating volume. Pediatric patients have smaller total blood volumes and, therefore, are at risk to lose a proportionately greater percentage of blood on an equivalent-volume basis during exsanguination compared to adults. The kidneys of children younger than 2 years are not mature; they have a blunted ability to concentrate solute. Younger children cannot conserve circulating volume as effectively as older children. Also, the body surface area is increased relative to the weight, allowing for rapid heat loss and early hypothermia, possibly leading to coagulopathy. Elderly people may have both altered physiology and preexisting medical conditions that may severely impair their ability to compensate for acute blood 2

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loss. Atherosclerosis and decreased elastin cause arterial vessels to be less compliant, leading to blunted vascular compensation, decreased cardiac arteriolar vasodilation, and angina or infarction when myocardial oxygen demand is increased. Older patients are less able to mount a tachycardia in response to decreased stoke volume because of decreased beta-adrenergic receptors in the heart and a decreased effective volume of pacing myocytes within the sinoatrial node. Also, these patients frequently are treated with a variety of cardiotropic medications that may blunt the normal physiological response to shock. These include beta-adrenergic blockers, nitroglycerin, calcium channel blockers, and antiarrhythmics. The kidneys also undergo age-related atrophy, and many older patients have significantly decreased creatinine clearance in the presence of near-normal serum creatinine. Concentrating ability may be impaired by a relative insensitivity to antidiuretic hormone. These changes in the heart, vessels, and kidneys can lead to early decompensation after blood loss. All of these factors in concert with comorbid conditions make management of elderly patients with hemorrhage quite challenging.

History
No single historical feature is diagnostic of shock. Some patients may report fatigue, generalized lethargy, or lower back pain (ruptured abdominal aortic aneurysm). Others may arrive by ambulance or in the custody of law enforcement for the evaluation of bizarre behavior. Obtaining a clear history of the type, amount, and duration of bleeding is very important. Many decisions in regard to diagnostic tests and treatments are based on knowing the amount of blood loss that has occurred over a specific time period. If the bleeding occurred at home or in the field, an estimate of how much blood was lost is helpful. For GI bleeding, knowing if the blood was per rectum or per os is important. Because it is hard to quantitate lower GI bleeding, all episodes of bright red blood per rectum should be considered major bleeding until proven otherwise. Bleeding because of trauma is not always identified easily. The pleural space, abdominal cavity, mediastinum, and retroperitoneum are all spaces that can hold enough blood to cause death from exsanguination. External bleeding from trauma can be significant and can be underestimated by emergency medical personnel. Scalp lacerations are notorious for causing large underestimated blood loss. Multiple open fractures can lead to the loss of several units of blood.

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Hemorrhagic Shock

Physical
The physical examination in patients with hemorrhagic shock is a directed process. Often, the examination will be paramount in locating the source of bleeding and will provide a sense of the severity of blood loss. Differences exist between medical patients and trauma patients in these regards. Both types of patients usually will require concurrent diagnosis and treatment. The hallmark clinical indicators of shock have generally been the presence of abnormal vital signs, such as hypotension, tachycardia, decreased urine output, and altered mental status. These findings represent secondary effects of circulatory failure, not the primary etiologic event. Because of compensatory mechanisms, the effects of age, and use of certain medications, some patients in shock will present with a normal blood pressure and pulse. However, a complete physical examination must be performed with the patient undressed. The general appearance of a patient in shock can be very dramatic. The skin may have a pale, ashen color, usually with diaphoresis. The patient may appear confused or agitated and may become obtunded. The pulse first becomes rapid and then becomes dampened as the pulse pressure diminishes. Systolic blood pressure may be in the normal range during compensated shock. The conjunctivae are inspected for paleness, a sign of chronic anemia. The nose and pharynx are inspected for blood. The chest is auscultated and percussed to evaluate for hemothorax. This would lead to loss of breath sounds and dullness to percussion on the side of bleeding. The abdominal examination searches for signs of intra-abdominal bleeding, such as distention, pain with palpation, and dullness to percussion. The flanks are inspected for ecchymosis, a sign of retroperitoneal bleeding. Ruptured aortic aneurysms are one of the most common conditions that cause patients to present in unheralded shock. Signs that can be associated with a rupture are a palpable pulsatile mass in the abdomen, scrotal enlargement from retroperitoneal blood tracking, lower extremity mottling, and diminished femoral pulses. The rectum is inspected. If blood is noted, take care to identify internal or external hemorrhoids. On rare occasion, these are a source of significant bleeding, most notably in patients with portal hypertension. Patients with a history of vaginal bleeding undergo a full pelvic examination. A pregnancy test is warranted to rule out ectopic pregnancy. Trauma patients are approached systematically, using the principles of the primary and secondary examination. Trauma patients may have multiple injuries 4

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Hemorrhagic Shock

that need attention concurrently, and hemorrhage may accompany other types of insults, such as neurogenic shock. The primary survey is a quick maneuver that attempts to identify life-threatening problems.

To assess the airway, ask the patient's name. If the answer is articulated clearly, the airway is patent. The oral pharynx is inspected for blood or foreign materials. The neck is inspected for hematomas or tracheal deviation. The lungs are auscultated and percussed for signs of pneumothorax or hemothorax. The radial and femoral pulses are palpated for strength and rate. A quick inspection is made to rule out any external sources of bleeding. A gross neurological examination is performed by asking the patient to squeeze each hand and dorsiflex both feet against pressure. Advanced trauma life support (ATLS) suggests that a "miniature" neurologic examination categorizes the patient's level of consciousness by whether the patient is alert, responds to voice, responds to pain, or is unresponsive (ie, AVPU). The patient then is exposed completely, taking care to maintain thermoregulation with blankets and external warming devices

The secondary examination is a head-to-toe, careful examination that attempts to identify all injuries.

The scalp is inspected for bleeding. Any active bleeding from the scalp should be controlled before proceeding with the examination. The mouth and pharynx are examined for blood. The abdomen is inspected and palpated. Distention, pain on palpation, and external ecchymosis are indications of intra-abdominal bleeding. The pelvis is palpated for stability. Crepitus or instability may be an indication of a pelvis fracture, which can cause life-threatening hemorrhage into the retroperitoneum. Long bone fractures are noted by localized pain to palpation and boney crepitus at the site of fracture. All long bone fractures should be straightened and splinted to prevent ongoing bleeding at the sites. Femur fractures are especially prone to large blood losses and should be immobilized immediately in a traction splint. Further diagnostic tests are warranted to diagnose intrathoracic, intraabdominal, or retroperitoneal bleeding.

Causes 5

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Hemorrhagic Shock

Hemorrhagic shock is caused by the loss of both circulating blood volume and oxygen-carrying capacity. The most common clinical etiologies are penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding.

Differentials Abdominal Trauma, Blunt Abdominal Trauma, Penetrating Abruptio Placentae Ampullary Carcinoma Angiodysplasia of the Colon Angiofibroma Angiosarcoma Aortic Dissection Benign Gastric Tumors Benign Neoplasm of the Small Intestine Bile Duct Tumors Biliary Trauma Bladder Trauma Blunt Chest Trauma Carcinoma of the Ampulla of Vater Cardiac Tamponade Colon Cancer, Adenocarcinoma Colonic Polyps Corpus Luteum Rupture Disseminated Intravascular Coagulation Diverticulosis, Small Intestinal Duodenal Ulcers Dysfibrinogenemia Dysfunctional Uterine Bleeding Ectopic Pregnancy Esophageal Varices Esophagitis Gastric Ulcers Gastritis, Acute Hemangioblastoma Hemangiomas, Hepatic Hemolytic Anemia Hemolytic-Uremic Syndrome Hemophilia, Overview Hemorrhoids Hemostatic Disorders, Nonplatelet Hemothorax 6

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Hemorrhagic Shock

Hypersensitivity Reactions, Immediate Immune Thrombocytopenic Purpura Inflammatory Bowel Disease Initial Evaluation of the Trauma Patient Intestinal Leiomyosarcoma Intestinal Perforation Intra-abdominal Sepsis Mallory-Weiss Tear Menorrhagia Myocardial Rupture Pancreatic Trauma Pancreatitis, Acute Penetrating Chest Trauma Penetrating Head Trauma Penetrating Neck Trauma Perioperative Anticoagulation Management Portal Hypertension Renal Artery Aneurysm Renal Trauma Septic Shock Shock, Distributive Splenic Rupture Toxic Shock Syndrome Trauma and Pregnancy Upper Gastrointestinal Bleeding

Laboratory Studies Generally, laboratory values are not helpful in acute hemorrhage because values do not change from normal until redistribution of interstitial fluid into the blood plasma occurs after 8-12 hours. Many of the derangements that eventually occur are a result of replacing a large amount of autologous blood with resuscitation fluids. Hemoglobin and hematocrit values remain unchanged from baseline immediately after acute blood loss. During the course of resuscitation, the hematocrit may fall secondary to crystalloid infusion and re-equilibration of extracellular fluid into the intravascular space. No absolute threshold hematocrit or hemoglobin level that should prompt transfusion exists. A hemoglobin concentration of less than 7 g/dL in the acute setting in a patient that was otherwise healthy is concerning only because the value most likely will drop considerably after re-equilibration. 7

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Hemorrhagic Shock

In the absence of preexisting disease, transfusions can be withheld until significant clinical symptoms are present or the rate of hemorrhage is enough to indicate ongoing need for transfusion. Patients with significant heart disease are at higher risk of myocardial ischemia with anemia, and transfusion should be considered when values drop below 7 mg/dL. Arterial blood gas may the most important laboratory value in the patient in severe shock. Acidosis is the best indicator in early shock of ongoing oxygen imbalance at the tissue level. A blood gas with a pH of 7.30-7.35 is abnormal but tolerable in the acute setting. The mild acidosis helps unload oxygen at the peripheral tissues and does not interfere with hemodynamics. A pH below 7.25 may begin to interfere with catecholamine action and cause hypotension unresponsive to inotropics. Although this is a time-honored concept, recent data do not find evidence of this phenomenon. Metabolic acidosis is a sign of underlying lack of adequate oxygen delivery or consumption and should be treated with more aggressive resuscitation, not exogenous bicarbonate. Life-threatening acidemia (pH < 7.2) initially may be buffered by the administration of sodium bicarbonate to improve the pH. However, be aware that no survival benefit to this practice has been documented. Coagulation studies generally produce normal results in the majority of patients with severe hemorrhage early in the course. The notable exceptions are patients who are on warfarin, low molecular weight heparin, or antiplatelet medications or those patients with severe preexisting hepatic insufficiency. If patients are unable to provide adequate medication histories, tests for primary and secondary hemostasis should be ordered. The prothrombin time (PT) and the activated partial thromboplastin time (aPTT) will identify major problems with secondary hemostasis. The best test for platelet function is the bleeding time. This test is difficult to perform in the patient with acute hemorrhage. An alternative is thromboelastography, which is at least equivalent, and possibly superior, to the bleeding time. This test is an ex vivo analysis of all of the components of clotting and has been used extensively in orthotopic hepatic transplantation, cardiac surgery, and trauma.

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Hemorrhagic Shock

Qualitative platelet dysfunction can be inferred in those patients with a clinical coagulopathy and normal PT and aPTT values. Obviously, abnormal PT or aPTT values should be corrected emergently in the context of severe hemorrhage. Electrolyte studies usually are not helpful in the acute setting. After massive resuscitation, certain abnormalities can occur. Sodium and chloride may increase significantly with administration of large amounts of isotonic sodium chloride. Hyperchloremia may cause a nonion gap acidosis and significantly worsen an existing acidosis. Calcium levels may fall with large-volume, rapid blood transfusions. This is secondary to chelation of the calcium by the ethylenediaminetetraacetic acid (EDTA) preservative in stored blood. Newer methods of blood banking avoid using EDTA, and the problem of hypocalcemia should be minimized. Likewise, potassium levels may rise with large-volume blood transfusions. Creatinine and blood urea nitrogen usually are within normal limits unless preexisting renal disease is present. Caution should be used when administering iodinated contrast in patients with elevated creatinine because the dye load could initiate a contrast-induced nephropathy in addition to chronic renal impairment. A blood specimen for type and crossmatch should be obtained as soon as the patient arrives. For patients who are actively bleeding, 4 U of packed red blood cells (PRBCs) should be prepared, along with 4 U of fresh frozen plasma (FFP). Platelets may be obtained as well, depending on the physician's estimation of the likelihood of the need for platelet transfusion (less commonly needed compared to FFP). Imaging Studies Imaging studies are aimed at identifying the source of bleeding. In many types of severe hemorrhage, therapeutic interventions, such as exploratory laparotomy, will preclude comprehensive diagnostic studies. Chest radiographs Chest radiographs indicate a diagnosis of hemothorax by showing a large opacity in one or both lung fields. Hemothoraces large enough to cause shock usually are obvious as a complete whiteout of one pleural space. Abdominal radiographs Abdominal radiographs are rarely helpful. Hemoperitoneum usually will not be visible on plain film. 9

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Occasionally, a radiograph will have a diffuse ground glass appearance, suggesting a large amount of intraperitoneal fluid, but this sign is not reliable. Rarely, a ruptured abdominal aortic aneurysm can be diagnosed by noting an incomplete shell (calcified wall) of a dilated aorta. Loss of the psoas shadow unilaterally also can suggest retroperitoneal blood. CT scan Computed tomography (CT) scan is sensitive and specific for diagnosing intrathoracic, intra-abdominal, and retroperitoneal bleeding. It is the test of choice for diagnosing bleeding in these cavities.

image 1. CT scan of a 26-year-old man after a motor vehicle crash shows a significant amount of intra-abdominal bleeding.

CT scan only has an adjunctive role in the diagnosis of GI bleeding when other tests have suggested a mass lesion as part of the disease process. Ultrasound is rapidly replacing CT scan as the diagnostic test of choice for the identification of hemorrhage in major body cavities. It is, of course, limited in its ability to evaluate the retroperitoneum. Retroperitoneal evaluation remains the purview of the CT scan. Esophagogastroduodenoscopy Esophagogastroduodenoscopy (EGD) is the test of choice for acute upper GI bleeding because it can provide a specific diagnosis and has therapeutic potential. Lavage the stomach with a large gastric tube before the procedure to remove as much clot as possible. 10

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Capabilities for epinephrine injection and bipolar circumactive probe (BICAP) cautery should be available. Aortoenteric fistulas are very rare and usually are caused by erosion of an aortic aneurysm into the duodenum. EGD may be able to diagnose this problem, but the false-negative rate in these cases is very high. Colonoscopy Colonoscopy is used to diagnose acute lower GI bleeding. It is considered by most to be difficult to perform in the acute setting and may fail to show the exact source of bleeding in cases of rapid hemorrhage. Although some experience exists with therapeutic interventions, such as cauterization for acute arteriovenous malformation bleeding, these techniques are not used widely. Ultrasound Ultrasound is a useful technique to diagnose intraperitoneal bleeding in the trauma patient. The focused abdominal sonographic technique (FAST) examination realistically has replaced diagnostic peritoneal lavage as the test of choice for identifying intraperitoneal fluid in the trauma patient. The FAST examination includes 4 anatomical views of the pericardium, abdomen, and pelvis that attempt to identify free intra-abdominal fluid. Bedside ultrasound can be performed by radiologists, surgeons, and emergency medicine physicians who have specialized training and certification. Angiography Angiography is extremely useful in the diagnosis of acute hemorrhage from many different sources. Its utility is limited by the availability of an angiographer on a timely basis. In cases of lower GI bleeding, angiography is one of the best tests to localize a bleeding source. Angiography usually can detect bleeding that is at least 1-2 mL/min. Selective angiograms of the celiac, superior mesenteric, and inferior mesenteric arteries are performed to locate the areas of bleeding. The best time to perform the examination is when the patient is actively bleeding. Once the source is identified, embolotherapy may be used as an acute means of arresting hemorrhage. This will allow resuscitation to proceed prior to operation. If embolotherapy is not used, then identifying the site of bleeding will allow a more limited bowel resection to be performed if surgery becomes indicated during the admission. 11

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Angiography can be used for diagnosis and management of severe bleeding from pelvic fractures. Although most bleeding from severe pelvic fractures is venous in origin, occasional significant arterial bleeding can be diagnosed and treated effectively with embolization. Severe liver injuries pose a challenge to the trauma surgeon because of the large amounts of blood loss and the difficulty in gaining surgical control quickly. Many severe liver injuries now are being diagnosed and treated with angiographic embolization. Angiography is increasingly considered first-line intervention (before laparotomy) for severe liver injuries in centers that are equipped to perform rapid angiography and angiographic intervention. Similar methods may be used for other solid organ injuries, such as the spleen and kidney. Angiography may be used in the diagnosis of massive hemoptysis of unclear etiology. Selective angiography of the bronchial arteries, combined with a selective pulmonary angiogram through a separate venous catheterization can localize bleeding. The role of angiography in upper GI bleeding is more limited. Hemobilia is a rare cause of upper GI bleeding. If blood definitely is observed emanating from the ampulla of Vater, angiography should be performed to localize and control the source of bleeding. Nuclear medicine scanning Nuclear medicine scanning can be used to localize GI bleeding. A tagged red blood cell scan may help differentiate upper from lower GI bleeding and may provide anatomic information, such as identifying bleeding from the right versus left colon. Overlap of structures will confound the utility and accuracy of this test. The test requires a significant amount of time to complete, but it is very sensitive, detecting bleeding as slow as 0.5 mL/min.

Procedures
Diagnostic peritoneal lavage is a bedside procedure that utilizes a small midline laparotomy and insertion of a catheter directly into the peritoneal cavity. Percutaneous insertion techniques are available but carry an increased risk of injury to underlying structures. The intent of diagnostic peritoneal lavage is to determine if significant intraabdominal bleeding or injuries to hollow organs are present. If more than 5 mL of blood is aspirated, the test result is said to be grossly positive and laparotomy usually is indicated. 12

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If blood is not aspirated, 1000 mL of warm lactated Ringers solution is infused into the abdomen and then allowed to drain out into the IV bag. The contents of the bag are examined in the lab. A red blood cell count of greater than 10,000 per LL is considered a microscopically positive test result. Other conditions that make the test results positive include the following: white blood cell count greater than 500/LL; high levels of amylase, lipase, or bilirubin; and particulate matter that may be from an intraluminal source. Central venous access Central venous access is considered an adjunct to large-bore (16- or 14-gauge) peripheral IV lines. Flow through a catheter is inversely proportional to the length and directly proportional to the diameter. Thus, long small-caliber lines, such as a standard triple lumen catheter, will deliver significantly less volume than a short largecaliber line, such as a peripheral IV. Large-bore (12F) central resuscitation lines This large-bore sheath introducer is used for volume resuscitation. Smaller sizes are less effective but are more effective than a standard multi-lumen central venous catheter. If significant intra-abdominal bleeding from a venous injury is suspected, volume lines should be avoided in the femoral veins. In general, access above and below the site of an injury is a good practice. This allows the operator to switch the primary resuscitation lines should one or more be ineffective or be positioned directly below an injury in the vessel in which the catheter resides. Chest tube The initial management of a hemothorax involves the insertion of a large-caliber chest tube for drainage, or open thoracotomy. In most patients with a hemothorax, tube thoracostomy alone is sufficient. Surgical exploration with open thoracotomy is mandated in the presence of persistent bleeding; the presence of more than 1500 mL of blood in the initial chest tube drainage; or drainage of more than 200 mL/h for 2-4 hours.

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Hemorrhagic Shock

Medical Care
The primary treatment of hemorrhagic shock is to control the source of bleeding as soon as possible and to replace fluid. In controlled hemorrhagic shock (CHS), where the source of bleeding has been occluded, fluid replacement is aimed toward normalization of hemodynamic parameters. In uncontrolled hemorrhagic shock (UCHS), in which the bleeding has temporarily stopped because of hypotension, vasoconstriction, and clot formation, fluid treatment is aimed at restoration of radial pulse or restoration of sensorium or obtaining a blood pressure of 80 mm Hg by aliquots of 250 mL of lactated Ringer's solution (hypotensive resuscitation). When evacuation time is shorter than 1 hour (usually urban trauma), immediate evacuation to a surgical facility is indicated after airway and breathing (A, B) have been secured ("scoop and run"). Precious time is not wasted by introducing an intravenous line. When expected evacuation time exceeds 1 hour, an intravenous line is introduced and fluid treatment is started before evacuation. The resuscitation should occur before, or concurrently with, any diagnostic studies. Crystalloid is the first fluid of choice for resuscitation. Immediately administer 2 L of isotonic sodium chloride solution or lactated Ringers solution in response to shock from blood loss. Fluid administration should continue until the patient's hemodynamics become stabilized. Because crystalloids quickly leak from the vascular space, each liter of fluid expands the blood volume by 20-30%; therefore, 3 L of fluid need to be administered to raise the intravascular volume by 1 L. Alternatively, colloids restore volume in a 1:1 ratio. Currently available colloids include human albumin, hydroxy-ethyl starch products (mixed in either 0.9% isotonic sodium chloride solution or lactated Ringers solution), or hypertonic saline-dextran combinations. The sole product that is avoided routinely in largevolume (>1500 mL/d) restoration is the hydroxy-ethyl starch product mixed in 0.9% isotonic sodium chloride solution because it has been associated with the induction of coagulopathy. The other products have not been so implicated. PRBCs should be transfused if the patient remains unstable after 2000 mL of crystalloid resuscitation. For acute situations, O-negative noncrossmatched blood should be administered. Administer 2 U rapidly, and note the response. For patients with active bleeding, several units of blood may be necessary. If at all possible, blood and crystalloid infusions should be delivered through a fluid warmer. A blood sample for type and cross should be drawn, preferably before blood transfusions are begun. Start type-specific blood when available. Patients who require large amounts of transfusion inevitably will become 14

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coagulopathic. FFP generally is infused when the patient shows signs of coagulopathy, usually after 6-8 U of PRBCs. Platelets become depleted with large blood transfusions. Platelet transfusion is also recommended when a coagulopathy develops. In a large, comprehensive cohort study by Levi et al, placebo-controlled trials of recombinant factor VIIIa (rFVIIa) were examined.[2] Off-label treatment with high doses of rFVIIa significantly increased the risk of arterial events but not venous thromboembolic events, especially among elderly patients.[3]

Surgical Care
The decision regarding whether to operate to control bleeding is complicated and beyond the scope of this article. Some generalities, however, may be advanced. Acute life-threatening bleeding within the abdominal or thoracic cavity is an indication for operation. Retroperitoneal bleeding is difficult to control operatively and generally is treated nonoperatively. Severe upper GI bleeds should be managed first by EGD, with the possibility of cauterizing or injecting the bleeding source with epinephrine. Failure of endoscopic management usually is an indication for surgery. Confirm the location of a lower GI bleed before operative intervention is performed. Severe vaginal bleeding should prompt early involvement of the gynecologist. Ectopic pregnancies are treated with immediate surgery. Abruptio placenta is a true emergency and should prompt immediate cesarean section.

Consultations
On occasion, consultation with a hematologist is essential. This is especially true if the coagulopathy fails to be corrected with standard measures. Increasingly recognized are the entities of heparin-induced thrombocytopenia and acquired antibodies to native clotting factors. Consultation is useful in identifying the correct tests to obtain, as well as the full range of useful modalities to correct the underlying defect. These may include IV gamma-globulin infusion, plasmapheresis, or, simply, large-volume clotting factor repletion.

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Further Inpatient Care

The remainder of care is determined by the proximate course of the hemorrhagic shock. Patients with hemorrhagic shock are at risk for acute tubular necrosis, acute lung injury, transfusion-related acute lung injury, infections (principally nosocomial and related to operative sites or indwelling catheters), and multiple organ dysfunction syndrome, with its attendant risk of death. Discussion of each of these entities is beyond the scope of this article.

Inpatient & Outpatient Medications

Patients with hemorrhagic shock are often unable to mount an appropriate bone marrow response in the acute setting with regard to red blood cell production. Using erythropoietin (40,000 U/wk) in combination with supplemental iron and vitamin C to boost production is useful. This strategy has been used successfully to decrease red blood cell transfusions in a large multicenter trial in Canada.

Transfer
in general, few indications exist to transfer a patient who is in shock to a specialized facility. Ideally, all hospitals and physicians should be prepared to initially treat and stabilize the patient with exsanguinating hemorrhage. After control of the bleeding and reversal of acute shock, patients may be transferred to facilities that can treat additional injuries. The patient should be transferred by an advanced life support unit with the capability of blood transfusion en route. The decision for air ambulance transport instead of ground transportation is one that involves consideration of proximity, difficulty with the ground route, time en route, weather conditions, and availability. Patients may be transferred for ongoing management of the initial injury when the injury complex demands care that exceeds the resources or capabilities of the initially receiving facility. This transfer should be made from the transferring physician to the receiving physician without intermediaries.

Complications
The primary complication is death. The entire spectrum of organ failures may be the sequelae of resuscitated hemorrhagic shock. The cascade of systemic inflammatory response syndrome (SIRS) progressing to multiple organ failure
syndrome (as described by the late Roger Bone, MD) complicates the cases of approximately 30-70% of patients who present with hemorrhagic shock and survive their initial resuscitation.

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Prognosis
Prognosis is related to the ability to be resuscitated from shock, as well as the underlying illness or injury, not the presentation of hemorrhagic shock. Patient Education For excellent patient education resources, visit eMedicine's Shock Centerand Public Health Center. Also, see eMedicine's patient education articlesShock and Cardiopulmonary Resuscitation (CPR).

Reference :
1. 2. 3. 4. 5. 6. 7. 8. 9. Blalock A. Principle of Surgical Care, Shock, and Other Problems. St Louis: Mosby; 1940. Levi M, Levy JH, Andersen HF, Truloff D. Safety of recombinant activated factor VII in randomized clinical trials. N Engl J Med. Nov 4 2010;363(19):1791-800. [Medline]. Aledort LM. Off-label use of recombinant activated factor VII--safe or not safe?. N Engl J Med. Nov 4 2010;363(19):1853-4. [Medline]. Ambrogi MC, Lucchi M, Dini P, et al. Videothoracoscopy for evaluation and treatment of hemothorax. J Cardiovasc Surg (Torino). Feb 2002;43(1):109-12. [Medline]. Barber AE, Shires GT. Cell damage after shock. New Horiz. May 1996;4(2):161-7. [Medline]. Brown MA, Casola G, Sirlin CB, et al. Blunt abdominal trauma: screening us in 2,693 patients. Radiology. Feb 2001;218(2):352-8.[Medline]. Butler K, Winters M. Shock: beyond the "golden hour". Emergency Medicine Reports. 2003;24:345356. Collins JA. The pathophysiology of hemorrhagic shock. Prog Clin Biol Res. 1982;108:529. [Medline]. Dizien O, Held JP, Eyssette M, et al. [Severe cranial trauma in the rehabilitation milieu. Management in the initial phase]. Rev Infirm. Mar 1993;43(5):33-8. [Medline].

10. Domsky MF, Wilson RF. Hemodynamic resuscitation. Crit Care Clin. Oct 1993;9(4):71526. [Medline]. 11. Falk JL, O'Brien JF, Kerr R. Fluid resuscitation in traumatic hemorrhagic shock. Crit Care Clin. Apr 1992;8(2):323-40. [Medline]. 12. Hollenberg SM. Cardiogenic shock. Crit Care Clin. Apr 2001;17(2):391-410. [Medline]. 13. Kemp SF. Current concepts in pathophysiology, diagnosis, and management of anaphylaxis. Immunol Allergy Clin North Am. 2001;21:611-634. 14. Ketcham EM, Cairns CB. Hemoglobin-based oxygen carriers: development and clinical potential. Ann Emerg Med. Mar 1999;33(3):326-37. [Medline]. 15. Kramer GC, Kinsky MP, Prough DS, et al. Closed-loop control of fluid therapy for treatment of hypovolemia. J Trauma. Apr 2008;64(4 Suppl):S333-41. [Medline]. 16. Krausz MM. Initial resuscitation of hemorrhagic shock. World J Emerg Surg. Apr 27 2006;1(1):14.

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Advanced Trauma Life Support_Journal@2011

Hemorrhagic Shock

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Published By : Rickky Kurniawan,MD (member of MedScape)