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HEMORRHAGIC SHOCK Shock is a momentary pause in the act of dying CASE FOR DISCUSSION 27 y.o. construction worker fell from the 17 feet ladder. He was brought to ER by paramedics. On arrival, his BP-105/55, HR-130, O2Sat-97(Face mask). He is agitated, blood in the mouth, right ankle open fx., head laceration. QUESTIONS 1.Differential diagnosis? 2.What are you going to do first? 3.Is patient in shock? WHAT IS SHOCK? A medical condition, not a diagnosis. Types: Hypovolemic (Hemorrhagic) Cardiogenic Distributive Obstructive TYPES OF SHOCK More then 100 types of shock have been described. -classified by the cause of the syndrome -two or more types are often combined hypovolemia may occur with septic shock hemorrhagic shock, combined with neurogenic shock The 3 essential patterns of circulatory shock I II III SHOCK REGARDLESS OF CLASSIFICATION THE UNDERLYING DEFECT IS ALWAYS INADEQUATE TISSUE PERFUSION!!!!!! SHOCK SYNDROM Shock is a condition in which the CV system fails to perfuse tissues adequately. An impaired cardiac pump,circulatory system, and/or volume can lead to compromised BF to tissues. Inadequate tissue perfusion can result in: -generalized cellular hypoxia(starvation) -widespread impairment of cellular metabolism -tissue damage>organ failure>death DIAGNOSIS OF SHOCK MAP<60 Clinical s/s of hypoperfusion of vital organs ECG changes Mental disturbances Drop in UO Jaundice etc. CAUSES OF HYPOVOLEMIC SHOCK Anything that causes rapid fluid loss -Most commonly rapid blood loss. -Also be caused by fluid loss. diarrhea,vomiting,water deprivation, third spacing ets. HEMORRHAGIC SHOCK Caused by the loss of both circulating blood volume and oxygen carrying capacity. PATHOPHISIOLOGY OF HYPOVOLEMIC SHOCK Impaired tissue perfusion is the result of imbalance between cellular O2 supply and cellular O2 demand. PATHOPHISIOLOGY Acute hemorrhage results in activation of following compensatory mechanisms: -Hematologic(coagulation) -Cardiovascular -Renal(increase renin production) -Neuroendocrine(ADH release) COMPENSATORY MECHANISMS Sympathetic Nervous System Response. Acute hemorrhage results in a decreased CO and BP, which is sensed by receptors in the aortic arch and atrium. – Stimulated by baroreceptors Increasing HR Increasing contractility Vasoconstriction (SVR-Afterload) Increased preload COMPENSATORY MECHANISMS Mediated by renin-angiotensin system Decreasing renal perfusion Activation of renin-angiotensin system Angiotensin II is a very potent vasoconstrictor IN ADDITION Aldosteron released by adrenal cortex produces sodium and water retention COMPENSATORY MECHANISMS Mediated by antidiuretic hormone Osmoreceptors in hypothalamus stimulated ADH released by posterior pituitary gland – Vasopressor effect – Acts on renal tubules to retain water COMPENSATORY MECHANISMS Mediated by adrenal cortex Anterior pituitary releases adrenocorticotropic hormone (ACTH) ACTH stimulates adrenal cortex to release glucocorticoids Blood sugar increase to meet increased metabolic needs – In addition hyperglycemia is caused by glucagon and growth hormone- induced increase in gluconeogenesis and glycogenesis. Circulating catecholamines inhibit insulin release and activity, leading to increased plasma glucose. COMPENSATORY MECHANISMS In addition, the brain has remarkable autoregulation that keeps cerebral BF constant over a wide range of blood pressures The kidneys can tolerate a 90% decrease in total BF for short period of time With decreases in circulatory volume, intestinal BF is reduced by splanchnic vasoconstriction. FAILURE OF COMPENSATORY RESPONSE Decreased blood flow leads to cellular hypoxia→ cells switch for anaerobic from aerobic metabolism→ lactic acid production→ cell swells (function ceases) membrane becomes permeable→ electrolytes and fluids seep in and out of cells→ Na+/K+ pump impaired, mitochondria damage, cell death. STAGES OF SHOCK Compensated shock Decompensated shock Irreversible shock STATES OF SHOCK Compensated shock – Decreased tissue perfusion, but the body’s compensatory responses overcome the decrease in intravascular volume – CO and l BP are normal due to adrenal compensatory response STAGES OF SHOCK Compensated Shock – RR and TV increase (this is a result of metabolic acidosis, caused by tissue hypo perfusion and chemoreceptors activation) – Acidosis is decreased by of hyperventilation STAGES OF SHOCK Sympathetic stimulation – Constriction of veins leading to ↑ BP and ↑ CO (increased preload) – ↑ HR and ↑ contractility – Arterial constriction leading to ↑ PVR (peripheral vasoconstriction-cool skin) – Bronchodilatation (improved air exchange) STAGES OF SHOCK Compensated shock Progression of shock to microcirculation produces a sequence of changes in capillary perfusion Oxygen delivery to the cells supplied by these capillaries decreased → anaerobic metabolism ↓ leaky capillary syndrome ↓ A-V shunts open in the skin, muscles, GI tract, to causing less flow to the arterials and less flow through capillaries ↓ Blood is shunted to the heart, brain, and kidneys Stages of Shock Compensated shock – If the underlying cause of shock is untreated the compensatory mechanisms eventually collapse. STAGES OF SHOCK Decompensated Shock – Marked increase in HR – BP and CO decrease – Blood flow to critical organs drops ↓UO Altered mental status ECG changes STAGES OF SHOCK Decompensated Shock – As the shock continues, the precapillary sphincters relax with expansion of the vascular space and capillary engorgement STAGES OF SHOCK Decompensated shock – Hypotension and closing of the A-V shunts results in more BF through capillaries. More of capillary engorgement. STAGES OF SHOCK Decompensated Shock – Increased hypoxemia and acidosis lead to additional vasodilatation. The vascular bed expands greatly. STAGES OF SHOCK Decompensated Shock – The capillary and venule capacity may become great enough to reduce the volume of available blood for the great veins. Decreased venus return and a fall in CO STAGES OF SHOCK Decompensated shock – The viscera (lungs, kidneys, and GI mucosa) become congested due to stagnant blood flow. STAGES OF SHOCK Decompensated shock – The respiratory system attempts to compensate for the acidosis by increasing ventilation to blow off CO2 Partially compensated metabolic acidosis STAGES OF SHOCK Decompensated Shock – Clotting mechanisms are also affected: hypercoagulability (DIC) – This stage progresses to irreversible shock if fluid resuscitation is inadequate STAGES OF SHOCK Irreversible shock – Systolic and diastolic pressure drop. – Pulse pressure narrows to the point of no detection. STAGES OF SHOCK Irreversible shock – S/S. Bradicardia Dysrhythmias Hypotension Evidence of multiple organ failure Pale, cold and clammy skin Noticeably delayed capillary refill STAGES OF SHOCK Irreversible shock – Myocardial contractility decreases from ischemia secondary to A reduction of Hb A reduction in SO2 A reduction in coronary perfusion Myocardial necrosis STAGES OF SHOCK Irreversible shock – DIC – Pulmonary capillaries become permeable leading to pulmonary edema Absorption of O2↓ Elimination of CO2↓ ARDS STAGES OF SHOCK Irreversible shock – Multiple organ failure Usually hepatic failure occurs, followed by renal failure and heart failure GI bleeding and sepsis may result from GI mucosal necrosis Pancreatic necrosis may lead to further clotting disorders and severe pancreatitis VARIATIONS IN RESPONSE TO SHOCK Hemorrhagic shock is tolerated differently depending on – Pre-existing physiological state – Age HEMORRHAGIC SHOCK IN CHILDREN Pediatric patients have smaller blood volumes and, therefore ,are at risk to lose a proportionately greater percentage of blood on an equivalent-volume basis. HEMORRHAGIC SHOCK IN CHILDREN The kidneys of children younger then 2 years are not mature; they have blunted ability to concentrate solute. The body surface area is increased relative to the weight, allowing for early hypothermia, leading to coagulopathy. HEMORRHAGIC SHOCK IN ELDERLY Elderly people may have both altered physiology and may pre-existing medical conditions that may severely impair their ability to compensate for acute blood loss. HEMORRHAGIC SHOCK IN ELDERLY Atherosclerosis and decreased elastin cause arterial vessels to be less compliant leading to blunted vascular compensation, decreased cardiac arteriolar vasodilatation and infarction. HEMORRHAGIC SHOCK IN ELDERLY Older patients are less able to mount a tachycardia in response to decreased stroke volume because of: – decreased beta-adrenergic receptors in the heart – Decreased effective volume of pacing myocytes within the SA node – These patients are treated with a variety of cardiac meds that may blunt the physiological response to shock HEMORRHAGIC RESPONSE IN ELDERLY Many older patients have significantly decreased creatinine clearance in the presence of near-normal serum creatinine. Concentrating may be impaired by relative insensitivity to ADH ASSESMENT OF HEMORRHAGIC SHOCK S/S vary depending on severity of fluid loss: 15%[750ml]- compensatory mechanism maintains CO 15-30% [750-1500ml- Hypoxemia, decreased BP & UOP 30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis 40-50% - refactory stage: Clinical Classification of Shock EVALUATION/HISTORY Obtaining a clear history of the type, amount, and duration of bleeding is very important. Many decisions are based on knowing the amount of blood loss that has occurred over a specific time period EVALUATION/HISTORY 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 Inquire about hematemesis, melena, drinking history, NAID use, coagulopathies EVALUATION/HISTORY 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 Closed femoral fx fractures can cause major bleeding into the tissues Scalp lacerations are notorious for causing large underestimated blood loss EVALUATION/HISTORY If GYN cause is being considered, gather information about the following – Last menstrual period – Risk factors for ectopic pregnancy – Vaginal bleeding – Vaginal passage of products of conception – Pain EVALUATION/PHYSICAL Differences exist between medical patients and trauma patients The very nature of shock dictates how difficult or impossible is to find a pathognomonic sign/symptom which is is invariably associated with the presence of shock Remember BP and HR are unreliable indicators of rapid deterioration in trauma patients Most important is the trend of the pulse and BP EVALUATION/PHYSICAL (MEDICAL PATIENTS) The general appearance of a patient in shock is very dramatic. The skin will have a pale, ashen color, usually with diaphoresis. The patients may appear confused or agitated and may become obtunded EVALUATION/PHYSICAL (MEDICAL PATIENT) The pulse first becomes rapid and then becomes dampened as the pulse pressure diminishes. Systolic BP may be in the normal range during compensated shock EVALUATION/PHYSICAL (MEDICAL PATIENT) 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. The abdominal examination searches for signs of abdominal bleeding (distention, pain with palpation, and dullness to percussion) EVALUATION/PHYSICAL (MEDICAL PATIENT) The flanks are inspected for ecchymosis, a sign of retroperitoneal bleeding. Ruptured aortic aneurisms can present with shock, palpable pulsatile mass in the abdomen, scrotal enlargement from retroperitoneal blood tracking, diminished femoral pulses. Rectum is inspected for internal or external hemorrhoidal bleeding. Patients with vaginal bleeding undergo full pelvic examination, including pregnancy test to rule out ectopic pregnancies EVALUATION/PHYSICAL (TRAUMA PATIENT) Primary survey is a quick exam to identify life threatening problems – Airway (ask the patients name. If answers clearly the airway is patent) – Oral pharynx is inspected for blood/foreign bodies – Neck inspected for hematomas/ tracheal deviation – Lungs inspected for pneumo/hemothorax – Radial and femoral pulses – Quick inspection to rule out any external sources of bleeding – Gross neurological examination (AVPU- alert, response to voice, response to pain, unresponsive) EVALUATION/PHYSICAL (TRAUMA PATIENT) The secondary survey is a head to toe careful examination to identify all injuries. DON’T FORGET In the patient with trauma, hemorrhage is usually the presumed cause of shock. However it must be distinguished from other causes of shock – Cardiac tamponade (muffled heart tones, distended neck veins) – Tension pneumothorax (deviated trachea, decreased breath sounds) – Spinal cord injury (warm skin, lack of expected tachycardia, neurological deficits EVALUATION/LAB STUDIES Generally, lab 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 occur are a result of replacing a large amount of blood with fluids. EVALUATION/LAB STUDIES Hb and hct unchanged from baseline immediately after acute blood loss. During the course of resuscitation, the hct may fall secondary to crystalloid infusion and re- equilibration of extracellular fluid in the intravascular space. No absolute threshold hct/Hb level that should prompt transfusion exists. (Physician’s judgment/patient’s comorbidity) EVALUATION/LAB STUDIES Arterial blood gas is the most important lab value in the patient with severe shock – Acidosis is the best indicator of ongoing O2 imbalance at the tissue level. – A pH < 7.25 may begin to interfere with catecholamine action and cause hypotension unresponsive to inotropes. – Metabolic acidosis must be treated aggressively. – Life threatening acidemia (pH < 7.2) initially may be buffered by the administration of sodium bicarbonate (be aware that no survival benefit to this practice has been documented). EVALUATION/LAB STUDIES Coagulation studies produce normal results in the early course Electrolyte studies are not helpful in the acute setting. After massive resuscitation: – Na and chloride may increase with administration with large amounts of isotonic sodium chloride. Hyperchloremia may cause a non-ion gap acidosis and worsen an existing acidosis. – Ca levels may fall w/ large volume blood transfusion – K levels may rise with large volume blood transfusion EVALUATION/LAB STUDIES A blood specimen for type and cross should be obtained on arrival. For patients who are actively bleeding 4 U of PRBC and 4 U of FFP should be prepared. Platelets may be obtained depending on physicians judgment. EVALUATION/IMAGING STUDIES Chest X-ray (useful to dx. Hemothorax/pneumothorax) Abdominal x-rays are not helpful CT scan (sensitive and specific for dx. Intrathoracic, intra- abdominal, and retroperitoneal bleeding). Ultrasound is rapidly replacing CT scan as the diagnostic test of choice for ID of hemorrhage in major body cavities. EGD is the test of choice for upper GI bleeding Colonoscopy is used to diagnose acute lower GI bleeding. Angiography is one of the best tests to localize a bleeding source. Diagnostic peritoneal lavage. TREATMENT Medical care of hemorrhagic shock consists of resuscitation. The resuscitation should occur before, or concurrently with any diagnostic studies. The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care. TREATMENT 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). 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 the injury is a good practice. TREATMENT Crystalloid is the first fluid of choice for resuscitation. Fluid administration should continue until the patient’s hemodynamics becomes stabilized. Because crystalloids leak from the vascular space, 3 liters of fluid need to rise the intravascular volume by one liter. TREATMENT Alternatively, colloids restore volume in 1:1 ratio. Current colloids include human albumin, hydroxy-ethyl starch products, and hypertonic saline-dextran combinations. Hydroxy-ethyl starch product in large volumes has been associated with coagulopathy. TREATMENT PRBC’s should be transfused if the patient remains unstable after 2-3 liters of crystalloid resuscitation. – Blood n crystalloid infusions should be delivered through the fluid warmer. – Patients who require large amounts of transfusion inevitably will become coagulopathic (consider platelets and FFP) TREATMENT Intravenous access and fluid resuscitation are standard.However it has become controversial. For many years,agressive fluid administration has been advocated.Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions. TREATMENT Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage,disloge clots and dilute existing clotting factors. Findings from animal studies support these postulates. TREATMENT These provocative results raise possibility that moderate hypotension may be physiologically protective and should be permitted. TREATMENT These findings should not yet be clinically extrapolated.Permissive hypotension in humans remains speculative. TREATMENT Surgical care (just in general) – 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 be EGD – Severe vaginal bleeding should prompt early involvement of GYN Ectopic pregnancies are treated with immediate surgery Abruptio placenta is a true emergency and should prompt c-section – Consultation with a hematologist is essential when coagulopathy fails to be corrected with standard measures. (He may offer gamma-globulin infusion, plasmapheresis, or large-volume clotting factor repletion). COMPLICATION OF HEMORRHAGIC SHOCK Patients often are unable to mount bone marrow response in the acute setting. Using erythropoieten is useful. This strategy has been successful in decreasing RBC transfusions in multicenter trials in Canada Acute tubular necrosis Acute lung injury Transfusion related acute lung injury Infections (nosocomial and related to operative sites or indwelling catheters). Multiple organ dysfunction The cascade of systemic inflammatory response syndrome (SIRS) progressing to organ failure will complicate 30-70% of patients with hemorrhagic shock Death PROGNOSIS OF HEMORRHAGIC SHOCK Related to the ability to be resuscitated from shock as well as the underlying illness or injury, not the presentation of hemorrhagic shock.
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