Shock Chapter 40 PDF

CHAPTER 40 Shock 157 of the patient. External support of oxygenation and ventilation may be provided by noninvasive ventilation methods (heated humidified high-flow nasal cannula, continuous positive air- CHAPTER 40 way pressure, biphasic positive airway pressure, or neg...

CHAPTER 40 Shock 157 of the patient. External support of oxygenation and ventilation may be provided by noninvasive ventilation methods (heated humidified high-flow nasal cannula, continuous positive air- CHAPTER 40 way pressure, biphasic positive airway pressure, or negative pressure ventilation) or through invasive methods (traditional Shock mechanical ventilation, high-frequency oscillatory ventila- tion, or extracorporeal membrane oxygenation). Elimination ETIOLOGY AND EPIDEMIOLOGY of CO2 is achieved through manipulation of minute ventilation Shock is the inability to provide sufficient perfusion of oxygen- (tidal volume and respiratory rate). Oxygenation is improved ated blood and substrate to tissues to meet metabolic demands. by altering variables that affect oxygen delivery (fraction of Oxygen delivery is directly related to the arterial oxygen con- inspired oxygen) or mean airway pressure (positive end- tent (oxygen saturation and hemoglobin concentration) and expiratory pressure [PEEP], peak inspiratory pressure, inspi- to cardiac output (stroke volume and heart rate). Changes in ratory time, gas flow). metabolic needs are met primarily by adjustments in cardiac output. Stroke volume is related to myocardial end-diastolic fiber length (preload), myocardial contractility (inotropy), and COMPLICATIONS resistance of blood ejection from the ventricle (afterload; see The major complication of hypoxic respiratory failure is the Chapter 145). In a young infant whose myocardium possesses development of organ dysfunction. Multiple organ dysfunc- relatively less contractile tissue, increased demand for cardiac tion includes the development of two or more of the follow- output is met primarily by a neurally mediated increase in ing: respiratory failure, cardiac failure, renal insufficiency/ heart rate. In older children and adolescents, cardiac output failure, gastrointestinal or hepatic insufficiency, disseminated is most efficiently augmented by increasing stroke volume intravascular coagulation, and hypoxic-ischemic brain injury. through neurohormonally mediated changes in vascular tone, Mortality rates increase with increasing numbers of involved resulting in increased venous return to the heart (increased organs (see Table 38.3). preload), decreased arterial resistance (decreased afterload), Complications associated with mechanical ventilation and increased myocardial contractility. include pressure-related and volume-related lung injury. Once the initial assessment of an acutely ill child is com- Both overdistention and insufficient lung distention (loss of pleted, the constellation of clinical characteristics can suggest functional residual capacity) are associated with lung injury. one of the five broad classifications of shock: hypovolemic, dis- Pneumomediastinum and pneumothorax are potential com- tributive, cardiogenic, obstructive, and dissociative. plications of both the disease process and iatrogenic over- distention. Inflammatory mediators may play a role in the development of chronic fibrotic lung diseases in ventilated HYPOVOLEMIC SHOCK patients. Acute hypovolemia is the most common cause of shock in children. It results from loss of fluid from the intravascu- lar space secondary to inadequate intake or excessive losses PROGNOSIS (vomiting and diarrhea, blood loss, capillary leak syndromes, Prognosis varies with the etiology of respiratory failure. Less than or pathologic renal fluid losses) (Table 40.1). Reduced blood 1% of previously healthy children with bronchiolitis die. Asthma volume decreases preload, stroke volume, and cardiac output. mortality rates, although still low, have increased. Population- Hypovolemic shock results in increased sympathoadrenal based studies report a variable mortality rate for pediatric ARDS activity, producing an increased heart rate and enhanced myo- from 18–35% depending on the study population. cardial contractility. Neurohormonally mediated constriction of the arterioles and capacitance vessels maintains blood pres- sure, augments venous return to the heart to improve preload, PREVENTION and redistributes blood flow from nonvital to vital organs. If Prevention strategies are explicit to the etiology of respi- hypovolemic shock remains untreated, the increased heart ratory failure. Some infectious causes can be prevented rate may impair coronary blood flow and ventricular filling, through active immunization against organisms causing while elevated systemic vascular resistance increases myocar- primary respiratory disease (pertussis, pneumococcus, dial oxygen consumption, resulting in worsening myocardial Haemophilus influenzae type b, seasonal influenza) and sep- function. Ultimately, intense systemic vasoconstriction and sis (pneumococcus, H. influenzae type b). Passive immuni- hypovolemia produce tissue ischemia, impairing cell metab- zation with respiratory syncytial virus immunoglobulins olism and releasing potent vasoactive mediators from injured prevents severe illness in highly susceptible patients (prema- cells. Cytokines and other vasoactive peptides can change turity, bronchopulmonary dysplasia). Primary prevention of myocardial contractility and vascular tone and promote traumatic injuries may decrease the incidence of pediatric release of other inflammatory mediators that increase capil- ARDS. Compliance with appropriate therapies for asthma lary permeability and impair organ function further. may decrease the number of episodes of respiratory failure (see Chapter 78). DISTRIBUTIVE SHOCK Distributive shock results from a relative inadequacy of intra- PEARLS FOR PRACTITIONERS vascular volume caused by venous or arterial vasodilation. This See The Acutely Ill or Injured Child: Pearls for Practitioners at maldistribution of blood flow can result in profound inade- the end of this section. quacies in tissue perfusion, even in the presence of a normal 158 SECTION 8 The Acutely Ill or Injured Child CARDIOGENIC SHOCK TABLE 40.1 |  lassification of Shock and Common C Underlying Causes Cardiogenic shock is caused by an abnormality in myocardial function and is expressed as depressed myocardial contractility PRIMARY and cardiac output with poor tissue perfusion. Compensatory CIRCULATORY mechanisms may contribute to the progression of shock by TYPE DERANGEMENT COMMON CAUSES depressing cardiac function further. Neurohormonal vasocon- Hypovolemic Decreased Hemorrhage strictor responses increase afterload and add to the work of circulating blood the failing ventricle. Tachycardia may impair coronary blood volume Diarrhea flow, which decreases myocardial oxygen delivery. Increased Diabetes insipidus, central blood volume is caused by sodium and water retention diabetes mellitus and by incomplete emptying of the ventricles during systole. Burns This results in elevated left ventricular volume and pressure, which then impairs subendocardial blood flow. As compen- Adrenogenital syndrome satory mechanisms are overcome, the failing left ventricle Capillary leak produces increased ventricular end-diastolic volume and pressure, which leads to increased left atrial pressure, resulting Distributive Vasodilation → Sepsis in pulmonary edema. This sequence also contributes to right venous pooling → decreased preload ventricular failure because of increased pulmonary artery pressure and increased right ventricular afterload. Maldistribution of Anaphylaxis Primary cardiogenic shock may occur in children who regional blood flow CNS/spinal injury have congenital heart disease. Cardiogenic shock also may occur in previously healthy children secondary to viral myo- Drug intoxication carditis, dysrhythmias, toxic or metabolic abnormalities, or Cardiogenic Decreased Congenital heart disease after hypoxic-ischemic injury (see Chapters 142, 145, and 147; myocardial see Table 40.1). contractility Arrhythmia Hypoxic/ischemic injuries OBSTRUCTIVE SHOCK Cardiomyopathy Obstructive shock results from mechanical obstruction of Metabolic derangements the great vessels or of the heart itself. The pathophysiology of Myocarditis obstructive shock can be classified according to the location of the obstruction within the vascular system in relation to the Drug intoxication heart. These extravascular, intravascular, or luminal obstruc- Kawasaki disease tions result in a shock state due to reduced cardiac outflow and the associated critical drop in global oxygen supply. Etiologies Obstructive Mechanical Cardiac tamponade of obstructive shock include both congenital lesions (such as obstruction to ventricular filling or Massive pulmonary coarctation of the aorta, interrupted aortic arch, and severe outflow embolus aortic valvular stenosis) and acquired diseases (such as pul- monary embolus and cardiac tamponade) (see Table 40.1). Tension pneumothorax Cardiac tumor DISSOCIATIVE SHOCK Dissociative Oxygen not Carbon monoxide appropriately poisoning Dissociative shock refers to conditions in which tissue perfu- bound or released Methemoglobinemia sion is normal, but cells are unable to utilize oxygen because from hemoglobin the hemoglobin has an abnormal affinity for oxygen, prevent- CNS, Central nervous system. ing its release to the tissues (see Table 40.1). or high cardiac output. Septic shock is the most common type CLINICAL MANIFESTATIONS of distributive shock in children. Other causes include ana- All forms of shock produce evidence that tissue perfusion and/ phylaxis, neurologic injury, and ingestion of certain drugs or or oxygenation are insufficient (increased heart rate, abnormal poisons (see Table 40.1). blood pressure, alterations of peripheral pulses). The etiology Distributive shock may present with the systemic inflam- of shock may alter the initial presentation of these signs and matory response syndrome (SIRS), defined as two or more symptoms. of the following: temperature greater than 38°C or less than 36°C; heart rate greater than 90 beats/min or more than two standard deviations above normal for age; tachypnea; or Hypovolemic Shock white blood cell count that is greater than 12,000 cells/mm3, Hypovolemic shock is distinguished from other causes of less than 4,000 cells/mm3, or has greater than 10% immature shock by history and the absence of signs of heart failure or forms. Although SIRS is part of the criteria for pediatric sepsis sepsis. In addition to the signs of sympathoadrenal activity (SIRS + proven or suspected infection = sepsis), it can also be (tachycardia, vasoconstriction), clinical manifestations include seen in non-infectious states such as trauma or postoperatively. signs of dehydration (dry mucous membranes, decreased  CHAPTER 40 Shock 159 urine output) or blood loss (pallor). Recovery depends on the degree of blood loss in the early acute phase of hemorrhagic degree of hypovolemia, the patient’s pre-existing status, and shock). Electrolyte measurements in patients with hypovole- rapid diagnosis and treatment. The prognosis is good, with a mic shock may identify abnormalities from losses. Patients low mortality in uncomplicated cases. presenting in septic shock require appropriate bacterial and viral cultures to aid in identification of a causative pathogen. If cardiogenic or obstructive shock is suspected, an echocar- Distributive Shock diogram assists with the diagnosis and, in the case of tampon- Patients with distributive shock usually have tachycardia and ade, assists with placement of a pericardial drain to relieve alterations of peripheral perfusion. In early stages, when cyto- the fluid. Patients with dissociative shock require detection kine release results in vasodilation, pulses may be bounding and of the causative agent (carbon monoxide, methemoglobin). vital organ function may be maintained (an alert patient, with The management of shock also requires ongoing monitoring rapid capillary refill and some urine output in warm shock). As of mixed venous oxygen saturations and arterial blood gases the disease progresses untreated, extremities become cool and for assessment of oxygenation, ventilation (CO2), and degree mottled with a delayed capillary refill time. At this stage, the of acidosis. Frequent re-assessment of serum electrolytes and patient has hypotension and vasoconstriction. biochemical markers of end-organ impairment, such as liver and renal function panels as well as coagulation factors and CBC, may aid in subsequent therapeutic interventions. Cardiogenic Shock Cardiogenic shock results when the myocardium is unable to supply the cardiac output required to support tissue perfusion DIFFERENTIAL DIAGNOSIS and organ function. Because of this self-perpetuating cycle, See Table 40.1. heart failure progressing to death may be rapid. Patients with cardiogenic shock have tachycardia and tachypnea. The liver is TREATMENT usually enlarged, a gallop is often present, and jugular venous distention may be noted. Because renal blood flow is poor, General Principles sodium and water are retained, resulting in anasarca. The key to therapy is the recognition of shock in its early, par- tially compensated state, when many of the hemodynamic and metabolic alterations may be reversible. Initial therapy for Obstructive Shock shock follows the ABCs of resuscitation (see Chapter 38). Later, Restriction of cardiac output results in an increase in heart therapy can then be directed at the underlying cause. Therapy rate and an alteration of stroke volume. The pulse pressure is should minimize cardiopulmonary work, while ensuring car- narrow (making pulses harder to feel), and capillary refill is diac output, adequate perfusion, and gas exchange. Intubation, delayed. The liver is often enlarged, and jugular venous disten- combined with mechanical ventilation with oxygen supple- tion may be evident. mentation, improves oxygenation and decreases or eliminates the work of breathing but may impede venous return if dis- tending airway pressures (positive end-expiratory pressure Dissociative Shock [PEEP] or peak inspiratory pressure) are excessive. Blood The principal abnormality in dissociative shock is the inability pressure support is crucial in promoting adequate end-organ to deliver oxygen to tissues. Symptoms include tachycardia, perfusion. tachypnea, alterations in mental status, and ultimately cardio- Monitoring a child in shock requires maintaining access vascular collapse. to the arterial and central venous circulation to record pres- sure measurements, perform blood sampling, and measure systemic blood pressure continuously. These measurements LABORATORY AND IMAGING STUDIES facilitate the estimation of preload and afterload. Regional Shock requires immediate resuscitation before obtaining monitoring with near infrared spectroscopy (NIRS) may allow comprehensive laboratory or diagnostic studies. Following early, noninvasive detection of alterations in perfusion. initial stabilization (including glucose administration if hypo- glycemia is present), the type of shock dictates the necessary Organ-Directed Therapeutics laboratory studies. Patients with shock may benefit from the determination of a baseline pH via arterial blood gas and Fluid Resuscitation blood lactate level to assess the degree of tissue oxygenation Alterations in preload have a dramatic effect on cardiac out- impairment. Measurement of a central mixed venous oxygen put. In hypovolemic and distributive shock, decreased preload saturation aids in the assessment of the adequacy of oxygen significantly impairs cardiac output. In these cases, early and delivery. Notably, in contrast to other forms of shock, patients aggressive fluid resuscitation is important and greatly affects with vasodilated distributive shock (such as in gram-negative outcome. In cardiogenic shock, an elevated preload contrib- rod sepsis) often have high mixed venous saturation values utes to pulmonary edema. due to impairment of mitochondrial function and inability of Selection of fluids for resuscitation and ongoing use is dic- tissues to extract oxygen. A complete blood count (CBC) can tated by clinical circumstances. Crystalloid volume expanders reveal altered bone marrow function or provide evidence of are generally recommended as initial choices because they are disseminated intravascular coagulation (DIC) and may also aid effective, inexpensive, and often readily available. Most acutely in assessing the severity of blood loss following equilibration ill children with signs of shock may safely receive, and usually in hemorrhagic shock (of note, a CBC may not reveal the true benefit greatly from, rapid administration of a 20 mL/kg bolus 160 SECTION 8 The Acutely Ill or Injured Child TABLE 40.2 | Medications Used to Improve Cardiac Output POSITIVE POSITIVE DIRECT INOTROPE CHRONOTROPE PRESSOR VASOCONSTRICTOR VASODILATOR Dopamine ++ + ± ++ (high dose) + (low dose) Dobutamine ++ ± − − + Epinephrine +++ +++ +++ ++ (high dose) + (low dose) Norepinephrine +++ +++ +++ +++ − Milrinone + − − − + of an isotonic crystalloid. This dose may be repeated until a Renal Salvage response is noted. Colloids contain larger molecules that may Poor cardiac output accompanied by decreased renal blood stay in the intravascular space longer than crystalloid solu- flow may cause prerenal azotemia and oliguria/anuria. tions and exert oncotic pressure, drawing fluid out of the tis- Severe hypotension may produce acute tubular necrosis sues into the vascular compartment. However, the long-term and acute renal failure. Prerenal azotemia is corrected when risks of colloids may exceed the benefits. Care must be exercised blood volume deficits are replaced or myocardial contractil- in treating cardiogenic shock with volume expansion as the ity is improved, but acute tubular necrosis does not improve ventricular filling pressures may rise without improvement or immediately when shock is corrected. Prerenal azotemia is with deterioration of cardiac performance. Careful monitoring associated with a serum blood urea nitrogen (BUN)–to-cre- of cardiac output via vital signs, clinical exam (repeatedly evalu- atinine ratio of greater than 10:1 and a urine sodium level ate for development of rales and/or hepatomegaly), and central less than 20 mEq/L; acute tubular necrosis has a BUN-to- venous pressure (if available) guides safe volume replacement. creatinine ratio of 10:1 or less and a urine sodium level between 40 and 60 mEq/L (see Chapter 165). Aggressive fluid Cardiovascular Support replacement is often necessary to improve oliguria associated In an effort to improve cardiac output after volume resusci- with prerenal azotemia. Because the management of shock tation, or when further volume replacement may be danger- requires administering large volumes of fluid, maintaining ous, a variety of inotropic and vasodilator drugs may be useful urine output greatly facilitates patient management. (Table 40.2). Therapy is directed first at increasing myocardial Prevention of acute tubular necrosis and the subsequent contractility, then at decreasing left ventricular afterload. The complications associated with acute renal failure (hyperka- hemodynamic status of the patient dictates the choice of the lemia, acidosis, hypocalcemia, fluid overload) is important. agent. The use of pharmacologic agents to augment urine output is Therapy may be initiated with dopamine at 5–20 µg/kg indicated when the intravascular volume has been replaced. per minute; however, epinephrine or norepinephrine may be The use of loop diuretics, such as furosemide, or combina- preferable in patients with decompensated shock. In addition tions of a loop diuretic and a thiazide agent, may enhance to improving contractility, certain catecholamines cause an urine output. Nevertheless, if hyperkalemia, refractory aci- increase in systemic vascular resistance. The addition of a vaso- dosis, hypervolemia, or altered mental status associated dilator drug may improve cardiac performance by decreasing with uremia occurs, dialysis or hemofiltration should be the resistance against which the heart must pump (after- initiated. load). Afterload reduction may be achieved with dobutamine, milrinone, amrinone, nitroprusside, nitroglycerin, and angiotensin-converting enzyme inhibitors. The use of these COMPLICATIONS drugs may be particularly important in the later stages of Shock results in impairment of tissue perfusion and oxygen- shock, when vasoconstriction is prominent. ation and activation of inflammation and cytokine pathways. The major complication of shock is multiple organ system Respiratory Support failure, defined as the dysfunction of more than one organ, The lung is a target organ for inflammatory mediators in including respiratory failure, renal failure, liver dysfunction, SIRS and shock. Respiratory failure may develop rapidly and coagulation abnormalities, or cerebral dysfunction. Patients become progressive. Intervention requires endotracheal intu- with shock and multiple organ failure have a higher mortal- bation and mechanical ventilation accompanied by the use ity rate and, for survivors, a longer hospital stay. of supplemental oxygen and PEEP. Care must be taken with the process of intubation as a child with compensated shock may suddenly decompensate upon administration of sedative PROGNOSIS medications that reduce systemic vascular resistance or with Early recognition and goal-directed intervention in patients converting to positive pressure ventilation. Severe cardiopul- with shock improves survival. Delays in treatment of hypoten- monary failure may be managed with inhaled nitric oxide and, sion, however, increase the incidence of multiple organ failure if necessary, extracorporeal membrane oxygenation. and mortality.  CHAPTER 42 Major Trauma 161 PREVENTION EDUCATION FOR PREVENTING INJURIES Prevention strategies for shock are focused, for the most The recognition that much of the morbidity and mortality part, on shock associated with causative exposures (infec- are determined at the scene of an injury has stimulated the tion, trauma, and ingestion). Some forms of septic shock development of prevention measures. The Haddon matrix can be prevented through the use of immunizations (such as combines the epidemiologic components (host, agent, physi- Haemophilus influenzae type b, meningococcal, pneumococ- cal and social environments) with time factors (before, during, cal vaccines). Decreasing the risk of sepsis in a hospitalized and after the event) to identify effective interventions focused patient requires adherence to strict handwashing, isolation on different aspects of the injury event. Primary strategies practices, and minimizing the duration of indwelling devices. (preventing the event), secondary strategies (minimizing Measures to decrease pediatric trauma do much to minimize the severity of injury), and tertiary strategies (minimizing hemorrhage-induced hypovolemic shock. Preventative health long-term impact) can be targeted for each epidemiologic measures surrounding environmental toxins (carbon mon- component. Such strategies typically fall into one of three oxide) and medication storage/administration can aid in the areas: education, enforcement, and environment (including prevention of some forms of dissociative, distributive, and engineering). cardiogenic shock (see Table 40.1). Education is often the first strategy considered, but it requires behavioral change and action on the part of people. Most educational strategies are not well evaluated. PEARLS FOR PRACTITIONERS Despite the reliance on an action by the individuals See The Acutely Ill or Injured Child: Pearls for Practitioners at involved, some active strategies benefit from enforcement. the end of this section. Children wearing bicycle helmets experience a significantly lower incidence of traumatic brain injury and death. The enforcement of seatbelt laws increases seatbelt use and may decrease injuries. Automatic strategies require no action on the part of the CHAPTER 41 population and often change the environment (speed bumps) or involve engineering (child-resistant pill bottles, air bags). Injury Prevention Automatic strategies have more consistently resulted in a sig- nificant reduction in injuries. The most successful approaches EPIDEMIOLOGY AND ETIOLOGY to preventing injury have combined strategies (education, Unintentional injury is the leading pediatric cause of death in environmental changes, and engineering changes focused on the developed world. In 2017, unintentional injury accounted the host, agent, and environment in all three time phases). for 17,000 deaths of children, adolescents, and young adults 0–24 years of age in the United States. Between 2000 and 2009, the unintentional injury death rate for children under 19 years PEARLS FOR PRACTITIONERS declined by 29% in the United States (from 15.5 to 11 per See The Acutely Ill or Injured Child: Pearls for Practitioners at 100,000). In 2016, this rate declined even further to 10.1 per the end of this section. 100,000. This decline has been attributed to increased use of child safety seats and seat belts, increased use of child-resistant packaging, reduction in drunk driving, enhanced safety awareness, and improved medical care. The most common causes of fatal injuries differ among age CHAPTER42 groups. For instance, suffocation is the most common type of fatal injury among infants (84% of unintentional deaths in Major Trauma 2017); however, it accounts for only 1% of unintentional fatali- ties among 15- to 19-year-olds. Conversely, motor vehicle col- ASSESSMENT AND RESUSCITATION lisions account for 6% of fatal injuries among infants, whereas The general goal of prehospital trauma care is rapid assess- they account for 66% of adolescent fatal injuries. Drowning ment, support of the ABCs (airway, breathing, and circu- is the most common cause of fatal injury among children lation), immobilization, and transportation. Outcomes of ages 1–4 years (31%), while it accounts for 7% of fatal injuries patients with major or life-threatening trauma are significantly among adolescents. Notably, differences in geography, climate, improved when they receive care in a pediatric trauma center population density (access to care), and population traits affect or in an adult center with pediatric trauma certification com- the frequency, etiology, and severity of these injuries. pared with level I or II adult trauma centers. However, many Injury occurs through interaction of the host (child) children live too far from a pediatric trauma center to seek with the agent (e.g., car and driver) through a vector and an care at those facilities so it is imperative that all emergency environment (e.g., roadways, weather) that is conducive to providers understand the unique aspects of pediatric trauma exposure. The age of the child may determine the exposure patients. to various agents and environments. For example, most inju- Once the injured child arrives at the emergency department, ries in infants and toddlers occur in the home as the result of the trauma team must initiate an organized and synchronized exposure to agents found there (water heaters, bathtubs, soft response. The initial assessment of a seriously injured child bedding). Gender affects exposure to injury, with boys having should involve a systematic approach, including a primary a fatal injury rate greater than that of girls. survey, resuscitation, secondary survey, post-resuscitation