Shock

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Chapter 4 Shock

Brent R. King, MD, FACEP, FAAEM, FAAP

1 What blood pressure defines shock in the pediatric patient?

Shock is not defined by the blood pressure or by any other vital sign. Shock exists when the patient’s metabolic demand exceeds the body’s ability to deliver oxygen and nutrients. This occurs most commonly when metabolic demand is normal or slightly elevated but delivery of oxygen and nutrients is dramatically reduced. Examples include excessive blood loss (hemorrhage) or excessive fluid loss (diarrhea). The shock state can and often does exist in the presence of a “normal” blood pressure.

Bell LM: Shock. In Fleisher GM, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 51–62.

KEY POINTS: DEFINITION OF SHOCK

1 Shock is a condition in which the patient’s metabolic requirements are unmet.

2 The shock state is a complex interplay between the physiologic insult and the host’s response to that insult; both play a role.

3 In its earliest phase, shock might be recognized only by abnormal results of laboratory tests that measure tissue acid–base status (e.g., serum lactate). Overt clinical signs are seen as the shock state progresses.

2 How can shock be recognized?

To recognize shock, consider both the consequences of inadequate perfusion and the patient’s compensatory mechanisms. The clinical manifestations of shock are those of inadequate perfusion and compensation. Inadequate perfusion of the brain results in an alteration in the child’s level of consciousness. Inadequate perfusion of the kidneys results in decreased urine output.

As perfusion decreases, compensatory changes occur. These changes improve delivery of oxygen and nutrients and direct blood flow to the vital organs. The first compensatory mechanism is usually an increased heart rate. Since cardiac output is equal to the rate multiplied by the stroke volume, an increased heart rate can maintain cardiac output in the face of decreased stroke volume. Additionally, peripheral vasoconstriction helps to maintain blood flow to the central organs and to the brain. The patient therefore has pale, cool extremities and a delayed capillary refilling time. This increased vascular tone also affects the measured blood pressure. The diastolic pressure is slightly elevated, so the difference between the systolic and diastolic pressures—the pulse pressure—is smaller. This is referred to as a “narrowed” pulse pressure.

To compensate for both the decreased oxygen delivery and the acidosis created by underperfusion of peripheral tissues, the respiratory rate increases. The blood pressure eventually falls, but this is a late finding and may signal that the shock state is irreversible.

3 What are the stages of shock?

Shock is a spectrum of illness, so any division into discrete segments is somewhat artificial. However, shock is usually divided into two stages: compensated shock and uncompensated shock.

4 What is compensated shock?

In early shock, various physiologic changes allow continued delivery of oxygen and nutrients to the heart, kidneys, brain, and other vital organs. Tachycardia is usually the first compensatory mechanism. The increased heart rate helps to maintain cardiac output in the face of low blood volume, excessive vasodilation, or pump failure. Increased vasomotor tone shunts blood away from the skin and the extremities to more vital organs. In compensated shock, the patient is able to continue to meet his or her metabolic demand, even if only marginally.

5 Are there exceptions to the compensatory mechanisms described above?

Yes. In septic shock the patient sometimes develops so-called warm shock or warm distributive shock. In this state the patient has flushed skin and bounding pulses associated with a hyperdynamic precordium. This state can be explained by the cascade of inflammatory mediators that is responsible for the condition called septic shock. Likewise, in neurogenic shock, loss of sympathetic tone can result in bradycardia in the face of profound hypotension.

6 What is uncompensated shock?

If the shock state progresses without interruption, the patient’s compensatory mechanisms eventually fail. Hypoperfusion of organ systems causes acidosis and further release of inflammatory mediators. As blood flow to the brain decreases, the patient can become irritable or stuporous and eventually slips into coma. Likewise, decreased renal blood flow causes decreased urine output and finally results in anuria. The gastrointestinal tract is similarly affected, so the patient often has decreased bowel motility followed by distention and edema of the bowel wall. As tissue ischemia and acidosis progress, the inflammatory mediators cause diffuse vascular injury and capillary leakage. The pulmonary bed is especially sensitive to this type of injury. Damage to the pulmonary tissues exacerbates tissue hypoxemia. The ultimate result of progressive shock is multiorgan system failure and acute respiratory distress syndrome. At some point during this process the patient’s blood pressure falls.

7 What are the types (or mechanisms) of shock?

There are multiple mechanisms for shock. These include:

Hypovolemic shock: Hypovolemia, such as might occur with blood loss, vomiting, and/or diarrhea, decreases perfusion to the tissues and leads to shock.

Distributive or vasodilatory shock: This type of shock is the final common pathway of a variety of conditions that result in vasodilation. Neurogenic distributive shock is caused by a spinal cord injury that eliminates sympathetic innervation to the blood vessels, causing profound vasodilation and bradycardia. Accidental ingestion of vasodilating medications can also result in distributive shock. Anaphylaxis results in vasodilation, and, although anaphylaxis has many other components, shock is a part of the clinical picture. Septic shock is largely distributive in nature but is a complex process (see below).

Cardiogenic shock: Pump failure is the primary mechanism for cardiogenic shock. Decreased myocardial contractility makes adequate delivery of oxygen and nutrients impossible. Since children are very dependent on a normal heart rate to produce an adequate cardiac output, drugs and other conditions that cause bradycardia can lead to shock. The patient will have evidence of congestive heart failure, such as rales on pulmonary auscultation and peripheral edema. Viral myocarditis, hypertrophic cardiomyopathy, and certain myocardial depressant drugs can cause cardiogenic shock.

Septic shock: Many consider septic shock to be another form of distributive shock. In septic shock, a stimulus causes the formation of inflammatory mediators that result in profound vasodilation and shock. However, some of these mediators also directly depress myocardial activity; thus, septic shock can have features of both distributive and cardiogenic shock.

Jones AE, Craddock PA, Tayal VS, Kline JA: Diagnostic accuracy of left ventricular function for identifying sepsis among emergency department patients with nontraumatic, symptomatic, undifferentiated hypotension. Shock 24:513–517, 2005.

8 Is the pathophysiology of shock really that simple?

No, it is exceedingly complex. What we refer to as “shock” is the final common pathway for a variety of physiologic insults. Whether the process starts with acute blood loss or with an overwhelming infection, eventually the host mounts a response to the insult, and this response—at least in some cases—seems to contribute to the shock state.

9 What usually initiates septic shock?

The most common and potent initiator of the inflammatory cascade called septic shock is exposure to endotoxin. Endotoxin is the lipopolysaccharide (LPS) coat of gram-negative bacteria. Other bacterial and viral agents can also start this process. Examples include certain viral proteins and teichoic acid.

10 Is septic shock caused by gram-positive organisms different from septic shock caused by gram-negative organisms?

Yes, gram-negative septic shock is more severe. The expected mortality from gram-negative septic shock is 20–50%, while that from gram-positive septic shock is 10–20%.

11 How do proteins such as endotoxin cause septic shock?

This is a trick question. Endotoxin and the other bacterial and viral proteins do not actually cause septic shock. Instead, their presence in the body leads to a response from the host. This response involves a cascade of inflammatory mediators that are responsible for most of the symptoms of shock.

12 What are these inflammatory mediators called?

They are called cytokines.

13 Which of the cytokines is the most important?

Tumor necrosis factor appears to be the most important of the cytokines. Its formation seems to initiate and propagate the remainder of the inflammatory cascade.

Glauser MP: The inflammatory cytokines: New developments in the pathophysiology and treatment of septic shock. Drugs 52(2 Suppl):9–17, 1996.

14 Describe how the cascade of septic shock begins.

Most commonly, endotoxin (LPS) is bound by a plasma protein called LPS-binding protein (LBP). The LPS–LBP complex then binds to the CD14 receptor on the surfaces of macrophages. This process stimulates the formation of both tumor necrosis factor and interleukin. These two cytokines begin the cascade that leads to septic shock.

15 What is the role of activated protein C in the treatment of pediatric septic shock?

Sadly, this agent does not have a role in the treatment of pediatric septic shock. While studies of adults showed that activated protein C conferred a modest survival advantage, a large phase IIIb pediatric trial was terminated following a recommendation by the Data Monitoring Committee based on “futility due to an unfavorable benefit/risk profile.”

16 Which is more important in the management of the child with septic shock: aggressive resuscitation at the referring hospital or excellent care at the tertiary care center?

While both are important, a recent study demonstrated that children in shock from sepsis who are aggressively resuscitated at the referring hospital have better outcomes than those who do not receive such care. Theses results support the notion that management of shock must begin as soon as it is recognized.

Han YY, Carcillo JA, Dragotta MA, et al: Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome. Pediatrics 112:793–799, 2003.

17 What is the most common cause of shock in children?

Hypovolemia is the most common cause of shock in children.

18 What is the usual cause of hypovolemia?

Throughout most of the world, hypovolemia is caused by diarrheal illness. Millions of children die of hypovolemia caused by diarrhea each year.

19 What are some ways in which trauma can cause shock?

Posttraumatic hemorrhage is the most common way that trauma causes shock. Because young children have abdominal wall muscles that are poorly developed, they are at risk for liver and spleen injury after blunt abdominal trauma.

In addition to hemorrhagic shock, blunt chest trauma can result in a tension pneumothorax. Tension pneumothorax causes increased intrathoracic pressure, which in turn reduces venous return to the heart and causes shock. Similarly, blunt chest trauma can result in pericardial tamponade (essentially a form of restrictive cardiomyopathy).

Finally, cervical spine injury can result in neurogenic shock.

20 How does isolated head trauma cause shock?

It doesn’t. If a patient has shock after what appears to be isolated head trauma, there must be another explanation for the shock.

KEY POINTS: ETIOLOGY OF SHOCK IN CHILDREN

1 Hypovolemia (not enough circulating volume to deliver oxygen and nutrients)

2 Impaired cardiac function (ineffective pumping of the circulating volume)

3 Inappropriate vasodilation (the circulating volume exists primarily in the venous capacitance system and is unavailable to deliver oxygen and nutrients)

21 How is hemorrhage classified?

Hemorrhage is divided into four classes based on the amount of blood loss. Class I hemorrhage produces the least amount of blood loss, and class IV, the greatest.

22 How do the classes of hemorrhage relate to shock?

There is no direct relationship. In fact, a patient can experience class I hemorrhage without demonstrating signs of shock. However, as patients experience greater degrees of hemorrhage, they are more likely to have symptoms of shock.

23 What are the classes of hemorrhage?

Class I hemorrhage: The patient has lost up to 15% of his or her blood volume. Otherwise healthy patients are likely to have minimal tachycardia and no other symptoms. Unless there is ongoing hemorrhage, the patient should require no treatment.

Class II hemorrhage: The patient has lost 15–30% of his or her blood volume. Loss of this amount of blood stimulates the compensatory mechanisms usually associated with early, compensated shock. Tachycardia, increased respiratory rate, and narrowed pulse pressure are seen. Urine output is usually maintained, but the patient may have signs of early central nervous system impairment. Such signs may include fright or anxiety.

Class III hemorrhage: The patient has lost 30–40% of his or her blood volume. This amount of blood loss is clearly associated with signs of compensated shock but may also be associated with uncompensated shock. Even healthy individuals may have a drop in systolic blood pressure with this degree of blood loss. Urine output is likely to be decreased, and the patient may be very anxious or confused.

Class IV hemorrhage: This represents loss of more than 40% of the circulating blood volume. This degree of hemorrhage is uniformly fatal if untreated. The shock state may, in some cases, be irreversible. The patient has a markedly decreased blood pressure. He or she can be expected to have complete peripheral vasoconstriction, extreme tachycardia, and little or no urinary output. Mental status is very depressed, and the patient may be unconscious.

24 How can emergency physicians make a presumptive diagnosis of cardiogenic shock?

Recent studies have demonstrated that emergency physicians using bedside ultrasonography can correctly identify cardiac wall motion abnormalities. This technology makes it easy for the emergency physician to identify patients with abnormal cardiac function.

Dey I, Sprivulis P: Emergency physicians can reliably assess emergency department patient cardiac output using the USCOM continuous wave Doppler cardiac output monitor. Emerg Med Austr 17:193–199, 2005.

Hollenberg SM, Kavinsky CJ, Parrillo JE: Cardiogenic shock. Ann Intern Med 131:47–59, 1999.

25 How can neurogenic shock be distinguished from hemorrhagic shock?

The patient with hemorrhagic shock has a rapid and possibly irregular pulse, while the patient with neurogenic shock has a slow and regular pulse.

26 In general, what is the initial treatment for shock?

There is no single treatment for shock: Therapy is aimed at the cause. That being said, most types of shock respond well to fluid therapy, so if the cause cannot be identified, a single bolus of 20 mL/kg of either normal saline or lactated Ringer’s may be helpful and, at worst, is unlikely to cause serious harm. Additionally, the patient should receive supplemental oxygen and may require assisted ventilation to ensure that oxygen delivery is maximized.

27 Which treatments should be avoided?

The greatest error that you can make in the treatment of shock is to use pressor agents to treat hypovolemia. Even in cases of distributive shock, fluids should be used for initial treatment. Note that excessive fluid administration can be harmful in cardiogenic shock.

28 How should hypovolemic shock be treated?

Treat hypovolemia with volume. Initial therapy is usually crystalloids. Acceptable crystalloids are lactated Ringer’s and normal saline. Give boluses of 20 mL of fluid per kilogram of body weight. Up to 60 mL/kg can be given before considering other therapy. Patients with severe (class III and IV) hemorrhage usually require blood replacement therapy.

29 What is the treatment for neurogenic shock?

In neurogenic shock, injury to the spinal cord results in decreased sympathetic input to the vascular system. Most of the patient’s blood supply is left in the venous or capacitance system. Fluid therapy is an appropriate initial treatment, but pressor agents may also be needed. Norepinephrine is a powerful α-agonist and is often recommended for neurogenic shock. Metaraminol is an excellent alternative to norepinephrine. If the patient has profound bradycardia, atropine may be used to increase the heart rate and, therefore, the cardiac output.

In field situations or as a temporizing measure in the emergency department, a military antishock garment (MAST) can be applied to patients with neurogenic shock. The garment increases peripheral vascular resistance and thus compensates for some of the loss of sympathetic innervation.

Chiles BW III, Cooper PR: Current concepts: Acute spinal injury. N Engl J Med 334:514–520, 1996.

30 Is the MAST garment useful in other kinds of shock?

The MAST garment has been the subject of intense research since it was introduced during the Vietnam War. The available literature suggests that the MAST garment has a very limited role in the management of shock. It may help to stabilize pelvic fractures and may be of some use in patients who require prolonged transport to a definitive care center. As discussed, it may also be useful in the management of certain patients in neurogenic shock.

31 When should the MAST garment be avoided?

There is only one absolute contraindication to the use of the MAST garment. The garment increases peripheral vascular resistance (afterload) and therefore is contraindicated in patients with cardiogenic shock or potential cardiogenic shock (pulmonary edema). In general, it should be avoided in patients with impaled objects in the chest or abdomen, evisceration of the abdominal contents, and pregnancy. There is strong evidence against the use of MAST garments in patients with penetrating injuries to the chest, particularly in cases of penetrating cardiac injury.

32 How should the patient with septic shock be treated?

Treatment of septic shock is difficult and complex. Fluid therapy is usually employed first, but pressor agents are often required. Treatment with antibodies directed against the inflammatory mediators has not proven to be effective, but as our understanding of this complex process evolves, effective immunomodulator therapy may be developed. Interestingly, although antibiotics are needed to limit the infectious process, they alone are not sufficient treatment for septic shock. In certain cases, they may actually increase the antigen load in the system by destroying gram-negative organisms, which results in more LPS in the circulatory system. However, patients who do not receive adequate antibiotic therapy have a higher mortality than those receiving such therapy.

Carcillio JA, Fields AI, Task Force Committee Members: Clinical practice parameters for hemodynamic support of pediatric and neonatal patients in septic shock. Crit Care Med 30:1365–1378, 2002.

33 How should I choose an appropriate antibiotic for the patient in septic shock?

Septic shock is a severe and life-threatening condition and should be treated promptly. It may, however, be impossible to identify the causative organism in a timely fashion. Therefore, empirically administer antibiotic therapy. In most cases, it is prudent to choose broad-spectrum agents that are effective against a wide range of likely pathogens.

Schexnayder SM: Pediatric septic shock. Pediatr Rev 20:303–308, 1999.

34 Under what circumstances might the drug phenylephrine be useful in the management of shock?

Phenylephrine causes vasoconstriction without causing excessive tachycardia. In the patient whose shock state is caused primarily by vasodilation, phenylephrine might be indicated.

35 What is early, goal-directed therapy?

Early, goal-directed therapy is a management scheme that has been shown to be effective in the treatment of adult patients with sepsis and septic shock. There are four basic components of early, goal-directed therapy: (1) early recognition of the patient who is at risk for physiologic compromise using metabolic markers such as serum lactate; (2) correction of hypovolemia and cardiovascular function using predetermined goals or endpoints (e.g., fluid resuscitation until the central venous pressure has reached 8–12 mmHg); (3) prevention of sudden cardiopulmonary dysfunction; and (4) interruption of the inflammatory cascade created by cellular hypoxemia.

Rivers E, Nguyen B, Havstad S, et al: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 345:1368–1377, 2001.

36 How should anaphylactic shock be treated?

Most manifestations of anaphylaxis, including hypotension, respond well to intramuscular epinephrine. Epinephrine has both α- and β-receptor agonist effects, so it can effectively treat bronchospasm and hypotension.

American Heart Association: 2005 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 10.6: Anaphylaxis. Circulation 112:143–145, 2005.

37 What is toxic shock syndrome (TSS)?

TSS is an illness characterized by fever, erythroderma, hypotension, and involvement of several other organ systems. It is caused by strains of Staphylococcus aureus that produce an exotoxin (TSST-1, enterotoxin B, enterotoxin C). It is most often associated with prolonged use of tampons, but young children (boys and girls) with open skin wounds or minor abrasions can also develop toxic shock syndrome.

38 How do the exotoxins cause shock?

TSST-1 and the other exotoxins are profound vasodilators, and their effect causes distributive shock. Additionally, vasodilation seems to cause rapid movement of fluids and serum proteins to the extravascular space, leading to intravascular volume depletion. Exotoxins also have a direct effect upon the heart that results in decreased myocardial function. Finally, many patients with TSS experience vomiting or diarrhea, which leads to further volume depletion.

39 Are there other forms of TSS?

Yes, a clinical syndrome very similar to TSS has developed in association with group A streptococcal infections (Streptococcus pyogenes). Group A streptococci produce exotoxins very similar to those produced by staphylococci. These toxins are called streptococcal pyogenic exotoxins (SPEs). There are three of these: SPEs A, B, and, C. SPE A has long been associated with the clinical features of scarlet fever. Exactly why these toxins have recently become more virulent is unknown.

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