Trauma Care 1: Shock Portal
Introduction
Shock is a state of inadequate oxygen delivery and inadequate tissue perfusion. If prolonged, shock may lead to general impairment of cellular function.
The initial step in the management of shock is to recognize its existence. The second step is to identify the cause of shock. The causes are diverse, and patient signs and symptoms vary. At times, shock may be obvious (eg, the trauma patient with significant hemorrhage), but often the reason is more obscure (a patient with unknown diabetes exhibiting diabetic ketoacidosis (DKA) or a geriatric patient in early septic shock).
The goal of treatment is to restore adequate cellular and organ perfusion with sufficiently oxygenated blood.
Etiology of Shock
Cardiac output and systemic vascular resistance combine to produce arterial pressure. A significant decrease in either will affect arterial pressure unless there is a compensatory elevation of the other.
Cardiac output may be affected by hypovolemia (hemorrhage), myocardial failure (cardiogenic shock), or circulatory obstruction (pulmonary embolus).
Reduction in systemic vascular resistance by decreased peripheral vasomotor tone (neurogenic shock) or redistribution of blood into the venous capacitance bed (septic shock) causes decreased preload and can reduce cardiac output.
The causes of shock are divided into cardiac and non-cardiac. The cardiac causes are further broken down into rate problems, impaired contractility/excessive preload, decreased preload, and excessive afterload. Non-cardiac causes are separated into volume loss or decreased vascular resistance. As with all classification schemes, there is some overlap, and in many patients, multiple factors may be involved, particularly in the later stages of shock.
The mnemonic SHRIMPCAN is
helpful in creating a differential diagnosis for evaluation and
treatment of a patient in shock.
S—Septic:
gram-negative infection or other overwhelming infection
H—Hypovolemic:
hemorrhage, vomiting, diarrhea, dehydration, burns, peritonitis,
pancreatitis
R—Respiratory:
massive pulmonary embolus, tension pneumothorax
I—Ingestions:
drug overdoses
M—Metabolic:
diabetes mellitus or diabetes insipidus, myxedema, Addison's disease
P—Psychiatric: psychological
manifestation
C—Cardiogenic:
acute MI, cardiomyopathies, cardiac tamponade, arrhythmias, severe CHF,
obstructive outflow lesions, myxomas
A—Anaphylactic: immediate
hypersensitivity to a specific antigen
N—Neurogenic:
severe CNS injury or spinal cord injury
Patient Assessment
Hypotension and hypoperfusion are the 2 main clinical manifestations of shock. Hypotension is best defined as a decrease of 30 mm Hg or greater below baseline of the mean arterial blood pressure.
Manifestations of hypoperfusion are altered mental status, agitation, restlessness, obtundation, cool and clammy skin, and reduced or absent urinary output. Tachycardia is one of the earliest sign of hypoperfusion. Diaphoresis, nausea, vomiting, and diarrhea may also occur. Symptoms vary based on the stage of shock, the extent of hypoperfusion, and the underlying cause.
Obtain a SAMPLE history and begin to monitor and assess the patient. Measure BP, heart rate, respiratory rate, temperature, neck vein distension, mental status evaluation, and skin characteristics. Monitor the mental status, vital signs, cardiac status, and urinary output frequently. Clinical conditions may change rapidly.
Estimating Blood Loss Using Vital Signs
Blood volume is about 7% of body weight. A 70 kg male has a blood volume of about 5 L (70 kg x 0.07 = 4.9 kg). In obese adults, use ideal body weight to make this calculation.
PEDS: In children, blood volume is 80 to 90 mL/kg.
Class I hemorrhage: A loss of 15%
of blood volume (about 750 mL in a healthy adult) can be tolerated with
few hemodynamic signs. Mild tachycardia may be seen.
Class II hemorrhage: A loss of 15% to 30%
of blood volume (about 1000 mL in an adult) results in tachycardia and
decreased pulse pressure. Systolic BP may not change, and urinary
output is only mildly affected.
Class III hemorrhage: A loss of 30% to 40% of blood volume (about 2000 mL in an adult) produces signs of decompensation including marked tachycardia, mental status changes, and a fall in systolic BP.
Class IV hemorrhage: A loss of more than 40% of blood volume (about 2500 mL in an adult) results in marked tachycardia, significantly low systolic BP, very narrow pulse pressure, obtundation, and loss of normal skin color and temperature. The patient becomes unconscious, and the pulse is not obtainable when more than 50% of blood volume is lost.
Order an ECG, chest x-ray, ABG, CBC, electrolytes, BUN, creatinine, and arterial blood lactate level. Other tests are necessary and important but vary according to the underlying causes of the shock. Tests to consider include echocardiogram, CT or MRI, V/Q lung scan, pulmonary angiography, endoscopy, and possibly others, depending on suspected etiologies and potentially some test results.
Exceptions: When the Clinical Picture Differs from What’s Expected
Geriatric patients decompensate earlier and insidiously with fewer warning signs. PEDS: Children decompensate relatively later because of their resilient vascular trees.
Preexisting conditions may lessen the patient's ability to compensate. These include pacemakers, alcohol and other drug ingestions, pregnancy, seizure activity, hypothermia and hyperthermia, and anemia.
Some injuries—such as pelvic fractures, femur fractures, and liver ruptures—are associated with a wide range (from minor to major) of possible hidden blood loss.
Obligatory edema formation during and following resuscitation may require the infusion of electrolyte solution beyond the replacement of lost blood volume alone.
Treatment
Regardless of the cause, tailor initial treatment toward prompt restoration of tissue perfusion and cardiac output. Initial management of the airway and respiratory system is paramount. Adequate oxygenation may improve an already compromised cardiac output. Consider early ET intubation. Appropriate venous access is important. Invasive hemodynamic monitoring is usually necessary. Advanced treatment requires an intensive care unit. CVPs and pulmonary capillary wedge pressures may need to be monitored to adjust the therapy regimen.
How to Restore Blood Volume
The best method is to select a safe volume, infuse it rapidly through large bore IVs, then stop and reassess. A bolus of 1 to 1.5 L of NS is generally safe in hypovolemic adults. PEDS: In children, 20 mg/kg is generally safe. If instability persists, a second bolus of 20 mg/kg or 10 mg/kg of blood is recommended. Be aggressive, but use caution.
Avoid hemodilution with resulting coagulopathy, hypothermia, and loss of blood viscosity. Obtain compatible blood (type O or type specific) early. (You do not need to use it if the patient stabilizes with the initial bolus, but have it ready.)
Administer fluids through a high-volume fluid warmer. Be careful to avoid air embolism. In adults, if using NS for fluids, switch to Ringer’s lactate solution after 2 liters of NS to avoid hyperchloremic acidosis. Add NS to bags of packed RBCs to speed delivery to the patient.
When hemothorax is present, be prepared to collect shed blood for possible autotransfusion.
In the presence of head injury, contused lung, and advanced age, volume overload is dangerous. Do not hesitate to obtain central venous access in these patients so that CVP may be used to gauge the adequacy of fluid replacement.
Presume that the patient has continuing hidden blood loss until proven otherwise. Obtain surgical consultation for any trauma patient where shock is present. Continuing blood loss is manifested by instability refractory to fluid and blood replacement and by the loss of stability once achieved. Surgical intervention is needed as quickly as possible.
If cardiac failure with increased central venous and pulmonary vascular pressure is present, direct treatment toward restoring cardiac function. Rapid volume infusion in this setting may cause or exacerbate pulmonary edema.
Cardiac Causes
Cardiac Arrhythmias: A heart rate between 50 and 150 in a healthy adult is unlikely to be the cause for a patient developing shock. Parameters must be adjusted for children and preexisting conditions. The following table indicates parameters outside of which heart rate may be pathological and require correction.
Age |
Lower |
Upper |
Infant Child Adult |
<70 <60 <50 |
>200 >160 >150 |
Rapid correction of any dysrhythmia often leads to prompt improvement of a patient’s hemodynamic status. Follow ACLS guidelines to treat bradyarrythmias (Vol III—CV10 Bradycardia) and tachyarrythmias (Vol III—CV8 Tachycardia) quickly and effectively. Pay close attention to hypoxemia or metabolic abnormalities that may precipitate tachyarrhythmias.
Decreased Preload or Vascular Obstruction: Most common in this group is right ventricular infarction, pulmonary embolus, tension pneumothorax, and cardiac tamponade. Right ventricular infarction occurs in as many as 30% of patients with acute inferior infarction. Half of these patients may develop hemodynamic complications due to the infarction. Direct treatment toward fluid therapy to improve the left ventricular filling pressure. Dobutamine may also be helpful by its inotropic effect on the right ventricle. Avoid vasodilatory drugs such as nitroglycerine and morphine.
Cardiac tamponade and tension pneumothorax result in inadequate cardiac filling. Volume infusion improves cardiac function.
Massive pulmonary embolus may cause right heart failure and subsequent shock. The accompanying shock from pulmonary embolus may be treated with correction of hypoxemia, possible intubation, IV fluid support, and pressors (if necessary) to support BP.
Impaired Contractility/Excessive Preload: Cardiogenic shock following acute MI is the most common reason for impaired contractility.
Other causes include ventricular septal rupture, free wall rupture, acute mitral insufficiency, or papillary muscle/chordae dysfunction.
When extensive myocardial necrosis (> 30% to 40% of myocardial surface area) causes shock, the prognosis is particularly poor. Aggressive treatment such as cardiac catheterization, PTCA, intra-aortic balloon pump, and coronary artery bypass grafting may result in better short- and long-term survival.
Prognosis also improves for those patients who receive prompt surgical treatment of complications such as ventricular septal rupture and papillary muscle dysfunction. Patients with preserved left ventricular function but severe coronary artery disease causing cardiogenic shock also benefit from early surgical intervention.
As many as 20% of patients in cardiogenic shock have a relative hypovolemia (left ventricular filling pressure < 15 mm Hg) and benefit from fluid support. If acute pulmonary edema is not present, give a fluid challenge of 250 to 500 mL NS. If the hypotension doesn't respond to fluid support, initiate pressor support. A combination treatment regimen may be necessary to improve the pumping function. The American College of Cardiology and the American Heart Association have created guidelines for the early management of patients with hypotension, shock, and acute pulmonary edema.
Inotropic support from dopamine, dobutamine, or norepinephrine is usually first-line therapy. In addition, vasodilator therapy to reduce afterload, diuretic or vasodilator therapy to reduce preload, mechanical assistance such as an intra-aortic balloon pump, or even surgery may be necessary. The best chance for survival for patients suffering from cardiogenic shock after an acute MI is with the use of angioplasty and intra-aortic balloon counterpulsation.
Consider early transfer to a facility capable of cardiac catheterization, angioplasty, and cardiovascular surgery if patients are seen within the first 12 to 24 hours of symptom onset. Most studies indicate marked improvement of mortality if revascularization occurs within 16 hours of symptom onset in this patient subset.
Excessive Afterload: Conditions fitting into this category include aortic stenosis, certain types of cardiomyopathies, and coarctation of the aorta.
Non-Cardiac Causes
Volume Loss: Quickly identify the hypovolemic patient and detect any occult blood loss. Signs include orthostatic vital sign changes and a narrowed pulse pressure. In shock due to hemorrhage, seek the source carefully and quickly. A complete history and physical is essential. Important components of the physical exam include chest percussion for dullness, palpation of the abdomen, thigh girth measurement, and digital rectal exam. In some patients, nasogastric aspiration and peritoneal lavage may be needed to locate the source of hemorrhage.
Treatment begins with establishment of an adequate airway and administration of oxygen. Apply direct pressure to any external wounds to help control bleeding. If necessary, properly place a nasogastric tube. Promptly obtain vascular access (usually with 2 large-bore IV catheters). Maintain the patient's body temperature; monitor frequently.
Ringer's lactate solution or NS are the preferred fluid choices. The first fluid bolus is usually 1 to 2 L for adults or (PEDS:) 20 mL/kg for pediatric patients. The exact amount depends on the patient's signs and symptoms. Warm all fluids to body temperature. Determine the rate by the magnitude of the preexisting loss and how fast blood loss is continuing.
Close observation to the response of this initial bolus determines further therapeutic and diagnostic decisions. Monitor urinary output for determination of adequate replacement.
If blood transfusion is necessary, fully crossmatched blood is preferable. If time does not allow the use of crossmatched blood, type-specific blood can usually be provided in 10 minutes. If the patient is exsanguinating and type-specific blood is not available, use type O Rh-negative packed cells. (If O-negative blood is unavailable, un-crossmatched O-positive blood may be used in extreme emergencies for males and for females past reproductive age.)
For patients en route to the operating room or being transferred to another facility, consider using a pelvic stabilizer (1) for pelvic fractures causing continuing hemorrhage and hypotension and (2) for intra-abdominal trauma with severe hypovolemia.
Obtain surgical consultation and evaluation early.
Decreased Vascular Resistance: Three common types of shock in this category are septic, anaphylactic, and neurogenic.
Neurogenic shock results from a severe midbrain or spinal cord injury. Neurogenic shock is not caused by an isolated head injury. Shock occurs when there is a loss of vasomotor tone because of relaxation of the vascular smooth muscle. Typically, hypotension is present without tachycardia or cutaneous vasoconstriction. Treat patients initially for hypovolemia. If necessary, administer vasoactive drugs after volume has been restored.
Anaphylactic shock often causes severe respiratory distress and profound shock. Laryngeal edema and/or bronchospasm are often present. The preferred drug for initial treatment is epinephrine. (See Vol III—AIR8 Anaphylaxis for details about the use of epinephrine in anaphylactic shock.) An adequate airway is essential. Due to possibly severe laryngeal edema, more advanced airway management may be necessary. For bronchospasm, give nebulized albuterol or give aminophylline at a loading dose of 6 mg/kg and infuse intravenously over 20 to 30 minutes. Volume replacement IV may be needed to restore and maintain tissue perfusion. Consider a vasopressor (dopamine) if hypotension does not respond to volume infusion. Antihistamines and corticosteroids may also play a role in the ongoing treatment of anaphylactic shock.
Septic shock is caused by the action of bacterial toxins on the circulatory system. Although usually caused by gram-negative organisms, shock may also occur with gram-positive, anaerobic, fungal, or viral infections. Treatment and evaluation must address the underlying infection as well as the results of the circulatory compromise.
Two phases usually occur in septic shock. The first phase (warm) is characterized by an increase in cardiac output and a decrease in peripheral vascular resistance. During this phase, the patient is warm and diaphoretic. The second (cold) phase is manifested by decreased cardiac output, normal or increased peripheral vascular resistance, and cool, vasoconstricted skin.
Large volumes of IV fluids are frequently required to achieve a normal BP. If necessary, give vasopressor drugs. Ensure ventilation and correct electrolyte and acid-base disorders.
Specific therapy for septic shock involves antibiotic administration, surgical intervention (drainage of an abscess or removal of an obstruction), and correction of nutritional deficits. The choice of antibiotics involves using those with sensitivities that are most effective against the pathogens likely to invade a specific site. If a likely pathogen is unknown, begin broad-spectrum antimicrobial therapy (Vol III—IN3 Sepsis in Adults). The use and efficacy of corticosteroids remains controversial.
Special Considerations
PEDS: Evaluate shock in infants and children in much the same way as pediatric respiratory failure. Progressive deterioration from either condition may result in cardiopulmonary failure. Even though shock and respiratory failure may begin as separate entities, they both progress to an indistinguishable state of cardiopulmonary failure and even possibly cardiac arrest.
As in adults, clinical features in infants and children are caused by insufficient oxygen delivery to tissues and reduced clearance of metabolites. Clinical signs are caused by end-organ dysfunction due to tissue hypoxia and acidosis.
Signs include altered LOC, hypotonia, tachycardia, and weak central pulses with absent peripheral pulses. Late and ominous signs include hypotension, bradycardia, and irregular respirations.
Evaluate any infant or child with respiratory distress, severe multiple or blunt trauma, a reduced LOC, cyanosis, or pallor. Treat aggressively to determine the presence of cardiopulmonary failure and to prevent any progression toward cardiopulmonary arrest.
Conclusion
The causes of shock at any age are diverse. While the scope of this text does not allow full discussion of evaluation and treatment decisions for every cause of shock, hopefully a differential diagnosis can be generated to aid in evaluation and treatment. Initial treatment, regardless of the cause of shock, is directed toward prompt restoration of tissue perfusion and cardiac output. Most important is to initially recognize the existence of shock.