SECTION 7: Immediate Life-Threatening Events

Robert D. Greenberg, Stephen McConnell

INTRODUCTION

Respiratory failure is the inability of the lungs to perform the vital function of gas exchange, and may be caused by an inability to either obtain sufficient oxygen or eliminate carbon dioxide. Numerically, respiratory failure may be defined on arterial blood gas measurement as hypoxemia, with a PaO₂ <60 mmHg, or as hypercarbia, with a PaCO₂ >45 mm Hg.¹ Acute respiratory failure may be divided into four types. Type 1 respiratory failure is caused by acute hypoxia, and may be seen in patients with pulmonary edema, pneumonia, pulmonary hemorrhage, or acute respiratory distress syndrome. Type 2 respiratory failure may be seen with hypoventilation and an inability to rid the body of carbon dioxide. Examples of disease processes where this may be seen include central nervous system disorders where the respiratory drive is diminished, neuromuscular disorders where the muscles of respiration are not sufficiently able to produce ventilation, as well as in pulmonary conditions such as pneumothorax, airway obstruction, or pleural effusions. Significant atelectasis is the cause for Type 3 respiratory failure, and is most commonly seen after mechanical ventilation. Type 4 respiratory failure is seen in patients who have hypoperfusion of the muscles of respiration caused by another process, such as shock.² Identifying the incidence of acute respiratory failure in the United States is extremely difficult but has been estimated near 140 cases per 100,000 individuals over the age of 5. Of the patients with acute respiratory failure, approximately 36% will not survive to hospital discharge. There seems to be a correlation with increased mortality seen in patients with increase in age, presence of multisystem organ failure, cancer, underlying liver disease, and HIV infection.³

OBJECTIVES

Describe the causes of respiratory failure and anaphylaxis.
Describe interventions used in the prehospital environment to treat respiratory failure and anaphylaxis.
Delineate equipment useful in the prehospital management.
Outline some easy-to-use mnemonics for airway assessment in the field.
Describe unique challenges encountered in the prehospital environment.
Delineate medications that are appropriate for use in airway interventions in the prehospital environment.

CAUSES OF ACUTE RESPIRATORY FAILURE

There are many causes of acute respiratory failure, and oftentimes more than one in any given patient. Understanding the underlying disease process may better direct treatment and management of the patient in both the prehospital and hospital environments. Appropriate early interventions may have a significant effect on patient outcome and subsequent management.

NEUROMUSCULAR

Communication from the medullary respiratory center to the muscles of respiration is crucial in the mechanics of respiration. Disruption of neurotransmission may occur by several mechanisms. Severe intoxication or overdoses may decrease the intrinsic capability of the medullary respiratory center to function. Environmental clues may allow for the detection of organophosphate induced respiratory failure, which occurs within the first 4 days of exposure. It is believed that the central nervous action of the organophosphate has a larger role inducing respiratory failure compared to the peripheral effect.⁴ Myasthenia gravis, an autoimmune disease with an incidence of approximately 18 individuals out of 1 million,⁵ may also present as respiratory distress. Other diseases, such as Guillain-Barre or Eaton-Lambert syndrome may also present with weakness of the respiratory muscles. Trauma may result in damage to the brain or the cervical spinal cord that may also disrupt neurotransmission. A vital capacity less than 20 mL/kg or peak inspiratory pressures greater than −30 cm H₂O combined with bulbar dysfunction are strong predictors of which patients may require mechanical ventilation for neuromuscular dysfunction.⁶

VASCULAR

Gas exchange in the pulmonary vasculature depends on diffusion of both oxygen and carbon dioxide across the alveolar membrane and may be affected by several conditions. Interstitial lung disease, such as pulmonary fibrosis or sarcoidosis in addition to others, may destroy and cause a reduction in capillary-alveolar units. Pulmonary embolism is another vascular process that can lead to respiratory distress and failure, depending on the thrombus location and size. Pulmonary embolism creates a ventilation/perfusion mismatch and can lead to hypoxia, with massive pulmonary embolism creating significant cardiac dysfunction. Additional vascular causes of acute respiratory failure can be related to pulmonary hypertension or iatrogenic interventions secondary to pulmonary artery dissection. This can be seen following catheterization as well as cardiac valve replacement. Other disease processes affecting blood flow through the pulmonary vasculature include right-to-left mechanical shunts and may be found during a workup for another pathological finding, such as an ischemic stroke.

ENVIRONMENTAL AND TOXIC

One of the challenges of prehospital patient care is some of the austere environments that may be encountered. Working in enclosed environments with limited air ventilation, some patients may have exposure to hypoxic environments or be exposed to chemicals which may alter the body's ability to appropriately exchange carbon dioxide and oxygen. Poisoning by carbon monoxide, a byproduct of fossil fuel combustion, may result from intentional or unintentional means. Carbon monoxide with an increased affinity for both hemoglobin and myoglobin, effectively decreases the amount of oxygen available for tissue delivery and can interfere with mitochondrial cytochrome oxidase. Carbon monoxide exposures account for approximately 15,000 emergency department visits and up to 500 deaths annually in the United States.⁷ Caring for patients exposed to carbon monoxide should focus on removing the patient from the environment while taking care not to unnecessarily expose prehospital providers. High flow supplemental oxygen should be administered and hyperbaric oxygen therapy, although controversial, may be indicated. Pulse oximetry may not be accurate in patients with carbon monoxide poisoning but an arterial blood gas with cooximetry will give more accurate values. Cyanide poisoning, commonly seen in fire-related injuries, can also result from iatrogenic exposure from prolonged nitroprusside infusion.⁸ The primary toxic effect of cyanide is inhibition of mitochondrial cytochrome oxidase.⁹ Several antidotes to cyanide toxicity exist, each having a unique mechanism of action and with varying degrees of side-effects from the antidote.¹⁰

IMPAIRED VENTILATION

Chronic obstructive pulmonary disease (COPD) is increasing in prevalence and incidence throughout the United States and contributes to approximately 5% of deaths annually. Tobacco smoking has been attributed in up to 75% of COPD cases.¹¹ Airflow obstruction seen in COPD is not completely reversible and is caused by small airway disease as well as parenchymal disease in varying degrees. The hallmark of outpatient management for COPD has remained β-agonist as well as steroid therapy with supplemental oxygen needed in the more severe cases.¹² Approximately 10% of patients with COPD who experience an acute exacerbation will require hospitalization. Etiology of exacerbations may be related to bacterial or viral infections, with Moraxella catarrhalis, Haemophilus influenza, and Streptococcus pneumonia being the most common organisms. Cardiac dysfunction may be seen as a concomitant disease process and may be the underlying process worsening respiratory status. In patients without an explained cause for the acute exacerbation, pneumothorax and pulmonary embolism should be considered, noting that pulmonary embolism may have a prevalence as high as 25% in unexplained exacerbations.¹³ Treatment for the acute exacerbation may require an increase in oxygen, inhaled β-agonist and anticholinergic, as well as systemic glucocorticoids, and possibly noninvasive positive pressure ventilation. Reactive airway disease, such as asthma, may affect individuals of any age, but has a higher prevalence among children than adults. Overall, the prevalence in the United States is slightly higher than 8% and increasing.¹⁴ Asthma symptoms occur when the airway diameter is decreased due to smooth muscle contraction, development of bronchial secretions and bronchial wall edema, as well as with vascular congestion. Exacerbations are due to a variety of causes including environmental temperature, exercise, as well as allergens. Management depends on the degree of the disease process, but typically includes short-acting β-agonists, anticholinergics, steroids, noninvasive positive pressure ventilation, and severe acute exacerbations may also include magnesium and/or endotracheal intubation and mechanical ventilation.^15,16

REDUCED PULMONARY VOLUME

With some patients, an acute presentation of respiratory distress or failure may be caused by a potentially reversible structural cause. For example, a patient with a spontaneous or traumatic pneumothorax may present with chest pain or dyspnea, which may progress rapidly to a tension pneumothorax. Aeromedical transportation is not an absolute contraindication when considering the entire clinical picture. If tension physiology is encountered, emergent thoracostomy is indicated, with some prehospital providers performing both needle and/or tube thoracostomy¹⁷ (Figure 34-1). Successful placement of a needle thoracostomy depends on several factors including length and physical properties of the catheter. Thoracostomy appears to have more of a role in penetrating thoracic trauma, but can also successfully be employed in blunt trauma.^18,19

FIGURE 34-1.

Needle thoracostomy. Tension pneumothorax with return of air bubbling through blood out of a large-bore IV catheter placed through the anterior chest wall at the second intercostal space, midclavicular line. (Reproduced with permission from Corbett SW, Stack LB, Knoop KJ. Chest and abdomen. In: Knoop KJ, Stack LB, Storrow AB, Thurman R, eds. The Atlas of Emergency Medicine. 3rd ed. New York, NY: McGraw-Hill; 2010:chap 7.)

Reduction of the thoracic cavity volume, by either compression from the abdominal cavity as in severe cirrhosis with ascites or extrapulmonary thoracic conditions such as pleural effusions, may result in reduced total lung capacity and cause respiratory distress. Many of these conditions do not develop suddenly, but are more insidious. Understanding the underlying disease process allows for targeted therapy, although procedures such as thoracentesis and paracentesis are not performed in the prehospital environment, knowledge that they may be indicated may direct destination determination. Supportive measures including supplemental oxygen, patient positioning, and noninvasive positive pressure ventilation^20,21 may assist in improving symptoms until definitive care can be obtained.

INFECTION

Pneumonia has the highest overall mortality of any infectious disease in the United States. Annually, approximately 5.5 million cases of community-acquired pneumonia are diagnosed with around 20% requiring hospitalization. Streptococcus pneumoniae remains the primary causative organism of bacterial pneumonia. One of the challenges in treating patients with pneumonia is the coinfection with other organisms as well as bacterial drug resistance.²² Patients with pneumonia may present with cough, sputum production, chest pain, or shortness of breath, with elderly patients having fewer or nonspecific symptoms.²³ Management in the prehospital setting should focus on general supportive measures addressing hemodynamic stability and oxygenation. If the patient shows evidence of shock, appropriate measures should be employed including fluid resuscitation and possibly airway management as indicated.

ANAPHYLAXIS

Anaphylaxis is a Type 1 hypersensitivity immune-mediated reaction based on IgE-mediated effects with multisystem involvement including urticaria, angioedema, hypotension, or bronchospasm. Identified etiologies include food, medications (specifically antibiotics), as well as envenomation.²⁴ Diagnosis of anaphylaxis is based on clinical presentation and history, with laboratory values having no clinical importance in the immediate treatment phase. Epinephrine administered intramuscular is the emergent intervention of choice with no absolute contraindication. Intravenous resuscitation with isotonic fluids and other medications including antihistamines and corticosteroids may be administered, but definitive treatment still relies on administration of epinephrine. Respiratory failure may be seen in anaphylaxis as a result of bronchospasm, angioedema, or hypotension with a systemic lack of perfusion.²⁵

DIAGNOSTIC APPROACH TO ACUTE RESPIRATORY FAILURE

Prompt recognition of patients requiring respiratory support is crucial. Oftentimes, the history obtained from the patient or others will provide the most clues as to how patient care should be approached and which interventions, if any, will help improve symptoms. Identifying the underlying etiology of the respiratory distress may prove more challenging but is of secondary importance. Reviewing a patient's medical history and obtaining an accurate list of medications for review may prove helpful. A patient may have wheezing on examination and review of their medications may show treatments for chronic obstructive pulmonary disease, congestive heart failure, asthma, or other etiologies that could guide management. Sometimes, patients may be in extremis and not able to contribute, but family members present may be able to help significantly. Environmental exposures are also good clues as to the underlying disease process. If the patient is at a chemical plant or found near a pesticide, this could easily direct management and help the prehospital providers take extra precautions so as not to contaminate themselves or anyone else. Removing a patient from an environment may be the simplest intervention needed to improve a patient's symptoms. Clothing may serve as a reservoir for chemical agents, and these should be removed quickly. Physical examination is helpful in evaluating all patients, but especially those who are not able to contribute verbally or answer questions appropriately. Physical examination is not reliable to exclude pneumothorax or hemothorax, as patients still may have breath sounds.²⁶ Reduced air movement may also not allow for breath sounds to be adequately auscultated. Work of breathing may change in patients who are improving or deteriorating necessitating serial observation and continuous monitoring.

MANAGEMENT OF RESPIRATORY FAILURE IN THE PREHOSPITAL SETTING

Management of respiratory distress, insufficiency, and failure in the prehospital setting may be affected by the uncontrolled environment but has the potential to greatly improve patient outcome. A patient may require anything from supplemental oxygen to aggressive invasive airway control during treatment and transport. Continuous monitoring will allow the provider to determine if an intervention is sufficient or if more support is necessary. Prehospital airway management is an ongoing challenge, which requires close attention from EMS physicians.²⁷

OXYGEN

The use of oxygen is widely accepted in a variety of patient conditions. The routine use of pulse oximetry in the prehospital setting allows for identification of patients who are hypoxic and can guide therapy. The use of oxygen in patients with chronic obstructive pulmonary disease is still debated regarding the target oxygenation level with concern related to eliminating the hypoxic respiratory drive and worsening hypercapnia.²⁸ Waveform capnography is another tool available to the prehospital provider to identify hypercapnia and initiate other treatments such as noninvasive positive pressure ventilation.

NONINVASIVE POSITIVE PRESSURE VENTILATION

Select populations of patients with hypoxemic respiratory failure may benefit by noninvasive positive pressure ventilation (NIPPV) with a reduced intubation rate and decreases in intensive care unit stay and mortality²⁹ and has been used and advocated for in the prehospital setting.^30,31 NIPPV has been shown to reduce the need for intubation in patients with pulmonary edema, chronic obstructive pulmonary disease, and asthma.³² Individuals with COPD as well as acute pulmonary edema may benefit from continuous positive airway pressure (CPAP), a form of NIPPV. Utilizing CPAP for patients with severe acute pulmonary edema improves oxygenation,³³ decreases hospital mortality, and decreases need for intubation.³⁴ Overall hospital length of stay did not significantly decrease, but duration of intensive care unit stay did.³⁵

INVASIVE AIRWAY DEVICE

In the event that a patient has decreased mental status, or will not tolerate other forms of airway support, invasive devices may be indicated. The classic airway involves placement of an endotracheal tube by direct laryngoscopy, but multiple other devices are becoming available to the prehospital provider.

BLIND INSERTION AIRWAY DEVICE

Many different manufacturers have created various forms of blind insertion airway devices that are passed through the oropharynx and occlude the esophagus while allowing ventilation to occur. These devices are deployed quickly and can be used as a primary³⁶ or backup airway device.³⁷ In the case of cardiac arrest, these devices may be preferred, as placement does not require interruption of chest compressions.³⁸

ENDOTRACHEAL INTUBATION

Endotracheal intubation is considered the gold standard for airway management. Prehospital intubation success has been reported with a rate as low as 50% and as high as 98%, with success increased by using rapid sequence algorithms.³⁹ Video laryngoscopy is also becoming an option for increasing numbers of prehospital providers.⁴⁰ There are several different video laryngoscopes available, and some have suggested this as a primary tool in patients with cervical spine injuries or expected difficult airway.⁴¹ Using a video laryngoscope during cardiopulmonary resuscitation with chest compressions may decrease the time needed for definitive airway control.⁴²

SURGICAL AIRWAY

Airway management in the prehospital environment is not always easily attainable. In some circumstances, multiple devices may be required to appropriately ventilate a patient. Surgical airway management has primarily been reserved as an option in the failed airway algorithm, and rarely is the primary method for obtaining an airway. A failed airway has been proposed as either the inability to ventilate and oxygenate a patient or three unsuccessful attempts at placement of an endotracheal tube by an experienced operator.⁴³ It is important to note that in some circumstances proper bag-valve-mask ventilations may provide sufficient oxygenation and ventilation. A number of devices are commercially available to help perform a cricothyroidotomy from surgical kits to those using the Seldinger technique. Providers should be familiar with the technique and equipment available to them to obtain a surgical airway (Figure 34-2). Consider transtracheal jet ventilation in children under the age of 10 given anatomic differences between pediatric patients and adults.⁴⁴

FIGURE 34-2.

Percutaneous cricothyroidotomy. One option to obtain a surgical airway is to utilize a percutaneous device such as the QuickTrach^®.

INITIAL APPROACH TO AIRWAY MANAGEMENT IN THE PREHOSPITAL SETTING

Many patients who utilize emergency medical services will do so because of respiratory distress and prehospital providers should be ready and capable to respond and care for them. Frequent reassessments should identify if further interventions are required in managing the patient with respiratory distress. Using equipment such as a pulse oximetry, electrocardiogram, end-tidal or waveform capnography may help direct therapy toward the underlying cause of respiratory distress. Evaluating the airway is crucial in managing patients in respiratory distress. If the patient can converse appropriately without distress, the airway is likely intact. If the patient has a muffled voice, one may suspect an obstruction. Stridor may be another physical examination finding that can signal a patient with potential airway compromise. Auscultation of the lungs may allow the provider to notice abnormal or diminished lung sounds. Medications such as bronchodilators may improve lung sounds as well as the patient's symptoms. Absence of lung sounds, in addition to other physical examination findings, may signify a tension pneumothorax that may necessitate immediate intervention. Anaphylaxis and allergic reactions pose a challenge to prehospital providers. Provider safety is essential but the patient may need to be moved quickly from the environment in which they are found. Anaphylaxis is a true emergency, and when suspected, treatment should not be delayed.

IDENTIFICATION AND APPROACH TO THE DIFFICULT AIRWAY

Identification and preparation for airway management oftentimes will lead to a greater success rate. Understanding the limitations to airway management in the prehospital environment is crucial, as is evaluating the patient and circumstances surrounding the working environment. Several mnemonics⁴⁵ have been developed for the rapid evaluation of potential difficulties in bag-valve-mask-assisted ventilations, intubation, blind insertion airway devices, and cricothyroidotomy.

MOANS

All providers should maintain competence in the basic airway technique of bag-valve-mask (BVM) ventilation (Figure 34-3). The ability to effectively oxygenate and ventilate a patient using a BVM may be crucial and can be potentially lifesaving. Assist devices such as nasopharyngeal or oropharyngeal airway placement may improve the effectiveness of BVM ventilations. There are several rapid assessment areas that focus on setting up for success utilizing a BVM and can be easily remembered by the MOANS mnemonic.

FIGURE 34-3.

Bag-valve-mask (BVM) ventilation. Here the classic one-handed “c-hold” helps maintain the seal and allow for BVM ventilation.

Mask seal. Facial fractures or deformities, either congenital or from prior trauma, may impede the ability to form an airtight seal. Facial hair may also limit the quality of seal that can be obtained. Appropriate mask and bag size selection is also crucial, especially in the pediatric population.

Obesity or Obstruction may make ventilation more challenging and not provide for sufficient tidal volumes. Obese individuals have an increase in weight that must be displaced for adequate ventilation and may have redundant pharyngeal tissue that may lead to an airway obstruction. Other factors for consideration include the presence of foreign bodies or anatomical upper airway obstructions.

Age-related factors also need to be taken into account. Both the young and old may have a lack of supporting skeletal structures needed to create a good mask seal. Elderly patients may also lack muscle tone in the upper airway and tend to an obstruction.

No teeth limits the ability to create a good mask seal. If present, leaving dentures in place provides more support to obtain a good seal.

Snoring, Stiff lungs, or Spinal precautions may also make BVM ventilation more challenging. Individuals who are suspected of having cervical spine injuries are frequently placed in a cervical collar which will limit the ability of the provider to open the airway by mechanical manipulation. Patients with various lung pathology may have reduced pulmonary compliance, while other disease processes may require adjusting the inspiratory to expiratory ratio to prevent air trapping.

RODS

Blind insertion airway devices have become more common in medical practice. Although there are a variety of devices available, the principal design is relatively similar: obstruct entry into the esophagus and allow outflow through the pharynx so ventilation may occur. Placement of these devices depends largely on which device is being used; however, patient evaluation remains similar. Utilizing the RODS mnemonic, one can anticipate which patients will be more challenging for appropriate blind insertion airway device placement.

Restricted mouth opening. This is most commonly caused by a small oral aperture either through the patient's anatomy or injury.

Obstruction of the upper airway either through a foreign body, trauma, or swelling. Consider development of an obstruction or airway dislodgement in a patient who becomes more difficult to ventilate.

Distorted airway anatomy either from trauma, mass effect, or previous surgery may only become evident after attempted placement. These devices work well on normal anatomy, but significant variations may cause the device not to function appropriately.

Spinal precautions and Stiff lungs. Elevated airway pressures may reduce the effectiveness of the seal and allow air to enter the stomach or escape from the pharynx. Some devices allow passage of a gastric tube to help reduce the risk of aspiration.

LEMON

Correct placement of an endotracheal tube is still considered the definitive airway device. Many factors combine to make placement of an endotracheal tube successful, and preparation is one of the most important. The LEMON mnemonic was developed to help determine which patients may be more challenging to intubate.

Looking at the external anatomy and features of the patient is paramount. Individuals with significant facial hair may obstruct a provider's view. An abundance of oral secretions or trauma may obscure vocal cord visualization. Patients with prominent incisors may also pose a challenge with direct laryngoscopy.

Evaluate using the 3-3-2 rule will allow for prediction of alignment of the oral, pharyngeal, and laryngeal axis. This is performed by seeing if the patient can open their mouth three fingerbreadths, if there is a distance of three fingerbreadths from the chin to the hyoid bone, and if there is a distance of two fingerbreadths from the hyoid bone to the thyroid.

Mallampati score refers to the four-classification system for ease of visualization of the posterior pharynx (Figure 34-4). Class one allows for visualization of the posterior pharynx, soft palate, entire uvula, and tonsil pillars while class two allows for visualization of the soft palate and uvula. Both of these Mallampati classifications should allow for good visualization with direct laryngoscopy. Class three allows for visualization of the soft palate and the base of the uvula while class four allows visualization of the hard palate only. Both class three and four predict a difficult airway. In the prehospital setting, complete Mallampati evaluation is not always appropriate prior to attempting endotracheal intubation.

FIGURE 34-4.

Mallampati classification. A: Class I. B: Class II. C: Class III. D: Class IV. (Reproduced with permission from Reichman EF. Essential anatomy of the airway. In: Reichman EF, ed. Emergency Medicine Procedures. 2nd ed. New York, NY: McGraw-Hill; 2013:chap 6.)

Obstruction including foreign bodies, soft tissue swelling, and trauma may also pose a challenge to endotracheal intubation. The provider may need to be ready with alternative airway devices or adjuncts in order to secure the airway in patients with suspected obstruction. Patients with pronounced soft tissue swelling may need a smaller diameter endotracheal tube which may allow for smoother passage.

Neck mobility is a concern for all patients requiring airway management in the prehospital setting. Victims of trauma with possible or suspected cervical spine injuries should have cervical spine precautions when feasible. Without the ability to extend the patient's neck, endotracheal intubation may be more challenging. Also consider neck mobility in patients with previous fusion and those with a history of spondyloarthropathies.

SHORT

If a patient cannot be intubated, and ventilation cannot occur even with the assistance of BVM or other devices, consideration of a surgical airway such be entertained, specifically cricothyroidotomy. In children, transtracheal ventilation may be a better option depending on the age of the patient. Performing a cricothyroidotomy on a patient with laryngotracheal injuries is a relative contraindication as attempting the procedure may worsen the injury.⁴⁶ There are no absolute contraindications to performing a surgical airway if the patient is in extremis and there are no other means of establishing an airway.

Scars and previous Surgery to the anterior aspect of the neck may interfere with normal anatomy and make the surgical procedure more difficult. Also, the presence of subcutaneous emphysema may signify a disruption to the trachea.

Hematoma formation may be evidence of a vascular injury displacing the trachea from midline and also make the procedure more difficult if active bleeding is ongoing. Obesity will obscure the normal landmarks and oftentimes provide excess subcutaneous tissue to go through before reaching the anterior aspect of the trachea.

Radiation therapy may distort normal anatomy and cause scar tissue formation which may make blunt dissection more difficult.

Tumors and other masses pose an issue in terms of landmark identification, tracheal deviation, and the possibility of bleeding complications if the tumor is violated.

CHALLENGES OF AIRWAY MANAGEMENT IN THE PREHOSPITAL SETTING

There are several challenges when caring for patients in acute respiratory distress or failure. Some of these may be anticipated and prepared for through simulations, continuing education, or experience obtained in an alternative environment such as the operating rooms or cadaver laboratory experiences. Physical obstacles may be encountered in the prehospital environment. Attempting to manage a patient's airway in the controlled environment of the emergency department or operating room is dramatically different than having a patient in a motor vehicle collision or in a small room in a residence. Maintaining cervical spine stabilization during attempted airway management may make the procedure more difficult. Environmental exposures to elements such as rain, extreme heat, and other elements may also provide additional challenges to appropriate airway management.

Equipment available to the prehospital provider may be limited to direct laryngoscopy for placement of an endotracheal tube or a supraglottic airway device. Utilizing a tool such as a gum elastic bougie may increase endotracheal intubation success rates⁴⁷ (Figure 34-5). With the introduction of video laryngoscopes, some prehospital providers have additional tools to assist with airway management.⁴⁸ Supraglottic airway devices are also becoming widely used throughout prehospital medicine (Figure 34-6). One impetus for this is the low frequency of endotracheal intubations performed by prehospital providers,⁴⁹ as well as some studies showing an improvement in time to ventilation with supraglottic devices in patients requiring airway management.⁵⁰ In patients with cardiac arrest, reinforcing the importance of early defibrillation and early and high-quality chest compressions remain vital to improved outcomes.^51,52 Utilizing supraglottic airway devices may minimize interruptions to chest compression while performing cardiopulmonary resuscitation.⁵³ Other equipment challenges encountered in the prehospital environment include lack of backup or supporting devices and personnel.

FIGURE 34-5.

Limitations in neck mobility may require advanced techniques. The EMS provider is using a bougie to enter the airway due to the use of spinal immobilization.

FIGURE 34-6.

Supraglottic airway device. The EMS provider is placing a supraglottic airway device (Combitube) as a rescue airway device after failed intubation.

MEDICATIONS FOR AIRWAY MANAGEMENT IN THE PREHOSPITAL SETTING

Correctly identifying a patient's underlying medical condition will allow prehospital providers to properly choose and implement medications to assist in patient management. Understanding appropriate indications and utilization of these medications in the prehospital environment is paramount in patient safety and outcome. Although the availability of medications may differ depending on the experience of the provider, level of training, and the guidance of the medical director, it is important to understand and be familiar with different medications for managing acute respiratory complaints and respiratory failure.

ADRENERGIC AGONIST

Management of acute bronchospasm, either in the setting of reactive airway disease or another cause continues to rely on the use of short-acting β-adrenergic agonists for dilation of the bronchioles.^54,55 Primarily, this is accomplished through stimulation of the β₂ receptor found within the smooth muscle of the bronchioles promoting relaxation of those structures. Several different medications fall into this category and are classified based on their duration of action. Long-acting β-agonists with duration of action over 12 hours, such as formoterol and salmeterol, are used primarily as maintenance medications by individuals who have known chronic obstructive pulmonary disease. The role of these medications in the acute setting is very limited and has been shown in some studies to be harmful. However, short-acting β-agonists such as albuterol and terbutaline, commonly given either through a nebulized solution or via metered-dose inhaler, with onset of action within several minutes and a duration of 4 to 6 hours, are classically used to treat an acute exacerbation of bronchospasm.⁵⁶ Albuterol is the most prescribed short-acting β-agonist in the United States.⁵⁷ Terbutaline may also be given subcutaneously, but this route of administration is commonly reserved for patients who do not respond to inhaled therapy or those in extremis.⁵⁸ Management of anaphylaxis and anaphylactic shock focuses on early administration of epinephrine.⁵⁹ Nonselectively activating both α- and β-adrenergic receptors, epinephrine has many systemic effects including vasoconstriction and increasing cardiac output. Epinephrine also acts to reduce the release of chemical mediators of anaphylaxis.⁶⁰ Epinephrine may be given subcutaneously, intramuscularly, or intravenously with the preferred route being intramuscular.⁶¹

ANTICHOLINERGIC

Anticholinergic agents work by inhibiting muscarinic-mediated bronchoconstriction and mucous production in the central airways and have been used effectively in the maintenance therapy of chronic obstructive pulmonary disease.⁶² The synergistic effect seen with the combination of an anticholinergic and a β₂ agonist may be related to the effects at both the central (anticholinergic) and peripheral (β₂ agonist) airways.⁶³ The combination has also shown a trend toward improvement in pulmonary function for individuals with both reactive airway disease and COPD.⁶⁴ Today, there are both short-acting and long-acting anticholinergic medications available for inhalation with both having low systemic effects.⁶⁵ The short-acting anticholinergic ipratropium is also available commercially in combination with albuterol and may be given as either a metered dose inhaler or nebulized solution.

MAGNESIUM

Another agent that is available for the treatment of reactive airway disease or bronchospasm is magnesium. It is believed that giving magnesium will reduce the amount of intracellular calcium in the smooth muscle, reduce contraction, and cause smooth muscle relaxation.⁶⁶ Current recommendation for magnesium therapy is limited to those with severe acute asthma⁶⁷ or those who have not responded to conventional management. Slow administration via the intravenous route is preferred but some reports of nebulized magnesium do exist.⁶⁸

CORTICOSTEROID

A hallmark of inflammatory disease management has been the administration of corticosteroids and has been used in the treatment of reactive airway disease and chronic obstructive pulmonary disease. In order for corticosteroids to work, they must cross the cellular membrane and combine with intracellular receptors. Following this combination enters the cell nucleus and decreases production of inflammatory mediator proteins. For patients with moderate to severe asthma, administration of systemic corticosteroids within 1 hour of presentation has been shown to reduce hospital admission rates.⁶⁹ Small studies have also shown that moving administration to the prehospital environment has a reduction in hospital admission rates as well.⁷⁰ Similarly, patients with exacerbations of chronic obstructive pulmonary disease appear to have improved clinical outcomes, improvement in spirometry,⁷¹ and decrease in treatment failure and relapse rates.⁷² Corticosteroid management still appears as a treatment option in patients with anaphylaxis although the routine administration of this medication is not supported.⁷³

VASODILATOR AND DIURETIC

Nitroglycerin is routinely utilized in the prehospital setting for the treatment of acute coronary syndrome. In the treatment of decompensated congestive heart failure with pulmonary edema, nitroglycerin has also been used, historically administered in combination with other medications including opiates and diuretics. Nitroglycerin is believed to have vasodilatory properties through the relaxation of smooth muscle by the local creation of nitric oxide⁷⁴ causing a reduction in preload. When used in the prehospital environment for the treatment of pulmonary edema, nitroglycerin has been shown to improve outcome related to dyspnea and hospital morbidity. As important, if the diagnosis of pulmonary edema is incorrect, which occurs up to 40% of the time, nitroglycerin was not associated with adverse events.⁷⁵ Other medications such as angiotensin-converting enzyme (ACE) inhibitors are currently being used in the prehospital setting.⁷⁶ Administration of ACE inhibitors has been associated with a decrease of intensive care admissions as well as a decrease in the need for intubation when administered in the emergency department for patients with acute pulmonary edema.⁷⁷ Prehospital administration of diuretics such as furosemide is not appropriate. The effects of furosemide are delayed and potentially increase morbidity or mortality if given to a patient with a different disease process such as pneumonia or sepsis.⁷⁸

RAPID SEQUENCE INTUBATION

Performing endotracheal intubation in patients who still maintain protective reflexes, including the gag reflex, may require the administration of a sedative and paralytic to optimize intubating conditions, improve success rates and patient outcome. Classically, positive pressure ventilation is not administered to patients undergoing rapid sequence intubation (RSI) if possible, but is a controversial issue.⁷⁹

PRETREATMENT

Several medications have been administered prior to induction and paralysis in the attempt to blunt the physiologic response to direct laryngoscopy including stimulation of the sympathetic and parasympathetic nerves of the larynx and hypopharynx, increase in intracranial pressure, and bronchospasm. The routine use of some of these medications, usually administered 3 minutes prior to induction, is not well supported.

LIDOCAINE

Lidocaine administration as a pretreatment to patients undergoing RSI due to asthma has been suggested to prevent bronchospasm from direct laryngoscopy and endotracheal tube placement. Studies with patients undergoing general anesthesia have suggested that the addition of lidocaine does not reduce postintubation bronchospasm.⁸⁰ Lidocaine has also been suggested to blunt the increase in intracranial pressure which some suggest is mediated by an increase in cardiac output and arterial pressure. Studying lidocaine use in RSI and the effect on intracranial pressure is difficult although some studies in the intensive care unit or elective neurosurgical cases have been performed. Some of the research is limited by confounding issues including other medications administered as well as the clinical setting. It is unclear if the routine use of lidocaine for pretreatment in the setting of acute traumatic head injury reduces intracranial pressure or has a positive effect on patient outcome.^81,82

FENTANYL

Ultrashort-acting opiates such as fentanyl have been suggested and used as pretreatment medications prior to RSI because they may decrease the sympathetic response seen with direct laryngoscopy. Fentanyl is hemodynamically neutral. When given as a pretreatment medication at 3 µg/kg, fentanyl was able to blunt the hypertension seen with laryngoscopy, but did not have an effect on heart rate.^83,84 In bolus doses higher than those used in RSI, studies have linked fentanyl to an increase in intracranial pressure and a decrease in cerebral perfusion pressure in patients who already have elevated intracranial pressure.⁸⁵

ATROPINE

Atropine administered as part of the pretreatment for a pediatric patient undergoing RSI is still common. The thought is to reduce reflex bradycardia in pediatric patients, but the data are conflicting. Bradycardia has been seen in both patients who do and do not have atropine administered prior to laryngoscopy.⁸⁶ Few adverse events have been reported with administration of atropine.

SEDATIVES

As part of RSI, a sedative agent is given prior to neuromuscular blockade. A variety of medications are available for sedation. Understanding the different options for sedation, as well as the appropriate clinical use, is very important. Selecting the appropriate agent may help improve patient outcome, whereas inappropriate sedative agents may have a detrimental effect.

Etomidate

Etomidate is an imidazole derivative which has no analgesic properties but is a potent sedative hypnotic agent. The onset of action in induction doses (0.2-0.4 mg/kg) is within 15 seconds with a duration of action up to 15 minutes. Few cardiovascular and respiratory effects are seen after its administration, making it an ideal induction agent. Unlike other induction agents, etomidate reduces intracranial pressure without reducing arterial blood pressure or cerebral perfusion pressure.^87,88 One of the concerns regarding routine use of etomidate for RSI is its potential to cause adrenal suppression. The continuous use of etomidate for sedation is not recommended because of this effect, and the single use for induction in patients has been investigated. Studies suggest that the adrenal suppression is transient and appears to resolve within 12 hours of administration⁸⁹ with no significant effect on patient mortality.⁹⁰

Benzodiazepine

Benzodiazepines are a class of medication that function through stimulation of the GABA receptors. Of the benzodiazepine agents, midazolam is the most commonly used for induction during RSI. The recommended dose for induction is 0.1 mg/kg to 0.3 mg/kg and may take up to 2 minutes for full effects to occur. When evaluating its use in RSI, midazolam is frequently underdosed in both the pediatric and the adult population.⁹¹ Use of short-acting benzodiazepines, such as midazolam, is limited in part due to the time for effect as well as the dose-dependent decrease in systemic vascular resistance and resultant hypotension.⁹²

Barbiturate

Ultrashort-acting barbiturates, such as thiopental and methohexital, have been used for induction as part of RSI in patients with suspected elevation of intracranial pressure or with status epilepticus. Barbiturates, similar to benzodiazepines, exert their effect through GABA receptors. Barbiturates have a negative cardiovascular effect and reduce both cardiac output and mean arterial pressure, but appear to have preservation of the cerebral perfusion pressure. Of the ultrashort-acting, methohexital has been reported to be less cardiac depressive. Other negative effects that have been seen with barbiturate administration include laryngeal spasm.⁹³ Both ultrashort-acting barbiturates have an onset less than 30 seconds and last up to 5 minutes.⁹⁴

Ketamine

Ketamine is considered a dissociative anesthetic with analgesic properties although it also causes stimulation of the sympathetic nervous system, resulting in an increase in heart rate, blood pressure, and cardiac output. Other effects of ketamine include bronchial dilation by smooth muscle relaxation. The effects of ketamine work through antagonism of the NMDA receptor.⁹⁵ Typical induction dosages of ketamine are 1 to 2 mg/kg when administered intravenously. The use of ketamine has been avoided in patients with suspected head injury due to concern for increase in intracranial pressure, but further research shows that this concern may not be justified.⁹⁶

Propofol

Propofol is a sedative hypnotic which also exerts effects by mediating the GABA receptors. Widely used in procedural sedation procedures, propofol has also been used in RSI with dosages of 1.5 to 2.5 mg/kg. Onset of action is approximately 30 seconds with a duration of up to 5 minutes. Propofol has been shown to reduce cerebral blood flow, cerebral oxygen consumption, and decreases intracranial pressure.⁹⁷ The role of propofol has been limited in rapid sequence intubation due to the cardiac depressant effect and noted hypotension.

Neuromuscular Blockade

With RSI, the administration of a neuromuscular blocking agent assists in optimizing intubation success. There are two different types of neuromuscular blocking medications available currently and differ in the mechanism of action: depolarizing and nondepolarizing. The nondepolarizing neuromuscular blockers may be reversed by administration of acetylcholinesterase inhibitors.

Depolarizing Agents

Depolarizing neuromuscular blockers, such as succinylcholine, work by depolarizing the postsynaptic acetylcholine receptors, thus making them resistant to further stimulation by acetylcholine. Succinylcholine has long been used as the neuromuscular blocker of choice in RSI due to the extremely quick time of onset (approximately 30-45 seconds) and its short duration of action (less than 10 minutes). However, there are many relative contraindications which should be well understood by the prehospital provider.

Hyperkalemia has been associated with the administration of succinylcholine with peak increase occurring between 2 and 5 minutes following neuromuscular blockade. The increase in potassium levels has been reported between 0.5 and 1 mEq/L, and is transient over a period of 10 to 15 minutes.⁹⁸ It is believed that this increase is caused by an upregulation of the acetylcholine receptor, leading to potassium efflux. Caution should be exercised in patients who may be predisposed to the hyperkalemic side effect of succinylcholine including patients with burns and crush injuries (although in the acute setting, succinylcholine may be administered), chronic peripheral denervation either from stroke or spinal cord injury, severe infections, prolonged immobility with resultant atrophy, certain myopathies, and those who are hyperkalemic or at risk for being hyperkalemic.^99,100

Succinylcholine has been reported to increase intraocular pressure and it has been propagated that an open globe injury is a contraindication to administration, but there have been no cases of vitreous extrusion or blindness linked to succinylcholine.¹⁰¹

Nondepolarizing Agents

Nondepolarizing neuromuscular blockers, such as rocuronium and vecuronium, work by blocking the binding of acetylcholine to the postsynaptic receptors in a competitive fashion. There are many different nondepolarizing neuromuscular blockers available, with differing properties in terms of onset as well as duration. Rocuronium has a recommended dosing of 0.6 mg/kg with onset of approximately 1 minute and duration near 1 hour, while vecuronium has a recommended dosing of 0.1 mg/kg with onset of approximately 2 minutes and a duration near 2 hours. Nondepolarizing neuromuscular blockers do not have the same adverse effects as seen in succinylcholine, but the longer onset and duration of action¹⁰² make them less favorable for RSI. Reversal of neuromuscular blockade is possible with acetylcholinesterase inhibitors such as neostigmine, as well as other commercially available medications that are not currently available in the United States, but are currently in use in other countries.¹⁰³

Early comparison studies looking at the difference between success rates of neuromuscular blockade for rapid sequence intubation with succinylcholine compared with rocuronium do not show significant difference.¹⁰⁴

KEY POINTS

Respiratory failure and anaphylaxis are acute life-threatening conditions that can and must be addressed by prehospital providers.
Causes of respiratory failure and anaphylaxis are numerous and of varied etiologies.
Treatment options for respiratory failure and anaphylaxis are effective and can range from minimally invasive to invasive.
Assessment of the airway is important to optimize successful management.
There are many useful medications and equipment options available to the prehospital provider treating respiratory failure and anaphylaxis.

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Shock and Hemorrhage

Christopher J. Fullagar

INTRODUCTION

The evaluation and treatment of shock in the prehospital environment presents unique challenges to the EMS physician. Decisions regarding the balance between sophisticated field treatment and minimizing transport time to definitive care must continually be evaluated. The benefit of advanced care in the field has been questioned.^1–3 Some studies have demonstrated that the addition of the physician on the scene may increase scene time in certain scenarios, while other studies have not observed this effect.³ This is likely related to the prehospital training and experience of the physician. Balancing physician intervention with scene time is an important part of the care of the patient in shock and must be explored during the EMS education of residents and fellows.

OBJECTIVES

Describe the identification of shock in the field.
Describe the initial management of shock in the field.
Analyze the causes of shock.
Examine how to treat specific causes of shock while in the prehospital setting.
Present the use of advanced vascular access and pressors in the field.
Discuss the use of tourniquets and hemostatic agents for severe hemorrhage.

CARE OF SHOCK IN THE FIELD

Physician participation in the field is routine in the Franco-German model of prehospital care and is becoming more common in the United States. Participation in the field also allows the physician to gain a first-hand perspective on how the system works. The physician is often in a position to have an effect on protocols, provider education, and operational matters that affect patient care. For those in training, participation in the field provides them with critical insight into the challenges and limitations of caring for patients in the out-of-hospital setting. Without an understanding of the differences inherent in the provision of prehospital emergency care, it is often less than productive to apply in-hospital evaluation and treatment techniques in the field environment. To treat a patient in shock effectively in the field environment requires a knowledge base specific to EMS.

Shock is a state of decreased perfusion resulting in inadequate delivery of oxygen to the tissue. Typically, the body has exhausted its ability to compensate for the stressors it is experiencing. The principles for management of shock include the maintenance of perfusion while supporting ventilation and oxygenation. The precise degree of resuscitation of the patient depends on a number of factors and has been the topic of significant discussion in the literature.⁴ The prehospital environment presents unique challenges when treating a patient in shock. Equipment and supplies are typically limited in the field environment. Austere conditions such as temperature extremes, darkness, and precipitation may hamper care of the patient in shock. Temperature control is a significant factor. Initial studies indicated that therapeutic hypothermia may have beneficial effects on patients after return of spontaneous circulation (ROSC), although further evaluation of this is required.⁵ Alternatively, trauma patients requiring massive transfusion with a core temperature less than 34°C is associated with a mortality rate >85%. Maintaining an adequate environment in the ambulance may be challenging. Factors as simple as opening the doors to the back of the ambulance on a cold day may have a significant effect on the cabin temperature. Warmed saline may not be as readily available in the field. For hypothermic patients, interventions such as invasive warming may not be practical or even possible in the field environment. This is to say nothing of the patient who cannot be removed from the elements such as is the case with vehicle entrapment or patients in remote locations.

SHOCK RECOGNITION

Identification of the patient in shock may not be as apparent in the field environment as it may be in the hospital. Equipment is limited and environmental factors such as temperature and vibration may affect the accuracy of that equipment. Skin color and temperature that is consistent with shock may be difficult to differentiate from a normal response to outdoor environmental factors. Peripheral vasoconstriction in colder environments may render distal SaO₂ monitors useless. Other equipment such as EtCO₂ detectors and prehospital ultrasound, which can indicate poor ventilatory exchange and ventricular collapse respectively, may not be available to assist in the diagnosis of shock.

SHOCK TYPES

Shock is generally divided into four main categories: hypovolemic, cardiogenic, obstructive, and distributive. While the overarching goal of shock management is to support adequate perfusion, specific interventions tailored to each type of shock are important.

HYPOVOLEMIC SHOCK

Hypovolemic shock results from decreased intravascular volume. Decreased preload leads to a compensatory increase in both cardiac output and systemic vascular resistance. Etiologies may include hemorrhage or other fluid losses such as gastrointestinal, insensible losses, burns, and third spacing.

CARDIOGENIC SHOCK

Cardiogenic shock is secondary to a failure of the cardiac pump itself. Systemic vascular resistance increases to compensate for diminished cardiac output. Etiologies include arrhythmias, cardiomyopathies, and mechanical abnormalities such as valve dysfunction. In all of these cases the ability of the heart to maintain adequate cardiac output is overwhelmed, leading to inadequate systemic perfusion.

OBSTRUCTIVE SHOCK

Obstructive shock is sometimes classified as a type of cardiogenic shock as the heart is unable to maintain output due to an extracardiac etiology. This type of shock is secondary to mechanical impedance of forward flow such as saddle pulmonary embolism (PE) or tension pneumothorax.

DISTRIBUTIVE SHOCK

In distributive shock, systemic vascular resistance is compromised. Cardiac output is increased in an effort to compensate for the vasodilatory effects that cause distributive shock. Distributive shock includes septic shock, anaphylaxis, and other systemic inflammatory processes. Neurogenic shock may fall into this broader category.

COMBINED SHOCK

In addition to the broad categories above, a particular process may produce different types of shock simultaneously. Sepsis is an excellent example of this. In addition to the vasodilatory effects of the inflammatory mediators (distributive shock), the septic patient may also have a component of hypovolemic shock secondary to decreased oral intake, insensible losses, and GI losses. Myocardial irritability may also result in cardiac arrhythmias inducing a component of cardiogenic shock.

GENERAL CONSIDERATIONS IN THE MANAGEMENT OF SHOCK

Initial management of the patient in shock follows the typical mantra of critical care patient management. Consideration of the primary survey with the establishment of high flow oxygen administration, cardiac monitoring, and establishment of IV access, typically two large bore IVs, is compulsory in the field as it is in the hospital. Limitations of equipment, space, or personnel may limit interventions to those that have the highest priority, but, in general, all of these are critical initial steps in the general field management of the patient in shock. While the necessity of establishing two large bore IVs has been challenged, it warrants consideration that in the chaotic scene environment one should anticipate that a single IV may become inadvertently dislodged by a combative patient or patient moving mishap.⁶ With any advanced procedure the understanding of when not to perform an intervention is often as critical as knowing when to perform one. Any intervention must be weighed against scene time, provider safety, and issues of sterility.

BASIC LIFE SUPPORT

Initial interventions need not be advanced to have a significant beneficial effect on the patient in shock. It is important not to overlook or underestimate the effect of basic life support (BLS) intervention on a critical patient. Simple positioning of a patient in supine or slightly elevating the feet can be beneficial to maintaining perfusion. The importance of BLS care is amplified in an environment where advanced equipment is limited. Aggressive basic hemorrhage control with direct pressure and tourniquets, when needed, can have a profound effect on patient outcome. Other BLS maneuvers, such as proper basic stabilization of a pelvic fracture, are essential. Overlooking basic interventions such as these could prove fatal during transport if not properly implemented.

PARENTERAL FLUID HYDRATION

Normal saline solution is a satisfactory choice for initial resuscitation. Lactated Ringer's has also been suggested in the treatment of trauma- induced shock. Lactated Ringer's fails to show significant benefit over normal saline in the immediate phases of resuscitation and may not be available in the field.⁴ Rapid administration of fluid must be tempered with the risks of volume overload which may result in pulmonary edema and hemodilution. In addition, the cooling effect of unwarmed saline administration may compound hypothermia in a patient in shock. According to the Hagen-Poiseuille equation of fluid dynamics flow is inversely proportional to length and exponentially proportional to diameter (Figure 35-1). Rapid instillation fluids are best administered via a short, large bore line. Hence, shorter peripheral IVs are preferable to longer central lines for rapid volume administration. The question whether to administer large quantities of fluid rapidly or to delay fluid administration continues to be unanswered. There is no definitive evidence for or against the use of rapid or high-volume administration of fluid in patients with uncontrolled hemorrhage in trauma.⁴ Many practitioners will titrate fluid hydration in trauma to various end points such as maintenance of the patient's mental status or an arbitrary systolic blood pressure such as 90mm Hg or mean arterial pressure of 60 mmHg.

FIGURE 35-1.

Fluid catheter radius and length effect on flow. Adaptation of the Hagen-Poiseuille equation demonstrating the relationship among the catheter radius (r), catheter length (L), and rate of fluid flow.

VOLUME EXPANDERS

The determination of colloid versus crystalloid infusion in the treatment of shock has long been discussed. Albumin and hetastarch are two common examples of colloids. Initially, there were theoretical advantages of colloid infusion including less risk of pulmonary edema and faster volume expansion. A number of studies failed to demonstrate that colloids provided any significant benefit over crystalloid.⁷ The use of colloid in trauma resuscitation has fallen out of favor due to poor efficacy and higher cost compared to crystalloid.

VASOPRESSORS

The decision regarding when and how to administer vasopressors in the field to a patient in shock depends, in part, on the cause of the shock itself (Table 35-1). Patients who are fluid overloaded, for example, may require vasopressors sooner than those who can tolerate volume resuscitation. Pressor choices are often limited in the field and relatively infrequently used. This coupled with cost and other factors such as shelf life or need for temperature control further contribute to limit the choices of pressors in most advanced life support (ALS) ambulances. There may be additional choices, however, in critical care transport units or in EMS physician vehicles. These units may handle a higher proportion of critical calls and cover a wider geographic area. Vasopressors are often recommended to be administered via a central line. This is mainly because of the sclerotic complication should extravasation of the pressor occur in the periphery. In the prehospital environment placement of a central line is often not practical for a number of reasons. Space is limited and, in an uncontrolled environment, it may be difficult to maintain sterility. This is not to mention the potential for injury to the providers from the sharps required to perform this procedure. In the field vasopressors are often started peripherally until after arrival to the hospital, when a central line can safely and more practically be placed. The choice of vasopressor agents used in EMS may vary. In most cases, the choice is often limited to one or perhaps two agents. While no individual agent has been determined to be superior to another, there are some differences among the available agents⁸ (Table 35-2). In addition, certain agents may be associated in a greater number of adverse events such as increase incidence of arrhythmias with dopamine compared with norepinephrine.⁹

TABLE 35-1

Common Vasopressors

TABLE 35-1

Common Vasopressors

Drug

Dose

Dopamine

• Low dose: <5μg/kg/min

• Moderate dose: 5-10μg/kg/min

• High dose: >10μg/kg/min

Dobutamine

2.0-20μg/kg/min

Epinephrine

• For refractory hypotension

• Typical dosing is 1-4μg/min (1:10,000 solution)

• For anaphylaxis, the dose and route change, based on the presence of shock:

• Without evidence of shock: 0.3-0.5mg (300-500μg) IM q 5-10min (1:1000)

• With evidence of shock: 0.1mg (100μg) IV, which is 1.0mL of 1:10,000 dilution IV given slowly over 3-5 min or infused at 5-15μg/min

Norepinephrine

0.03-3.0μg/kg/min

Vasopressin

• 0.04U/min

• Not titrated

Phenylephrine

• 0.5-8μg/kg/min

• 100-180μg/min IV drip

Isoproterenol

2-10μg/min

Milrinone

50μg/kg bolus, and then 0.25-1μg/kg/min

Reproduced with permission from Marshall JP, Rollstin A, Chiu W, Chiu WC. Vasopressors and inotropes. In: Farcy DA, Chiu WC, Flaxman A, Marshall JP, eds. Critical Care Emergency Medicine. New York, NY: McGraw-Hill; 2012:chap 16.

TABLE 35-2

Physiological Effects of Vassopressors

TABLE 35-2

Physiological Effects of Vassopressors

Drug

MAP

SVR

Dopamine (moderate–high dose)

Increased

Dobutamine

Variable

Decreased

Increased

Epinephrine

Variable

Increased

Norepinephrine

Increased

0 → decreased

Increased

Vasopressin

Increased

Phenylephrine

Increased

0 → decreased^a

0 → increased

Isoproterenol

Decreased

Increased

Variable

Milrinone

Variable

Decreased

Increased

CO, cardiac output; HR, heart rate; MAP, mean arterial blood pressure; SVR, systemic vascular resistance

^aPhenylephrine can produce reflex bradycardia as a side effect of hypertension. Reproduced with permission from Marshall JP, Rollstin A, Chiu W, Chiu WC. Vasopressors and inotropes. In: Farcy DA, Chiu WC, Flaxman A, Marshall JP. eds. Critical Care Emergency Medicine. New York, NY: McGraw-Hill; 2012:chap 16.

BLOOD

Carrying of blood in the field poses a number of challenges. Blood supply is limited and the lack of availability of type and crossmatch necessitates the use of O negative blood. Blood has a limited shelf life and must be kept within a narrow temperature range. This limits blood to some air and ground critical care transport units. In some areas, blood is carried in a designated physician response unit. This potentially allows a larger potential response area than placing the blood on a unit that covers a single jurisdiction.¹⁰

TRANEXAMIC ACID

Tranexamic acid (TXA), an antifibrinolytic agent, has garnered significant attention as studies have indicated a significant reduction in mortality when used in trauma patients. The use of TXA has been advocated in a wide spectrum of patients with traumatic bleeding, not simply those who are most severely injured.¹¹ TXA is classified as an antifibrinolytic agent, antihemophilic agent, hemostatic agent, and lysine analog. The exact mechanism of action responsible for the observed decrease in mortality among trauma patients is not known.¹² The recommended infusion of TXA is 1 g over 10 minutes followed by 1 g over 8 hours. It is suggested that TXA be started as soon as practical, making this an attractive adjunct for the prehospital phase of trauma resuscitation. In the CRASH-2 trial, TXA (or placebo) was started within 3 hours of the trauma.⁸ As the use of TXA is becoming more widespread it will be interesting to see how the results compare with use on a larger scale.

BICARBONATE

There remain varying opinions regarding the use of bicarbonate for acidotic patients in shock. Studies have failed to show a benefit from bicarbonate administration in morbidity, mortality, or improved cellular function in the acidotic patient.¹³ In the field it would be rare to have precise knowledge of a patient's pH. While there is no evidence that bicarbonate has a significant effect on the patient in septic shock, many practitioners will administer bicarbonate for a profoundly low pH. Generally, correction beyond a pH of 7.25 is not recommended, although some prefer lower values. While typically available in the prehospital setting, the use of bicarbonate in the field for this indication is further limited by lack of patient data and utility.

PNEUMATIC ANTISHOCK GARMENT

Recent literature regarding the use of pneumatic (PASG) and nonpneumatic antishock garments has centered on use in areas of the world with limited medical resources, particularly associated with the treatment of postpartum hemorrhage. In the United States, many EMS systems have reduced or eliminated the use of PASGs citing a number of drawbacks and lack of evidence showing definitive benefit for the patient in shock. Some of the issues include the amount of time required to properly deflate the garment once the patient arrives at the trauma center. There has also been discussion regarding increased mortality in patients with penetrating chest trauma with and general questions about the shunting of blood to uncontrolled internal injuries. Furthermore, inflation of the abdominal compartment may compromise ease of breathing. The position statement of the National Association of EMS physicians entitled “Use of the Pneumatic AntiShock Garment (PASG)” has been moved to the “historical” section of the page.

TRANSPORT DECISIONS

The transport of a patient in shock is in part determined by the etiology underlying the shock presentation. Decisions regarding hospital capabilities versus proximity must be considered. Since trauma outcomes revealed that bypassing a local hospital in favor of a trauma center improved outcomes, this concept has since been applied to other etiologies of shock. For example, a patient in cardiogenic shock secondary to ST-segment elevation myocardial infarction (STEMI) may be best served at a facility that can provide emergent percutaneous transluminal coronary angioplasty (PTCA) intervention. States may designate certain centers for particular presenting conditions such as strokes. Other presentations may be more difficult to triage in this way as the extent of the assessment of the patient may be limited in the ambulance. EMS physicians may be able to anticipate the needs of the patient and determine the best facility based on patient presentation and hospital specialty service availability.

TREATMENT OF SPECIFIC CAUSES OF SHOCK

HYPOVOLEMIC SHOCK

The mainstay of the treatment of hypovolemic shock is generally fluid repletion. Administering fluids in this instance is preferred over the use of vasopressors as the former helps correct the underlying problem. While specific end points are somewhat controversial, and will vary depending on the particular scenario such as trauma, objective signs can be used to determine the adequacy of treatment. Perhaps more important than a particular blood pressure number, signs such as mental status and skin color should facilitate in determining whether further fluid therapy is warranted. While not all trauma patients may warrant aggressive fluid resuscitation, those that are in severe shock require some volume repletion. Initial administration of isotonic saline is the typical starting point in prehospital emergency care. If more than 2 or 3 L are required, blood can be considered if it is available. In the absence of blood, TXA may be an alternative in the setting of severe hemorrhage if started in a trauma system that uses it. Colloids are generally not recommended. Surgical intervention is the definitive treatment for major trauma and rapid transport to an appropriate trauma center should not be delayed.

CARDIOGENIC SHOCK

The prehospital treatment of cardiogenic shock is best managed according to the underlying etiology. In some cases, such as STEMI, destination decisions may come into play. Although many hospitals can provide fibrinolytic medication, not all can provide PTCA capability. There is evidence to suggest that patients fare better when transported to a facility that can provide PTCA providing the transport is less than 90 minutes.¹⁴ The EMS physician, either on scene or remotely, can influence destination and mode of transport decisions on a case-by-case basis. For patients in remote locations, air medical transport may be the only practical way to deliver the patient to the best-suited facility or, in some cases, the only advanced care available. While there are no uniform national utilization guidelines for air medical transport at this time, the EMS physician may assist in identifying which patients might be most appropriate for this intervention. Acute decompensated heart failure may also be treated effectively in the field. Medications to reduce preload and diurese, such as nitroglycerin and furosemide, are often carried on advanced life support units. Particular caution must be exercised in patients with aortic stenosis. The availability of prehospital noninvasive positive pressure ventilation (NPPV) has also expanded in many regions. Patients with acute pulmonary edema and dyspnea may benefit significantly from NPPV in the prehospital setting. Patients with hypercarbia appear to fare particularly well with NPPV. Mortality seems to be reduced more significantly in patients with acute decompensated heart failure secondary to acute myocardial ischemia or infarction.¹⁵

OBSTRUCTIVE SHOCK

Treatment of obstructive shock, such as pulmonary embolism, is somewhat limited in the prehospital setting. Initial treatment is centered on resuscitation and hemodynamic stabilization of the patient in shock. The mainstay of treatment is the prevention of recurrent embolism in the acute setting after the initial event. Anticoagulation is rarely available in the field. Fluids, vasopressors, and respiratory support are the mainstay of field treatment of PE.

DISTRIBUTIVE SHOCK

Anaphylactic reaction is a true medical emergency and prompt intervention in the prehospital setting is paramount to survival. Initial intervention is intramuscular (IM) epinephrine injected into the thigh.¹⁶ Epinephrine administration for anaphylaxis should be instituted prior to second-line treatments such as antihistamines and corticosteroids. There are no absolute contraindications to epinephrine administration in the setting of anaphylaxis.¹⁷ For patients who are refractory to repeated IM administration of epinephrine, some suggest the use of intravenous epinephrine. If this is considered, it must be done with the utmost caution in the prehospital setting, as it is not the ideal setting to administer IV epinephrine. Often the advanced provider is working alone and multitasking. The epinephrine dose must be carefully calculated and, in some cases, mixed. IV pumps are often not available. One recommendation is to draw up 0.1mg (0.1mL of the 1:1000 solution) into 10cc of normal saline. This provides a concentration of 1:100,000 which may be administered over 10 minutes.¹⁸ Ideally, this should be administered by IV pump and titrated to effect. Continuous cardiac monitoring is required and the infusion should be stopped if the patient develops arrhythmia or chest pain. Patients with anaphylaxis may have upper airway involvement as manifested by stridor, lower airway involvement/bronchospasm and/or hypotension. IV fluid bolus may be initiated after initial epinephrine administration if distributive hypotension is present. Allergic bronchospasm may benefit from bronchodilators. EMS physicians may also consider addition of inhaled anticholinergics or magnesium sulfate administration in refractory cases. Magnesium sulfate is often carried on the ambulance. For this indication, magnesium sulfate should be administered 2 g IV over 20 to 30 minutes in adults. Another consideration for physicians is the administration of glucagon for patients on β-blockers therapy in the setting of refractory anaphylactic hypotension. While glucagon supply may be limited in the ambulance, initial dose of 1mg IV every 5 minutes is a reasonable starting point, although starting doses as high as 5mg or more have been recommended, and may be considered as the situation and medication supply allows.

SEPTIC SHOCK

The choice for the best sedative agent to use in the field may still spur some controversy.¹⁹ While a single dose of etomidate has been shown to suppress adrenal secretion of cortisol, there has been no evidence linking this with increased mortality.²⁰ Many still feel as though etomidate is the best choice given the potential drawbacks of the alternatives. Others prefer ketamine as an alternative to etomidate in such instances.²¹ One of the mainstays of the treatment of septic shock is the administration of IV fluid.²² Some patients require 5 L of IV fluid in the first 6 hours of treatment. Patients will need to be monitored closely for the development of pulmonary edema particularly if there are underlying comorbidities that predispose them to this. Dividing the fluid administration into smaller boluses interspersed with clinical evaluation for pulmonary edema is possible without compromising the overall rapid infusion of needed fluids.

Vasopressors are the next line of intervention although they should be avoided until the patient's fluid deficit has been properly corrected. There are instances in the field, however, when vasopressors must be initiated before the fluid balance is completely corrected, particularly in the cases of profound hypotension or the development of pulmonary edema. While there is no definitive evidence to suggest a particular vasopressor in the setting of sepsis, there are some data to suggest that norepinephrine, if available, should be considered over dopamine. This is primarily because dopamine has been associated with an increased incidence of arrhythmias.⁷

ADVANCED VASCULAR ACCESS

INTRAOSSEOUS VASCULAR ACCESS

The availability of adult intraosseous (IO) access is now widely available in the prehospital setting. For rapid and safe vascular access in the field environment the IO may be the most practical method when intravenous (IV) access is difficult or impossible. Incidence of infection such as osteomyelitis is uncommon following IO access. Complications are generally considered minimal.²³ IO insertion techniques and locations may vary among the available devices. Removal may also be different based on the particular device used. Generally, the IO device should be left in place for no more than 24 hours. Although limited, this provides ample time to secure alternate vascular access in the hospital. Medications given via the IO route have been shown to have rapid systemic absorption.²⁴ Medications that can be given via the IV route may also be administered IO.

VENOUS CUTDOWN

With the increased availability of IO access in the field, venous cutdown is not often required for rapid access in the out-of-hospital environment. While saphenous vein cutdown may be of use in the pediatric population, IO access may be preferred in critical field situations.

CENTRAL VENOUS ACCESS

Central venous access has traditionally been practiced by some air medical and ground critical care transport agencies. Physicians with experience establishing these lines in the hospital may be inclined to initiate central lines in the field. Again, with the availability of adult IO access, central venous access has become less relied on in critical care scenarios in the field. Concerns regarding complications such as pneumothorax and sepsis may be more of a risk in the field setting. Ultrasound may not be available and difficulty may be encountered attempting to maintain strict sterility. The time it takes to perform the procedure may prolong delivery of the patient to definitive care. In addition, central venous access generally requires multiple sharps such as a scalpel, and needles for suture, lidocaine administration, and initial vascular access, all of which may pose a hazard to the providers in the austere field environment.

UMBILICAL VEIN CUTDOWN

The EMS physician faced with a critical premature or term newborn may consider performing an umbilical vein cutdown if peripheral or IO access is unsuccessful or unavailable.²⁵ This decision is tempered by the complications that may occur (Table 35-3).²⁶ In addition, proper equipment, such as the appropriate catheter, may not be available. Generally a 5-French catheter for term infants and 3.5-French catheter for preterm infants are recommended. Typically, 4 to 5 cm of catheter length is required for emergency access. With any procedure done on a newborn it is important to consider hypothermia and maximize heat retention in the field environment.

TABLE 35-3

Complications of Umbilical Vein Cutdown

TABLE 35-3

Complications of Umbilical Vein Cutdown

Thromboembolic events

Bacteremia/sepsis (particularly heart and liver)

Intracardiac placement or migration

Arrhythmias
Cardiac perforation
- Pericardial effusion
- Cardiac tamponade

Portal vein placement

Thrombosis of hepatic vein
Infusion of hypertonic or vasospastic solution
- Hepatic necrosis
Necrotizing enterocolitis
Perforation of colon

SPECIAL ISSUES IN HEMORRHAGE CONTROL

TOURNIQUETS

The management of massive trauma in the field has developed from our experience with military and civilian tactical medical support. Not long ago tourniquets were a last resort for hemorrhage to be used only after all other methods of bleeding control failed. Now, in many areas, the use of tourniquets has been moved up on the algorithm as we have learned the importance of aggressive hemorrhage control and the relative safety of limited-time tourniquet application. The overstated concern of the complications of tourniquet use in the field expressed by previous EMS teaching contrasted with the experience in the operating room when tourniquet use occurs routinely for relatively extended periods. In this setting, it is not uncommon for a tourniquet to be on for 1 to 2 hours. The 2-hour upper limit for surgical patients is customary and likely derived from animal studies that show changes at the 2- to 3-hour mark. These changes, however, are typically temporary and there is no evidence to suggest that leaving a tourniquet up for greater than 2 hours should necessarily be contraindicated in the rare instances in which it is necessary.²⁷ Some EMS protocols recommend loosening the tourniquet periodically for brief intervals if prolonged use is required. On the other hand, if severe bleeding is not adequately controlled by the initial tourniquet, a second tourniquet may be added proximal to the first. Accurate documentation of the time of tourniquet application is recommended, and in prehospital settings, is often written on the patient's forehead or on the commercially available tourniquet on the provide tag (Figure 35-2).

FIGURE 35-2.

Combat application tourniquet (CAT).

HEMOSTATIC BANDAGES

The use of hemostatic bandages has been well demonstrated in the combat environment. EMS and combat medicine share many similarities. Operating in critical situations with limited resources in austere environments is reciprocally applicable. The drawbacks of hemostatic bandages have largely been addressed. Exothermic reactions, localized tissue necrosis, and difficulty corralling the loose granulations have been remedied by revised formulations packaged in self-contained bandages. Hemostatic bandages are particularly useful to control severe bleeding in areas where tourniquet use would not be possible such as the head, neck, and trunk. These bandages may also be used as adjunct to tourniquets in severe extremity bleeding and should be considered when assembling EMS physician field equipment (Figure 35-3).

FIGURE 35-3.

Some hemorrhage control devices. From top to bottom: wound stapler, CAT, disposable cautery, hemostatic gauze.

PROTOCOL DEVELOPMENT

There has been a general push to standardize the care that EMS provides across systems. When developing protocols it is important to consider the national standards. There are, however, variations that may contribute to differences among protocols of different regions. Transport times, availability of resources (equipment and personnel), overall geography, and availability of other transport modalities, such as air medical services, may influence individual protocols. Considering the capabilities of the receiving hospitals in a system contributes to the optimization of care that is provided to the patient.

Physical space and financial resources are practical limitations that warrant consideration when developing protocols. Anything that is added to the EMS repertoire might be done at the expense of some other intervention, equipment, or procedure that might have a more beneficial impact for a greater number of patients. For example, it may not be practical to equip every ambulance in a particular system with TXA or blood for the few times that it will be used in massive hemorrhagic shock. An alternative may be to equip a special vehicle with expanded capacity to manage low-volume high-acuity patients which is available to augment a larger geographic area such as a supervisor's vehicle, physician response unit, or air medical service. That would allow limited resources on the general EMS units to be dedicated to more practical and beneficial capabilities. Alternatively, it may not be practical for an EMS physician (or other specialized unit) to carry all of the medications that are available in the system particularly if the model is such that the physician will typically be meeting with an ALS ambulance. There should, however, be sufficient equipment with the physician vehicle to allow at least initial management of any medical emergency should the physician arrive on scene before the ambulance.

Capacity to maintain competency in rarely used procedures is another limited resource to consider when developing protocols. There may be instances in which it would not be practical to train an entire EMS system for certain, rarely used procedures but having an EMS physician available to perform that intervention may be reasonable. An EMS physician may draw on experience and training not available to many EMS providers. In addition, a single physician could potentially cover many smaller jurisdictions.

SUMMARY

The EMS physician has a number of roles in the field management of the patient in shock. Patient care, education, and administrative responsibilities such as protocol development and quality improvement measures are all part of those roles. Shock management in the prehospital environment necessitates an evaluation of the underlying etiology with limited diagnostic resources and effective initiation of a plan based on the inciting process. In the field, the EMS physician has the skills and equipment to perform many interventions. This must be tempered with the wisdom of knowing what must be done on scene, during transport or deferred until arrival at the hospital. Often, basic life support interventions will take precedence and have the most profound effect on the management of the patient in shock. Advanced interventions are secondary and should be employed at the right time, for the right patient, in the right setting. A properly educated, proficient EMS physician who works well as part of the EMS team can have a profound effect on many direct and indirect aspects of the out-of-hospital care of the patient in shock.

KEY POINTS

There are four categories of shock: cardiogenic, hypovolemic, obstructive, and distributive.
Normal saline is the preferred crystalloid for volume resuscitation.
Blood products are preferred for hemorrhagic shock but technical challenges prevent widespread deployment of blood products in many EMS systems.
Tourniquets, tranexamic acid (TXA), intraosseous (IO) access, and hemostatic dressings are being deployed more frequently in the civilian EMS environment.
Medical antishock trousers (MAST) or pneumatic antishock garments (PASG) are infrequently utilized for resuscitation of hemorrhagic shock due to lack of proven benefit and presence of potential for harm in some circumstances. The NAEMSP has relegated its previous MAST/PASG position statement to historical interest only, and no longer recommends their use.

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Stiell IG., Spaite DW, Field B, et al. Advanced life support for out-of-hospital respiratory distress. N Engl J Med. 2007;356: 2156–2164. [PubMed: 17522399]

Kwan I, Bunn F, Roberts I. Timing and volume of fluid administration for patients with bleeding. Cochrane Database Syst Rev. 2003;3:1–16.

Reynolds BR, Forsythe RM, Harbrecht BG, et al. Hypothermia in massive transfusion: have we been paying enough attention to it? J Trauma Acute Care Surg. 2012;73:486–491. [PubMed: 23019675]

Merlin MA, Kaplan E, Schlogl J. Study of placing a second intravenous line in trauma. Prehosp Emerg Care. 2011;15:208–213. [PubMed: 21294630]

Finfer S, Bellomo R, Boyce N, et al. A comparison of albumen and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350:2247–2256. [PubMed: 15163774]

Havel C, Arrich J, Losert H, et al. Vasopressors for hypotensive shock. Cochrane Database Syst Rev. 2011;5:1–81.

De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362:779–789. [PubMed: 20200382]

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Merlin MA, Grembowicz JJ, Cortacans HP, et al. Docs on demand. EMS Magazine. 2008;37:44–45.

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Roberts I, Perel P, Prieto-Merino D, et al. Effect of tranexamic acid on mortality in patients with traumatic bleeding: prespecified analysis of data from randomized controlled trial. BMJ. 2012;345e5839.

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Shakur H, Roberts I, Bautista R. Effects of tranexamic acid on death, vascular occlusive events, and blood pressure in trauma patients with significant haemorrhage (CRASH-2): a randomized, placebo=controlled trial. Lancet. 2010;376:23–32. [PubMed: 20554319]

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Kraut JA, Madias NE. Treatment of acute metabolic acidosis: a pathophysiological approach. Nat Rev Nephrol. 2012;8:589–601. [PubMed: 22945490]

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DeJaegere PP, Serruys PW, Simoons ML. Should all patients with an acute myocardial infarction be referred for direct PTCA? Heart. 2004;90:1352–1357. [PubMed: 15486147]

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Weng CL, Zhao YT, Liu QH. Meta-analysis: noninvasive ventilation in acute cardiogenic pulmonary edema. Ann Intern Med. 2010;152:590–600. [PubMed: 20439577]

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Simmons FER, Gu X, Simmons KJ. Epinephrine absorption in adults: intramuscular versus subcutaneous injection. J Allergy Clinical Immunol. 2001;108:871–873.

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Kemp SF, Lockey RF, Simons FE. Epinephrine: the drug of choice for anaphylaxis. A statement of the World Allergy Organization. Allergy. 2008;63:1061–1070. [PubMed: 18691308]

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Brown SGA, Blackman KE, Stenlake V, et al. Insect sting anaphylaxis; prospective evaluation of treatment with intravenous adrenaline and volume resuscitation. Emerg Med J. 2004;21:149–154. [PubMed: 14988337]

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Schenarts CL, Burton JH, Riker RR. Adrenocortical dysfunction following etomidate injection in emergency department patients. Acad Emerg Med. 2001;8:1–7. [PubMed: 11136139]

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Hohl CM, Kelly-Smith CH, Yeung TC, et al. The effect of a bolus dose of etomidate on cortisol levels, mortality, and health service utilization: a systematic review. Ann Emerg Med. 2010;56:105–113. [PubMed: 20346542]

21.

Jabre P, Comber X, Lapostolle F, et al. Etomidate versus ketamine for rapid sequence intubation in acutely ill patients: a multicenter randomized controlled trial. Lancet. 2009;97:293–300.

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Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and shock. N Engl J Med. 2001;345: 1368–1377. [PubMed: 11794169]

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Voigt J, Waltzman M, Lottenberg L. Intraosseous vascular access for in-hospital emergency use: a systematic clinical review of the literature and analysis. Pediatr Emerg Care. 2012;185-199.

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Tan BKK, Chong S, Koh ZX, et al. EZ-IO in the ED: an observational, prospective study comparing flow rates with proximal and distal tibia intraosseous access in adults. Am J Emerg Med. 2012;30:1602–1606. [PubMed: 22244227]

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Abe KK, Blum GT, Yamamoto LG. Intraosseous is faster and easier than umbilical venous catheterization in newborn emergency vascular access models. Am J Emerg Med. 2000;18:126–129. [PubMed: 10750913]

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Decreased Consciousness and Severe Agitation

Noel Wagner

INTRODUCTION

It is common for an EMS physician to encounter patients experiencing an alteration in their level of consciousness. This can present as a decrease in the level of consciousness in which the patient will exhibit confusion or a more significant alteration to the point of coma. An individual may also present with acute agitation, confusion, and violent and uncontrollable behavior.

Traditionally decreased consciousness and acute agitation are often viewed as separate entities. In reality, both states are divergent points on a continuum. For example, a hypoglycemic patient may be simply confused, comatose, or combative and dangerous. The acutely agitated patient may require restraint and sedation prior to receiving care that may be very similar to that given to a patient with decreased consciousness.

The EMS physician is a tremendous asset in caring for a patient with an altered mental status. He or she brings a breadth and depth of knowledge that will provide a significant differential diagnosis list while having the ability to provide physician level care in the unusual circumstances that require such care.

The purpose of this chapter is to develop an understanding of these altered states, identify causes, and develop treatment plans that can be employed in the field whether a cause is identified or not. This chapter also gives particular attention to the acutely agitated state and the approach and treatment that is required to attempt to prevent a police or EMS provider–related death.

Although an overview of the approach and treatment of the altered state is provided, it must be emphasized that individual conditions may require different or modified treatment depending on the situation.

OBJECTIVES

Identification of conditions causing altered level of consciousness.
Discuss treatment priorities and plans.
Discuss current understanding of excited delirium and treatment.
Discuss restraint and takedown techniques.
Overview chemical restraint and sedation.

PROVIDER SAFETY CONCERNS

When attempting treatment of an altered patient, provider safety is paramount. Not only must the EMS physician be aware of direct danger from a combative patient, or an unconscious patient who suddenly regains consciousness, he or she must also maintain vigilance to the surrounding scene. Dangerous factors that may have contributed to the patient's condition may still be present. Refer to Chapter 30 for a full discussion on this topic.

CAUSES

There are many potential causes of altered mental status. The classic mnemonic is AEIOU TIPS (see Box 36-1). This provides a concise overview of multiple entities that may lead to altered consciousness. This section will focus on specific conditions that may be identified and corrected in the field setting. This section will also discuss conditions that may require presumptive treatment based on suspicion alone in the absence of field diagnostics.

Box 36-1 Altered Mental Status (AEIOU TIPS)

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Alcohol

Endocrine, Electrolytes, Encephalopathy

Insulin

O₂, Opiates

Uremia

Toxidromes, Trauma, Temperature

Infection

Psychiatric, Pharmacy

Space occupying CNS lesion, Subarachnoid hemorrhage, Stroke, Sepsis, Shock

The ABCs are as applicable in the altered mental status patient as any other patient, if not more. Airway and breathing issues may readily account for alterations in mental status. Hypoxia, hypoventilation, hypercapnia, and carbon monoxide poisoning are high on the list of initial concerns. Pulse oximetry is now ubiquitous in the prehospital setting and readily assists in diagnosing hypoxia. Less common, but gaining in popularity, are end-tidal CO₂ detectors which are a tremendous asset in evaluating ventilatory status and impending respiratory failure. A more recent addition to the prehospital environment is the CO monitor. Its presence is still sporadic, but when available it is able to give a confirmation of suspected CO exposure as well as a quantifiable number by which the EMS physician can evaluate the level of poisoning and possibly affect the destination hospital if hyperbaric treatment facilities are available.

If circulation, measured as blood pressure of perfusion status, is altered, then this etiology must be addressed. These scenarios are beyond the scope of this chapter and are fully discussed in other chapters such as Chapter 35 or Chapter 39. Acute blood loss is addressed in the chapters on gastrointestinal emergencies (Chapter 41), blunt and penetrating trauma (Chapter 54), and wounds and hemorrhage (Chapter 57).

Blood glucose problems are rapidly detectable in the field and low levels are easily corrected. IV administration of D50 has long been the mainstay for correcting hypoglycemia in adults that is not amenable to more basic interventions such as oral intake of foods or liquids that are high in sugar content. Recently there has been investigation on the use of alternative IV dextrose solutions.¹ D10 administration in adults showed equal time to regain consciousness without the characteristic posttreatment hyperglycemia that is present with D50 administration. Currently, D50 remains the standard of care in this country, but more dilute solutions are apparently efficacious and may be administered to adults at the discretion of the EMS physician. D10 (<1 year old) and D25 (1-12 years old) are recommended for children.² Some EMS systems utilize D12.5 in place of D10³ for ease of conversion which should hopefully increase safety. If IV access is unobtainable, IM/SQ glucagon may be administered. The dose is 1 mg IM/SQ for patients greater than 20 kg (44 lb). Patients below approximately 20 kg should receive 0.5 mg IM/SQ.

Electrolyte abnormalities are not easily identifiable in the field and usually require a significant level of presumption. Traditionally, a patient undergoing heavy exertion in a hot environment and who has been ingesting only free water would be suspected of hyponatremia, especially if a new onset seizure is observed. This should be expanded to any excessive fluid consumption during strenuous activity, regardless of fluid type.⁴ Psychogenic polydipsia could result in hyponatremia in the setting of a psychiatric patient who has unrestricted water consumption. Treatment for uncomplicated hyponatremia would consist of 0.9% NS IV. Three percent NS could be considered if the patient is in extremis, is experiencing repetitive or protracted seizures unresponsive to benzodiazepines, or has lapsed into a comatose state. In such situations where cerebral edema and herniation is suspected, 50 to 100 mL of 3% saline may be bolused^5,6 followed by up to 200 mL over the next 4 to 6 hours. Three percent saline should be stopped once signs of cerebral edema and herniation have ceased.

Hypernatremia and severe dehydration are suspected by a history of decreased fluid intake and by clinical presentation. The treatment of both entities would be 0.9% NS IV. Dehydration to the point of mental status changes would require significant boluses of NS due to significant volume depletion. As long as the patient remains symptomatic from dehydration, there is no upper limit on NS administration, as long as pulmonary edema and other signs of fluid overload are monitored. Acute hypernatremia may also be corrected quickly. However, a slower correction should be employed, in the hospital setting, for sodium levels that are suspected to have been high for a longer time.

Hyperkalemia is most often suspected in a dialysis patient. Altered mental status is not the hallmark of hyperkalemia, but its presence could lead to arrhythmias which could induce an altered mental status prior to progression into cardiac arrest. The ECG may be beneficial in diagnosing peaked T waves or a sine wave, but it may be nondiagnostic if the patient has a sinus tachycardia or PSVT that precludes thorough examination of the morphology. Suspicion of hyperkalemia is enough to warrant treatment with IV calcium chloride with or without sodium bicarbonate.

Alcohol consumption is a common practice in this country and ethanol intoxication is always a high concern in a patient with an altered mental status. No specific antidote exists and support of the airway and respiratory status is warranted. This is the ideal patient to employ not only pulse oximetry, but end-tidal CO₂ monitoring as well to monitor for changes in the respiratory status that may not be appreciated by physical examination alone. This approach would also apply to other sedative medications. Blood glucose abnormalities should not be overlooked in someone who is intoxicated, or just appears intoxicated.

Opiates are a classic cause for altered mental status.^7,8 Pinpoint pupils and decreased consciousness are the hallmarks, although a person occasionally may present in an agitated state. The treatment is naloxone (Narcan) IV, IM, or IN. The usual starting dose is between 0.4 and 2 mg, but there is no upper limit on the amount of naloxone that may be administered and large doses may be required in large overdoses and in certain opiates.⁹ Since narcotic overdose does not have a test in either the field or hospital, the EMS physician must have an index of suspicion, or a blanket treatment plan, to utilize Narcan (naloxone). Usage in patient with compromised respiratory status is unquestionable. Usage in patient with a lesser degree of alteration is less clear. The EMS physician must remain cognizant about the potential for mixed drug overdoses. Removal of the opiate effect and its sedative properties may result in unopposed effects of cocaine, methamphetamine, PCP, or something similar. It may also precipitate acute narcotic withdrawal which may create a combative and uncooperative patient. In these situations, the EMS physician is usually best served by weighing the patient's airway and ventilatory status along with the perceived safety of the patient and providers. If any of these are compromised, administration is warranted. If none are compromised, diagnostic trials of naloxone in the field are unwarranted and supportive care is recommended until this patient arrives at the hospital. However, it is important to consider that there is a growing availability of public access naloxone programs, and that the patient may have already received 2 mg of naloxone prior to arrival of EMS providers.^10–13

On a related note, flumazenil (Romazicon) should not be utilized in the prehospital setting for suspected benzodiazepine overdoses or overdoses of unknown etiology. The safety of its usage in such situations is questionable^14–16 and should be avoided. Fatal, intractable seizures are possible and are a significant concern. Supportive airway and breathing management are safer options.

Other substances such as cocaine, methamphetamines, or PCP may also be encountered and usually present with agitation but may also include hallucinations, aggression, and violence. No specific antidote exists, but benzodiazepines are appropriate and large amounts may be necessary for effect in such patients. If the patient progresses into excited delirium, then more aggressive measures may be indicated and will be discussed later in this chapter.

CNS injury is often suggested by history provided by the patient or bystanders. Sometimes, the mechanism is less clear and requires a high index of suspicion. Stroke, both hemorrhagic and ischemic, may mimic CNS injury. No specific prehospital intervention is available to the EMS physician and supportive care and transport to the most appropriate facility is warranted.

Psychiatric conditions are widespread and more commonly lead to agitation rather than a depressed level of consciousness. An acute psychotic episode is characterized by abrupt disturbance of thought, behavior, and mood.¹⁷ Anxiolysis and mild sedation may be required to provide comfort to the patient, provide safety, and prevent deterioration. When the acute psychotic episode includes agitation and violence, the patient has crossed into excited delirium, which will be discussed in more detail later in this chapter. Other specific psychiatric conditions are discussed in Chapter 51.

Temperature regulation issues and environmental exposure can lead to alterations in consciousness and can be addressed in the field. Thermometers may or may not be available so presumptive treatment may be required. Patient and environmental clues can be used to develop a suspicion of hyper- or hypothermia. Warming or cooling as needed is appropriate and can be accomplished in the prehospital environment and is discussed in Chapter 37.

While temperature abnormalities undeniably need treatment, acidosis treatment is less clear. An acidotic state is not reliably identified in the field setting so the EMS physician must be presumptive to suspect this state. Patients exhibiting hyperventilation may be showing a clinical sign of respiratory compensation, or the increased respiratory rate may be attributed to something entirely unrelated. Behavior such as vigorous fighting and physical exertion or history obtained from bystanders may lead the EMS physician to suspect an acidotic state. Some acidotic conditions such as DKA are usually best treated with ventilatory support, fluids, ensuring adequate volume status and transport. Infection and sepsis also benefit from similar care.

EXCITED DELIRIUM

Excited delirium has recently gained increased attention in the emergency medicine and EMS literature. The National Association of Medical Examiners has accepted excited delirium syndrome as a legitimate diagnosis for some time. Recently, the syndrome (ExDS) has been recognized by the American College of Emergency Physicians.¹⁸ It is of interest that this condition is not universally acknowledged and there is continued debate as to the existence of such a condition. This disagreement occurs in the lay press¹⁹ as well as in some fractions of the medical community. For example, the American Psychiatric Association does not list excited delirium as a diagnosis.²⁰

Of those that do agree with its existence, some minor semantics are noted. Some state that excited delirium is the event that a patient experiences and the term excited delirium syndrome only applies when death is the outcome.¹⁷ Others use the term excited delirium syndrome to refer to the premortem state as well as the postmortem diagnosis.¹⁸ Regardless, certain characteristics of the condition are appreciated (see Box 36-2). Excited delirium syndrome results in a patient who is out of control, psychotic, untiring, and violent. This patient invariably has law enforcement contact and a resultant struggle. Control techniques such as chemicals (pepper spray or mace), conducted energy devices (CED), or restraint holds may be employed. Occasionally, the patient deteriorates and the result is death.

Box 36-2 Features of Excited Delirium

Pain tolerance
Tachypnea
Sweating
Agitation
Tactile hyperthermia
Police noncompliance
Lack of tiring
Unusual strength
Inappropriately clothed

The exact causative etiology of excited delirium is unknown, but there is a strong prevalence of substance abuse and, to a lesser extent, mental illness. The main substances involved are cocaine, methamphetamine, PCP, and alcohol. Mental illness makes up a smaller proportion of those affected, often with concurrent substance abuse, but occasionally without. Most patients are male and young.

The actual cause of death is uncertain. It is postulated that death is due to severe acidosis, hyperthermia, and undefined cardiac arrhythmias.¹⁸ Di Maio and Di Maio postulate that the cardiac abnormality is torsades de pointes (TdP) due to QT-interval prolongation.¹⁷ They believe that the intense struggle resultants in massive catecholamine release. The struggle also produces significant hyperkalemia. The hyperadrenergic state protects against the effects of hyperkalemia but as the struggle stops the potassium level starts to fall. The patient then experiences a sudden and severe drop in potassium and may be suddenly significantly hypokalemic. This may trigger torsades de pointes and resultant cardiac arrest.

The best treatment for excited delirium is rapid and aggressive intervention.^17,18 Minimizing the amount of struggle through decisive physical control, rapid sedation, and chemical restraint may be lifesaving. Sodium bicarbonate use is tempting when faced with the marked acidosis that is invariably present, but a word of caution is in order. Simply treating the apparent acidosis cannot be supported as there is no specific literature in regard to this plan of action. Many conditions present with acidosis and sodium bicarbonate is not an appropriate treatment. Examples include diabetic ketoacidosis and traditional cardiac arrest. Also, Di Maio and Di Maio's theory of hypokalemic-induced TdP should give pause. The logic of giving medications traditionally used to counter the effects of potassium (sodium bicarbonate and calcium) must be questioned in the absence of any scientific literature to indicate their use.

The worst possible outcome of excited delirium syndrome is cardiac arrest. Since most excited delirium-induced cardiac arrests are asystolic arrests,^21–23 vasopressin should be the first-line therapy.^24,25 Additionally, the patient is already in a hyperadrenergic state and providing additional epinephrine has not proven successful in resuscitating prior ExDS cardiac arrests. Magnesium should be administered early in the arrest since torsades de pointes is strongly suspected as an etiology.

PATIENT EVALUATION/ AIRWAY MONITORING

As for all patients, those with decreased consciousness and severe agitation must be evaluated. The patient who is comatose or altered yet cooperative will not pose much of an evaluation dilemma. Traditional examination techniques and equipment (pulse oximetry, blood glucose monitor, cardiac monitor, stethoscope, etc) can be employed and information can be obtained.

Evaluation of a patient usually starts with an assessment of their mental status. This invariably is the first observation that is obtained since it is often accomplished while approaching the patient. Formal GCS testing is likely to be impractical in the agitated patient. It is not a first-line assessment in the patient with decreased consciousness as other evaluations and treatments must be considered first. The AVPU scale (see Box 36-3) has emerged as both a quick and accurate method to assess mental status. It can be assessed in a few seconds and often can occur in synchronization with the ABC assessment. It can be easily monitored and provides an easily interpreted piece of information for the prehospital team as well as the receiving facility.

Box 36-3 AVPU Scale

A—Alert
V—Responsive to verbal stimuli
P—Responsive to painful stimuli
U—Unresponsive

Monitoring the patient's airway is simplified in a patient with decreased consciousness. Conventional methods of auscultation, pulse oximetry, CO₂ and visual observation are easily employed. Whether the patient is intubated or not, ongoing assessment is relatively simple and straightforward.

The traditional methods of examination and airway monitoring are not practical when the patient will not cooperate or even allow you to be safely in their presence. A much more rudimentary form of assessment must be employed. The EMS physician will have to visualize the respiratory status from afar. Effort and sounds will be appreciated from a distance without the aid if a stethoscope or pulse oximetry. Unfortunately, respiratory rate, effort, and sounds are often confusing information in the presence of acute agitation, physical activity, and fighting. A decrease in physical activity can signal a lessening desire to fight and resist or be an ominous sign of impending collapse. This distinction is not always readily apparent and the worst outcome must be anticipated and preparations made. Positioning may offer some clue to airway and breathing status if the patient is in an unusual position (ie, tripod). The ability to speak only in few word phrases could be due to severe respiratory compromise or a sign of a psychiatric condition or intoxicants. Skin color can potentially be appreciated and a bluish hue to the lips or extremities may be the only supportive piece of information that the EMS physician is afforded.

One of the most important observations for physical examination and airway monitoring is to note the respiratory status and its stability or change over time. While rate and effort may be deceiving due to the agitation, an acute change may signal deterioration and herald impending doom. Significantly increased or decreased rate or effort may signal that there is new airway and ventilation issue, a worsening of a preexisting one, or a worsening of the patients underlying medical condition. This change, if appreciable, should signal the EMS physician that immediate action is needed. Once an agitated patient is calmed or sedated, conventional measures for airway monitoring can be employed.

A complication of caring for such patients is that they may attempt to bite or spit at the care providers. Surgical masks and commercially available spit shields run the risk of becoming wet and impeding air exchange. A nonrebreather mask properly placed and attached to an oxygen source will provide some impedance to airborne saliva. Devices designed for oxygen administration such as nonrebreather masks should always be attached to an oxygen source. Any method used must be continually monitored as part of your ongoing airway assessment.

TREATMENT PRIORITIES

After scene safety is assessed and maximized, the ABCs are the next priority. Full details of these procedures are discussed in other chapters. Proper attention to adequate air exchange and control of serious hemorrhage is important. Decreased blood pressure requires treatment for shock (Chapter 35) in the absence of response to the rapidly correctable conditions discussed below.

Cervical spine immobilization has been a cornerstone of prehospital care in this country for decades. Recently debate has evolved regarding the appropriateness of cervical immobilization in certain subsets of patients (see Chapter 55). This debate will likely continue and develop over time. The current recommendation is to guard against a potential unstable cervical spine injury in a patient with decreased consciousness or a comatose state by utilizing a cervical collar and immobilization on a long backboard.²⁶ The agitated patient presents a different concern. The benefit of a cervical collar and immobilization on a backboard in a patient who is actively fighting and resisting spinal precautions is probably dubious at best. Additionally, agitated patients fighting against restraints may worsen their condition. A patient so combative and uncooperative that physical force is required for immobilization should probably have this modality deferred.

Rapidly correctable conditions should be the next focus. These include hypoxia, hypoglycemia, and narcotic overdose. In the absence of a functioning pulse oximeter, or the inability for a patient to cooperate with its usage, presumptive oxygen should be administered. Hypoglycemia is also easily detected in the prehospital environment and should be treated with IV dextrose or glucagon. A potential narcotic overdose can then be addressed with administration of naloxone (Narcan). Hypotension, fluid depletion, dehydration, and electrolyte abnormalities can then be addressed.

After rapidly correctable conditions are addressed, or if the patient's condition makes addressing these impossible, then focus shifts to restraint and control of an agitated patient. Physical and chemical restraints should be employed if safety is jeopardized and are discussed in more depth later in this chapter.

Core temperature abnormalities can then be addressed. If a thermometer is not available, the EMS physician will have to rely on environmental and historical clues as well as physical examination findings and consider presumptive treatment. Since the patient has an altered mental status it is advised that the physician be aggressive in treating even suspected temperature abnormalities.

At the end of the list of interventions, the EMS physician must decide if an acidotic state is suspected and whether presumptive treatment is in order.

PATIENT SAFETY ISSUES

Patient safety is both extremely important and difficult to ensure for the altered patient. Not only is the patient unable to communicate needs and concerns or cooperate with your care plan, they are often actively resisting attempts to help them and may be acting in a fashion that is dangerous to themselves as well as others.

Positional asphyxia has been a concern. This includes the prone position, hog tying, hobble tying, and pressure applied to a patient's upper torso. Some earlier observers and researchers discussed the dangers and condemned these practices.^27–30 More recent research has cast significant doubt on the theory that positional asphyxia is caused by routine practices utilized by police and other providers.^31–33

Conducted energy devices, commonly referred to as tasers, have become a popular tool in law enforcement. They utilize electricity to incapacitate an uncooperative person.^34,35 They have been condemned in the lay press^36,37 and their use has resulted in lawsuits.³⁸ Proponents cite that taser use in itself is not dangerous and has proven innocuous in controlled laboratory trials.^39,40 The concern about arrhythmias seems dubious since it has been noted that time of collapse is remote from the application of the CED making an electricity-induced arrhythmia highly unlikely.^41,42 Additionally, the US Department of Justice recently concluded:

Law enforcement need not refrain from using CEDs to place uncooperative or combative subjects in custody, provided the devices are used in accordance with accepted national guidelines and appropriate use-of-force policy. The current literature as a whole suggests that deployment of a CED has a margin of safety as great as or greater than most alternatives. Because the physiologic effects of prolonged or repeated CED exposure are not fully understood, law enforcement officers should refrain, when possible, from continuous activations of greater than 15 seconds, as few studies have reported on longer time frames.⁴³

The bottom line is that tasers are present in modern law enforcement and the will have to be factored into the care for the uncooperative patient. The EMS physician will often receive care of a patient who has been tased. This will factor into the plan of immediate care as well as continued care.

Once the patient is cooperative, in control and calm, there does not appear to be a delayed effect of the taser. A literature search by Vilke et al covering 22 years (1988-2010) showed that the routine performance of laboratory studies, electrocardiograms, or ongoing cardiac monitoring in asymptomatic, awake, and alert patients could not be supported.⁴⁴ The review does caution that this applies only to asymptomatic patients. Anyone experiencing symptoms, exposure >15 seconds, intoxication, or symptoms of excited delirium may require additional evaluation and treatment as warranted. The patient's condition leading up to the tasing, the events surrounding the tasing, and the patient's complaints and findings after the event are factors in determining the need for evaluation. The act of tasing in itself, viewed independently of any other information, does not mandate hospital evaluation. The EMS physician can provide this information to EMS providers or law enforcement if a question of disposition arises. If EMS or police policy dictates transport, this information may be used to utilize a BLS resource or even law enforcement transport.

Chemical sprays have also received some controversy. The most common of these is oleoresin capsicum, commonly known as pepper spray. As with other control modalities, they have been denounced.^45,46 Various studies have failed to show negative effects.^47,48

RESTRAINT/TAKEDOWN

A patient who is merely upset or mildly agitated should not be treated with aggressive measures. Calming techniques and mild sedation are probably all that is required. This is all dependent on the patient not being dangerous or in danger. When a patient is severely agitated, uncontrollable, and violent, then restraint becomes necessary. The National Association of EMS Physicians states that patient restraint should be employed when a patient becomes dangerous to themselves or others.⁴⁹ This decision should be made with a thought to balancing a patient's dignity and liberty with a concern about their safety and the safety of others.⁵⁰

The levels of restraint start with a progression that provides attempts at verbal calming, a show of force, physical take down and restraint, ending with chemical restraint. This restraint hierarchy does not need to proceed to the highest level if a lower level of restraint is effective in preventing patient and provider injury and provides safety to all. Likewise, just as physical and chemical restraint should be considered last resorts, they should not be shied away from in a patient in extremis and who is an immediate danger to themselves or others. A dire situation may require going to the last steps first if danger to the patient, providers, or others is evident.

Performing physical restraint in the field is a challenging task. A team will need to be assembled, usually in an expeditious fashion. The assembled ad hoc team may include not only the EMS physician, but also EMS, fire, and law enforcement personnel. Regardless of the composition of the restraint team, it is beneficial that all have previous training in patient restraint although this is not always possible. All members should perform a quick huddle to establish goals and roles of all members. Tactics and phrases can be communicated so that everyone understands the desired progression of the takedown and restraint. This can be brief lasting less than a minute or can be more detailed if time allows.

An adequate number of providers are important for a proper takedown. The traditional teaching is there should be a minimum of five providers for the restraint and takedown: one for each limb and one for the head. An additional team member would be ideal to safely apply restraints or administer medication. Two persons should approach from the front and two from the rear. This allows for some indecision on the part of the patient should they decide to attack. If they do attack in any direction, then there are two members of the team that will be behind the patient to restrain him or her. Extremities should be controlled at the joint.

This approach is under optimal circumstances and may need to be modified as the situation demands. A paucity of providers may result in a decision to wait for more persons to arrive or to attempt a modified take down. Also, a large or extremely active patient may require more than the traditional five providers. Each situation will be different and the EMS physician is in an ideal position to help with this decision.

The EMS physician is probably a more valuable resource if he or she is not part of the restraint team. This is contingent on the number of available bodies allowing this. The EMS physician is more beneficial in that they have airway and examination expertise and can serve as the safety person in watching for potential restraint complications (see Box 36-4). As the person on scene with the highest level of medical training, this keeps them in the position to continuously observe and monitor the patient and alter the treatment plan as needed. Additionally, the EMS physician is then in the position to administer medications to provide sedation and chemical restraint. If a rapidly acting sedative is selected (ie, ketamine),⁵¹ then the patient may be safely immobilized by the restraint team until sedate and then safely transferred to physical restraints without a struggle. This enhances both patient and provider safety as there is no additional struggle to place the patient in restraints. It also allows for the patient to receive sedation as soon as possible and limits the time of struggle.

Box 36-4 Restraint Checklist

Airway
- Difficulty
- Unusual sounds
- Vomitus/other obstructions
Breathing
- Adequate
- Color appropriate
Pressure remove
- Chest
- Neck
- Abdomen
Position
- Make sure patient is in the position that you intended
Appropriate limb restraints
- Monitor circulation

The proper position of restraint has had much controversy. As discussed earlier, the theory of positional asphyxia has waxed and waned. There is no unanimous consent on the proper position. One benefit of having EMS involved is that there is usually a stretcher available that can be utilized for patient restraint and treatment. It appears that sitting on the stretcher with the upper torso in an upright position is the most desirable position. This avoids the controversy of the prone and other positions and theoretically provides the least impediment to respiratory effort. Four-point restraints can then be employed. It is commonly suggested that one arm be restrained above the patients head to prevent the patient from either tipping the stretcher or moving and assuming a position other than what was intended.

Leather restraints are preferred to other devices in that they are secure and will offer the most protection to the patient and providers, but they are difficult to remove quickly in the event of clinical deterioration. Soft restraints are the next most desired. They are not as secure and patients have been known to rip through soft restraints in an acutely agitated state. They can be quickly cut in an emergency. Improvised gauze dressings and handcuffs or zip ties are a last resort. Gauze (or similar) restraints can tighten and compromise circulation or loosen and become ineffective. Handcuffs and zip ties are not designed for a patient who does not have the mental status to stop moving while they are inflicting damage to underlying structures. These may be better than no restraint when patient safety is at stake, but other restraint methods should be employed if available. They should be considered temporary restraints (at best) when there use in unavoidable.

Once restrained, monitoring is of the utmost importance. Priorities include airway preservation and guarding against impingement of the chest, abdomen, and neck (Figure 36-1).

FIGURE 36-1.

Suggested technique for medication administration in an acutely agitated and out-of-control patient. Grasping the syringe in this fashion will maximize both control of a sharp object as well as speed of administration.

SEDATIVES/CHEMICAL RESTRAINT

Sedation, or chemical restraint, is the final modality on the restraint hierarchy. A patient who continues to struggle while physically restrained is at risk of injuring themselves. This is particularly true if improvised restraints have been used. Also, the act of physical restraint does nothing to address the patients underlying medical or psychiatric condition. It has been shown that struggling against restraints is a detriment to normal physiology with pH levels as low as 6.25 being experienced.⁵² It is unclear if sedation will prevent bad outcomes in cases of acute agitation, but excited delirium has an often fatal endpoint if left untreated. It is strongly encouraged that aggressive treatment be employed when the diagnosis of excited delirium is entertained. Such treatment may still be met with an undesirable outcome, but the lack of treatment is not appropriate as this does not offer any attempt to redirect a fatal cascade while it is in progress. Simply stated, the possibility of a bad outcome in spite of sedation and chemical restraint does not justify failure to utilize it in an attempt to correct metabolic worsening and potential cardiopulmonary collapse.

When sedation is administered, benzodiazepines have a long-standing tradition as first-line agents. They enjoy a considerable safety margin with virtually no medication or drug interactions that would preclude its use in an agitated patient. Additionally, benzodiazepines have a positive effect on the seizure threshold which is advantageous in many agitated conditions. The classic benzodiazepine is diazepam. It offers rapid onset IV. There is a considerable history of its use and safety. Its main drawback is that it is not a reliable intramuscular medication due to erratic absorption.⁵³ Lorazepam offers the same advantages of valium and provides consistent IM absorption. The major drawback of lorazepam is that it requires refrigerated storage, something not uniformly found in an ambulance or EMS physician vehicles.

Possibly the most versatile benzodiazepine is midazolam. It offers the advantages of diazepam and lorazepam when given IV, is absorbed well IM, and does not need refrigeration. It has the most rapid onset of all benzodiazepines. Its main drawback is that it is considered to have more respiratory depression (at high doses) than other benzodiazepines. The respiratory depression effect of benzodiazepines is felt to likely be due to the rapidity of onset and administration. With midazolam having the most rapid onset, this most likely accounts for this trait.

A drawback of all benzodiazepines is the wide variation in dosages required for effect. There can be a 10-fold difference or more in the effective doses between various patients. Sometimes massive doses may be required to achieve the desired effect. This may be up to 15 to 20 mg of lorazepam, 200 to 500 mg of diazepam, and 30 to 40 mg of midazolam.⁵⁴ Additionally, although they do not usually have direct hemodynamic effects, they may contribute to hemodynamic instability in large doses or in combination with previously ingested substances. This is particularly true with alcohol or narcotics. Finally, when administered IM midazolam and lorazepam still have and onset time of 10 minutes or greater. This can seem like an eternity in an acutely agitated patient.

Ketamine, a dissociative anesthetic, has emerged as a potent tool in the sedation of the acutely agitated patient. There is little literature to support its use in the acutely agitated patient,⁵⁵ but it does offer many theoretical and practical advantages. It provides rapid and consistent control without the wide variation in dosage seen with benzodiazepines. It is also rapidly effective IM which is a tremendous attribute when faced with an actively struggling and acutely agitated patient. Ketamine has no negative effects on blood pressure. It is also a bronchodilator and respiratory drive is preserved even at the height of its dissociative effect. Seizures are possible but infrequent.

Haloperidol has a long tradition of safe use in the acutely agitated patient. It provides sedation and control while preserving respiratory drive. It has recently come under scrutiny for cardiac side effects and the FDA has issued a warning for the use of haloperidol.⁵⁶ This is primarily due to documented cases of QT interval prolongation and torsades de pointes. It is of note that over 70% of deaths attributed to TdP after haloperidol administration were from IV administration which is an off label use and not FDA approved. Higher doses are also noted to have higher risk of QT prolongation and TdP. The FDA advises caution in patients who have other QT-prolonging conditions, including electrolyte imbalance (particularly hypokalemia and hypomagnesaemia), have underlying cardiac abnormalities, hypothyroidism, familial long QT syndrome, or are taking drugs known to prolong the QT interval. It is often impossible to definitively exclude many of these conditions in the prehospital setting especially in a patient who is acutely agitated and uncooperative. Some authors go as far as to say that haloperidol should never be used.¹⁷ Others are strong supporters and note that its historical track record, lack of respiratory effects, and lack of hypotension are strong indications for its continued usage.⁵⁷ This author does not recommend the use of haloperidol for control of excited delirium. It makes little sense to use a medication with documented arrhythmia risks in a subset of patients already at risk for cardiac arrhythmias. Even if a bad outcome is unrelated to haloperidol, this fact may not be appreciated. If the EMS physician decides to use haloperidol it should be given IM and in recommended starting dosages (see Table 36-1).

TABLE 36-1

Chemical Restraint Medications

TABLE 36-1

Chemical Restraint Medications

Medication

Class

Dose^a

Route

Onset

Duration

Advantages

Disadvantages

Versed (midazolam)

Benzodiazepine

5 mg every 5 m

IM, IV, IN

1-2 m IV

10-15 m IM

2 h IV

4-6 h IM

IM absorption, most rapid benzodiazepine onset

Respiratory depression at higher doses^b

Valium (diazepam)

Benzodiazepine

10-20 mg every 5 m

IV^c

1-5 m

15-60 m

Classic, well-established track record

IV only

Ativan (lorazepam)

Benzodiazepine

2-4 mg every 5 m

IM, IV,IN

5-20 m IV

20-30 m IM

6-8 h

IM absorption

Slowest benzodiazepine onset, refrigeration required

Ketalar (ketamine)

Dissociative anesthetic

1-2 mg/kg IV

5 mg/kg IM/IN

IM, IV, IN

30 s IV

3 m IM

5-10 m IV

15-25 m IM

Rapid, reliable IM results

Seizure potential (low incidence)

Amidate (etomidate)

Anesthetic agent

0.3-0.6 mg/kg

1 m

3-5 m

Very short acting, lowers ICP

IV only, uncommonly used in severe agitation

Haldol^d (haloperidol)

Typical antipsychotic

5 mg

20 m

hours

Long history of safe use, preserves respiratory drive

Arrhythmia concerns, lowers seizure threshold, long onset, rare hypotension

^aConventionally accepted starting doses. Some situations will require higher starting doses and total requirements may be significantly higher.

^bBenzodiazepine-induced respiratory depression is possibly due to rapidity of onset. With midazolam having the most rapid onset of all benzodiazepines, this may explain the higher incidence of respiratory depression.

^cDiazepam may be given IM, but erratic absorption precludes this as a viable and reliable route.

^dThe author of this chapter does not endorse haloperidol if excited delirium is suspected.

The ultimate chemical restraint would be the use of paralytics. Their dose and administration are discussed in Chapter 34. The benefit of paralytics is that they offer definitive and predictable control of an agitated, combative patient when given IV. A potential downside is that they eliminate the respiratory drive in a severely acidotic patient who may be at the limits of respiratory compensation. The window for safe intubation is likely markedly narrowed and the need to support ventilation (not just oxygenation) during the procedure is paramount due to the likelihood of severe acidosis and the tenuous respiratory compensation that is occurring. Additionally, paralytics require IV administration for rapid, uniform onset. While IM administration is pharmacologically possible, the onset curve will be longer. How this affects a combative and uncooperative patient is unknown. There is potential to decrease respiratory function in a graduated fashion while the patient is still uncooperative with oxygenation, ventilation, or even airway monitoring. No information exists to guide the EMS physician as to whether this is problematic beyond the theoretical.

Etomidate deserves mention since the EMS physician may have access to this medication for airway control. It is a medication not traditionally utilized for rapid control of an agitated and potentially violent patient so extensive evaluation of its use in unavailable. It may provide immediate, short duration sedation of a patient, allowing for proper restraint and treatment. Its main disadvantage is that it only works IV, and this is often problematic in the setting of acute agitation. Due to it being administered IV and its lack of track record in acute agitation, it is probably not preferred to other medications listed in this text, but it should not be eschewed for definitive patient control and protection if other agents are not available. At best, it is a segue medication for rapid control, but must be immediately followed by another medication. It may be useful for immediate control, advanced airway placement and then be followed by massive doses of benzodiazepines (since the airway is controlled) and consideration of paralytic medication.

Sedation and chemical restraint must be individualized based on the patient presentation. A patient who is only mildly to moderately agitated is best served with a benzodiazepine in moderate amounts. When the patient crosses into excited delirium, more aggressive control is indicated and ketamine is the desired medication. Massive doses of benzodiazepines may also be employed. Paralytics are a last resort when the patient is uncontrollable by other medications and their safety is still in peril. The discussed medications are summarized in Table 36-1.

PRACTICAL CONSIDERATIONS

A few practical notes regarding how to administer medications are in order. One question that arises is how to administer medication IM in a combative, struggling patient. Clothing is often in place and obstructs the safest and most convenient site of IM administration: the vastus lateralis muscle (the midanteriolateral thigh). Epinephrine is a medication that is recommended to be given IM through clothing as necessary in life-threatening situations.⁵⁸ Insulin has also received support in the literature for administration through clothing.⁵⁹ Consequentially, all of the medications in this chapter should be given through clothing if necessary, especially since they are being administered in critical, life-threatening situations.

Additionally, the standard 3- to 5-mL injection limit for IM medication administration should not apply to a patient who is agitated making medication administration dangerous. The purpose of the limit on injections is patient comfort and the prevention of fibrosis due to muscle damage from larger volume injections. Neither of these concerns are valid in a patient who is possibly about to deteriorate into cardiopulmonary arrest. IM medications should be given quickly and without regard to amount. Grasping the barrel of the syringe with the fingers and palm and using the thumb on the plunger (see Figure 36.1) will provide both maximum injection speed and control over the sharp object. Aspiration of the needle is not necessary as almost all medications administered IM can also be given IV (the exception being haloperidol). A needle that is slightly larger than what would be used for a typical injection can be used. Up to a 19-gauge needle can be employed if necessary to administer medication more quickly to help remove a sharp object from the vicinity of a combative patient. The needle length should be at least 1.5 in to ensure reaching the muscle belly. Longer needles may be needed for markedly obese patients.

Intranasal (IN) medication administration has been gaining popularity. Most of its usage has been for seizure control^60,61 or sedation in the hospital setting.⁶² How this technique will fare in an acutely agitated, uncooperative patient is unclear. The clear advantage of not having to bring a sharp object near a fighting patient is a significant factor that makes this an attractive route to consider. This advantage may be offset by the EMS physician needing to put his or her hand in the vicinity of the combative patient's mouth. Medications of appropriate concentration will need to be selected that conform to the 2 mL maximum volume (1 mL per naris) of this administration method. Amounts that exceed this could run out and be lost or be swallowed and relegated to PO ingestion and the resultant delay in onset.

Intraosseous access is also an alternative route that may be considered. It is difficult to accomplish in a combative patient, but may prove easier than IV access in some situations. Medication needs as well as personnel resources available will dictate whether the EMS physician should attempt this route of access.

KEY POINTS

Hypoxia, hypoglycemia, and narcotic overdose are rapidly correctable causes of altered mentation in the prehospital environment.
Neither conducted energy devices such as tasers, nor chemical sprays ever been scientifically proven to be causative of patient mortality or severe morbidity.
Physical and chemical restraints can be accomplished in a humane manner and can prevent injury or death.
The EMS physician should be knowledgeable about and prepared to treat a broad differential of causes of mental status changes that range from decreased consciousness to severe agitation.
The EMS physician should be aware of potential complications that can arise from different types of physical restraint and should allow for appropriate chemical restraint to mitigate the risk of these complications.
Excited delirium is a medical emergency with potential for severe morbidity and mortality. It must be recognized and managed rapidly and appropriately with use of fast-acting sedatives followed by assessment and treatment of potential medical or toxic causes.

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Drowning, Hypothermia, and Hyperthermia

Peter Tilney

INTRODUCTION

Environmental exposures lead to numerous emergency calls throughout the United States and beyond each year and result in potentially devastating conditions. Appropriate prehospital care may make the difference for patients experiencing these serious, and sometimes fatal, exposures. By knowing the risks and recognizing the signs, early detection and proper intervention can be instituted.

OBJECTIVES

Define and differentiate between the terms: drowning and near drowning.
Describe the signs and symptoms that occur during the drowning process and the prognosis of individuals who have undergone this process.
Describe the general management of drowning victims.
Comment on the inherent risks associated with water operations (covered in greater detail in Chapter 72).
Describe the cardiovascular and neurological findings of severe hypothermia.
Detail the initial management of life-threatening hypothermia and list deviations from usual ACLS during cardiac arrest or periarrest scenarios.
Describe the cardiovascular and neurological findings of severe hyperthermia.
Detail the management of life-threatening hyperthermia.

DROWNING

EPIDEMIOLOGY AND DEFINITIONS

Although substantial efforts have been taken by health care advocates and public health providers to develop appropriate prevention strategies, drowning remains a significant cause of morbidity and mortality in not only the United States, but also worldwide. The global statistics vary widely on the annual number of deaths from submersion injuries, but depending on sources cited, annual death rates range from 150,000 to 500,000 deaths per year.^1,2,3–5 For each death that occurs, there are two to four other related water-related injuries that require hospitalization.⁶

In the United States, drowning is the second leading cause of death in children only surpassed by deaths from motor vehicle accidents.² Of those who survive the drowning episode, one-third will suffer from significant morbidity due to irreversible anoxic brain injuries.⁷ The populations most at risk for submersion injuries are infants and toddlers aged 1 to 4 years. Children in this age bracket account for approximately 27% of all deaths due to submersion.¹ Of those patients, males are more apt to suffer from drowning injuries when compared to their female counterparts.⁷

Most submersion injuries occur in freshwater, even in states with large areas of coastal access. The sites of drowning also vary with age. In the young infant population (<1 year), 55% of drownings occur in the bathtub.¹ In older children, up to 50% occur in local swimming pools, followed by freshwater bodies of water (lakes, rivers, and streams).^1,2,6,7 It is important to note in older children and adults that greater than 50% of submersion injuries are associated with the concurrent use of alcohol and drugs.^1,6,7

For many years, the specific definitions of the types of submersion injuries have been blurred. In 2002, the First World Congress on Drowning met in Amsterdam to delineate definitions based on the mechanism of injury and subsequent physiologic sequelae.² At the meeting, members defined drowning as the process of experiencing respiratory impairment from submersion or immersion. Patients who have had a mechanical obstruction due to a liquid medium regardless of outcome are said to have been involved in a drowning incident.

Since 2002, the definition of near drowning is slowly being phased out of use by medical professionals due to fact that it is imprecise and has a high level of interpretation by providers. However, it is worth defining due to fact that it is still common verbiage. Near drowning is defined as surviving, at least initially, after being submerged in a liquid medium. Since the decision in 2002 for a standard definition, further delineations have become increasingly irrelevant and for the sake of simplicity have not been included in the text.

As defined by the World Congress on Drowning in 2002²:

Drowning is a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium. Implicit in this definition is that a liquid/air interface is present at the entrance of the victim's airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a drowning incident.

PATHOPHYSIOLOGY

The process and subsequent continuum of drowning begins the moment the airway is obstructed by the noted liquid medium. Initially, victims are able to hold their breath briefly. This short period is immediately followed by laryngospasm due to the presence of liquid in the posterior oropharynx. This choking response represents the first anoxic insult that the patient experiences in the drowning process. If uncorrected, the patient will become even more hypoxic and hypercarbic due to the fact that gas exchange is inhibited. Depending on multiple physiologic factors and the mechanism of injury, 90% to 98% of cases, the laryngospasm will resolve resulting both swallowing and aspirating the liquid into the pulmonary tissues.²

In earlier literature, providers would describe those patients who had aspirated water, detritus, and vomitus to have suffered a “wet drowning.” Those who had limited abnormal findings on examination or autopsy were to have suffered from a “dry drowning” due to persistent laryngospasm. However, given the fact that the amount of water that can be found in drowning victim's pulmonary tissues can vary widely with no definable pattern, the differentiation between dry and wet drownings has also been discarded. The reason for this is due to the fact that most victims have a degree of fluid in the pulmonary tissues if the mechanism of death is associated with a submersion injury. It is important to note, however, that if the victim has no fluid in the lungs or respiratory tissues, the cause of death is not due to drowning. Fluid will not infiltrate the lungs or associated tissues without active respiratory effort.^2,6

The initial hypoxemia that the victim suffers secondary to the apnea of submersion is then exacerbated by a variety of factors including surfactant washout, pulmonary hypertension, and intrapulmonary shunting. As fluid is aspirated, profound alterations in arterial oxygenation occur. Left uncorrected, alveolar collapse, atelectasis, or mechanical obstruction leads to acute lung injury and acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema.

The debate concerning whether respiratory collapse is exacerbated depending on the fluid in which the patient is submerged, salt versus fresh water, continues. Multiple studies have been completed examining the effects of hyper- and hypotonic fluids on blood volume and electrolyte abnormalities in this population, and it has been found that only a small population of less than 15% of individuals has documented physiologic electrolyte changes from the aspiration of the surrounding liquid medium.² The end result, however, is the same. Whether it is due to mechanical obstruction, dilution of surfactant, loss of osmotic gradient, a ventilation and perfusion mismatch occurs, leading to profound hypoxemia.

Dysrhythmias and complete cardiovascular collapse can occur at the time of the initial hypoxic insult or several minutes after the noted laryngospasm has abated. If the victim is rescued prior to a prolonged period of submersion, the hypoxemia, acidosis, and subsequent electrolyte abnormalities will resolve with basic resuscitation. It is uncommon for drowning patients to suffer a primary ventricular fibrillation or ventricular tachycardic arrest giving the mechanism of injury. However, isolated events have been described anecdotally in lab models or in those patients who aspirate large volumes of fluid.

In the first several minutes of a drowning injury, cerebral ischemia occurs due to the cardiovascular compromise that occurs with submersion. The degree of injury to the brain and the remainder of the nervous system are dependent on the duration and severity of the initial hypoxic-ischemic injury. If the patient is extracted from the liquid medium and resuscitated appropriately, secondary ischemic injuries, including cerebral edema, can occur further exacerbating the initial insult. More than 10% of drowning survivors suffer permanent effects.^1,6

Recovery of victims of drowning events vary widely based on duration of submersion injures, associated trauma, other medical conditions, and surrounding environmental factors. In young healthy patients, periods of submersion between 2 and 5 minutes are moderately well tolerated. However, submersions for greater than 25 minutes for all patients are associated with high morbidity and mortality rates.^6,7 Many drowning patients present with associated hypothermia due to the immersion in the surrounding environment. Hypothermia as a whole can be indicative of prolonged duration in the water and is associated generally with a much poorer prognosis. In some cases, the cold temperature can limit end-organ perfusion and is associated with some anecdotal cases of prolonged submersion with little to no long-term deficits.⁶ Given the variability of factors, overall prognosis in victims of drowning incidents is difficult to predict.⁷

In patients who still have physiologic signs of spontaneous circulation at the time of rescue, the prognosis of recovery is variable. In those victims who are awake and oriented at the time of arrival in the emergency department, they typically survive without neurologic deficits if there is no respiratory compromise at the time of evaluation.^1,6,7 Those patients who arrive with altered mental status, but responsive to pain (ie, a GCS of 6 or greater) also typically survive without neurologic sequelae greater than 90% of the time.^6,7 However, those patients who arrived and were noted to be obtunded (with a GCS of 5 or less) tended to have poor outcomes.^2,6,7 Between 10% and 23% of those patients were neurologically affected and of those impaired patients, 39% died soon after their arrival and 17% had irreversible and incapacitating brain injuries.²

TREATMENT

Drowning emergencies can occur in a variety of environments. Proper initiation of prehospital care can heavily impact the overall morbidity and mortality in many cases. Bystander interventions, especially in children, are not uncommon. The role of the prehospital provider is to begin the initial resuscitation promptly to restore normal ventilation and circulation as quickly as possible. Concurrently, rescuers must not only begin basic cardiopulmonary resuscitative measures, but must also consider simultaneously the mechanism of injury and provide cervical spine precautions if applicable and prevent further heat loss if the patient is affected by the surrounding environment.

The initiation of the resuscitation will begin the assessment and establishment of an airway if indicated. If the patient is spontaneously breathing and there is no evidence of any traumatic injury, the patient should be placed in the left lateral decubitus position with supplemental oxygen. However, in most cases, the patient will be apneic and require clearing of the airway and subsequent positive pressure ventilation. As discussed previously, most patients will swallow large amounts of water during the drowning process, which can lead to significant gastric distention. Rescuers should be prepared for an abundance of vomiting and plan for immediate treatment to minimize further risk of an additional pneumonitis. In this early portion of the resuscitation, abdominal thrusts and the “Heimlich” maneuver are contraindicated. They have not shown to be beneficial and can precipitate further vomiting and are associated with additional complications.^1,2,6 If the patient remains hypoxemic or continues to be obtunded, placement of a definitive airway (endotracheal intubation, Combitube, or King Airway) will prevent further aspiration and will continue to facilitate appropriate oxygenation and ventilation.

The resuscitation should continue with appropriate cardiac monitoring. As per advanced cardiac life support (ACLS) protocols, pulses should be routinely assessed, and if are not present, CPR should continue. Bystanders and prehospital providers have a variety of monitoring devices available. Automated external defibrillators are available at a variety of locations and have been used in many resuscitations successfully. Advanced Life Support EMS providers routinely use manual defibrillators and monitoring devices, thus demonstrating further benefits for activating a 9-1-1 response.

Once the patient arrives in an appropriate receiving facility, treatment is focused minimizing further hypoxia. If the patient remains obtunded, and a definitive airway has not been established, rapid sequence intubation is required. Patients who are able to protect their airway can be supported with supplemental oxygen or BiPAP. Positive pressure ventilation can aid in minimizing the respiratory effort of the patient until the respiratory status improves. FiO₂ and PEEP should be titrated appropriately to maintain oxygen saturations of greater than 96%.

Additional sequelae following a drowning episode are common. Pulmonary edema and subsequent ARDS is a routine finding due to variety of factors including surfactant washout. These patients benefit from elevated PEEP or BiPAP levels to increase alveolar recruitment and ventilation. Diuretics have been used with some success, but it is important to assess the patient's fluid status prior to their routine administration. Lastly, the use of antibiotics is indicated when there is concern for immersion in grossly contaminated fluids. Their routine use is not indicated unless signs and symptoms occur. Other complications including traumatic injuries, hypothermia, and underlying comorbidities need to be addressed during each individual resuscitation. Overall outcomes are dependent on the quality and efficiency of the initial resuscitation and subsequent restoration of optimal oxygenation and ventilation.

WATER RESCUE OPERATIONS

When a water rescue team is activated for deployment, operations must be conducted in a safe and efficient manner. These specialty-trained teams undergo vigorous training and preparation to not only rescue victims, but also to conduct the deployments in a safe and efficient manner. Members adequately prepare for missions by not only perfecting skills as individual members by taking swiftwater rescue technician (SRT) courses and education on prehospital emergency care, but they will continuously train as a team to establish clear pathways and effective methods of recovery to minimize risk to the team and maximize the beneficial outcome.

During the course of rescue operations, standard operating procedures (SOPs) are typically defined prior to deployment to minimize adverse outcomes and mission failure. These protocols follow similar guidelines utilized in other rescue situations and are based on the Incident Command System (ICS). Once the mission is activated, staff must make rapid decisions during the course of the initial scene evaluation:

What is the nature of the call?
Is the activation for a rescue of living individual(s) or recovery of deceased victims?
What are the hazards?
Is there a need for additional resources beyond the scope of the first responders?

Once the initial scene assessment is completed, rescue operations can commence. Despite its simplicity, the standard Talk-Reach-Throw-Row-Go is still the standard in water rescue operations.⁸ Most scenarios requiring rescue personnel require the active intervention of providers, but all attempts should be made to minimize risk. There are clear examples when the standard operation procedures of water rescue cannot retrieve the victim without harming either the victim or placing the team at extreme risk. Helicopter utilization may be appropriate for patient extrication in these situations.

Once the patient is in a safe environment, trained personnel must complete rapid assessment for injuries and illnesses. In most cases, these patients are likely to have multiple complaints including traumatic injuries, hypothermia, and potentially, respiratory distress from inhalation of water. They will require aggressive management and transport to the nearest appropriate facility for evaluation and treatment.

HYPOTHERMIA

EPIDEMIOLOGY AND PATHOPHYSIOLOGY

The maintenance of the normal core body temperature is dependent on the body's inherent metabolism as well as the interaction with surrounding environmental conditions promoting heat loss. The human body functions optimally with a core temperature between 36.4°C and 37.5°C. Hypothermia is defined as an unintentional decrease in core temperature to less than 35°C (95°F) with severe hypothermia categorized as a body core temperature less than 28°C (82.4°F). At this temperature, body systems responsible for maintenance of homeostasis begin failing and further insult can occur easily.

Hypothermia occurs primarily due to three factors: decreased heat production, increased heat loss, and impaired thermoregulation. In order to maintain “normothermia,” multiple body systems must be operating optimally to ensure homeostasis. To promote cellular respiration and metabolism, sufficient quantities of fuel (ie, food) must be available for consumption. Hypoglycemia can further exacerbate the inability of body temperature maintenance. Heat production can also be limited due to endocrinologic inadequacies including hypothyroidism and hypopituitarism. Other systemic failures can also further impair thermoregulation, including the inability to shiver, extremes of age, and inactivity.

The most common reason, however, for hypothermia is due to heat loss.^9,10 Each year, there are multiple cases of fatalities due to environmental exposure with greater than 50% of these fatalities occurring in elderly patients in urban areas.⁹ It is important to identify the causative factors associated with primary hypothermia (accidental hypothermia) in order to treat patients effectively. Heat loss occurs as a result of the patient's interaction with surrounding environment through evaporation (cooling by conversion of fluid to vapor), conduction (transfer of heat by direct contact), convection (transmission of heat by moving particles), and radiation (nonparticulate heat emission). Heat loss can be further exacerbated through vasoactive medications, including illicit drugs, as well as damage to the skin seen in large-scale burns.

When treating patients with cold-related injuries, it is important to identify that there is a spectrum of illness seen with a decrease in body temperature. Mild and moderate hypothermia will be discussed in further detail in later chapters. Severe hypothermia is defined as a core temperature of less than 28°C (or 82.4°F). Patients with severe hypothermia have significant alterations in critical body systems. These patients typically will present obtunded and comatose with noted global loss of cerebral reflexes. EEG activity, if measured, will be minimal or completely silent with temperatures less than 26°C.^9,10 Ocular reflexes will not be present concurrently.

As with all other body systems in hypothermia, the cardiovascular system will be significantly affected. Cardiac output will be decreased significantly and is readily apparent in noted hypotension that may not be correctable with vasoactive medications. As the temperature continues to drop, the myocardium will also have noted sequelae. Bradycardia occurs initially and is followed by myocardial irritability, as evidenced by cardiac dysrhythmias. These include Osborn waves and prolongation of the PR, QRS, and QT intervals.^9–11 (Figure 37-1). The 12-lead tracing shows Osborn waves (J waves) in leads II, V5, and V6. With further decreases in temperature less than 28°C, the myocardium is susceptible to ventricular fibrillation and eventually asystole.

FIGURE 37-1.

Noted Osborn or J waves in leads II, V5, and V6 in a 88-year-old male with hypothermia.

As patient's temperature decreases significantly, further organ system failures can occur. Similar to the effects categorized previously, patient's respiratory status deteriorates with additional cooling. Depression of the respiratory centers result in blunting of airway reflexes, bradypnea, and eventually, respiratory arrest occurs if the cooling is not corrected.^9–11 Pulmonary edema can occur with rewarming and reassessment is vital to maintain appropriate oxygenation and ventilation. Renal failure, hypoglycemia, frozen or poorly perfused extremities, coagulopathy are all additional sequelae seen in severe hypothermia (Table 37-1).

TABLE 37-1

Signs and Symptoms of Severe Hypothermia

TABLE 37-1

Signs and Symptoms of Severe Hypothermia

Organ System

Clinical Manifestations in Severe Hypothermia

Nervous system

Altered mental status, confusion

Obtundation, coma

Loss of ocular reflexes, and dilated/fixed pupils

Decrease in or loss of EEG activity

Cardiovascular system

Bradycardia, Osborn/J waves

Hypotension, loss of peripheral pulses dysrhythmias

Respiratory system

Bradypnea, apnea

Pulmonary edema

Renal system

Oliguria, loss of renal perfusion

Hematologic system

Thrombocytopenia, anemia, leucopenia, coagulopathy

Musculoskeletal system

Muscular rigidity, frostbite

TREATMENT

Management of the severely hypothermic patient requires an understanding of human pathophysiology combined with a rapid assessment of the insult that the patient has encountered. Initial actions focus on the removal of environmental stimulus, the prevention of further cooling, and evaluation of other associated conditions. Once placed in a safe environment, attention is then focused on aggressive rewarming. Similar to other types of resuscitations, initial assessment and treatment focuses on basic cardiopulmonary stabilization.

If the patient is obtunded at the time of initial patient contact, consideration must be made to ensure that the etiology of the patient's altered mental status is due to hypothermia. During the initial assessment, blood glucose and evaluation of pupils to assess the possibility of narcotic use may be completed while initiating other critical interventions. The determination of the patient's temperature should also occur early in the resuscitation. Esophageal probe placement or rectal temperatures are the most accurate means of assessing core temperature. Continuous temperature monitoring is required in patients with severe hypothermia during the rewarming process.

Immediate attention should be focused on determining whether patients have a patent airway and are oxygenating appropriately. If the patient is breathing on her or his own and is protecting the airway, warm humidified oxygen can be applied. In most cases of severe hypothermia, the patient will require endotracheal intubation for airway protection and establishment of a definitive airway. It is important to note that neuromuscular blockade used in rapid sequence intubation (ie, rocuronium and succinylcholine) will not work in patients with body temperatures less than 86°F and should be avoided.^9–11 If the jaw is clenched, nasotracheal intubation or other BLS maneuvers may be necessary to maintain the airway.

After the definitive airway is placed, an orogastric tube can be placed to relieve gastric distention. Lastly, a Foley catheter can be placed to monitor urine output during the course of the rewarming process. There are now several companies that manufacture catheters with temperature sensors to aid in monitoring body temperatures during the resuscitation.

Once the initial stabilization has occurred, aggressive active rewarming must then take place. Fluid resuscitation should immediately begin with intravenous fluids heated to 40°C - 42°C. These fluids will not actively rewarm the patient; rather they will prevent further heat loss.^9,10 In many cases, the crystalloid administered will treat associated hypotension. It has been recommended not to use lactated Ringer in these resuscitations due to liver's inability to metabolize lactate effectively when in a hypothermic state.¹⁰

Although the treatment for severe hypothermia is rewarming, there is little agreement in how to complete this task effectively without additional injury. In patients with severe hypothermia, there is little role for passive rewarming methods. As noted previously, initial treatment methods focus on arresting further hypothermic insult. Therefore, active rewarming methods are required to treat this subset of patients.

Active external rewarming utilizes a variety of methods to treat severe hypothermia.¹² Each method, however, has its controversies and side effects.^13–15 Devices used include hot water immersion, heated blankets, forced air rewarming, and heating pads. Immersion in hot water has been long utilized in patients with mild to moderate hypothermia. However, it is not typically used in severely affected patients due to the fact that appropriate monitoring and resuscitation cannot occur easily. Burns and thermal injuries can occur with the use of heating blankets, pads, and radiant heat sources. Forced air rewarming (ie, Bair Huggers) can be used appropriately, will prevent further heat loss, and provide radiant heat transfer. External rewarming techniques, however, can cause peripheral vasodilation, which can exacerbate noted hypotension. Further complications can occur due to the transport of cold blood to the core, resulting in a core temperature decrease (afterdrop) before results of treatment are seen.

Recent development in technology in the last several decades has focused on active core rewarming. These internal rewarming techniques began with the instillation of fluids into truncal cavities. Heated irrigation has been used in peritoneal dialysis as well as closed thoracic lavage.^10,11,16 Both methods instill large volumes of fluid into noted cavities; however, these require specialized training and knowledge of surgical techniques.

Additionally, there are other methods used in extracorporeal blood rewarming, including hemodialysis, arteriovenous rewarming, venovenous rewarming, and cardiopulmonary bypass. Dialysis has been used successfully in patients who not only require active core rewarming, but also concurrent treatment for severe renal dysfunction and the removal of certain ingested toxins. Cardiopulmonary bypass is the most efficient core rewarming technique and can raise temperatures 1°C to 2°C every 3 to 5 minutes, but is labor intensive and not available at all facilities.^10,11

As the human body core temperature drops in severe hypothermia, the patient's myocardium becomes more irritable and is prone to significant cardiac dysrhythmias, resulting in compromised cardiac output. As with other critical systems, the primary treatment is to rapidly warm the patient. Most dysrhythmias will resolve spontaneously once the core body temperature is increased toward baseline. Initially, circulatory support by health care providers is dependent on identifying whether a pulse is present. Nonlethal rhythms including bradycardia and atrial fibrillation require basic supportive care and careful handling. At temperatures less than 32°C (86°F), the possibility of converting a patient from a nonlethal rhythm to ventricular fibrillation, ventricular tachycardia, or asystole is increased according to the irritability discussed previously.^10,11 These patients require gentle handling to minimize risks of spontaneous conversion.

Those hypothermic patients without a pulse require aggressive rewarming in addition to extensive resuscitation measures. If the patient is found to be in ventricular fibrillation or ventricular tachycardia, an initial defibrillation is warranted. Typically, attempts will be unsuccessful at temperatures less than 32°C; however, aggressive rewarming should occur with concurrent CPR and airway management.¹¹ As the temperature is increased 1-2 degree Celcius, additional attempts at defibrillation can occur. Once the body temperature achieves 30°C to 32°C (86°F to 89.6°F), antidysrhythmic and vasoactive medications can be utilized successfully.^10,11 Given that the body's metabolism is altered at low temperatures, the lowest indicated dose is indicated in hypothermia patients. Higher levels of these medications can lead to systemic toxicity.

Antidysrhythmic and vasoactive medications are useful adjuncts in patients with severe hypothermia. However, their efficacy remains largely unknown. Treatment should focus on aggressive rewarming rather than standard advanced cardiac life support protocols.

If the patient continues to remain hypotensive during the resuscitation, warm intravenous fluids are indicated for volume replacement. Vasopressor therapy has minimal effect on persistent hypotension and can result in worsening dysrhythmias.

Patients with severe hypothermia require an efficient and multifaceted approach during resuscitation. Aggressive rewarming must occur simultaneously with other resuscitative techniques. With this combination of therapies, effects seen after a significant drop in core body temperature, specifically a core afterdrop, will be minimized. Even though the effects of the initial insult can be mitigated with initial treatment, numerous other complications can occur after the patient is rewarmed including rhabdomyolysis, electrolyte imbalance, ARDS, and disseminated intravascular coagulation. Continued monitoring and reassessments will be required to ensure a successful outcome.

HYPERTHERMIA

Hyperthermia is the elevation of core body temperature due to an excess of heat production, and inability to decrease heat transfer to the ambient environment. Similar to the continuum of severity of illness seen in hypothermia, heat-related effects occur in a like fashion, based on the degrees above normal body temperature. The key difference, however, is that once the core temperature reaches 105.8°F (41°C), cellular apoptosis occurs and complex proteins begin to break down.¹¹ If uncorrected, significant physical impairment and noted sequelae can occur. There is a significant morbidity and mortality related to thermal illness with heat stroke, resulting in the death of greater than 12% of adult patients with body temperatures in excess of 41°C.¹¹ Thus, aggressive treatment to minimize these effects is essential to ensure appropriate outcomes.

There is a significant difference between heat-related illness and basic fevers. Febrile illness is normal physiologic response by the body that results in an elevation of core body temperature by pyrogenic stimuli (ie, infection). This elevation remains under the control of thermoregulatory centers in the hypothalamus and brainstem and rarely exceeds 41°C.¹⁷ In heat-related illness, however, there is no thermoregulation and thus body temperatures increase unchecked, leading to significant physiologic injury. It is also critically important to differentiate between heat-related illness and that of malignant hyperthermia (MH) that occurs secondary to a triggering agent. These include such medications as volatile halogenated anaesthetic agents and depolarizing muscle relaxants. Malignant hyperthermia has also noted sequelae including rigidity, and hypercapnia which is not identified in patients with heat stroke. Lastly, MH can be corrected with the use of dantrolene, whereas heat stroke requires rapid cooling by traditional means.¹⁷

Heat-related illness occurs primarily in warm climates and is exacerbated by conditions affecting thermoregulatory control. These include mental illness, chronic medical conditions, occupational hazards, and insufficient acclimatization. Rapid increases in body temperature occur when heat production occurs unchecked, and heat dissipation is inhibited. Signs and symptoms occur at various degrees of severity ranging from the mild discomfort related to heat stress to the emergent sequelae of heat stroke. The mild to moderate conditions of heat-related illness are outlined in Chapter 47. The remainder of this section will focus on the identification and treatment of the emergent heat stroke.

Heat stroke is the third leading cause of death behind cardiac disorders and head/ neck trauma in athletes.^11,18 Between 350 and 400 deaths occur annually, of which almost 50% occur due to ambient weather conditions.¹⁸ All humans are at risk for heat-related illness; however, the population of the young, elderly, and those with chronic conditions, which inhibit appropriate thermoregulations, can be particularly affected. Heat stroke is defined as an elevation of core body temperature to greater than or equal to 41°C with accompanying alterations in the central nervous system (CNS), including altered mental status, ataxia, and other neurologic sequelae.

Heat stroke has been further delineated into classic and exertional, based on the mechanism of injury. Classic heat stroke occurs primarily in compromised patients over the course of several days, usually during environmental conditions which include elevated temperature and humidity. Typically, patients with classic heat stroke present with anhydrosis, but this is not a firm criterion. This population of patients will also present with CNS dysfunction that is manifested by altered mental status, seizures, or coma. In addition, patients can present with signs and symptoms consistent with systemic volume loss from earlier diaphoresis and other insensible losses. Tachycardia, hypotension, and respiratory alkalosis from hyperventilation can be seen in some of these patients.

Exertional heat stroke occurs primarily in poorly acclimatized young patients including athletes and military personnel who participate in strenuous activities and are not adequately prepared for the conditions. These patients present not only with elevated core body temperatures and CNS alteration, but they also demonstrate sequelae resulting from significant hypovolemia. Common manifestations include severe tachycardia, hypotension, and tachypnea. Gastrointestinal signs and symptoms make occur as well including nausea, vomiting, and diarrhea, thus exacerbating the noted dehydrated state even further.

As a result of these sequelae, patients with exertional heat stroke can develop significant lab abnormalities including acute renal failure (increased BUN and creatinine), rhabdomyolysis (elevated CPK), and in extreme cases disseminated intravascular coagulation (DIC). Alterations in electrolytes also occur as a result of the acute volume loss including hypokalemia, hypocalcemia, and hypoglycemia. Lactic acidosis and liver dysfunction can also occur.

When patients present with CNS dysfunction in a warm environment, it is critical that the provider differentiate between heat-related illness and acute hyponatremia. With serum sodium levels less than 130 mmol/L, alterations in sensorium, seizures, and obtundation can occur.¹⁸ Health care providers must assess core temperatures in order to differentiate between the two diagnoses. Exertional hyponatremia can occur in similar environments. However, the hyponatremia is due to an excessive amount of water intake prior to, during, and after physical exercise without attention to simultaneous salt loss. If the sodium is not corrected, persistent seizures, coma, and even death may occur (Table 37-2).

TABLE 37-2

Signs and Symptoms of Heat Stroke