circulationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinscirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinscirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinscirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinscirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinscirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & Wilkins 220820002208200022082000220820002208200022082000The most important and detrimental consequence of submersion without ventilation is hypoxia. The duration of hypoxia is the critical factor in determining the victim’s outcome. Therefore, oxygenation, ventilation, and perfusion should be restored as rapidly as possible. Immediate resuscitation at the scene is essential for survival and neurological recovery after submersion. This will require bystander provision of CPR plus immediate activation of the EMS system. Victims who have spontaneous circulation and breathing when they reach the hospital usually recover with good outcomes. Hypoxia can produce multisystem insult and complications, including hypoxic encephalopathy and acute respiratory distress syndrome (ARDS). These complications are relevant to the care of the victim after resuscitation and will not be addressed here. Victims of submersion may develop primary or secondary hypothermia. If the submersion occurs in icy water (<5°C [41°F]), hypothermia may develop rapidly and provide some protection against hypoxia. Such effects, however, have typically been reported only after submersion of small victims in icy water.1B Hypothermia may also develop as a secondary complication of the submersion and subsequent heat loss through evaporation during attempted resuscitation. In these victims the hypothermia is not protective (see Hypothermia earlier in this section). All victims of submersion who require resuscitation should be transported to the hospital for evaluation and monitoring. The hypoxic insult can produce an increase in pulmonary capillary permeability with resultant pulmonary edema. Definitions, Classifications, and Prognostic IndicatorsA number of terms are used to describe submersion. Clinicians and others who report about submersion often apply the misunderstood term drowning to victims who die within 24 hours of a submersion episode. They apply the term near-drowning to submersion victims who survive >24 hours after the episode if the victim also requires active intervention for one or more submersion complications. Complications can include pneumonia, ARDS, or neurological sequelae. Rescuers and emergency personnel find these definitions irrelevant, because the drowning versus near-drowning distinction often cannot be made for 24 hours. Pending the future recommendations of an ILCOR Task Force revising the Utstein Guidelines, the Guidelines 2000 Conference recommends these terms: Water rescue: a person who is alert but experiences some distress while swimming. The victim may receive some help from others and displays minimal, transient symptoms, such as coughing, that clear quickly. In general the person is left on shore and is not transported for further evaluation and care. Submersion: a person who experiences some swimming-related distress that is sufficient to require support in the field plus transportation to an emergency facility for further observation and treatment. Drowning: this is a “mortal” event; this refers to submersion events in which the victim is pronounced dead at the scene of the attempted resuscitation, in the Emergency Department (ED), or in the hospital. With drowning, the victim suffers cardiopulmonary arrest and cannot be resuscitated. Death can be pronounced at the scene, in the ED, or within 24 hours of the event. If death occurs after 24 hours, the term drowning is still used as in “drowning-related death.” Up until the time of drowning-related death, refer to the victim as a submersion victim. We recommend that the term near-drowning no longer be used. We recommend that clinicians, managers, and research teams stop the classification of submersion victims by submersion fluid (salt water versus fresh water). Although there are theoretical differences between the effects of salt-water and fresh-water submersion in the laboratory, these differences are not clinically significant. The single most important factor that determines outcome of submersion is the duration of the submersion and the duration and severity of the hypoxia. Although survival is uncommon in victims who have undergone prolonged submersion and require prolonged resuscitation,2B3B successful resuscitation with full neurological recovery has occasionally occurred in near-drowning victims with prolonged submersion in extremely cold water.4B5B6B Therefore, resuscitation should be initiated by rescuers at the scene unless there is obvious physical evidence of death, such as putrefaction, dependent lividity, or rigor mortis. The victim should be transported with continued CPR to an emergency facility. In many European countries a physician will be available on scene as part of the EMS team. Prognostic indicators after submersion in children and adolescents (up to 20 years of age) include 3 factors associated with 100% mortality in one study1B :
Additional factors associated with poor prognosis in the same study1B included
Modifications to Guidelines for BLS for Resuscitation From SubmersionNo modification of standard BLS sequencing is necessary. There are, however, cautions and emphasis that should be considered when beginning CPR for the submersion victim. Recovery From the WaterWhen attempting to rescue a near-drowning victim, the rescuer should get to the victim as quickly as possible, preferably by some conveyance (boat, raft, surfboard, or flotation device). The rescuer must always be aware of personal safety and should minimize the danger to the rescuer and the victim. Treat all victims as potential victims of spinal cord injury, and immobilize the cervical and thoracic spine. Spinal injury is particularly likely after submersion associated with diving or involving recreational equipment, but it should be suspected if the submersion episode was not witnessed. If first-responding rescuers suspect a spinal cord injury, they should use their hands to stabilize the victim’s neck in a neutral position (without flexion or extension). They should float the victim, supine, onto a horizontal back support device before removing the victim from the water. The rescue from the water should be done quickly to ensure timely application of CPR if required. If the victim must be turned, align and support the head, neck, chest, and body. Carefully log-roll the victim to a horizontal and supine position. Provide rescue breathing while maintaining the head in a neutral position, using the jaw thrust without head tilt or chin lift to open the airway. Rescue breathing should begin as quickly as possible (see below). Provision of chest compression typically will have to wait until the victim has been removed from the water. External chest compressions cannot be performed in the water unless the victim is extremely small and can be supported on the rescuer’s forearm or unless flotation devices are used. Proper use of in-water resuscitation flotation devices requires training. Rescue BreathingThe first and most important treatment of the near-drowning victim is provision of immediate mouth-to-mouth ventilation. Prompt initiation of rescue breathing has a positive association with survival.10B Start rescue breathing as soon as the victim’s airway can be opened and the rescuer’s safety ensured. This is usually achieved when the victim is in shallow water or out of the water. If it is difficult for the rescuer to pinch the victim’s nose and support the head and open the airway in the water, mouth-to-nose ventilation may be used as an alternative to mouth-to-mouth ventilation. Appliances (such as a snorkel for the mouth-to-snorkel technique or buoyancy aids) may permit specially trained rescuers to perform rescue breathing in deep water. But rescue breathing should not be delayed for lack of such equipment if it can otherwise be provided safely. Untrained rescuers should not attempt to use such adjuncts. Management of the airway and breathing of the submersion victim is similar to that of any victim with potential trauma in cardiopulmonary arrest. The airway can be managed with adjuncts in the near-drowning victim.2B11B There is no need to clear the airway of aspirated water.12B Some victims aspirate nothing because of laryngospasm or breath-holding.3B8B13B At most only a modest amount of water is aspirated by the majority of drowning victims, and it is rapidly absorbed into the central circulation.3B An attempt to remove water from the breathing passages by any means other than suction is unnecessary and dangerous. Abdominal thrusts, for example, cause regurgitation of gastric contents and subsequent aspiration and have been associated with other injuries.12B Do not routinely perform the Heimlich maneuver for resuscitation of submersion victims. It delays the initiation of ventilation and produces complications.12B Use of the Heimlich maneuver as the first step in resuscitation of submersion victims is not evidence-based. Use the Heimlich maneuver only if the rescuer suspects foreign-body airway obstruction.11B12B14B15B If foreign-body airway obstruction is suspected, consider chest compressions rather than the Heimlich maneuver. There is recent evidence that chest compressions are superior to the Heimlich maneuver in generating increases in intrathoracic pressure to assist with the expulsion of foreign material.16B Chest CompressionsAs soon as the victim is removed from the water, check for signs of circulation. The lay rescuer will look for general signs of circulation (breathing, coughing, or movement in response to the rescue breaths). The healthcare provider will look for signs of circulation, including the presence of a central pulse. The pulse may be difficult to appreciate in a near-drowning victim, particularly if the victim is cold. If signs of circulation (including a pulse, if appropriate) are not present, start chest compressions at once. Chest compressions should not be attempted in the water. If there are no signs of circulation, an AED should be used to evaluate rhythm for victims older than 8 years of age. Attempt defibrillation if a shockable rhythm is identified. If hypothermia is present in a victim of VF and the victim’s core body temperature is ≤30°C (86°F), give a maximum of 3 defibrillation attempts (shocks). If a total of 3 defibrillation attempts are unsuccessful, return to BLS and ACLS care until the core body temperature rises above 30°C (86°F). Vomiting During ResuscitationVomiting is likely to occur when chest compressions or rescue breathing is performed, and it will complicate efforts to maintain a patent airway. In fact, in a 10-year study in Australia, vomiting occurred in half of submersion victims who required no interventions after removal from the water. Vomiting occurred in two thirds of victims who received rescue breathing and 86% of victims who required compression and ventilation.17B If vomiting occurs, turn the victim’s mouth to the side and remove the vomitus with the finger sweep or use a cloth to wipe the mouth or use suction. If spinal cord injury is possible, log-roll the victim so that the head, neck, and torso are turned as a unit to remove the vomitus. Modifications to Guidelines for ACLS for Arrest After SubmersionThe submersion victim in cardiac arrest requires ACLS including intubation without delay. Every submersion victim, even one who requires only minimal resuscitation and regains consciousness at the scene, should be transferred to a medical facility for follow-up care. Monitoring of life support measures must be continued en route with oxygen administered in the transport vehicle. Victims in cardiac arrest may present with asystole, pulseless electrical activity, or pulseless VT/VF. PALS and ACLS guidelines should be followed for the treatment of these rhythms. If severe hypothermia is present (core body temperature ≤30°C [86°F]), defibrillation attempts are typically limited to 3, and intravenous medications are withheld until the core body temperature rises above these levels. If moderate hypothermia is present, intravenous medications are spaced at longer than standard intervals (see Hypothermia earlier in this section). In children and adolescents, VT/VF on initial ECG is an extremely poor prognostic sign.1B Attempts have been made to improve neurological outcome in the intensive care unit with the use of barbiturates, intracranial pressure (ICP) monitoring, induced hypothermia, and steroid administration. None of these interventions has been shown to alter outcome. In fact, signs of ICP serve as a symptom of significant neurological hypoxic injury, and there is no evidence that attempts to alter the ICP will affect outcome. This section of the International Guidelines 2000 focuses on near-fatal asthma. The recommendations deviate immediately from routine asthma care and address the sequence of action steps needed to prevent death. Some recommendations, such as use of aminophylline, permissive hypercarbia, and early tracheal intubation, do not reflect routine asthma attacks. Nevertheless, in the desperate race to prevent cardiopulmonary arrest, heroic measures must be considered and considered early. Severe exacerbation of asthma can lead to several forms of sudden death. One classification scheme categorizes asthma on the basis of the onset of symptoms. Signs of rapid-onset asthma develop in <2.5 hours, signs and symptoms of slow-onset asthma develop over several days.1C Cardiac arrest in patients with severe asthma has been linked to
Most asthma-related deaths occur outside the hospital. The number of patients with severe attacks of asthma who present to the Emergency Department at night is 10 times greater than the number presenting during the day.6C Multiple factors affect the outcome of therapy in asthmatic patients. Constantly review these issues during evaluation and treatment:
Key Interventions to Prevent ArrestThe major clinical action is to treat the severe asthmatic crisis aggressively, before deterioration to full arrest. The specific agents and the treatment sequence will vary according to local practice. Emergency treatment will include some combination of the agents and interventions discussed below. The challenge of most concern for the ALS provider is the patient who deteriorates progressively, unresponsive to multiple therapeutic efforts. OxygenUse a concentration of inspired oxygen to achieve a Pao2 of ≥92 mm Hg. High-flow oxygen by mask is sometimes necessary. In patients with an asthmatic crisis, the following signs indicate that the need for rapid tracheal intubation is imminent:
Nebulized β2-AgonistsAlbuterol (salbutamol) is the cornerstone of therapy for acute asthma in most of the world. Standard practice in Emergency Departments is a dose of 2.5 to 5.0 mg every 15 to 20 minutes given up to 3 times in 1 hour (total dose of 7.5 to 15 mg/h). Patients who do not respond to albuterol may respond well to subcutaneous epinephrine or terbutaline.12C Intravenous CorticosteroidsBy 2000 it became a common practice in accident and emergency departments to begin corticosteroid therapy early (in the first 30 minutes) for patients with life-threatening asthma. Corticosteroids should be started early, but oxygen and β-agonists always have priority as the initial agents. Clinicians typically use 125 mg of methylprednisolone (or equivalent hydrocortisone 200 mg IV) as a starting dose in cases of severe asthma.13C14C15C Doses can range as low as 40 mg to as high as 250 mg IV or its equivalent. Nebulized AnticholinergicsUse ipratropium, an inhaled anticholinergic agent, as a moist nebulizing agent in combination with albuterol at a dose of 0.5 mg.16C Unlike β2-agonists, which have an immediate onset of action, nebulized anticholinergic agents have a delayed onset of approximately 20 minutes. Intravenous AminophyllineAminophylline, now used as secondary therapy after β2-agonists and corticosteroids, can enhance the effects of those agents. As a bronchodilator aminophylline is approximately one third as potent as β2-agonists. Clinicians use aminophylline much more frequently in children than in adults. A loading dose of 5 mg/kg is given over 30 to 45 minutes followed by an infusion of 0.5 to 0.7 mg/kg per hour, but this loading dose is not advised in people already taking theophylline, who should receive either half loading doses or maintenance doses. Addition of this agent to high doses of β2-agonists is thought to increase side effects more than it increases bronchodilation. This is most evident in patients already taking theophyllines. The risk-benefit ratio may be different in patients not taking theophyllines.17C Intravenous Magnesium SulfateA number of authors have reported success with magnesium sulfate in patients refractory to inhaled adrenergic agents and corticosteroids. Although not consistently effective, magnesium is widely available and can be administered with few if any side effects at a dose of 2 to 3 g IV at rates as fast as 1 g/min (1 g magnesium sulfate=98 mg of elemental magnesium).18C19C Parenteral or Subcutaneous or Intramuscular Epinephrine or TerbutalineSubcutaneous administration of epinephrine or terbutaline may prevent the need for artificial ventilation in cases of life-threatening asthma, especially in patients who do not respond to inhaled β2-agonists. The total epinephrine dose (at a concentration of 1:1000) is 0.01 mg/kg, usually divided into 3 doses at 20-minute intervals. For convenience and easy recall a non–weight-based dose of 0.3 mg usually is given to adults. This dose of epinephrine (0.3 mg) can be repeated twice at 20-minute intervals to a total of 3 injections. The dose of terbutaline is 0.25 mg SC every 30 minutes; up to 3 doses may be given. At this time there is no good evidence of advantages for IV β-agonists over inhaled bronchodilators.20C The value of IV bronchodilators, however, compared with that of inhaled bronchodilators merits further study. KetamineKetamine is a parenteral dissociative anesthetic that has been found to be a useful bronchodilator. Most experts think that ketamine is the anesthetic agent of choice for intubation of severe asthmatics. Ketamine potentiates catecholamines and directly induces relaxation of smooth muscle. It also increases bronchial secretions and can cause emergent reactions. Because of the effect of ketamine on bronchial secretions, atropine (0.01 mg/kg, minimum dose of 0.1 mg) also should be administered if this agent is used. Benzodiazepines help to minimize emergent reactions, although hallucinations may occur after the patient awakes. The initial dose of ketamine is 0.1 to 0.2 mg/kg followed by an infusion of 0.5 mg/kg per hour. In intubated patients or in those being prepared for intubation, the usual dose of ketamine is a bolus of 0.5 to 1.5 mg/kg, repeated 20 minutes later, or infusion of 1 to 5 mg/kg per hour.21C HelioxHeliox is a mixture of helium and oxygen (usually 70:30) that may delay the need for intubation by decreasing the work of breathing while the other medications are beginning to take effect.22C Bilevel Positive Airway PressureBilevel positive airway pressure intermittently provides assisted ventilation. Like a combination of positive-pressure ventilation and PEEP, bilevel airway pressure helps to delay or abort the need for tracheal intubation. This ventilation counteracts the effects of auto-PEEP, thereby reducing the work of breathing. Begin with an inspiratory positive airway pressure of 8 to 10 cm H2O and an expiratory positive airway pressure of 3 to 5 cm H2O.23C Tracheal Intubation With Artificial VentilationIn some patients oxygenation and ventilation can be achieved only after sedation, general anesthesia, muscle paralysis, and tracheal intubation. Patients with severe asthma experience some obstruction of inspiration and marked obstruction of expiration. This results in auto-PEEP, which is secondary to air trapping and “breath stacking” (breathed air entering and being unable to escape). The following critical points relate to tracheal intubation for life-threatening asthma:
Steps to Take Immediately After IntubationTracheal intubation only provides more external mechanical power to the patient’s failing ventilation efforts; it does not solve the problem. Patients with severe asthma may be extremely difficult to preoxygenate manually before intubation and even once the tube is in place. Because breathing efforts may be uncoordinated, the patient may not have inhaled an adequate amount of β2-agonist before intubation. Immediately after intubation inject 2.5 to 5.0 mg of albuterol directly into the tracheal tube. Confirm correct placement of the tracheal tube by the following newly recommended sequence:
Ventilate the patient with 100% oxygen. The absence of any significant obstruction to airflow immediately after intubation suggests that the diagnosis of acute asthma may have been incorrect, and the problem may have been more in the upper airway (eg, vocal cord dysfunction, tumor, or a foreign body). The person who performs manual ventilation after intubation should be instructed beforehand to ventilate at a rate of only 8 to 10 breaths per minute to avoid auto-PEEP and its consequences (eg, sudden severe hypotension). The drop in blood pressure with hyperventilation may be extremely sudden. Prevention of this problem is clearly better than treatment of it. Acute asthma can be confused with exacerbation of emphysema, especially in the elderly. For different reasons hyperventilation immediately after intubation can cause dire consequences in elderly patients with emphysema. (See the textbook Advanced Cardiovascular Life Support for an in-depth discussion of this topic.) Intubated, Critically Ill Asthmatic: Ventilator-DependentPermissive HypercapniaAdequately sedate and paralyze the patient to allow a “passive” ventilator-patient interaction. Allow Pco2 to rise (permissive hypercapnia) to values as high as 80 mm Hg. The ensuing drop in pH can be controlled with bicarbonate if needed. To set the ventilator for permissive hypercapnia:
If the patient’s airway is extremely difficult to ventilate, perform the following procedures in order until ventilation is adequate:
Troubleshooting: Hypotension or Desaturation Immediately After Intubation26CEnsure that the tracheal tube is in the correct position. The tube should be inserted to 21 to 23 cm (measured at the incisors) in most men and to 20 cm in most women. These values may need to be reduced in a small person. Incorrect placement of the tube must be addressed immediately. Do not take the time to obtain a chest x-ray, although an x-ray of the chest after intubation is always appropriate. The immediate consequences of insertion of the tube incorrectly in a patient with severe refractory asthma may be fatal. If the patient is difficult to ventilate, check the patency of the tube for obstructions caused by kinking, mucous plugging, or biting. Aspirate the tube. The differential diagnosis of hypotension or desaturation immediately after intubation, once tube position is confirmed, includes tension pneumothorax and massive auto-PEEP buildup. In patients with severe refractory asthma the chest often is silent to auscultation because of poor airflow and hyperinflation of the chest wall. Tension PneumothoraxEvidence of a tension pneumothorax includes unilateral expansion of the chest wall, shifting of the trachea, and subcutaneous emphysema. The lifesaving action is to release air from the pleural space with needle decompression. Slowly insert a 16-gauge cannula in the second intercostal space along the midclavicular line, being careful to avoid direct puncture of the lung. If air is emitted, insert a chest tube. Caution! Insertion of a chest tube in a patient with severe refractory asthma without pneumothorax will have dire consequences because the visceral pleura of the hyperinflated lung could be punctured, iatrogenically producing pneumothorax. The person inserting the tube would not realize that this has occurred because puncture of the lung would cause a release of air under pressure through the needle catheter or thoracostomy tube, just as would occur with relief of tension pneumothorax. Because of the high pressures experienced by the contralateral mechanically ventilated lung and coexisting auto-PEEP, contralateral pneumothorax would be generated, most likely under tension. Massive Auto-PEEP BuildupThe most common cause of profound hypotension after intubation is a massive buildup of auto-PEEP. Stop ventilating the patient for a brief period (<1 minute) and allow the auto-PEEP to dissipate. At the same time observe the patient’s oxygenation. Hypotension may also be due to the intubation sedatives, which should respond to volume infusion. If high auto-PEEP is not present, reconsider alternative explanations.
Anaphylactic and anaphylactoid reactions lack universally accepted definitions.
IncidenceThe annual incidence of anaphylaxis is unknown. Recent US estimates have averaged 30 per 100 000.1D A study in the United Kingdom has reported a frequency of 1 of every 2300 attendees at a hospital Emergency Department.2D The annual international incidence of fatal anaphylactic reactions seems to be 154 per 1 million hospitalized patients per year.3D EtiologyInsect stings, drugs, contrast media, and some foods (milk, eggs, fish, and shellfish) are the most common causes of anaphylaxis. When hypersensitivity to insect stings is present, 35% to 60% of affected patients will experience anaphylaxis to a subsequent sting.4D Peanut and tree nut (Brazil, almond, hazel, and macadamia nuts) allergies have recently been recognized as particularly dangerous.5D Aspirin and other nonsteroidal anti-inflammatory agents, parenteral penicillins, many other drugs and toxins, vaccines, and beer have become notorious causes of anaphylaxis. Latex-associated anaphylaxis has become a major problem in medical centers. An exercise-induced anaphylaxis (especially after ingestion of certain foods) has been reported. Anaphylaxis may even be idiopathic, typically managed with long-term use of oral steroids. β-Blockers may increase the incidence and severity of anaphylaxis and can produce a paradoxical response to epinephrine. Signs and SymptomsThe manifestations of anaphylaxis are related to release of chemical mediators from mast cells. The most important mediators of anaphylaxis are histamines, leukotrienes, prostaglandins, thromboxanes, and bradykinins. These mediators contribute to vasodilation, increased capillary permeability, and airway constriction and produce the clinical signs of hypotension, bronchospasm, and angioedema. The location and concentration of mast cells determine the organ(s) affected. Typically 2 or more of the following systems are involved: cutaneous, respiratory, cardiovascular, and gastrointestinal. The sooner the reaction occurs after exposure, the more likely it is to be severe.
Differential DiagnosisThe diagnosis of anaphylaxis is challenging because there is a wide variety of presentations, and no single finding is pathognomonic. Many conditions, including vasovagal reactions (from parenteral injections), functional vocal cord dysfunction, and panic attacks, have been misdiagnosed as anaphylaxis, whereas patients with genuine anaphylaxis do not always receive appropriate therapy. Angioedema (diffuse soft-tissue swelling) is often present in anaphylaxis. It is typically associated with urticaria, with small to even giant-sized lesions observed. There are, however, many other potential causes of angioedema and urticaria that should be considered. Scombroid poisoning, which often develops within 30 minutes of eating spoiled tuna, mackerel, or dolphin (mahi-mahi), typically presents with urticaria, nausea, vomiting, diarrhea, and headache. It is treated with antihistamines. Hereditary angioedema (in which there is a family history of angioedema) presents with no urticaria, but gastrointestinal mucosal edema produces severe abdominal pain, and respiratory mucosal edema produces airway compromise. This form of angioedema is treated with fresh-frozen plasma. ACE inhibitors are associated with a reactive angioedema predominantly of the upper airway. This reaction can develop days or years after ACE inhibitor therapy is begun. The best medical treatment of this form of angioedema is unclear, but aggressive early airway management is critical.6D Finally, in some forms of panic disorder, functional stridor develops as a result of forced adduction of the vocal cords. In a panic attack there is no urticaria, angioedema, or hypotension. Key Interventions to Prevent Arrest7DThe approach to therapy is difficult to standardize because etiology, clinical presentation (including severity and course), and organ involvement vary widely. Few randomized trials of treatment approaches have been reported. The following recommendations are commonly used and widely accepted but are based more on consensus than on evidence:
Special ConsiderationsRapid Progression to Lethal Airway ObstructionClose observation is required during conventional therapy (see above). Early, elective intubation is indicated for patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling. If respiratory function deteriorates, perform semielective (awake, sedated) tracheal intubation without paralytic agents. Angioedema. Patients with angioedema pose a particularly worrisome problem because they are at high risk for rapid deterioration. Most will present with some degree of labial or facial swelling. Patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling are at particular risk for respiratory compromise. Early tracheal intubation. If intubation is delayed, patients can deteriorate over a brief period of time (0.5 to 3 hours), with development of progressive stridor, severe dysphonia or aphonia, laryngeal edema, massive lingual swelling, facial and neck swelling, and hypoxemia. At this point both tracheal intubation and cricothyrotomy may be difficult or impossible. Attempts at tracheal intubation may only further increase laryngeal edema or compromise the airway with bleeding into the oropharynx and narrow glottic opening. The patient may become agitated as a result of hypoxia and may be uncooperative with oxygen therapy. Paralysis followed by an attempt at tracheal intubation may prove lethal, because the glottic opening is narrow and difficult to see because of the lingual and oropharyngeal edema and the patient is iatrogenically apneic. If tracheal intubation is not successful, even bag-mask ventilation may be impossible, because laryngeal edema will prevent air entry and facial edema will prevent creation of an effective seal between the face and bag mask. Pharmacological paralysis at this point may deprive the patient of the sole mechanism for ventilation, ie, spontaneous breathing attempts. During Arrest: Key Interventions and Modifications of BLS/ALS TherapyDeath from anaphylaxis may be associated with profound vasodilation, intravascular collapse, tissue hypoxia, and asystole. No data is available on how cardiac arrest procedures should be modified, but difficulties in achieving adequate volume replacement and ventilation are frequent. Reasonable recommendations can be based on experience with nonfatal cases. Airway, Oxygenation, and VentilationDeath may result from angioedema and upper or lower airway obstruction. Bag-mask ventilation and tracheal intubation may fail. Cricothyrotomy may be difficult or impossible because severe swelling will obliterate landmarks. In these desperate circumstances, consider the following airway techniques:
Support of CirculationSupport of circulation requires rapid volume resuscitation and administration of vasopressors to support blood pressure. Epinephrine is the drug of choice for treatment of both vasodilation/hypotension and cardiac arrest.
SummaryThe management of anaphylaxis includes early recognition, anticipation of deterioration, and aggressive support of airway, oxygenation, ventilation, and circulation. Prompt, aggressive therapy may be successful even if cardiac arrest develops. Survival from out-of-hospital cardiac arrest secondary to blunt trauma is uniformly low in children and adults.1E2E3E In some out-of-hospital and Emergency Department settings, resuscitative efforts are withheld when patients with blunt trauma are found in asystole or agonal electrical cardiac activity. Survival after cardiac arrest resulting from penetrating trauma is only slightly better; rapid transport to a trauma center is associated with better outcome than resuscitation attempts in the field.4E BLS and ALS for the trauma patient are fundamentally the same as the care of the patient with a primary cardiac or respiratory arrest. In trauma resuscitation, a “Primary Survey” is performed, with rapid evaluation and stabilization of airway, breathing, and circulation. The trauma rescuer must anticipate, rapidly identify, and immediately treat life-threatening conditions that will interfere with establishing effective airway, oxygenation, ventilation, and circulation. Cardiopulmonary deterioration associated with trauma has several possible causes, and the management plan may vary for each. Potential causes of cardiopulmonary deterioration and arrest include
In cases of cardiac arrest associated with uncontrolled internal hemorrhage or pericardial tamponade, a favorable outcome requires that the victim be rapidly transported to an emergency facility with immediate operative capabilities.4E5E Despite a rapid and effective out-of-hospital and trauma center response, patients with out-of-hospital cardiopulmonary arrest due to multiple-organ hemorrhage (as commonly seen with blunt trauma) will rarely survive neurologically intact.5E6E7E8E Patients who survive out-of-hospital cardiopulmonary arrest associated with trauma generally are young, have penetrating injuries, have received early (out-of-hospital) endotracheal intubation, and undergo prompt transport by highly skilled paramedics to a definitive care facility.7E8E9E10E Extrication and Initial EvaluationWhen resuscitative efforts will be attempted, the victim should be rapidly extricated, with protection of the cervical spine. Immediate BLS and ALS interventions will ensure adequate airway, oxygenation, ventilation, and circulation. As soon as the victim is stabilized (and even during stabilization), prepare the victim for rapid evacuation to a facility that provides definitive trauma care. Use lateral neck supports, strapping, and backboards throughout transport to minimize exacerbation of an occult neck and spinal cord injury.5E When multiple patients receive serious injuries, emergency personnel must establish priorities for care. When the number of patients with critical injuries exceeds the capability of the EMS system, those without a pulse should be considered the lowest priority for care and triage. Most EMS systems have developed guidelines that permit the out-of-hospital pronouncement of death or withholding of cardiac resuscitative efforts when there are multiple patients with critical injuries or when there are injuries incompatible with life. EMS personnel therefore should work within such guidelines when available. BLS for Cardiac Arrest Associated With TraumaProvision of BLS requires assessment of responsiveness, establishment of a patent airway, assessment of breathing, support of oxygenation and ventilation if indicated, and assessment and support of circulation. Establish UnresponsivenessHead trauma or shock may produce loss of consciousness. If spinal cord injury is present the victim may be conscious but unable to move. Throughout initial assessment and stabilization, the rescuer should monitor patient responsiveness; deterioration could indicate either neurological compromise or cardiorespiratory failure. AirwayWhen multisystem trauma is present, or trauma isolated to the head and neck, the spine must be immobilized throughout BLS maneuvers. A jaw thrust is used instead of a head tilt–chin lift to open the airway. If at all possible, a second rescuer should be responsible for immobilizing the head and neck during BLS and until spinal immobilization equipment is applied. Once the airway is anatomically open, the mouth should be cleared of blood, vomitus, and other secretions. Remove this material with a (gloved) finger sweep or use gauze or a towel to wipe out the mouth. It may also be cleared with suction. Breathing/VentilationOnce a patent airway is established, the rescuer should assess for breathing. If breathing is absent or grossly inadequate (eg, agonal or slow and extremely shallow), ventilation is needed. When ventilation is provided with a barrier device, a pocket mask, or a bag-mask system, the cervical spine should be immobilized. If the chest does not expand during ventilation despite repeated attempts to open the airway with a jaw thrust, a tension pneumothorax or hemothorax may be present and should be ruled out or treated by ACLS personnel. Deliver breaths slowly to reduce the development of gastric inflation and possible regurgitation. CirculationIf the victim has no signs of circulation (no breathing, coughing, or movement) in response to the rescue breaths and if the healthcare provider detects no carotid pulse, chest compressions should be provided. If an AED is available, it is applied when absence of circulation is detected. The purpose is to check whether VF/VT occurred first, causing loss of consciousness, then the trauma. The AED will evaluate the victim’s cardiac rhythm and advise shock delivery if appropriate. Apply external compression to stop external hemorrhage. DisabilityThroughout all interventions, assess the victim’s response. The Glasgow Coma Scale is useful and can be assessed in seconds. Monitor closely for signs of deterioration. ExposureThe victim may lose heat to the environment through evaporation. Such heat loss will be exacerbated if the victim’s clothes are removed or the victim is covered in blood. When possible, keep the victim warm. ACLS for Cardiac Arrest Associated With TraumaALS includes continued assessment and support of airway, oxygenation and ventilation (breathing), and circulation. AirwayIndications for intubation in the injured patient include
Endotracheal intubation is performed with cervical spine outside the trachea. Generally orotracheal intubation is performed. Avoid nasotracheal intubation in the presence of severe maxillofacial injuries, because the tube may migrate outside the trachea during placement. Proper tube placement should be confirmed by clinical examination and use of oximetry and exhaled CO2 monitor immediately after intubation, during transport, and after any transfer of the patient (eg, from ambulance to hospital gurney). Unsuccessful tracheal intubation for the patient with massive facial injury and edema is an indication for cricothyrotomy. Cricothyrotomy will provide an emergent, secure airway that supports oxygenation, although ventilation will be suboptimal. Once a tracheal tube is inserted, simultaneous ventilations and compressions may result in a tension pneumothorax in an already damaged lung, especially if fractured ribs or a fractured sternum is present. Synchronized ventilations and compressions in a ratio of 1 to 5 may be required in the presence of a damaged thoracic cage. Unless severe maxillofacial injuries are present, a gastric tube can be inserted to decompress the stomach. In the presence of severe maxillofacial injuries, inserted gastric tubes can migrate intracranially. They should be placed with caution under these conditions, with confirmation of placement into the stomach. VentilationHigh concentrations of oxygen should be provided even if the victim’s oxygenation appears adequate. Once a patent airway is ensured, assess breath sounds and chest expansion. A unilateral decrease in breath sounds associated with inadequate chest expansion during positive-pressure ventilation should be presumed to be caused by tension pneumothorax until that complication can be ruled out. Perform needle decompression of the pneumothorax immediately, followed by chest tube insertion. In the absence of an immediate hemodynamic response to thoracic decompression or alternatively in the presence of a penetrating thoracic wound, surgical exploration is warranted.9E Rescuers should look for and seal any significant open pneumothorax. Tension pneumothorax may develop after sealing of an open pneumothorax, so decompression may be needed.5E Hemothorax may also interfere with ventilation and chest expansion; treat hemothorax with blood replacement and chest tube insertion. If hemorrhage is severe and continues, surgical exploration may be required. If the victim has a significant flail chest, spontaneous ventilation likely will be inadequate to maintain oxygenation. Treat flail chest with positive-pressure ventilation. CirculationOnce airway, oxygenation, and ventilation are adequate, circulation is evaluated and supported. As noted above, if pulseless arrest develops, outcome is poor unless a reversible cause can be immediately identified and treated (eg, tension pneumothorax). Successful trauma resuscitation is often dependent on restoration of an adequate circulating blood volume. The most common terminal cardiac rhythms observed in trauma victims are PEA, bradyasystolic rhythms, and occasionally VT/VF. Treatment of PEA requires identification and treatment of reversible causes, such as severe hypovolemia, hypothermia, cardiac tamponade, or tension pneumothorax.11E Development of bradyasystolic rhythms often indicates the presence of severe hypovolemia, severe hypoxemia, or cardiorespiratory failure. VF/VT is of course treated with defibrillation. Although epinephrine is typically administered during the ACLS treatment of these arrhythmias, it may be ineffective in the presence of uncorrected severe hypovolemia. Open thoracotomy does not improve outcome from out-of-hospital blunt trauma arrest, but open thoracotomy can be lifesaving for patients with penetrating chest trauma, particularly penetrating wounds of the heart.6E8E During concurrent volume resuscitation for penetrating trauma, prompt emergency thoracotomy will permit direct massage of the heart and indicated surgical procedures. Such procedures may involve relief of cardiac tamponade, control of thoracic and extrathoracic hemorrhage, and aortic cross-clamping.6E8E Penetrating cardiac injury should be suspected whenever penetrating trauma to the left chest occurs and whenever penetrating injury is associated with low cardiac output or signs of tamponade (distended neck veins, hypotension, and decreased heart tones). Although pericardiocentesis theoretically is useful, efforts to relieve pericardial tamponade due to penetrating injury should be undertaken only in the hospital. Cardiac contusions causing significant arrhythmias or impairing cardiac function are present in approximately 10% to 20% of victims of severe, blunt chest trauma.12E Myocardial contusion should be suspected if the trauma victim demonstrates extreme tachycardia, arrhythmias, and ST-T–wave changes. Serum creatinine phosphokines are often elevated in the patient with blunt chest trauma. An MB fraction >5% has been used historically to diagnose cardiac contusion, but this is not a sensitive indicator of myocardial contusion.13E The diagnosis of myocardial contusion is confirmed by echocardiography or radionuclide angiography. Volume resuscitation is an important but controversial part of trauma resuscitation. In the field, bolus administration of isotonic crystalloid is indicated to treat hypovolemic shock. Adequate and aggressive volume replacement may be necessary to obtain adequate perfusing pressures. For patients with penetrating chest trauma who are located a short distance from the trauma center, aggressive fluid resuscitation in the field can increase transport time and has been associated with lower survival than rapid transport with less aggressive fluid resuscitation.4E When massive penetrating trauma or severe hemorrhage is present, immediate surgical exploration is required. Aggressive volume resuscitation in the field will delay arrival at the trauma center, delay surgical interventions to close off bleeding vessels, increase the blood pressure, and consequently accelerate the rate of blood loss.4E14E Replacement of blood loss in the hospital is accomplished with a combination of packed red blood cells and isotonic crystalloids. Bleeding must be controlled as soon as possible by whatever appropriate means to maintain adequate blood volume and oxygen-carrying capacity. If external pressure does not stop bleeding or internal bleeding continues, surgical exploration is required. Indications for Surgical ExplorationResuscitation may be impossible in the presence of severe, uncontrolled hemorrhage or in the presence of some cardiac, thoracic, or abdominal injuries. In these cases surgical intervention is required. Urgent surgical exploration is indicated for the following conditions:
Most pregnant women have little interest in thinking about the prospect of death. Mortality related to the pregnancy itself is rare, occurring in an estimated 1 of every 30 000 deliveries.1F A cardiovascular emergency in a pregnant woman creates a special situation—the involvement of a second person, the in utero child. The child must always be considered when an adverse cardiovascular event occurs in a pregnant woman. The decision of whether to perform an emergency cesarean section must be made quickly. Emergency cesarean section has the highest chance of improving the outcome for both mother and child.2F Significant physiological changes occur in a woman during pregnancy. For example, cardiac output, blood volume, minute ventilation, and oxygen consumption all increase. Furthermore, the gravid uterus may cause significant compression of iliac and abdominal vessels when the mother is in the supine position, resulting in reduced cardiac output and hypotension. Causes of Cardiac Arrest Associated With PregnancyThere are many different causes of cardiac arrest in pregnant women. Cardiac arrest in the mother is most commonly related to changes and events that occur at the time of delivery, such as
It may also be related to the complex physiological changes associated with the pregnancy itself, such as
Finally, and tragically, pregnant women suffer the same problems of motor vehicle accidents, falls, assault, attempted suicide, and penetrating trauma (eg, stabbings and gunshot wounds) as the rest of modern society.3F Regrettably, this daily stream of violence and trauma causes many dramatic events that require heroic interventions. Our response has been to craft harsh phrases to guide emergency care, such as “postmortem C-section,” “perimortem delivery,” “sacrifice mother or child or save mother or child,” “harvest the fetus,” and “empty the uterus.” We walk a thin line between aiding our memory and demeaning our patients. These guidelines will not repeat such phrases.4F Key Interventions to Prevent ArrestIn an emergency the simplest action may be the most often ignored action. Many cardiovascular problems associated with pregnancy are due to nothing more than anatomy interacting with gravity. The pregnant woman’s uterus, great with child, may press down against the inferior vena cava, reducing or blocking blood flow. The ensuing failure of venous blood return can produce hypotension and even shock.5F6F To treat a distressed or compromised pregnant patient:
Modifications to BLS Guidelines for ArrestDo not forget the simple BLS actions you can take:
Modifications to ACLS Guidelines for ArrestThere are no changes to the standard ACLS algorithms for medications, intubation, and defibrillation. Assess and treat the pregnant woman who has a sudden cardiac arrest by using the Primary and Secondary ABCD Surveys of ACLS as modified for the pregnant woman (Table 1). Consider a wide variety of possible causes of arrest such as amniotic fluid embolism, magnesium sulfate toxicity, mishap in patients who received spinal anesthesia, drug overdose, drug abuse, medication toxicity, and iatrogenic events. Should You Perform an Emergency Cesarean Section to Reduce the Size and Weight of the Gravid Uterus?When Standard BLS and ACLS FailIf standard application of BLS and ACLS fail and there is some chance that the fetus is viable, consider immediate perimortem cesarean section. The goal is to deliver the fetus within 4 to 5 minutes after the onset of arrest. If at all possible involve obstetric and neonatal personnel.8F Why Reduce the Size and Weight of the Uterus?With the mother in cardiac arrest, the blood supply to the fetus rapidly becomes hypoxic and acidotic, causing adverse effects in the fetus. Return of blood to the mother’s heart, blocked by the uterus pressing against the inferior vena cava, must be restored. Consequently the key to resuscitation of the child is resuscitation of the mother. The mother cannot be resuscitated until blood flow to her right ventricle is restored. This results in the familiar admonition to immediately begin cesarean section and remove the baby and placenta when arrest occurs in a near-term pregnant woman. That single act allows access to the infant so that newborn resuscitation can be started. Cesarean section also immediately corrects much of the abnormal physiology of the full-term mother. The critical point to remember is that you will lose both mother and infant if you cannot restore blood flow to the mother’s heart.9F Advance PreparationTable 2 lists the multiple factors that must be considered in a very short time during an emotionally dramatic event. All Emergency Departments should rehearse their plan of action for this type of event, including location of supplies, sources of extra equipment, and best methods for obtaining subspecialty assistance. Most electric shock injuries to adults occur in the occupational setting.1G Pediatric electric shock injuries occur most commonly in the home, when the child bites electrical wires, places an object in an electrical socket, contacts an exposed low-voltage wire or appliance, or touches a high-voltage wire outdoors.2G Electric shock injuries result from the direct effects of current on cell membranes and vascular smooth muscle and from the conversion of electric energy into heat energy as current passes through body tissues. Factors that determine the nature and severity of electric trauma include the magnitude of energy delivered, voltage, resistance to current flow, type of current, duration of contact with the current source, and current pathway. Victims of electric shock can sustain a wide variety of injuries, ranging from a transient unpleasant sensation caused by low-intensity current to instantaneous cardiac arrest caused by exposure to high voltage or high current. High-tension current generally causes the most serious injuries, although fatal electrocutions may occur with household current (110 V in the United States and Canada, 220 V in Europe, Australia, Asia, and many other localities).3G Bone and skin are most resistant to the passage of electric current; muscle, blood vessels, and nerves conduct with least resistance.4G Skin resistance, the most important factor impeding current flow, can be reduced substantially by moisture, thereby converting what ordinarily might be a minor injury into a life-threatening shock.5G Skin resistance can be overcome with increased duration of exposure to current flow. Contact with alternating current at 60 cycles per second (the frequency used in most household and commercial sources of electricity) may cause tetanic skeletal muscle contractions and prevent self-release from the source of the electricity, thereby leading to prolonged duration of exposure. The repetitive frequency of alternating current also increases the likelihood of current flow through the heart during the vulnerable recovery period of the cardiac cycle. This exposure can precipitate VF, analogous to the R-on-T phenomenon.6G Transthoracic current flow (eg, a hand-to-hand pathway) is more likely to be fatal than a vertical (hand-to-foot) or straddle (foot-to-foot) current path.7G The vertical pathway, however, often causes myocardial injury, which has been attributed to the direct effects of current and coronary artery spasm.8G9G10G Lightning StrikeLightning strike kills hundreds of people internationally every year and injures many times that number. Lightning injuries have a 30% mortality rate, and up to 70% of survivors sustain significant morbidity.11G12G13G The presentation of lightning strike injuries varies widely, even among groups of people struck at the same time.14G In some victims symptoms are mild and may not require hospitalization, whereas others die from the injury.15G16G The primary cause of death in lightning-strike victims is cardiac arrest, which may be associated with primary VF or asystole.15G16G17G18G Lightning acts as an instantaneous, massive direct current countershock, simultaneously depolarizing the entire myocardium.16G19G In many cases cardiac automaticity may restore organized cardiac activity, and a perfusing rhythm may return spontaneously. However, concomitant respiratory arrest due to thoracic muscle spasm and suppression of the respiratory center may continue after return of spontaneous circulation. Thus, unless ventilatory assistance is provided, a secondary hypoxic cardiac arrest may occur.20G Lightning can also produce widespread effects on the cardiovascular system, producing extensive catecholamine release or autonomic stimulation. If cardiac arrest does not occur, the victim may develop hypertension, tachycardia, nonspecific ECG changes (including prolongation of the QT interval and transient T-wave inversion), and myocardial necrosis with release of creatine kinase-MB fraction. Right and left ventricular ejection fractions may also be depressed, but this injury appears to be reversible.18G Lightning can produce a wide spectrum of neurological injuries. Injuries may be primary, resulting from the effects on the brain. Effects may also be secondary, as a complication of cardiac arrest and hypoxia.12G The current can produce brain hemorrhages, edema, and small-vessel and neuronal injury. Hypoxic encephalopathy can result from cardiac arrest. Effects of a lightning strike on the peripheral nervous system include myelin damage.12G Patients most likely to die of lightning injury if no treatment is forthcoming are those who suffer immediate cardiac arrest. Patients who do not suffer cardiac arrest and those who respond to immediate treatment have an excellent chance of recovery because subsequent arrest is uncommon. Therefore, when multiple victims are struck simultaneously by lightning, rescuers should give highest priority to patients in respiratory or cardiac arrest. For victims in cardiopulmonary arrest, BLS and ACLS should be instituted immediately. The goal is to oxygenate the heart and brain adequately until cardiac activity is restored. Victims with respiratory arrest may require only ventilation and oxygenation to avoid secondary hypoxic cardiac arrest. Resuscitative attempts may have higher success rates in lightning victims than in patients with cardiac arrest from other causes, and efforts may be effective even when the interval before the resuscitative attempt is prolonged.20G Clinical EffectsImmediately after electrocution or lightning strike, the victim’s respiratory function, circulation, or both, may fail. The patient may be apneic, mottled, unconscious, and in cardiac arrest from VF or asystole. Respiratory arrest may be caused by a variety of mechanisms:
If respiratory arrest persists, hypoxic cardiac arrest may occur. Cardiopulmonary arrest is the primary cause of immediate death due to electrical injury.21G VF or ventricular asystole may occur as a direct result of electric shock. Other serious cardiac arrhythmias, including VT that may progress to VF, may result from exposure to low- or high-voltage current.22G Modifications of BLS Actions for Arrest Caused by Electric Shock or Lightning StrikeThe rescuer must be certain that rescue efforts will not put him or her in danger of electric shock. After the power is turned off by authorized personnel or the energized source is safely cleared from the victim, determine the victim’s cardiorespiratory status. Immediately after electrocution, respiration or circulation or both may fail. The patient may be apneic, mottled, unconscious, and in circulatory collapse with VF or asystole. Vigorous resuscitative measures are indicated, even for those who appear dead on initial evaluation. The prognosis for recovery from electric shock or lightning strike is not readily predictable because the amplitude and duration of the charge usually are unknown. However, because many victims are young and without preexisting cardiopulmonary disease, they have a reasonable chance for survival if immediate support of cardiopulmonary function is provided. If spontaneous respiration or circulation is absent, initiate the ABCD techniques outlined in parts 3 and 4 of these guidelines, including EMS system activation, prompt CPR, and use of the AED. The presenting cardiac ECG rhythm may be asystole or VF.23G As soon as possible, secure the airway and provide ventilation and supplemental oxygen. When electric shock occurs in a location not readily accessible, such as on a utility pole, rescuers must lower the victim to the ground as quickly as possible. Note: Actions that involve rescuer proximity to live current must be performed only by specially trained rescuers who know how to execute this task. If the victim remains unresponsive, rescuers should start the standard ABCD protocols, including AED use by lay responders. If the victim has no signs of circulation, start chest compressions as soon as feasible. In addition, use the AED to identify and treat VT or VF. Maintain spinal protection and immobilization during extrication and treatment if there is any likelihood of head or neck trauma.23G24G Electrical injuries often cause related trauma, including injury to the spine24G and muscular strains and fractures due to the tetanic response of skeletal muscles. Remove smoldering clothing, shoes, and belts to prevent further thermal damage. Modification of ACLS Support for Arrest Caused by Electric Shock or Lightning StrikeTreat VF, asystole, and other serious arrhythmias with ACLS techniques outlined in these guidelines. Quickly attempt defibrillation, if needed, at the scene. Establishing an airway may be difficult for patients with electric burns of the face, mouth, or anterior neck. Extensive soft-tissue swelling may develop rapidly and complicate airway control measures, such as endotracheal intubation. For these reasons, intubation should be accomplished on an elective basis before signs of airway obstruction become severe. For victims with hypovolemic shock or significant tissue destruction, rapid intravenous fluid administration is indicated to counteract shock and correct ongoing fluid losses. Fluid administration should be adequate to maintain diuresis to facilitate excretion of myoglobin, potassium, and other by-products of tissue destruction.19G Increased capillary permeability may develop in association with tissue injury, so local tissue edema may develop at the site of injury. Because electrothermal burns and underlying tissue injury may require surgical attention, we encourage early consultation with a physician skilled in treatment of electrical injury.
 August 22, 2000 |
During transport of a hypothermic patient who is alert and responding
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