arterial
pressure.
of marked depression of brain function.
. 2000;102(suppl I):I-229–I-252.
1.
Schneider SM. Hypothermia: from recognition to
rewarming.
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2.
Steinman AM. Cardiopulmonary resuscitation and
hypothermia. Circulation. 1986;74(suppl IV):IV-29–IV-32.
3.
Holzer M, Behringer W, Schorkhuber W, Zeiner A, Sterz
F, Laggner AN, Frass M, Siostrozonek P, Ratheiser K, Kaff A,
Hypothermia for Cardiac Arrest (HACA) Study Group. Mild hypothermia and
outcome after CPR. Acta Anaesthesiol Scand Suppl. 1997;111:55–58.[Medline]
4.
Sterz F, Safar P, Tisherman S, Radovsky A, Kuboyama K,
Oku K. Mild hypothermic cardiopulmonary resuscitation improves
outcome after prolonged cardiac arrest in dogs [see comments].
Crit Care Med. 1991;19:379–389.[Medline]
5.
Larach MG. Accidental hypothermia [see comments].
Lancet. 1995;345:493–498.[Medline]
6.
Gilbert M, Busund R, Skagseth A, Nilsen PA, Solbo JP.
Resuscitation from accidental hypothermia of 13.7 degrees C with
circulatory arrest. Lancet. 2000;355:375–376. Letter.[Medline]
7.
Woodhouse P, Keatinge WR, Coleshaw SR. Factors
associated with hypothermia in patients admitted to a group of inner
city hospitals [see comments]. Lancet. 1989;2:1201–1205.[Medline]
8.
Danzl DF, Pozos RS, Auerbach PS, Glazer S, Goetz W,
Johnson E, Jui J, Lilja P, Marx JA, Miller J, et al. Multicenter
hypothermia survey. Ann Emerg Med. 1987;16:1042–1055.[Medline]
9.
Gallaher MM, Fleming DW, Berger LR, Sewell CM.
Pedestrian and hypothermia deaths among Native Americans in New Mexico:
between bar and home [published erratum appears in JAMA. 1992;268:2378] [see comments]. JAMA. 1992;267:1345–1348.[Medline]
10.
Weinberg AD, Hamlet MP, Paturas JL, White RD, McAninch
GW. Cold Weather Emergencies: Principles of Patient
Management. Branford, Conn: American Medical Publishing Co;
1990:10–30.
11.
Romet TT. Mechanism of afterdrop after cold water
immersion. J Appl Physiol. 1988;65:1535–1538.[Medline]
12.
Reuler JB. Hypothermia: pathophysiology, clinical
settings, and management. Ann Intern Med. 1978;89:519–527.[Medline]
13.
Southwick FS, Dalglish PH Jr. Recovery after prolonged
asystolic cardiac arrest in profound hypothermia: a case report
and literature review. JAMA. 1980;243:1250–1253.[Medline]
14.
Hall KN, Syverud SA. Closed thoracic cavity lavage in
the treatment of severe hypothermia in human beings [see comments].
Ann Emerg Med. 1990;19:204–206.[Medline]
15.
Krismer AC, Lindner KH, Kornberger R, Wenzel V, Mueller
G, Hund W, Oroszy S, Lurie KG, Mair P. Cardiopulmonary
resuscitation during severe hypothermia in pigs: does
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16.
Reuler JB. Hypothermia: pathophysiology, clinical
settings, and management. Ann Intern Med. 1978;89:519–527.[Medline]
17.
Zell SC, Kurtz KJ. Severe exposure hypothermia: a
resuscitation protocol. Ann Emerg Med. 1985;14:339–345.[Medline]
18.
Althaus U, Aeberhard P, Schupbach P, Nachbur BH,
Muhlemann W. Management of profound accidental hypothermia with
cardiorespiratory arrest. Ann Surg. 1982;195:492–495.[Medline]
19.
Kristensen G, Drenck NE, Jordening H. Simple system for
central rewarming of hypothermic patients. Lancet. 1986;2:1467–1468. Letter.
20.
Moss J. Accidental severe hypothermia. Surg
Gynecol Obstet. 1986;162:501–513.[Medline]
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Safar P. Cerebral resuscitation after cardiac arrest:
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Emerg Med. 1993;22:324–349.[Medline]
22.
Danzl DF, Pozos RS, Auerbach PS, Glazer S, Goetz W,
Johnson E, Jui J, Lilja P, Marx JA, Miller J, et al. Multicenter
hypothermia survey. Ann Emerg Med. 1987;16:1042–1055.[Medline]
 |
Submersion or Near-Drowning
|
|---|
Submersion: Overview
The 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 Indicators
A 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,2B 3B successful resuscitation with full
neurological recovery has occasionally occurred in near-drowning
victims with prolonged submersion in extremely cold
water.4B 5B 6B 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 :
- Submersion duration >25 minutes
- Resuscitation duration >25 minutes
- Pulseless cardiac arrest on arrival in the ED
Additional factors associated with poor prognosis in the same
study1B included
- Presence of VT/VF on initial ECG (93% mortality)
- Fixed pupils noted in the ED (89% mortality)
- Severe acidosis (89% mortality) in the ED
- Respiratory arrest (87% mortality) in the ED
- In a more recent study of adults and children from the same
investigators, level of consciousness and responsiveness correlated
with survival. Deaths occurred only among victims who remained comatose
at the scene and comatose on arrival at the hospital. No deaths
occurred among victims who were alert or lethargic but responsive
either at the scene or in the hospital.7B
- A number of classification systems have been proposed to link
clinical findings with outcome of submersion victims.8B 9B
In a recent analysis of 1831 submersion episodes from the
beaches of Brazil, mortality was related to severity of
cardiopulmonary involvement as assessed by an on-scene
physician with the drowning response team needing only 4 variables:
coughing (yes or no), auscultation, blood pressure, and heart rate.
Unlike other researchers in this area, Szpilman9B did not
start with an implicitly derived classification scheme into which he
forces each case. Instead, the classification grades were derived
retrospectively by asking what simple list of criteria had the best
association with severe pulmonary compromise. As displayed in
the Table
, increasing mortality
correlated with ascending grades of clinical
severity.9B
- Auscultation of breath sounds will not be applicable to the BLS
provider. For the ACLS provider, however, auscultatory findings provide
a helpful classification of the severity of cardiopulmonary
failure after submersion. The algorithm we have developed
(Figure) is largely a translation of
Szpilman’s results and an algorithm he derived in a manner that can be
used by epidemiologists to support a prospective database of submersion
victims.
- Any prognostic approach should consider the temperature of the
submersion fluid (icy versus nonicy) and the size and age of the
victim. Aggressive attempts at resuscitation in the hospital may be
continued for the small victim of icy-water submersion and
hypothermia.
Modifications to Guidelines for BLS for Resuscitation From
Submersion
No 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 Water
When 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 Breathing
The 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.2B 11B
There is no need to clear the airway of aspirated
water.12B Some victims aspirate nothing because of
laryngospasm or breath-holding.3B 8B 13B 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.11B 12B 14B 15B 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 Compressions
As 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 Resuscitation
Vomiting 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
Submersion
The 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.
|
References
|
|---|
1.
Quan L, Kinder D. Pediatric submersions:
prehospital predictors of outcome [see comments].
Pediatrics. 1992;90:909–913.[Abstract]
2.
Quan L, Wentz KR, Gore EJ, Copass MK. Outcome
and predictors of outcome in pediatric submersion victims receiving
prehospital care in King County, Washington [see comments].
Pediatrics. 1990;86:586–593.[Abstract]
3.
Modell JH, Davis JH. Electrolyte changes in
human drowning victims. Anesthesiology. 1969;30:414–420.[Medline]
4.
Southwick FS, Dalglish PH Jr. Recovery after
prolonged asystolic cardiac arrest in profound hypothermia: a
case report and literature review. JAMA. 1980;243:1250–1253.[Medline]
5.
Siebke H, Rod T, Breivik H, Link B. Survival
after 40 minutes; submersion without cerebral sequelae.
Lancet. 1975;1:1275–1277.[Medline]
6.
Bolte RG, Black PG, Bowers RS, Thorne JK,
Corneli HM. The use of extracorporeal rewarming in a child submerged
for 66 minutes. JAMA. 1988;260:377–379.[Medline]
7.
Cummings P, Quan L. Trends in unintentional
drowning: the role of alcohol and medical care [see comments].
JAMA. 1999;281:2198–2202.[Medline]
8.
Modell J. Drowning. N Engl J
Med.. 1993;328:253–256.[Medline]
9.
Szpilman D. Near-drowning and drowning
classification: a proposal to stratify mortality based on the
analysis of 1,831 cases. Chest. 1997;112:660–665.[Abstract]
10.
Kyriacou DN, Arcinue EL, Peek C, Kraus JF.
Effect of immediate resuscitation on children with submersion injury.
Pediatrics. 1994;94:137–142.[Abstract]
11.
Heimlich HJ. Subdiaphragmatic pressure to expel
water from the lungs of drowning persons. Ann Emerg Med. 1981;10:476–480.[Medline]
12.
Rosen P, Stoto M, Harley J. The use of the
Heimlich maneuver in near drowning: Institute of Medicine report.
J Emerg Med. 1995;13:397–405.[Medline]
13.
Deleted in proof.
14.
Patrick EA. A case report: The Heimlich maneuver.
Emergency. 1981;13:45–47.
15.
Heimlich HJ. The Heimlich maneuver: first
treatment for drowning victims. Emerg Med Serv. 1981;10:27–30.[Medline]
16.
Langhelle A, Sunde K, Wik L, Steen PA. Airway
pressure with chest compressions versus Heimlich manoeuvre in recently
dead adults with complete airway obstruction. Resuscitation. 2000;44:105–108.[Medline]
17.
Manolios N, Mackie I. Drowning and near-drowning
on Australian beaches patrolled by life-savers: a 10-year study,
1973–1983. Med J Aust. 1988;148:165–167, 170–171.
|
Near-Fatal Asthma
|
|---|
Introduction
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
- Severe bronchospasm and mucous plugging leading to
asphyxia2C (this condition causes the vast majority of
asthma-related deaths).
- Cardiac arrhythmias due to hypoxia, which is the common
cause of asthma-related arrhythmia. In addition,
arrhythmias are caused by use of ß-adrenergic agonists. (In
rare instances these arrhythmias may be due to prolongation of
the QT interval resulting from ß-adrenergic agonists3C 4C 5C
or toxicity caused by medications such as theophylline.)
- Auto-PEEP (positive end-expiratory pressure) occurs in some
patients who are intubated and mechanically ventilated. Patients fail
to expire as much air as they took in; gradual buildup of pressure
occurs and reduces blood flow and blood pressure. Auto-PEEP is
secondary to air trapping and "breath stacking" (breathed air
entering and being unable to escape).
- Tension pneumothorax (often bilateral)
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:
- Determine whether the patient has true acute asthma. When a patient
presents with dyspnea in extremis you may not be able to obtain the
recent history.
- Depending on the patient’s history and medication use, other
conditions may be present. These include
—Cardiac disease (congestive heart failure, myocarditis),
pulmonary disease (emphysema, pneumonia, upper-airway
obstruction—structural or psychogenic), acute allergic bronchospasm or
anaphylaxis (aspirin, foods, or idiopathic), pulmonary
embolism, or vasculitis (Churg-Strauss
syndrome).7C —Medications and drugs of
abuse: bronchospasm as sequelae to medications
(ß-blockers)8C or drugs of abuse (cocaine and
opiates).9C 10C —Discontinuation of
corticosteroids. Patients who have used
corticosteroids for a long time may have relative
adrenal insufficiency. With the stress of discontinuation of the
steroids and the adrenal insufficiency, these patients may present
with near-fatal asthma.
Key Interventions to Prevent Arrest
The 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.
Oxygen
Use 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:
- Findings of obtundation
- Profuse diaphoresis
- Poor ("floppy") muscle tone (clinical signs of hypercarbia)
- Findings of severe agitation, confusion, and fighting against the
oxygen mask (clinical signs of hypoxemia)11C
- Elevation of the PCO2 by itself is
not indicative of a need for tracheal intubation. Elevated
PCO2 does indicate severity of the
episode. Reserve intubation for patients with the clinical findings
mentioned above or a clearly rising
PCO2. Treat the patient, not
the numbers.
Nebulized ß2-Agonists
Albuterol (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 Corticosteroids
By 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
ß-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.13C 14C 15C Doses can range as low as 40 mg to as high
as 250 mg IV or its equivalent.
Nebulized Anticholinergics
Use ipratropium, an inhaled anticholinergic agent, as a moist
nebulizing agent in combination with albuterol at a dose of 0.5
mg.16C Unlike ß2-agonists, which
have an immediate onset of action, nebulized anticholinergic agents
have a delayed onset of approximately 20 minutes.
Intravenous Aminophylline
Aminophylline, now used as secondary therapy after
ß2-agonists and
corticosteroids, can enhance the effects of those
agents. As a bronchodilator aminophylline is approximately one third as
potent as ß2-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 ß2-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 Sulfate
A 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).18C 19C
Parenteral or Subcutaneous or Intramuscular Epinephrine
or Terbutaline
Subcutaneous 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 ß2-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 ß-agonists over inhaled bronchodilators.20C The value
of IV bronchodilators, however, compared with that of inhaled
bronchodilators merits further study.
Ketamine
Ketamine 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
Heliox
Heliox 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 Pressure
Bilevel 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 Ventilation
In 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:
- Provide adequate sedation with ketamine, a benzodiazepine,
or a barbiturate.
- Paralyze the patient with succinylcholine or vecuronium.
- Once intubated some patients may need permissive hypercarbia with
elective hypoventilation.24C
- Inhaled volatile anesthetics, although no longer widely used or
available outside the operating room, are powerful relaxants of
bronchial smooth muscle. Agents such as halothane, isoflurane,
enflurane, and ether have been used to reverse status asthmaticus
refractory to all other treatments.25C Use these agents
with extreme caution because (except for ether) they are also
vasodilators and myocardial depressants. Some anesthetics sensitize the
myocardium to catecholamines, leading to
life-threatening arrhythmias.
- Extracorporeal membrane oxygenation has been used as a
lifesaving measure for severe refractory asthma when all else has
failed, but this technique is not generally available.
- For most experts ketamine is the intravenous
anesthetic of choice for patients with status asthmaticus. In titrated
doses ketamine has a mild bronchodilator effect and does not
cause vasodilatation, circulatory collapse, or myocardial
depression.
Steps to Take Immediately After Intubation
Tracheal 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 ß2-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:
- Primary tracheal tube confirmation. Visualize the tube
past the vocal cords; perform 5-point auscultation; watch chest rise;
condensation in tube. Auscultation can be misleading because poor
ventilation and air movement may result in inaudible breath sounds in
patients with severe refractory asthma.
- Secondary confirmation of tube placement. Qualitative
end-tidal CO2 detectors; esophageal detector
device; dynamic pulse oximetry readings; quantitative and continuous
CO2 measurements using capnometers or
capnographs.
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-Dependent
Permissive Hypercapnia
Adequately 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:
- Rate: provide mechanical ventilation, 8 to 10 breaths per minute
- Volume: tidal volume, 5 to 7 mL/kg
- Peak flow: 60 L/min with a decelerating pattern
- Inspired oxygen: FIO2, 1.0 (ie,
100%)
If the patient’s airway is extremely difficult to ventilate,
perform the following procedures in order until ventilation
is adequate:
- Ensure that the patient is adequately sedated or paralyzed
so that there is passive patient-ventilator interaction.
- Check the patency of the tube for obstructions caused by
kinking, mucous plugging, or biting. Aspirate the tube as
needed.
- To ensure that the patient is receiving adequate tidal volume,
increase the time for exhalation, decrease the time for inhalation, and
increase the peak pressure.
- Reduce the respiratory rate to 6 to 8 breaths per minute to
reduce auto-PEEP to 15 mm Hg.
- Reduce the tidal volume to 3 to 5 mL/kg to reduce auto-PEEP to
15 mm Hg.
- Increase peak flow to >60 L/min (90 to 120 L/min is commonly
used) to further shorten inspiratory time and increase the ratio of
inspired to expired air (I:E).26C
Troubleshooting: Hypotension or Desaturation Immediately After
Intubation26C
Ensure 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 Pneumothorax
Evidence 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 Buildup
The 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.
- Obtain an ECG: Exclude myocardial ischemia or infarction as
a consequence of acute respiratory failure (ie, hypoxemia, intubation,
and medications).27C 28C
- Request emergency consultation from a pulmonologist.
- Request emergency consultation from an anesthesiologist.
- Admit the patient to the Critical Care Unit.
|
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1.
Wasserfallen J, Schaller M, Feihl F, et al. Sudden
asphyxic asthma: a distinct entity? Am Rev Respir Dis. 1990;142:108–111.[Medline]
2.
Molfino NA, Nannini AN, Matelli A, et al. Respiratory
arrest in near-fatal asthma. N Engl J Med. 1991;99:358–362.
3.
Robin ED, Lewiston N. Unexpected, unexplained sudden
death in young asthmatic subjects. Chest. 1989;96:790–793.[Abstract]
4.
Robin ED, McCauley R. Sudden cardiac death in
bronchial asthma and inhaled ß-adrenergic agonists.
Chest. 1992;101:1699–1702.[Medline]
5.
Rosero SZ, Zareba W, Moss AJ, Robinson, Hajj ARH,
Locati EH, et al. Asthma and the risk of cardiac events in the long QT
syndrome. Am J Cardiol. 1999;84:1406–1411.[Medline]
6.
Brenner BE, Chavda K, Karakurum M, Camargo CA Jr.
Circadian differences among 4096 patients presenting to the emergency
department with acute asthma. Acad Emerg Med. 1999;6:523.[Abstract]
7.
Brenner BE, Tyndall JA, Crain EF. The clinical
presentation of acute asthma in adults and children. In:
Brenner BE, ed. Emergency Asthma. New York, NY:
Marcel-Dekker; 1999:201–232.
8.
Odeh M, Oliven A, Bassan H. Timolol eye-drop-induced
fatal bronchospasm in an asthmatic patient. J Fam Pract. 1991;32:97–98.[Medline]
9.
Weitzman JB, Kanarek NF, Smialek JE. Medical examiner
asthma death autopsies: a distinct group of asthma deaths with
implications for public health strategies. Arch Pathol Lab
Med. 1998;122:691–699.[Medline]
10.
Levenson T, Greenberger PA, Donoghue ER, Lifschultz BD.
Asthma deaths confounded by substance abuse: an assessment of fatal
asthma. Chest. 1996;110:604–610.[Abstract]
11.
Brenner BE, Abraham E, Simon RR. Position and
diaphoresis in acute asthma. Am J Med. 1983;74:1005–1009.[Medline]
12.
Appel D, Karpel JP, Sherman M. Epinephrine
improves expiratory flow rates in patients with asthma who do not
respond to inhaled metaproterenol sulfate. J Allergy Clin
Immunol. 1989;84:90–98.[Medline]
13.
Rowe BH. Effectiveness of steroid therapy in acute
exacerbations of asthma: a meta-analysis. Am J Emerg
Med. 1992;10:301–310.[Medline]
14.
McFadden ER Jr. Dosages of
corticosteroids in asthma. Am Rev Respir
Dis. 1993;147:1306–1312.[Medline]
15.
Rowe BH, Spooner CH, Ducharme FM, Bretzlaff JA, Bota
GW. Early emergency department treatment of acute asthma with systemic
corticosteroids (Cochrane Review). Cochrane Library,
Issue 2, 2000. Oxford: Update Software.
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Karpel JP, Schacter EN, Fanta C, Levey D, Spiro P,
Aldrich TK, Menjjoge SS, Witek T. A comparison of ipratropium and
albuterol vs albuterol alone for the treatment of acute asthma.
Chest. 1996;110:611–616.[Abstract]
17.
Littenberg B. Aminophylline treatment in severe, acute
asthma: a meta-analysis. JAMA. 1988;259:1678–1684.[Medline]
18.
Schiermeyer RP, Finkelstein JA. Rapid infusion of
magnesium sulfate obviates need for intubation in status asthmaticus.
Am J Emerg Med. 1994;12:164–166.[Medline]
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Rowe BH, Bretzlaff JA, Bourdon C, Bota GW, Camargo CA.
Systematic review of magnesium sulfate in the treatment of acute asthma
(Cochrane Review). Cochrane Library, Issue 4, 1998. Oxford: Update
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Gibbs NA, Camargo CA Jr, Rowe BH, Silverman RA. State
of the art: therapeutic controversies in severe acute asthma.
Acad Emerg Med. 2000;7:800–815.[Abstract/Full Text]
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Hemmingsen C, Kielsen P, Ordorico J. Ketamine
in the treatment of bronchospasm during mechanical ventilation.
Am J Emerg Med. 1994;12:417–420.[Medline]
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Panacek EA, Pollack C. Medical management of severe
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|
Anaphylaxis
|
|---|
Background
Anaphylactic and anaphylactoid reactions lack universally accepted
definitions.
- The term anaphylaxis is typically applied to hypersensitivity
reactions mediated by the IgE and IgG4 subclass of antibodies. Some may
be mediated by complement (eg, allergic reactions to blood
products). Signs of an anaphylactic reaction develop after
reexposure to a sensitizing antigen within minutes.
- Anaphylactoid reactions look exactly the same, but they are
not mediated by an antigen-antibody reaction.
- The manifestations and management of anaphylactic and anaphylactoid
reactions are similar so that the distinction is unimportant in
relation to treatment of an acute attack.
Incidence
The 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
Etiology
Insect 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. ß-Blockers may
increase the incidence and severity of anaphylaxis and can produce a
paradoxical response to epinephrine.
Signs and Symptoms
The 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.
- Upper airway (laryngeal) edema, lower airway edema (asthma), or both
may develop acutely and become life-threatening.
- Cardiovascular collapse is the most common
periarrest manifestation. It is caused by an absolute and a relative
hypovolemia. Vasodilation produces a relative hypovolemia, and the
intravascular volume loss associated with increased capillary
permeability contributes to the absolute volume loss. Cardiac
dysfunction is due principally to hypotension but may be complicated by
presence of underlying disease or development of myocardial
ischemia from epinephrine administration.
- Other symptoms include urticaria, rhinitis, conjunctivitis, abdominal
pain, vomiting, diarrhea, and a sense of impending doom.
- The patient may appear either flushed or pale.
Differential Diagnosis
The 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 Arrest7D
The 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:
- Position. Place victims in a position of comfort. If
hypotension is present, elevate the legs until replacement fluids
and vasopressors restore the blood pressure.
- Oxygen. Administer oxygen at high flow rates.
- Epinephrine. Administer epinephrine to all
patients with clinical signs of shock, airway swelling, or definite
breathing difficulty. Administer intravenous
epinephrine if anaphylaxis is profound and life-threatening and
vascular access is available. If vascular access is not available or if
anaphylaxis is not profound and life-threatening, administer
epinephrine by intramuscular injection. Subcutaneous
administration may be used but absorption and subsequent achievement of
maximum plasma concentration may be delayed with
shock.8D —The IM dose of 0.3 to 0.5 mg
(1:1000; 1 mL) may be repeated after 5 to 10 minutes if no clinical
improvement. —Intravenous
epinephrine (1:10 000; 10 mL) 1 to 5 mL or 0.1 to 0.5 mg over
5 minutes should be used only for profound, immediately
life-threatening manifestations and when there are no delays in
intravenous access. Epinephrine may be diluted to a
1:10 000 solution before infusion. An intravenous infusion
(1 mg in 250 mL D5W [4 µg/mL]) at rates of 1
to 4 µg/min may avoid frequent repeat epinephrine
injections.9D
- Antihistamines. Administer antihistamines slowly
intravenously or intramuscularly (eg, 25 mg of
diphenhydramine).
- H2 blockers. Administer H2
blockers, such as cimetidine (300 mg PO, IM, or IV).10D
- Isotonic solutions. Give isotonic crystalloid (normal
saline) if hypotension is present and does not respond rapidly to
epinephrine. A rapid infusion of 1 to 2 L or even 4 L may be
needed initially.
- Inhaled ß-adrenergic agents. Provide
inhaled albuterol if bronchospasm is a major feature. If hypotension is
present, administer parenteral epinephrine before inhaled
albuterol to prevent a possible further decrease in blood pressure.
Inhaled ipratropium may be especially useful for treatment of
bronchospasm in patients on ß-blockers.
- Corticosteroids. Infuse high-dose
intravenous corticosteroids slowly or
administer intramuscularly after severe attacks, especially for
asthmatic patients and those already receiving steroids. The beneficial
effects are delayed at least 4 to 6 hours.
- Envenomation. Rarely insect envenomation by bees, but
not wasps, leaves a venom sac. Immediately scrape away any insect parts
at the site of the sting.11D Squeezing is alleged to
increase envenomation. Judicious local application of ice may also slow
antigen absorption. The application of papain (available in meat
tenderizers) to the stinger site is a common home remedy that appears
to have no therapeutic value.12D
- Glucagon. For patients unresponsive to epinephrine,
especially those receiving ß-blockers, glucagon may be effective.
This agent is short-acting (1 to 2 mg every 5 minutes IM or IV).
Nausea, vomiting, and hyperglycemia are common side effects.
- Observation. Observe closely up to 24 hours. Many patients
do not respond promptly to therapy, and symptoms may recur in some
patients (up to 20%) within 1 to 8 hours despite an intervening
asymptomatic period.13D 14D 15D
Special Considerations
Rapid Progression to Lethal Airway Obstruction
Close 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
Therapy
Death 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 Ventilation
Death 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:
- Fiberoptic tracheal intubation
- Digital tracheal intubation, in which the fingers are used to guide
insertion of a small (7 mm) tracheal tube
- Needle cricothyrotomy followed by transtracheal ventilation
- Cricothyrotomy as described for the patient with massive neck
swelling16D
Support of Circulation
Support 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.
- Rapid volume expansion is an absolute
requirement. —When anaphylaxis occurs, it can produce
profound vasodilation that significantly increases intravascular
capacity. Very large volumes should be administered over very short
periods; typically 2 to 4 L of isotonic crystalloid should be
given.
- High-dose epinephrine IV (ie, rapid progression to
high dose) should be used without hesitation in patients in full
cardiac arrest. —A commonly used sequence: 1 to 3 mg IV (3
minutes), 3 to 5 mg IV (3 minutes), then 4 to 10 µg/min.
- Antihistamines IV. There is little data about the value of
antihistamines in anaphylactic cardiac arrest, but it is reasonable to
assume that little additional harm could result.
- Steroid therapy. Although steroids should have no effect if
given during a cardiac arrest, they may be of value in the
postresuscitation period.
- Asystole/PEA Algorithms. Because the arrest rhythm in
anaphylaxis is often PEA or asystole, the ILCOR panel recommended
adding the other steps in the Asystole and PEA Algorithms. These
include —Administration of atropine —Transcutaneous
pacing
- Prolonged CPR. Cardiac arrest associated with anaphylaxis
may respond to longer therapy than usual. —In these
circumstances the patient is often a young person with a healthy heart
and cardiovascular system. Rapid correction of
vasodilation and low blood volume is required.
—Effective CPR may maintain sufficient oxygen delivery until the
catastrophic effects of the anaphylactic reaction resolve.
Summary
The 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.
|
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Epidemiology of anaphylaxis in Olmsted County:
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Brazil E, MacNamara AF. "Not so immediate"
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J Accid Emerg Med. 1998;15:252–253.[Medline]
16.
Simon RR, Brenner BE. Emergency procedures and
techniques. In: Airway Procedures. Baltimore,
Md: Williams & Wilkins; 1994:79.
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Cardiac Arrest Associated With Trauma
|
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Introduction
Survival from out-of-hospital cardiac arrest secondary to
blunt trauma is uniformly low in children and adults.1E 2E 3E
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
- Severe central neurological injury with secondary
cardiovascular collapse
- Hypoxia secondary to respiratory arrest resulting
from neurological injury, airway obstruction, large open pneumothorax,
or severe tracheobronchial laceration or crush
- Direct and severe injury to vital structures, such as the
heart, aorta, or pulmonary arteries
- Underlying medical problems or other conditions that led
to the injury, such as sudden VF in the driver of a motor vehicle or
the victim of an electric shock
- Severely diminished cardiac output from tension
pneumothorax or pericardial tamponade
- Exsanguination leading to hypovolemia and severely
diminished oxygen delivery
- Injuries in a cold environment (eg, fractured leg)
complicated by secondary severe hypothermia
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.4E 5E 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.5E 6E 7E 8E
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.7E 8E 9E 10E
Extrication and Initial Evaluation
When 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 Trauma
Provision 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 Unresponsiveness
Head 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.
Airway
When 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/Ventilation
Once 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.
Circulation
If 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.
Disability
Throughout 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.
Exposure
The 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 Trauma
ALS includes continued assessment and support of airway,
oxygenation and ventilation (breathing), and
circulation.
Airway
Indications for intubation in the injured patient
include
- Respiratory arrest or apnea
- Respiratory failure, including severe hypoventilation, hypoxemia
despite oxygen therapy, or respiratory acidosis
- Shock
- Severe head injury
- Inability to protect upper airway (eg, loss of gag reflex,
depressed level of consciousness, coma)
- Thoracic injuries (eg, flail chest, pulmonary contusion,
penetrating trauma)
- Signs of airway obstruction
- Injuries associated with potential airway obstruction (eg,
crushing facial or neck injuries)
- Anticipation of the need for mechanical ventilatory support
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.
Ventilation
High 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.
Circulation
Once 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.6E 8E 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.6E 8E
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.4E 14E 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 Exploration
Resuscitation 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:
- Hemodynamic instability despite volume
resuscitation
- Excessive chest tube drainage (1.5 to 2.0 L or more total, or
>300 mL/h for 3 or more hours)
- Significant hemothorax on chest x-ray
- Suspected cardiac trauma
- Gunshot wounds to the abdomen
- Penetrating torso trauma, particularly if associated with
peritoneal perforation
- Positive diagnostic peritoneal lavage (particularly
with evidence of ongoing hemorrhage)
- Significant solid-organ or bowel injury
|
References
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1.
Rosemurgy AS, Norris PA, Olson SM, Hurst JM,
Albrink MH. Prehospital traumatic cardiac arrest: the cost of futility.
J Trauma. 1993;35:468–73; discussion 473–474.[Medline]
2.
Bouillon B, Walther T, Kramer M, Neugebauer E.
Trauma and circulatory arrest: 224 preclinical resuscitations in
Cologne in 1987–1990 [in German]. Anaesthesist. 1994;43:786–790.[Medline]
3.
Hazinski MF, Chahine AA, Holcomb GW III, Morris
JA Jr. Outcome of cardiovascular collapse in pediatric
blunt trauma. Ann Emerg Med. 1994;23:1229–1235.[Medline]
4.
Bickell WH, Wall MJ Jr, Pepe PE, Martin RR,
Ginger VF, Allen MK, Mattox KL. Immediate versus delayed fluid
resuscitation for hypotensive patients with penetrating torso injuries.
N Engl J Med. 1994;331:1105–1109.[Medline]
5.
Pepe PE. Emergency medical services systems and
prehospital management of patients requiring critical care. In: Carlson
R, Geheb M, eds. Principles and Practice of Medical Intensive
Care. Philadelphia, Pa: Saunders; 1993:9–24.
6.
Rozycki G, Adams C, Champion HR, Kihn R.
Resuscitative thoracotomy: trends in outcome. Ann Emerg Med. 1990;19:462.
7.
Copass MK, Oreskovich MR, Bladergroen MR,
Carrico CJ. Prehospital cardiopulmonary resuscitation of the
critically injured patient. Am J Surg. 1984;148:20–26.[Medline]
8.
Durham LA III, Richardson RJ, Wall MJ Jr, Pepe
PE, Mattox KL. Emergency center thoracotomy: impact of prehospital
resuscitation. J Trauma. 1992;32:775–779.[Medline]
9.
Kloeck WGJ, Kramer EB. Prehospital advanced CPR
in the trauma patient. Trauma Emerg Med. 1993;10:772–776.
10.
Schmidt U, Frame SB, Nerlich ML, Rowe DW,
Enderson BL, Maull KI, Tscherne H. On-scene helicopter transport of
patients with multiple injuries: comparison of a German and an American
system [see comments]. J Trauma. 1992;33:548–553;
discussion 553–555.[Medline]
11.
Kloeck WG. A practical approach to the aetiology
of pulseless electrical activity: a simple 10-step training mnemonic.
Resuscitation. 1995;30:157–159.[Medline]
12.
McLean RF, Devitt JH, Dubbin J, McLellan BA.
Incidence of abnormal RNA studies and dysrhythmias in patients with
blunt chest trauma. J Trauma. 1991;31:968–970.[Medline]
13.
Paone RF, Peacock JB, Smith DL. Diagnosis of
myocardial contusion. South Med J. 1993;86:867–870.[Medline]
14.
Solomonov E, Hirsh M, Yahiya A, Krausz MM. The
effect of vigorous fluid resuscitation in uncontrolled hemorrhagic
shock after massive splenic injury [see comments]. Crit Care
Med. 2000;28:749–754.[Medline]
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Cardiac Arrest Associated With Pregnancy
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Background
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
Pregnancy
There 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
- Amniotic fluid embolism
- Eclampsia
- Drug toxicity (eg, due to magnesium sulfate or epidural
anesthetics)
It may also be related to the complex
physiological changes associated with the pregnancy
itself, such as
- Congestive cardiomyopathy
- Aortic dissection
- Pulmonary embolism
- Hemorrhage due to a pregnancy-related pathological
condition
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 Arrest
In 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.5F 6F
To treat a distressed or compromised pregnant patient:
- Place the patient in the left lateral position or manually and
gently displace the uterus to the left.
- Give 100% oxygen.
- Give a fluid bolus.
- Immediately reevaluate the need for any drugs being
administered.
Modifications to BLS Guidelines for Arrest
Do not forget the simple BLS actions you can take:
- Relieve aortocaval compression by manually displacing the gravid
uterus.
- You can also use wedge-shaped cushions, multiple pillows,
overturned chairs, a rescuer’s thighs, or commercially available
foam-cushion wedges (eg, the Cardiff wedge) to displace the
uterus.7F
- Generally perform chest compressions higher on the sternum
to adjust for the shifting of pelvic and abdominal contents toward the
head. We lack clear guidelines on how far the compression point should
be shifted. Use the pulse check during chest compressions to adjust the
sternal compression point.
- Address the need for left-lateral tilt of the torso to
prevent compression or blockage of the vena cava. Foam-cushion wedges
work best because they provide a wide, firm, angled surface to support
the tilted torso during chest compressions. In the usual circumstances
surrounding a suddenly pulseless, gravid woman, however, such
single-purpose equipment will not be available.
- Two alternative means of support are the angled backs of
several chairs and the angled thighs of several rescuers. Overturn a
4-legged chair so that the top of the chair back touches the floor.
Align 1 or 2 more overturned chairs on either side of the first so that
all are tilted in the same manner. Place the woman on her left side,
align her torso parallel with the chair backs, and begin chest
compressions (see Figure).
Modifications to ACLS Guidelines for Arrest
There 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 Fail
If 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 Preparation
Table 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.
|
References
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1.
Wolcomir M, ed. Advanced Life
Support for Obstetrics. Kansas City, Mo: American Academy of
Family Physicians; 1996.
2.
Katz VL, Wells SR, Kuller JA, Hansen WF, McMahon
MJ, Bowes WA Jr. Cesarean delivery: a reconsideration of terminology.
Obstet Gynecol. 1995;86:152–153.[Medline]
3.
Kupas DF, Harter SC, Vosk A. Out-of-hospital
perimortem cesarean section. Prehosp Emerg Care. 1998;2:206–208.[Medline]
4.
Kam CW. Perimortem caesarean sections (PMCS).
J Accid Emerg Med. 1994;11:57–58.
5.
Page-Rodriguez A, Gonzalez-Sanchez JA. Perimortem
cesarean section of twin pregnancy: case report and review of the
literature. Acad Emerg Med. 1999;6:1072–1074.[Full Text]
6.
Cardosi RJ, Porter KB. Cesarean delivery of twins
during maternal cardiopulmonary arrest. Obstet
Gynecol. 1998;92:695–697.[Medline]
7.
Goodwin AP, Pearce AJ. The human wedge: a manoeuvre to
relieve aortocaval compression in resuscitation during late pregnancy.
Anaesthesia.. 1992;47:433–434.[Medline]
8.
Whitten M, Irvine LM. Postmortem and perimortem
caesarean section: what are the indications? J R Soc Med. 2000;93:6–9.[Medline]
9.
Lanoix R, Akkapeddi V, Goldfeder B. Perimortem
cesarean section: case reports and recommendations. Acad Emerg
Med. 1995;2:1063–1067.[Abstract]
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Electric Shock and Lightning Strikes
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Background
Electric Shock
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.8G 9G 10G
Lightning Strike
Lightning 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.11G 12G 13G
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.15G 16G
The primary cause of death in lightning-strike victims is cardiac
arrest, which may be associated with primary VF or
asystole.15G 16G 17G 18G Lightning acts as an instantaneous,
massive direct current countershock, simultaneously
depolarizing the entire myocardium.16G 19G 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 Effects
Immediately 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:
- Electric current passing through the brain and causing inhibition of
medullary respiratory center function
- Tetanic contraction of the diaphragm and chest wall musculature during
current exposure
- Prolonged paralysis of respiratory muscles, which may continue for
minutes after the electric shock has terminated
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 Strike
The 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.23G 24G 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 Strike
Treat 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.
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Top
Hypothermia
References
presents a recommended
hypothermia treatment algorithm with recommended actions that should be
taken for all possible victims of hypothermia. 
