PEM|BRS: Shock, Sepsis, & Resuscitation
Winter’s Formula is a way of calculating the expected pCO2 for a patient compensating
for metabolic acidosis: Expected pCO2 =1.5 x [serum HCO3] + 8 +/- 2
Example: patient has a serum HCO3 of 8; therefore the expected PCO2 would be 1.5 (8)
+ 8 +/- 2 = 18-22; The measured pCO2 on patient’s blood gas is 28 therefore this patient
has a combined metabolic and respiratory acidosis.
If a trauma comes in, starts to receive blood products, and suddenly develops
hypotension, wheezing, and hypoxia, think about possible anaphylactic reaction to the
blood products and first stop the transfusion immediately; then give IV Epi and IV
steroids, IV Benadryl, and normal saline; may also give nebulized albuterol
Septic Shock can be divided into 2 types, warm shock and cold shock; In warm shock
you can have normal pulses (even bounding) and normal capillary refill time along with
hypotension; In cold shock, you’d have cool/mottled extremities, diminished pulses, and
delayed capillary refill time and hypotension.
For a child presenting in septic shock that is refractory to aggressive fluid replacement
(still with poor perfusion and/or hypotension) and you’ve corrected hypoglycemia and
hypocalcemia and given antibiotics, the next step depends on the BP. If you are
normotensive, then give Dopamine. If you are hypotensive then you pick your
catecholamine based on whether you’re in warm or cold shock—if warm shock, start NE
drip, if cold shock, start Epi drip. If still in shock after titrating NE or Epi, then give
stress dose steroids (2mg/kg IV hydrocortisone, max 100mg); If cold shock is still
refractory after Epi drip, start Type III phosphodiasterase inhibitor (amrinone, milrinone)
(reduce afterload.) Likewise, if you have refractory cardiogenic shock, consider
Dobutamine for afterload reduction. If you have refractory warm shock, give vasopressin
(pressor effect only—similar to NE!)
Central venous lines should be in place for catecholamine infusions. Arterial line should
be in place when starting drugs like NE
FFP cannot be pushed rapidly because it causes hypotension
Self-Inflating bags can re-expand even without O2 source, thus can ventilate a patient
even if oxygen tank is empty; They do cause air entrainment during subsequent breaths.
Only use 3% NaCl for hyponatremia WITH seizures—NOT for use with hyponatremia
without seizures.
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For Cardiovascular Meds, you have 3 components to your system: the tank (CVP), the
pump (contractility) and your pipes (vascular tone)
 In hypovolemia you need to give fluid to fill the tank
 In Myocardial depression, you need to give inotrope to improve contractility
 In septic shock you need to do all 3: fill tank, give inotrope, & tighten the pipes
Medication
Receptor
Dose(mcg/kg/min)
Action
Dopamine
D1
2-5
Increase Renal perfusion
Beta 1 (heart)
5-10
Inotrope/chronotrope
Alpha 1 (periph)
10-20
Pressor
Beta1 ( heart)
Beta 2 (periph)
0.02-0.08
Inotrope/chronotrope
Vasodilator
Beta 1 (heart)
Alpha 1 (periph)
0.1-1
Inotrope/chronotrope
Pressor
Alpha 1,2 (periph)
>1
Pressor
NE
Alpha 1,2 (periph)
0.1-2
Pressor
Dobutamine
Beta 1 (heart)
Beta 2 (periph)
5-20
Inotrope/chronotrope
Vasodilator
Milrinone
PDE inhibitor
50-75 mcg/kg load
Over 60 min,
Then 0.5-0.75
Vasodilator
Inotrope (no inc. HR!)
Lusotrope (inc. dias. relax.)
Epinephrine
Pediatric length-based resuscitation tapes:
 Permit rapid determination of size-dependent resuscitation parameters
 Reduce the likelihood of medical errors
 One end of the tape aligns to patient’s head and the other to the patient’s heel
 Appropriate color & letter block identifies approp. drug doses & equipment sizes
 Can only be used for children who weigh up to 36 kg
In status asthmaticus, the best RSI drug is Ketamine due to its bronchodilator effect, but
it can also cause laryngospasm—the most effective treatment of that is continued PPV (as
the laryngospasm is usually transient. Continued PPV followed by administration of a
muscle relaxant and ET intubation would be the most appropriate next step of a patient
who needs continued assistance with ventilation. Benzo=bad—causes bronchospasm.
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If a functionally asplenic patient is septic appearing, you should give Vancomycin in
addition to ceftriaxone (because pneumococcus shows moderate resistence to
cephalosporins). If the patient is neutropenic as well, you’d give ceftazidime instead of
ceftriaxone.
Only time you should use high-dose epi (1:1000) in a resuscitation is down the ET tube.
Children can lose 25-30% of their blood volume with only minimal changes in vitals
Physiologic subtypes of shock are:
 Hypovolemic
 Cardiogenic
 Distributive
o Anaphylactic (start with 0.01mg/kg IM Epi)
 If very hypotensive, give 10 mcg/kg Epi IV over 3-10 minutes then
start drip at 0.1-1 mcg/kg/min
o Septic
o Neurogenic (hypotension, warm/flushed skin, good pulses, brady)
 Use phenylephrine (use NE, or high dose dopamine if need ino)
 Obstructive
All burns that total >15% BSA will require aggressive fluid management
Systemic inflammatory Response Syndrome (SIRS): presence of at least 2 of the
following criteria, one of which must be abnormal temperature or leukocyte count:
 Core temp of >38.5 or < 36 C.
 Tachycardia, or if < 1yo, bradycardia
 Tachypnea
 Leukocytosis or leucopenia
Sepsis: SIRS in the presence of suspected or proven infection
In anaphylaxis, rapid administration of IM Epi is first line therapy
Children with asthma are at increased risk for delayed and more severe reactions in
anaphylaxis.
Anaphylaxis is likely if you have an onset of an illness within minutes to hours after
exposure to a substance (at least 2 of the following): skin/mucosa changes, GI
symptoms, and either respiratory compromise or hypotension; only symptom can be
hypotension if after exposure to a known allergen for that patient.
Anaphylaxis is IgE mediated; Anaphylactoid reactions are not IgE mediated. In US
ED’s, anaphylaxis is most commonly due to foods (peanuts, tree nuts, fish, milk, eggs);
PCN is the most common drug induced cause of anaphylaxis, followed by ASA and
NSAIDs.
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Radiographic contrast material causes anaphylactoid reactions and does not require a
preceeding sensitization—moderate reactions to RCM occur in 1% of patients receiving
RCM and life-threatening reactions occur in < 0.1%
75% of the spina bifida population is sensitized to latex.
All children with an anaphylactic reaction should be observed for at least 8 hours after
resolution of symptoms or admitted overnight for monitoring. In Anaphylaxis, use Epi
IM 0.01 mg/kg 1:1000 concentration; if patient is in extremis or refractory shock, use IV
Epi 0.01 mg/kg of 1:10,000 over 2-5 minutes then start Epi drip; consider trendelenberg
positioning.
The outcome of resuscitation in situations in which there has been asystolic arrest is poor;
Trauma is the leading cause of death in childhood. In PALS, the many etiologies of
arrest follow one of two pathways:
·
Respiratory distress to respiratory failure to arrest (80%)
·
Circulatory compromise to circulatory failure to arrest (20%)
Causes of death < 1 year:
1. Perinatal conditions (LBW, RDS, preemie, etc.)
2. Congenital
3. SIDS
4. Injuries
5. Infections/Heart
Causes of death age 1-4 years:
1. Injuries
2. Congenital
3. Cancer
4. Homicide
5. Heart
Causes of death age 5-9 years:
1. Injuries
2. Cancer
3. Congenital
4. Homicide
5. Heart
Causes of death 10-19 years:
1. Injuries
2. Homicide
3. Suicide
4. Cancer
5. Heart
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In the ED, lack of an immediate patient response (to correction of hypoxia) usually
predicts a need for multiple drug interventions
The most common cardiac rhythms to be recognized and managed are sinus bradycardia
and asystole
Most airway obstruction is related to the mandibular block of tissue falling posteriorly
and lying against the posterior wall of the hypopharynx. This can be relieved manually
by pulling the jaw forward or doing jaw thrust--these always should be done first before
any other advanced airway procedures are tried.
Oropharyngeal Airways: used when manual manipulation cannot maintain airway.
Purpose is to stent the mandibular block of tissue off the posterior pharyngeal wall. The
size can be estimated by placing the airway alongside the face so the bite block portion is
parallel to the palate. The tip of the airway should just approximate the angle of the
mandible. Use in the unconscious patient. Place using a tongue depressor to press the
tongue into the floor of the mouth and then pass so the stent conforms to the contour of
the tongue.
Nasopharyngeal Airways: stent the tongue from the posterior pharyngeal wall; estimate
by measuring the distance from the nares to the tragus of the ear. It should not be so
large as to cause sustained blanching to the skin of the ala nasae; Pass it along the floor of
the nasopharynx; adenoidal hypertrophy and bleeding problems are relative
contraindications.
Endotracheal Tubes: inside diameter (in mm) = (16 + age in years)/4
Uncuffed tubes are used under the age of 10 because, in children, there is a normal
narrowing of the trachea at the level of the cricoid ring (serving as a functional seal if
using the above formula). At age 10 and over, cuffed tubes are used. By using a cuffed
tube, you are adding 0.5mm to the tube size.
Insertion Distance (cm mark at teeth) = 12 + age(years)/2
Straight blade (Miller)
Curved blade (MacIntosh)
On an AP film, the tip of the ETT should be at T2 or T3 vertebral level or 1 cm above the
carina, or directly between the lower edges of the medial aspect of the clavicles.
100% O2 by NC at 4-6L = 30-40% O2 delivered
Obtunded patient wearing a facemask is at risk for aspiration from vomitus and must be
closely observed
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Self-inflating resuscitators are the most commonly used bags (due to their ease of use)
but for gas to flow, the bag must be squeezed. Anesthesia bags depend on adequate gas
flow to maintain a compressible unit; advantage is that you can maintain PEEP;
disadvantage is that more experience is required.
The palpation of a strong femoral or brachial pulse indicates that cardiac output is
adequate (apical pulse is not meaningful)
In the arrested patient, IO access is the method of choice; IO’s can handle fluids,
catecholamines, all PALS drugs, and blood products
ETT route of drug delivery ok for LEAN (Lido, Epi, Atropine, Narcan); dilute all drugs
with 5cc NS and follow with 5 mechanical ventilations; Use 1:1000 Epi down ETT
Only use SDE (standard dose Epi in 1:10,000 concentration) via IV
Consider NaHCO3 in prolonged cardiopulmonary arrest, after adequate airway,
ventilation, epi, and chest compressions have been instituted. 1mEq/kg IV q 10min
(titrate to blood gas acidosis); Use 0.5mEq/kg in neonates; NaHCO3 also useful in
hyperkalemia, hypermagnesemia, tricyclic overdose, and Na channel blocker poisoning
Atropine useful in bradycardia that is known to be vagally mediated (i.e. with intubation);
Use when you have symptomatic bradycardia after airway and ventilation are
accomplished; 0.02mg/kg; minimum dose of 0.1mg; max dose in a child of 0.5mg and
1mg in an adolescent; may repeat q 5 minutes
Documented hypoglycemia treated with 0.5g/kg glucose (5cc/kg of D10NS or D10W)
Adenosine is the treatment of choice for stable SVT; 0.1mg/kg; maximum dose is 6mg; a
second dose of 0.2mg/kg with maximum dose of 12mg may be given; Give via rapid
bolus using two syringe technique; Effects occur within 15-30 seconds; SE=facial
flushing, chest pain, anxiety, dyspnea (all disappear within 10-20 seconds)
Amiodarone is a class III antiarrhythmic; blocks potassium channels; Load with 5mg/kg
over 50 minutes; In pulseless arrest, give as rapid bolus; adverse effects= bradycardia,
tachydysrhythmias, and hypotension
Lidocaine is a class I antiarrhythmic; blocks sodium channels; reduces slope of phase 4
repolarization of the myocyte thus decreasing automaticity (not as good as amiodarone)
Calcium does not improve outcome in patients with out-of-hospital asystolic arrest;
indicated in children with documented hypocalcemia and hyperkalemia (check for these
in septic children) as well as in hypermagnesemia and calcium channel blocker overdose
Give 0.2cc/kg of 10% CaCl as slow IV push; Give 0.6cc/kg of 10%CaGluconate
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Magnesium sulfate used in severe asthma with persistent respiratory distress despite
aggressive beta-agonist therapy; Use also in torsades de pointe and hypomagnesemia;
Give 25-50 mg/kg (maximum of 2g) IV over 10-20 minutes
In defibrillation and cardioversion, use adult paddles/pads over 1 year (10kg) of age;
always use electrode paste with paddles; may use AED’s with adult pads in children
>8yrs old; Use AED’s with Peds pads from 1-8 years old.
ABCDE’s of resuscitation: A (Airway/cervical spine/intubate); B (Breathing/ventilate); C
(Circulation/stop hemorrhage); D (Disability/GCS & Pupils/Dextrose/decontamination; E
(Exposure/remove all clothing/environment/check temp & warming blankets) all within
first 5-10 minutes of arrival; then tubes, lines, bloodwork, radiology studies are ordered;
Then head to toe secondary survey and call consultants and arrange for definitive care;
then reassess primary survey.
If no return of circulation after aggressive airway, ventilation, chest compressions and 2
doses of Epi, there is no chance for a successful resuscitation in the child who arrives to
the ED with cardiopulmonary arrest; Leader should do history, primary and secondary
surveys to scan for other treatable problems like hypothermia, overdose, or VT/VF; code
should be called at 20-30 minutes.
For the brain during arrest, oxygen stores are depleted within 20 seconds and glucose and
adenosine are depleted within 5 minutes; mild hypothermia in arrest victims shows
promise in attenuating brain damage.
Points to remember during codes: assign specific tasks, give directions without directly
performing tasks or procedures, do frequent reassessment following interventions, query
team for suggestions prior to terminating resuscitation efforts; correct ETT placement
should be continually confirmed via auscultation and ET CO2 monitoring; alternate chest
compressors frequently; debrief team following code.
Infusion of resuscitative medications and fluids through an intraosseous (IO) needle is a
rapid and safe intervention, particularly in patients who present in cardiopulmonary arrest
or in whom previous attempts at intravenous access have failed. Contraindications to IO
placement include fracture in the intended bone, prior unsuccessful attempts or placement
in the site, and any type of pre-existing bone disease at risk of fracture (eg, osteogenesis
imperfecta or osteopetrosis). A further relative contraindication is an overlying infection
or loss of skin integrity at the proposed insertion site.
Research has demonstrated that trained health-care providers can achieve a high rate of
successful IO placement within 1 to 2 minutes. The proximal tibia is recommended as the
primary IO needle insertion site in young children, but access also can be achieved at the
distal tibia, distal femur, and proximal humerus. Although the sternum is used
infrequently as an insertion site in adults, this site is not recommended in pediatric
patients because of potential interference with CPR and the risk to underlying structures.
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IO placement begins with proper identification of the anatomic site for insertion using
either a specialized IO needle, 16- to 20-gauge spinal needles, or bone marrow aspiration
needles. The area of insertion on the proximal tibia is the flat anteromedial section of the
bone, approximately 1 to 2 cm distal to the tibial tuberosity, angled approximately 10 to
15 degrees caudally to avoid damage to the physis (Fig. 1) in infants and young children.
An alternative site may be appropriate for older children (Fig. 2).
Figure 1. The proximal tibia along the flat anteromedial surface of the shaft, 1 to 2
cm below the tibial tuberosity, is the preferred site for intraosseous infusion in
infants and young children because of differences in cortical thickness. Reprinted
with permission from Zenel JA, Ibsen LM, Braner DAV, Hodo R, Goldstein B.
Technical tip: intraosseous infusion. Pediatr Rev. 2000;21:11-CD.
Figure 2: The distal one third of the femur along the midline at a point
approximately 3 cm above the femoral condyle is one site for intraosseous infusion
in older children. Reprinted with permission from Zenel JA, Ibsen LM, Braner
DAV, Hodo R, Goldstein B. Technical tip: intraosseous infusion. Pediatr Rev.
2000;21:11-CD.
After insertion of the IO needle into the soft tissue, a drilling/twisting motion should be
used to penetrate the bony cortex.
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The IO needle should be advanced slowly until a sudden decrease in resistance is felt as
the marrow cavity is entered. Successful placement can be confirmed by aspiration of a
small amount of bone marrow through the needle or by infusion of fluids and medications
without evidence of extravasation. Mechanical devices recently have become available to
aid in insertion.
Complications of IO placement can involve the overlying skin, soft tissues, and
underlying bone. Skin and soft-tissue complications include localized hematoma, fat
necrosis, cellulitis, and abscess formation. Extravasation of infused medications can lead
to localized effects on the surrounding tissues, such as necrosis from epinephrine or
calcium. In addition, extravasation of fluids under pressure possibly can lead to
compartment syndrome. Skeletal complications include injury to the bony growth plate,
osteomyelitis, and fracture of the underlying bone.
Shock:
Shock occurs when adequate oxygen and nutrients cannot be provided at the cellular
level to meet the metabolic demands of vital organs. Hypovolemic shock is the most
common type of shock in children and may be caused by gastrointestinal losses (eg, from
vomiting and diarrhea), especially in small infants. Other causes of hypovolemic shock
include hemorrhage (eg, due to trauma or gastrointestinal bleeding), loss of plasma from
the vascular space (eg, due to burns, peritonitis, or hypoproteinemia), and loss of water
(eg, due to an osmotic diuresis in a patient who has diabetic ketoacidosis). Other major
categories of shock are cardiogenic and distributive shock. Major categories of shock, the
underlying pathophysiology, expected signs and symptoms, and suggested treatments for
each are summarized in the Table.
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Table: Pathophysiology, Signs and Symptoms, and Treatment of the Various Forms
of Shock
Reprinted with permission from McKiernan CA, Lieberman SA. Circulatory shock in
children: an overview. Pediatr Rev. 2005;26:451-460.
The goal of therapy in this child is to increase the delivery of oxygen and other substrates
to the tissues. The initial therapy for any pediatric patient in shock (regardless of cause)
involves ensuring that the airway is open and maintained (including endotracheal
intubation, if needed) and that breathing is adequate. Intravascular access should be
obtained, with an intraosseous line placed in critically ill patients if other access cannot
be achieved readily. Once access has been attained, 20 mL/kg of isotonic crystalloid fluid
(0.9% sodium chloride or lactated Ringer solution) should be delivered as rapidly as
possible. Additional 20-mL/kg boluses of isotonic fluids should be provided, based on the
assessment of response to the initial therapy.
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One goal in the resuscitation of patients experiencing shock is to keep their hemoglobin
values at 10 mg/dL (100 g/L) or greater. Additional crystalloid should be administered
until packed red blood cells are available. When they become available, the patient
should receive a transfusion of 10 mL/kg over 1 to 2 hours. Coagulation studies should be
obtained because coagulopathy may develop as an effect of the shock state and the large
volume of resuscitation fluids required.
Defibrillation:
Ventricular fibrillation: Defibrillation at a dose of 2 J/kg is the intervention of choice.
Defibrillation is an unsynchronized electrical shock used to treat pulseless ventricular
tachycardia or ventricular fibrillation. The true mechanism of action behind defibrillation
is controversial, but one theory postulates that it prolongs the refractory period. The usual
initial energy dose is 2 J/kg, with subsequent doses of 4 J/kg if the initial shock is not
successful. The lower and upper limit energy doses used to defibrillate pediatric patients
successfully have not been determined.
Direct current cardioversion involves the synchronized delivery of the countershock and
is the treatment of choice for unstable, organized cardiac dysrhythmias, such as
supraventricular tachycardias, atrial flutter, or atrial fibrillation. The electrical shock is
electronically synchronized with the R wave of the QRS complex to avoid administering
the shock during the relative refractory period. Unsynchronized, lower-energy shocks
could induce ventricular fibrillation. Cardioversion works by depolarizing enough
myocardium to interrupt the re-entrant circuits, allowing the sinoatrial node to initiate a
normal rhythm. The usual initial energy dose is 0.5 to 1 J/kg, increased to 2 J/kg if the
initial dose is not successful.
Once ventricular fibrillation is identified, countershocks are given without delay,
followed by immediate resumption of cardiopulmonary resuscitation. Effective pump
activity may not be established immediately after successful conversion to an organized
electrical rhythm. Current Pediatric Advanced Life Support guidelines (2005)
recommend immediate resumption of chest compressions for a period of 2 minutes before
assessing for pulse. If elective cardioversion is deemed necessary, steps should be taken
to provide adequate pain control or sedation because this procedure causes discomfort.
Paddle/Pad placement: Optimal positioning directs the current through most of the
myocardial mass, with anterior-posterior placement on the chest in younger children and
right upper chest and cardiac apex placement in older children, similar to adults.
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Type of waveform: Biphasic waveforms demonstrate more effective defibrillation at
lower-energy doses than do single-polarity, monophasic waveforms.
Contraindications to cardioversion include a non-re-entrant tachycardia, such as sinus
tachycardia, multifocal atrial tachycardia, and junctional ectopic tachycardia.
Defibrillation is contraindicated in pulseless electrical activity and asystole and in
patients who have tachycardia and a pulse.
Potential complications of electrical countershock therapy include electrical injuries to
the patient or clinicians who are in close proximity. Electrical arcing injuries can occur in
the presence of excessive amounts of liquid or other conducting substances on the
patient's chest or if the paddles/pads touch. Increasingly higher doses of delivered energy
can damage the myocardium and cause thermal injury to the skin. Furthermore, the
administered shock can act as an igniting spark for combustible gases in the immediate
area. Pediatric Advanced Life Support protocols instruct the person delivering the
countershock to announce before administering: “One, I am clear. Two, you're clear,
oxygen's clear. Three, everybody's clear.” to increase safety for all health-care workers
involved in the resuscitation.
The most common causes of respiratory failure in newborns are respiratory distress
syndrome, meconium aspiration, and sepsis. Pneumonia is a common cause beginning in
the newborn period and continuing throughout childhood. In addition, infants are
susceptible to bronchiolitis, bronchopulmonary dysplasia, croup, and sepsis. Among
toddlers, asthma and near-drowning become important causes, with foreign body
aspiration also playing a role. Trauma and drug ingestions join asthma as the leading
causes of respiratory failure in teenagers.
Another method of categorizing respiratory failure is by anatomic/physiologic groupings.
The Pediatric Advanced Life Support curriculum teaches the need to identify the cause of
respiratory failure as either upper airway (eg, croup, epiglottitis, retropharyngeal abscess,
foreign body), lower airway (eg, bronchiolitis, asthma, foreign body), lung
tissue/parenchymal (eg pneumonia/empyema, interstitial disease, congestive heart failure
with pulmonary edema, near-drowning), or disordered control of breathing (metabolic,
toxicologic, neuromuscular, and central neurologic causes). Management differs
according to cause, but the potential need for emer. ventilatory support is common to all.
Neurogenic Shock:
Assessment and treatment of hypotension in this setting includes searching for and
treating any accompanying hemorrhagic injuries, standard administration of fluid and
blood products, and aggressive treatment to maintain an adequate blood pressure for
spinal cord perfusion that can minimize secondary spinal cord injury. Primary α-agonists
(norepinephrine or phenylephrine) have the advantage of maximizing vasoconstriction
with limited effect on cardiac performance.
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Complete spinal cord injuries often are followed by an immediate physiologic loss of all
spinal cord function caudal to the level of the injury. This state, which is associated with
flaccid paralysis, complete anesthesia, absent bowel and bladder control, and loss of
reflex activity that may be accompanied by priapism in males, is referred to as spinal
shock. There may be an initial period of hypertension due to a surge of catecholamine
release, followed by hypotension.
Neurogenic shock refers to hypotension, usually associated with bradycardia believed to
be due to the interruption of autonomic pathways in the spinal cord causing vasodilation
and decreased vascular resistance. It is a form of distributive shock. Spinal cord ischemia
is believed to be one of the major causes of neuronal injury and neurologic deficits after
spinal cord injuries. Although no human clinical trials have shown benefit from
aggressive treatment of hypotension in patients who have neurogenic shock, animal data
show that hypotension after spinal cord injuries is associated with worse neurologic
outcomes. Several case series in adult victims of spinal cord injury suggest better
neurologic outcome and a lack of adverse effects with similar aggressive management.
No evidence supports the superiority of a single approach to management of
cardiovascular derangements in this population. Hypovolemia should be corrected and
sources of blood loss sought and treated. Typical fluids for resuscitation should be
administered. Hypertonic saline and mannitol are used in patients who have severe brain
injuries and evidence of herniation, but there is no evidence or recommendation for their
use in spinal cord injuries. Blood should be used in patients exhibiting blood loss or
evidence of anemia.
The choice of vasoreactive agents has not been the subject of clinical trials. Initial
treatment with dopamine may be started. Agents that are primarily α-agonists, such as
norepinephrine or phenylephrine, have been recommended by some experts due to their
effect on vascular tone with fewer direct cardiac effects.
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