Shock Syndromes I

The potential offending agent should be discontinued (for medication-related reactions) and

potentially removed (in the setting of envenomation) for patients with immune-mediated

(anaphylactic) shock.

Treatment goals and end points of resuscitation are usually similar to those listed in section IV,

Resuscitation Parameters and End Points. In the setting of acute spinal cord injury, a MAP goal of

at least 85 mm Hg has been associated with improved outcomes in uncontrolled studies. As such, the

guidelines recommend an initial MAP goal of 85–90 mm Hg in patients with acute spinal cord injury

for 1 week after injury (level III recommendation).

Initial resuscitation

The treatment of choice is intravenous fluids, which restore effective circulating volume.

Crystalloids (e.g., lactated Ringer solution or normal saline) are typically the initial fluid of

choice compared with colloids (e.g., albumin or other blood products).

ii.

Fluid should be administered until the patient is no longer fluid responsive.

Vasopressors should be initiated for hypotension unresponsive to fluid administration.

Norepinephrine is usually considered the first-line vasopressor because of its ability to increase

SVR without decreasing CO.

ii.

Epinephrine is typically used for patients with immune-mediated (anaphylactic) shock to

provide mast cell stabilization, histamine suppression, bronchodilation, and vasoconstriction.

During initial treatment, intramuscular epinephrine (0.01 mg/kg; maximum 0.5 mg) into

the anterolateral thigh is preferred for speed and fewer adverse events, including overdoses,

compared with intravenous epinephrine. Intramuscular epinephrine may be repeated at 5-

to 15-minute intervals if the response is inadequate. Beyond initial management, in patients

who continue to be hypotensive despite intramuscular epinephrine, epinephrine infusions

(1–10 mcg/minute) are often used for ongoing shock, largely because of convention rather than

evidence. In patients with actual or impending cardiac arrest, slow, intravenous administration

of epinephrine 50 mcg may be necessary. Norepinephrine, vasopressin, and other vasopressor

agents have been used with refractory hypotension associated with anaphylaxis, though

it is unclear whether this strategy is superior to epinephrine alone. Dosing and route of

administration of epinephrine for anaphalaxis should be monitored closely and verified;

accidental overdoses involving decimal errors or confusing “mcg” with “mg” have led to

adverse events such as cardiac arrest.

iii.

In neurogenic shock, agents with combined vasoconstrictive and inotropic properties (e.g.,

norepinephrine, dopamine, epinephrine) are preferred. Phenylephrine may also be used, but a

concomitant inotropic agent (e.g., dobutamine) is often administered.

greater than 85 mm Hg for 1 week.

Additional therapies

Immune-mediated (anaphylactic) shock is also conventionally treated with concomitant histamine-1

and histamine-2 receptor antagonists and corticosteroids, though no strong data support the

use of these agents. Corticosteroids have a slow onset of action (4–6 hours) and are therefore

ineffective for acute management; however, they may decrease the risk of late symptoms. If used,

methylprednisolone 1–2 mg/kg or the equivalent is recommended.

The most recent guidelines regarding the treatment of patients with acute cervical spine and spinal

cord injuries recommend against administering methylprednisolone (level I recommendation).

Patients with vasodilatory shock secondary to adrenal insufficiency (Addisonian crisis) should

receive intravenous corticosteroids (typically hydrocortisone 50 mg every 6 hours).

outlined in the Hepatic Failure/GI/Endocrine Emergencies chapter.