Neurogenic ShockNRS 560

Definition

• Neurogenic shock- A form of distributive shock due to decreased peripheral vascular resistance.

• Rarest form of shock

Etiology

• Damage to either the brain or spinal cord (Above T6) inhibits transmission of neural stimuli to the arteries and arterioles, which reduce vasomotor tone.

• The decrease peripheral resistance result in vasodilatation and hypotension.

• Cardiac output diminishes due to the altered distribution of blood.

Pathophysiology

• Loss of sympathetic tone (parasympathetic �response) results in massive vasodilitation, inhibition of the baro-receptor response, and impaired thermo-regulation.

• Arterial vasodilitation = drop in BP�• Decrease in BP & drop in CO = impaired �

tissue perfusion.• Inhibition of baro-receptors = no reflex �

tachycardia, further compromising tissue perfusion

Clinical manifestation

• Hypotension• Bradycardia• Hypothermia• Warm/Dry skin (Loss ability to sweat)

Hemodynamic

• Decreased CO & CI�• Decrease in pre-load�• Decrease in RAP & PAWP�• Decrease in after-load =low SVR�

Causes of neurogenic shock

• Spinal cord injury (SCI)• Most prevalent cause; can be complete or

incomplete SCI• Location of the SCI lesion can be predictive of

the incidence and severity of neurogenic shock• Lesions at T1 and above can have complete

disruption of SNS outflow• Lesions from T1 to L3 can result in partial

disruption of SNS outflow• Spinal anesthesia• Autonomic blocking agents

Assessment

• Assess risk for neurogenic shock development (Guly et al).

• Assess vital signs as prescribed, including orthostatic blood pressure and oxygenation.

• Assess hemodynamic parameters as prescribed.

• Monitor strict intake and output.

Assessment

• Assess nutritional intake.• Assess neurological parameters (motor,

sensation, reflexes) to determine presence and level of SCI as prescribed.

• Assess skin temperature and skin integrity.• Assess for signs of anxiety, depression,

and coping skills.

Diagnosis

• Hypotension; bradycardia; and warm, dry skin are classic signs of neurogenic shock.

• Ongoing monitoring of vital signs is necessary to detect the changes in blood pressure and heart rate associated with the development of neurogenic shock that many not be present on initial presentation to the emergency department (ED).

Diagnosis

• Hypotension in the trauma patient warrants a thorough work-up to exclude other possible causes including hemorrhage.

• A diagnosis of neurogenic shock is properly rendered only when other causes of hypotension have been ruled out. A diagnosis of SCI is confirmed with radiographs, CT, and MRI studies.

Prevention

• To prevent or minimize secondary injury associated with SCI that can lead to neurogenic shock, trauma patients are considered at risk for cervical spinal instability.

Prevention

• Stabilization measures (use of a cervical collar, backboard, and careful positioning including logrolling) are implemented until cervical spine injury is ruled out by:– History– Examination– Radiographs– computed tomography (CT)– magnetic resonance imaging (MRI).

Acute Treatment : Airway

• Care focuses on maintaining or achieving a patent airway and providing ventilator support if indicated.

Acute Treatment : Hypotension

• A rapid infusion of crystalloid is given to maintain a mean arterial pressure (MAP) of 85 to 90 mm Hg. Insertion of a pulmonary artery (PA) catheter may be indicated to monitor for fluid overload in at-risk patients.

• Additionally, vasopressors may be necessary to maintain normal blood pressure and tissue perfusion.

• Positive inotropic medications including dopamine are indicated for hypotension in combination with bradycardia and decreased cardiac output.

Acute Treatment : Hypothermia

• Environmental temperature regulation is necessary, and warming blankets or other commercially available measures can be used.

• Surgical stabilization, if indicated

Management of neurogenic shock

Medical Management

• Goal : to treat or remove the cause, prevent cardiovascular instability and promote optimal tissue perfusion

Cardiovascular instability occur from :

1. Hypovolemia

2. Bradycardia

3. hypothermia

• Hypovolemia is treated with carefully fluid resuscitation

- the minimal amount of fluid is administered to ensure adequate tissue perfusion.

- Volume replacement is initiated for SBP lower than 90 mmhg, urine output less than 30 ml/hr, or changes in mental status that indicate decreased cerebral tissue perfusion.

- Carefully observed for evidence of fluid overload.

- Vasopressor are used as necessary to maintain BP and organ perfusion.

• Bradycardia should be treated with atropine when necessary.

• Hypothermia is treated with warming measures and environmental temperature regulation.

• Correction of the client’s hypotension and hypoperfusion through IV fluid administration, vasopressor, supplemental oxygen and respiratory support if needed

• patients with acute SCI have a high incidence of deep venous thromboembolism (DVT) if they do not receive venous thromboembolism (VTE)prophylaxis.

• Administer steroid such as methylprednisalone to reduce the inflammation and swelling around spinal cord

Nursing management• Elevate and maintain the head of the bed

at least 30 degree to prevent neurogenic shock during epidural or spinal anesthesia

• Applying anti-embolism stocking and elevate the foot to minimize the pooling of blood in the legs.

• Continues stabilization and immobilization of the patient’s spinal is critical, concomitant spinal injury frequently accompanies with neurogenic shock.

• Collaborate with physician regarding the administration of Iv fluid replacement at a sufficient rate to maintain urinary output greater than 30 ml/hr.

• Colloid solution is avoided in the initial phase to prevent risk of edema formation as a result of the increased capillary permeability.

Hypothermia

• Monitor core body temperature continuously

• Heated air and oxygen can be added to rewarm the body core

• Do not hyperventilate the hypothermic patient because carbon dioxide production is low and this action may induce severe alkalosis and precipitate ventricular fibrillation.