Emergency management of shock

EMERGENCY MANAGEMENT OF SHOCK

By Prof. Srour Yina

I.     INTRODUCTION:

Shock is defined as a state of inadequate tissue perfusion due to poor circulatory flow or increased cellular needs. A series of compensatory mechanisms are activated to cope with the initial shock state which results in clinical manifestations. Untreated, shock states can rapidly deteriorate into failure of multiple organ systems and eventually irreversible shock. Recognition of pre-shock states is important so early goal-directed therapy can be instituted. The regime of resuscitation includes fluid boluses, airway intervention and inotropic support. The key is early shock recognition and prompt action.

II.     DIAGNOSIS

1.   Recognize some of the following:

•      Sick-looking/lethargy

•      Tachypnoea

•      Tachycardia/Hypotension

•      Pallor

•      Cyanosis  (if Haemoglobin (Hb) adequate)

•      Poor capillary refill

•      Acidemia (metabolic or mixed acidosis)

•      CNS disturbance

•      Oliguria

•      Agitation or depression

2.   Investigations

•      Blood:

§    FBC

§    Blood gases and acid base

§    Electrolytes, Blood Urea Nitrogen (BUN), creatinine

§    Coagulation profile

§    Group and cross-match, if necessary

•      CXR

•      Cultures from blood, urine, respiratory secretions; full septic workup if appropriate

•      Consider:

§    Disseminated Intravascular Coagulation (DIC) screen

§    Liver Function Test

§    Serum cortisol

§    Serum lactate

§    Mixed venous saturation

•      Further management based on diagnostic clues and response to initial therapy

 III.     FORMS OF SHOCK

•      Hypovolemic

•      Septic

•      Cardiogenic

•      Anaphylactic

•      Neurogenic

IV.     IMMEDIATE TREATMENT

1.   Improve Oxygenation and Ventilation

•      Oxygen by mask, nasal cannula or hood

•      Consider intubation

•      Ventilate if there is severe hypoxia, respiratory failure, severe respiratory distress or marked acidaemia. Ventilation will reduce work of breathing and cardiac demands, especially in cardiogenic and septic shock

2.   Volume Replacement

•      Establish IV access; perform blood work including microbiological cultures

•      Replete circulating blood volume with normal saline, plasma, albumin or blood in hypovolaemic shock

•      In septic shock, volume status must be restored quickly and should be given before starting inotropes

•      In cardiogenic shock, fluid resuscitation should be given with caution.

Dobutamine or epinephrine is usually started once volume state is optimised

•      Start with aliquots of 10–20ml/kg and reassess

•      In early resuscitation, both colloids and crystalloids can be given.

•      Subsequent fluid therapy in post-resuscitation stabilisation period will usually require a combination of colloids and crystalloids, depending on the clinical state and disease pathophysiology. Blood products should be considered in cases of anaemia, ongoing blood loss or bleeding tendency

•      Rate of infusion depends on clinical state; in acute resuscitation, volume should be given as IV push/bolus; in shock states, each fluid bolus can be given over 15 minutes; in less acute situations, the timing may be prolonged to one hour

3.   Increase Cardiac Contractility

•      Correct pH:

-    Ventilate if respiratory acidosis

-    NaHCO3 if pH is still < 7.20 and ventilation is adequate

[(Weight) x (Base Deficit) x 0.15]mEq

-    Repeat if necessary

•      Inotrope infusion (see appendix) : Inotrope therapy is usually indicated if the perfusion remains poor after fluid state is restored or there is poor or no response after fluid therapy of 60ml/kg in septic shock. In cardiogenic shock, inotropes should be considered early:

-    Dopamine 5–10μg/kg/min

-    Dobutamine 5–10μg/kg/min

-    Milrinone 0.3–0.7μg/kg/min

-    Noradrenaline 0.1–1.0μg/kg/min

-    Adrenaline 0.1–1.0μg/kg/min

•      In patients with cardiogenic shock whose cardiac contractility is decreased, adrenaline should be started. Afterload reduction agents (dobutamine and/or milrinone) are useful to decrease the work against which the ventricles must perform, thereby decreasing myocardial oxygen consumption and increasing cardiac output

•      Paediatric septic shock, unlike adults, presents usually as cold shock rather than warm shock. In cold shock, circulatory flow is decreased either from poor myocardial effort or increased systemic vascular resistance. When BP is decreased, epinephrine can be titrated to achieve normal BP limits. When BP is normal, an afterload reduction agent e.g. dobutamine or milrinone can improve cardiac output by decreasing systemic vascular resistance (SVR)

•      In warm shock, the cardiac output is increased but end organ perfusion is diminished because the SVR is low. Using a vasopressor agent will increase SVR and improve flow. Noradrenaline at lower doses (< 0.5μg/kg/min) or adrenaline at high doses (>

0.4μg/kg/

min) will have such effects. In adult studies, dobutamine with noradrenaline have been shown to improve splanchnic flow

•      When high doses of inotropes are needed or the shock state does not respond to inotrope therapy, other therapeutic measures should be considered:

-    Vasopressin at low dose of 0.001μg/kg/min

-    Hydrocortisone should be given initially to all patients who are at risk of adrenal insufficiency e.g. prolonged steroid use. This group of patients will require stress doses of hydrocortisone. In addition, certain patients with septic shock who require high catecholamine support may have relative adrenal insufficiency. These patients have low baseline cortisol levels (< 18mg/dl) or poor Adrenocorticotrophic Hormone (ACTH) stimulation response (< 9mg/dl increase after ACTH). These patients may benefit from hydrocortisone given at higher doses

•        Inotropes, with the exception of dobutamine and milrinone, should always be administered through a central line, though in an emergency lower doses (dopamine <

10μg/kg/min, noradrenaline and adrenaline < 0.1μg/kg/min) may be administered

peripherally for a short period until central venous access is established

4.   Monitoring

•      All patients with shock who require > 20ml/kg fluid resuscitation should be

considered for CICU admission. Upon admission, they should be on hourly parameters, saturation monitoring and strict input-output (I/O) charting

•      Urinary catheterisation is needed to quantify output and for initial urine cultures

•      Arterial line should be inserted for invasive BP monitoring

•      Central venous pressure can be trended via central venous access

•      Nasogastric tube and empty stomach to decrease risk of aspiration

•      Mixed venous saturations and serum lactate levels may be useful to gauge end-organ oxygen deficit

•      Serum cortisol levels should be taken before hydrocortisone treatment

V.    FURTHER MANAGEMENT

•      Detailed history, best obtained by another doctor during initial resuscitation

•      Detailed physical examination should proceed as the resuscitation process progresses

•      Assess neck veins, fontanelle, mucous membranes, skin turgor for signs of hypovolaemia

Note: beware pneumothorax and/or cardiac tamponade if full neck veins and shock are both present

•      Fever, focal signs of infection (may be minimal); beware rash consistent with meningococcemia

•      Signs of heart failure, especially gallop rhythm, cardiomegaly, pulse differential, lung crackles, hepatomegaly.

•      Urticaria, mucosal oedema, bronchospasm in anaphylaxis

Approach to the initial management of shock in children

* For possible cardiogenic shock with hypovolemia, give 5 to 10mL/kg, infused over 10 to 20 minutes. Evaluate target end points and slowly give another 5 to 10 cc/kg if there has been improvement or no change.

** For patients with DKA who do not improve with 20 mL/kg, look for another cause of shock before administering additional crystalloid. For possible cardiogenic shock, slowly give another 5 to 10 mL/kg if

there has been improvement or no change.

***Dopamine if normotensive, noradrenaline if hypotensive and vasodilated, and adrenaline if

hypotensive and vasoconstricted.

                                 Management of suspected septic shock

Reference

1-  Task Force of the American college of Critical Care Medicine, Society of Critical Care

Medicine. Practice parameters for hemodynamic support of sepsis in adult patients. Crit Care

Med. 1999;27(3):639–660.

2-    Carcillo JA, Fields AI, American College of Critical Care Medicine Task Force Committee.

Members. Clinical practice parameters for hemodynamic support of paediatric and neonatal patients in septic shock. Crit Care Med. 2002;30(6):1365–1378.

Thanks