Diagnosis and Management of Neonatal Shock

Introduction Shock is defined as a state of impaired cellular energy (ATP) synthesis when tissue oxygen delivery no longer satisfies tissue oxygen demand (Kleinman etal., 2012)

Shock is an independent predictor of early neonatal mortality and more often a problem in preterm infants than in term infants, even late preterm infants are at much higher risk (Femitha and Bhat, 2012)

In the first phase of shock, perfusion and oxygen delivery is maintained towards the so-called vital organs (heart, brain, and adrenal glands) by selective regional vasodilation in combination with vasoconstriction to non-essential tissues, such as muscles, skin, kidneys, and the splanchnic tissues. This is the compensated stage of shock. As the product of cardiac output (which falls) and systemic vascular resistance (which increases), blood pressure actually remains in the normal range in a compensated shock. When this redistribution fails, perfusion and oxygenation of the vital organs will become impaired, resulting in multi-organ dysfunction. In this phase of uncompensated shock, systemic hypotension might be expected (Willem etal., 2018)

Echocardiography is one of the emerging technologies that can be used to measure cardiac output in critically ill newborn infants, especially since the clinical estimation of cardiac output is rather inaccurate (de Boode, 2010)

Diagnosis of Shock

The clinical diagnosis of shock in the early compensated phase often depends on assessment of peripheral perfusion,pulse volume, heart rate changes, metabolic acidosis and urine output.

Ideally, shock should be diagnosed at this stage. In the later uncompensated phase, blood pressure (BP) becomes a key parameter for monitoring and for titrating inotropes and fluids Willem etal.,2018). )

Clinicians rely on BP measurements to diagnose hypotension and to titrate therapy. Hypotension in preterm infants has been associated with an increased risk of intraventricular hemorrhage (Vishnu and Plakkal, 2015)

Treatment of Shock:

1. Volume Expanders

   It is common practice to give one or two normal saline boluses when neonates present in shock, before assessing the need for inotropes.

   Apart from saline, albumin or other colloids are also sometimes used for volume expansion.

2. Drug Therapy of Neonatal Shock

Dopamine is an endogenous catecholamine and has been shown to raise the blood pressure in hypotensive infants better than either albumin or dobutamine (Osborn and Evan, 2005) Cardiac arrhythmias And extravasation injury are potential adverse effects (Osborn etal., 2004)

Dobutamine, unlike dopamine, does not have endocrine effects and does not depend on the release of endogenous catecholamines for effect. It is predominantly inotropic, with some vasodilator effects, Indeed, there is some evidence that dobutamine is better than dopamine at increasing and maintaining systemic blood flow in preterm infants with low systemicblood flow (Subhedar and Shaw, 2003).

Epinephrine is usually used when shock is refractory to dopamine and dobutamine, although some use it as a first line drug, especially when septic shock is suspected (Maria etal., 2004)

Norepinephrine use in neonates is uncommon due to its vasoconstrictive effects, resulting in organ hypoperfusion and increased myocardial work (Pierre etal., 2008)

Hydrocortisone is most commonly used in catecholamine resistant shock in treatment of hypotension in very low birth weight infants (vishnu and plakkal, 2015). Hyperglycemia can be a troublesome short-term side effect (Ng etal., 2006)

Vasopressin is a potent vasoconstrictor and useful in vasodilatory shock (Brierley etal., 2009).

Supportive Treatment:

Pulmonary Support. Most neonates with shock requiring inotropic support will also require mechanical ventilation.(especially \<28 wk) (Saugstad and Aune, 2014].

Antibiotics.

• Empirical antibiotics should be chosen based on prevailing infection patterns in each NICU (Adrienne etal., 2003)

Newer Developments in the Management of Neonatal Shock

Milrinone and amrinone are phosphodiesterase III inhibitors. they are vasodilators, hypotension can result. However, they are excellent inotropes and can also reduce pulmonary pressures (Nick etal., 2009)

Levosimendan is a newer drug which causes vasodilatation and improves calcium coupling to troponin, resulting in an increase in myocardial contractility (Papoff etal., 2012)