Shock in Neonates

Shock in Neonates

PREPARED BY
MAGED ZAKARIA
NICU RESIDENT

Neonatal Vasoregulation

 Blood pressure (BP) measures the pressure in the walls

of arteries created by the activity of the myocardium.

 This measurement consists of 2 numerical values:

1. Systole is the force exerted on the vessel wall during

the myocardium contraction.

2. Diastole is the pressure that remains on the blood

vessels when the myocardium relaxes.


 Blood pressure is affected by several factors:

1. The integrity of the myocardium.
2. The elasticity of blood vessels.

3. Blood volume.

4. Blood viscosity.

 The nervous system maintains adequate organ perfusion
through sympathetic/parasympathetic nervous system which
is necessary for hormone secretion to maintain homeostasis.


 The neonatal myocardium has unique features:

1. It lacks sarcoplasmic reticulum.

2. It has an  fibrous non-contractile tissue.

3. It possess diminished sympathetic intervention.

 These structural differences are evident in the high output and lack

of contractile reserve shown by the premature neonatal
myocardium. Consequently, the premature neonate displays a
relative tachycardia when compared with that of the term neonate.


 The Frank–Starling law states that stroke volume (and
therefore, COP) is  when the myocardium relaxes and
stretches to allow more blood to fill in the chambers during
diastole.

 The Frank–Starling law has a limited application to neonatal
physiology; because of the  amounts of fibrous non-
contractile tissue. This fibrous tissue does not have the
capacity to stretch adequately to  COP.


 When the neonate perceives a stressor, hormones

that trigger receptors to manipulate vasculature,
cardiac contraction, and smooth muscle tone are
released.

 These hormones are known as catecholamines.


 The 3 major catecholamines are:

1. Dopamine
2. Epinephrine (adrenaline)
3. Norepinephrine (noradrenaline)

 These biologically active chemical compounds are released by the
adrenal glands during times of stress.

 The following discussion will be confined to catecholamines effects
in relation to blood pressure.


 There are 4 types of receptors that accept catecholamine.

 These “acceptors” are known as α1, α2, β1, and β2

receptors.

 They are classified according to their location in the body

and the alterations elicited by stimulation.

Table 1: ɑ And β Receptors

Catecholamine
Site Action
Receptor
Smooth muscles in BVs • VC of coronary arteries
• VC of peripheral veins
α1 including mesenteric •  Smooth muscle motility/blood
BVs flow in the GI tract

• VC of coronary artery
• VC of peripheral veins
α2 Pre-postsynaptic nerve
•  Myocardial conduction velocity
terminals •  Muscle motility/blood flow in the
GI tract
•  HR
β1 Cardiac muscles
•  Contractility of the atrium
• Dilates smaller BVs
β2 • Blood vessels • Dilates hepatic artery
• Bronchi • Dilates the arteries to skeletal ms
• Bronchodilation

Clarifying Terminology

 Neonatal care does not specifically aim to avoid
hypotension but is more concerned in preventing shock.

 Shock occurs when organs experience inadequate blood
flow to meet aerobic, cellular metabolism. Cellular
oxygen requirements must be maintained for efficient
energy production, and its absence results in cellular
death.


 When the myocardium fails to produce adequate COP, or the
nervous system detects a hypoxic state, catecholamines are
released in an attempt to compensate for poor perfusion.

 This can be observed in patients who exhibit tachycardia and
yet have a stable BP.

 However, without normal COP, a normotensive state can be
maintained only for a limited amount of time.

 In fact, hypotension is a late sign of shock.


 The first phase of shock is the “compensated phase.”

 Signs include HR and UOP with no change in BP.

 It is important to understand that HR does not mean
tachycardia and UOP is not synonymous for oliguria;
both are simply deviations from the patient’s baseline.


 The second stage of neonatal shock is the
“uncompensated phase.” It is in this stage that the
blood flow to major organs becomes compromised.

 The HR remains  from the baseline, UOP continues
to , and BP  as well.


 The final stage of shock is known as the “irreversible

phase.”

 The cellular damage encountered leads to cellular

death with severe organ damage.


 A hemodynamically significant PDA in the 1st postnatal week

can cause inadequate tissue perfusion due to failure of a
compensatory  COP secondary to myocardial immaturity and
the ductal steal phenomenon, which accounts for uniform
reduction in systolic and diastolic blood pressure.

 A significant  in systolic BP occurs only when the PDA shunt

is moderate or large, yet a  in diastolic and mean BP can
occur when the shunt is small.


 The classic clinical picture of hypovolemia is that of a

baby who is pale, hypotensive and tachycardic with
very slow CRT.

 Each of these signs is non-specific for circulatory

compromise and could reflect anything from sepsis
to congenital heart disease.

Clinical Monitoring
of Systemic Hemodynamics
in Critically Sick Newborns

Clinical monitoring of hemodynamics

1. Capillary refill time (CRT) :

 The accepted upper normal time is < 3 sec.

 A study of 469 preterm and term healthy neonates at 1-7
days of age demonstrated significant site and observer
variations when CRT was measured on the
chest, forehead, palm, and heel.

 CRT is more reliable when measured on the chest but not
the forehead, palm or heel.

Strozik KS, Pieper CH and Roller J (1997): Capillary refilling time in newborn babies: normal values. Arch
Dis Child Fetal Neonatal Ed;76(3):F193–6.


 A positive predictive value of CRT for SBF was

found only when the refill time was over 6 s.

 When the refill time is this long, the clinician

generally does not need to press the skin to know
that something is wrong.

Tibby SM, Hatherill M, Murdoch IA (1999): Capillary refill and core–peripheral temperature gap as
indicators of haemodynamic status in paediatric intensive care patients. Arch Dis Child;80(2):163–6.


2. Central–peripheral temperature difference (CPTd):

 Under normal conditions, CPTd will be < 1 °C

during the 1st postnatal days in ELBW infants.

 In a thermoneutral environment (secondary to poor

peripheral perfusion in shock), peripheral VC will 

skin temperature and thus lead to an  CPTd.


 CPTd depends largely on body

temperature, environmental temperature and

the use of vasoactive drugs.

 However, no relation was observed between

CPTd and SBF or SVR.

Tibby SM, Hatherill M, Murdoch IA (1999): Capillary refill and core–peripheral temperature gap as
indicators of haemodynamic status in paediatric intensive care patients. Arch Dis Child;80(2):163–6.


3. Blood Pressure:

 Vascular resistance is increased as a
compensatory response to hypovolemia.

 So, hypotension may be a relatively late sign.


 Three different definitions of neonatal hypotension

are in widespread use:

1. BP < the 10th (or 5th) percentile of normative BP
values derived from a reference population with
regard to GA, BW and postnatal age.


2. The lower border of normal Mean BP equals the numeric
value of GA (provided no signs exist of hypoperfusion e.g.
a high serum lactate or oliguria).

For example, the lowest acceptable Mean BP for a 26 wk
neonate would be 26 mmHg.

This is only valid during the 1st 3-5 days of life, since
Mean BP  during the 1st 3 days of life with a magnitude
of 2-10 mmHg.
Nuntarumit P, Yang W and Bada-Ellzey HS (1999): Blood pressure measurements in the newborn. Clin
Perinatol;26(4):981-996.


3. Mean BP < 30 mmHg.

This is based on the assumption that cerebral

blood flow becomes pressure dependent at a

MAP around 30 mmHg.

Dammann O, Allred EN, Kuban KCK, et al. (2002): Systemic hypotension and white matter damage in
preterm infants. Dev Med Child Neurol;44(2):82-90.


 BP is not linearly related to systemic blood flow, which is

not unexpected, since BP is not only determined by
COP, but also by SVR.

 The consequence of using BP to diagnose low systemic

blood flow will be that too many patients will be
undertreated or overtreated, both with substantial risk of
adverse effects and iatrogenic damage.


 When a low Mean BP is detected; test for accuracy of the

reading.

 It is the nurse’s responsibility to ensure that the BP cuff covers

two-thirds of the extremity that is used to derive the
measurement.

 When the BP cuff is too large, the BP will be falsely low.

 Inversely, when the BP cuff is too small, the measurement will

be falsely high.


4. Heart Rate:

 Ventricular output is determined by SV and HR.

 SV is considered to be at a fixed level in neonates

without much variation. Supposing that, COP is

almost entirely dependent on HR.


  HR for compensation of COP can only be effective
when EDV is maintained.

 When the HR is too high, diastolic coronary blood
flow can be impeded due to insufficient filling time,
which might result in  contractility.

 Children have a limited reserve in HR, because of a
basic high HR.


 HR can be influenced by many factors, such as
body temperature, stress, pain, medication, etc.

 This means that a single HR value poorly
reflects systemic perfusion, but that large
changes in HR may indicate relevant changes in
COP.


5. Urine Output:

 UOP is  in shock because of  renal perfusion.

 UOP is a poor marker of circulatory failure in the absence of a
direct relationship with systemic blood flow.

 Persistent oliguria after the 2nd day of life or anuria indicates
poor renal perfusion after exclusion of congenital
malformations and administration of nephrotoxic drugs.


 Urine production may be in the normal range,

despite a compromised renal perfusion:

1. Renal tubular immaturity.

2. Septic shock with hyperglycemia (osmotic

diuresis).


 Normally, UOP changes during the 1st days of life with
an initial phase of low urine production (first 24
h), followed by a period of transient polyuria (2nd and 3rd
days of life), after which diuresis stabilizes and depends
on fluid intake.

 These physiologic changes in UOP are difficult to
differentiate from oliguria due to impaired renal
perfusion.


6. Lactate:
 There is an important difference between lactate and lactic
acid.

 Lactic acid is a strong ion, which dissociates into lactate and
H+ at the physiological pH.

 Lactate itself is not an acid. Moreover, the conversion of
pyruvate to lactate is not coupled with  H+.

 This means that hyperlactatemia is not synonymous to lactic
acidosis.


 Only when H+, cannot be recycled in the
mitochondria, hyperlactatemia results in lactic
acidosis.

 Possible causes of an  lactate production in

neonates are anaerobic metabolism (such as in
circulatory failure), 
glycogenolysis, sympathomimetic drugs and IEM.


 Blood lactate concentration is not  during

circulatory failure when lactate clearance is in

balance with lactate production and when oxygen

delivery meets the oxygen demand in the tissues by 

oxygen extraction.


 Beyond the 1st 6 hrs after birth the lactate concentration

in umbilical arterial blood of healthy infants is often <
2.5 mmol/L.

 There is a good agreement between lactate concentration

in arterial, venous and capillary blood, although the
difference between arterial and capillary lactate
concentration is  with the use of vasoactive drugs and in
sepsis.


 To differentiate between transient dysoxia and IEM in

newborns with persistent hyperlactatemia during the 1st
2 days of life, serum alanine concentration can be
measured.

 Neonates with transient hyperlactatemia did not have 

serum alanine, whereas  serum alanine turned out to be
a sensitive marker in neonates with an IEM.
Morava E, Hogeveen M, De Vries M, Ruitenbeek W, de Boode WP and Smeitink J (2006): Normal
serum alanine concentration differentiates transient neonatal lactic acidemia from an inborn error of energy
metabolism. Biol Neonate;90: 207–9.


 The predictive value of lactate as an isolated

indicator of circulatory failure is poor. When lactate

is used in conjunction with other markers of poor

perfusion it may improve the accuracy of the

identification of circulatory failure


7. Acid–base balance:

 Blood gas parameters, like pH and BE, are used

as indirect indicators of tissue acidosis.

 This is based on the assumption that metabolic

acidosis reflects tissue hypoxia secondary to

inadequate perfusion and/or oxygenation.


8. Color:

 The adequacy of peripheral perfusion and/or
oxygenation is often evaluated by clinical assessment of
the patient's color.

 An infant's color is influenced by many factors, such as

oxygenation, Hb concentration, skin temperature, skin
thickness, peripheral perfusion, race, GA, ambient
temperature and light.


 The determination of the color of newborn

infants has been proven to be very subjective

with large inter-observer variability.


9. Combination of different clinical hemodynamic

variables:

 Combination of different hemodynamic

variables can improve the predictive value for

the detection of neonatal circulatory failure.

Echocardiography

 Ventricular outputs can be assessed using Doppler

echocardiography. These outputs may reflect SBF.

 However, this is not true in the transitional

circulation, particularly in very preterm babies, in whom

shunts through the ductus arteriosus and foramen ovale

may cause ventricular output to overestimate SBF.

Echocardiography

 Because of this, the measure of superior vena cava (SVC) flow is

developed because it is not corrupted by intracardiac shunts.

 Normal SVC flow in preterm babies is 50-110 ml/kg/min.

 A low upper body blood flow is common in 1st day of life in preterm

infants < 30 weeks' gestation; this has strong correlation with
periventricular or intraventricular hemorrhage.

Echocardiography

 The other potential echocardiographic assessment of

hypovolemia is ventricular filling, which can be assessed
by left ventricular end-diastolic diameter (LVEDD).

 Normal mean LVEDD increases

from 12 mm at 26–28 weeks to

17 mm at term.

Etiology

A. Abnormal peripheral vasoregulation:

i.  or Dysregulated endothelial nitric oxide (NO)
in perinatal period, particularly in preterms

ii. Immature neurovascular pathways

iii. Pro-inflammatory cascades with vasodilation

Etiology

B. Hypovolemia may be:

1. Absolute; loss of intravascular volume.

2. Relative; vasodilatation (such as in septic shock) and

inadequate volume to fill the expanded intravascular
compartment.

 The result is inadequate filling pressure (or preload) on

the heart. If the condition is severe enough, COP will fall.

Etiology

B. Hypovolemia:

1. Placental hemorrhage (abruptio placentae, placenta
previa or delayed cord clamping).

2. Fetal-to-maternal hemorrhage (diagnosed by the
Kleihauer-Betke test of the mother's blood for fetal
erythrocytes).

3. Acute twin-to-twin transfusion (the donor twin).

4. Intracranial hemorrhage.

Etiology

5. Massive pulmonary hemorrhage (i.e. PDA).

6. DIC or other severe coagulopathies.

7. Plasma loss into the extravascular compartment, as seen
with low oncotic pressure states or capillary leak
syndrome (e.g. sepsis).

8. Excessive extracellular fluid losses, as seen with volume

depletion from IWL or inappropriate
diuresis, commonly seen in ELBW infants.

Etiology

C. Myocardial dysfunction:

1. Intrapartum asphyxia can cause poor contractility and papillary

muscle dysfunction with TR, resulting in low COP.

2. Secondary to infectious agents (bacterial or viral) or metabolic

abnormalities such as hypoglycemia.

3. Cardiomyopathy can be seen in IDMs with or without
hypoglycemia.

Etiology

4. Obstruction to blood flow resulting in  COP:
a. Inflow obstructions:

• Total anomalous pulmonary venous return.
• Cor triatriatum.
• Tricuspid or Mitral atresia.
• Acquired inflow obstructions can occur from IV air
or thrombotic embolus, or from  intrathoracic
pressure caused by high airway pressures or air-leak
syndromes (e.g. pneumothorax).

Etiology

b. Outflow obstructions:

• Pulmonary stenosis or atresia.
• Aortic stenosis or atresia.
• Hypertrophic subaortic stenosis seen in IDMs with
compromised left ventricular outflow, particularly
when cardiotonic agents are used.
• Coarctation of the aorta or interrupted aortic arch.
• Arrhythmias, if prolonged. SVT such as paroxysmal
atrial tachycardia are most common.

Treatment Options

 Correction of negative inotropic factors such as
hypoxia, acidosis, hypoglycemia, and other metabolic derangements will
improve COP.

 In clinical practice, the re-establishment of proper organ perfusion is

generally approached in a stepwise.

 The first step is to fill the vasculature by way of volume expanders.

 The second is to tighten the vasculature with the use of catecholamines.

 The final step is to compensate for the immature vasculature with steroids.

First Tier: Volume Expanders

 Fluid boluses are used only when there is physiological

evidence of external hemorrhage/fluid loss.

 An infusion of 10-20 mL/kg isotonic saline solution or

Ringer’s lactate over 30-60 min is used to treat suspected

hypovolemia if Hct ≥ 40% and cardiogenic process

unlikely.


 In previous years, clinicians have administered colloids, such as
albumin, in order to replace the intravascular loss.

 However, studies have proven that:

1. When albumin and crystalloids (normal saline) are compared in
terms of cost, availability, safety, and effective therapeutic outcome,
normal saline becomes the agent of choice for volume expansion.
2. Abnormal neurodevelopment is present in neonates who were
given albumin as compared to those given crystalloids.

Oca MJ, Nelson M and Donn SM (2003): Randomized trial of normal saline versus 5% albumin for the
treatment of neonatal hypotension. J Perinatol;23(6):473-476.

Dempsey EM and Barrington KJ (2007): Treating hypotension in the preterm infant: when and with what: a
critical and systematic review. J Perinatol;27(8):469-478.


 Unwarranted volume expansion has been linked with  mortality in
the preterm neonate population.

 Generous fluid administration in preterm infants  the likelihood
of:
1. PDA
2. NEC
3. Abnormal neurodevelopmental outcomes
4. Death.


 When endogenous or exogenous blood loss has

occurred, prompt transfusion with “whole blood” is
appropriate.

 It can be administered in aliquots of 5-10 mL/kg

over 5 min until signs of adequate perfusion are
present.

Engle WD and LeFlore JL (2002): Hypotension in the Neonate. NeoReviews;3;157


 Measurement of CVP may help fluid management, especially in term or late preterm infants. It

is measured using a catheter with its tip in the right atrium or in the intrathoracic SVC.

 Catheter can be placed through the UV or percutaneously through the EJV, IJV or subclavian

vein.

 CVP should be maintained at 5-8 mmHg. If CVP > 5-8 mmHg, additional volume will usually

not be helpful.

 CVP is influenced by other factors:

1. Noncardiac factors such as ventilator pressures

2. Cardiac factors such as tricuspid valve function

Cloherty JP, Eichenwald EC and Stark AR (2008): Manual of Neonatal Care, Lippincott Williams &
Wilkins, 6th ed.


 Hypocalcemia frequently occurs in infants with
circulatory failure, especially if they have received large
amounts of volume resuscitation.

 Calcium gluconate 10% (1 mL/kg) can be infused slowly

if ionized calcium levels are low. In this setting, calcium
frequently produces a positive inotropic response.

Wilkins, 6th ed.

Second Tier: Vasoactive Drugs (the Catecholamines)

 While volume expanders “fill the pump” vasoactive drugs “tighten
the pump” to assist the vasculature in providing blood to organ
systems.

 The administration of dopamine, dobutamine, and epinephrine act
in accordance with adrenergic receptors to mediate an alteration in
vascular tone.

 Once these receptors are stimulated, changes in blood pressure can
be observed in the form of higher Mean BP, shortened CRT,  HR,
improved oxygenation, and  UOP.

Second Tier: Vasoactive Drugs (Dopamine)

 Dopamine is an endogenous hormone synthesized and

released by the nervous tissues and adrenal medulla.

 The increase in myocardial contractility depends in part on

myocardial norepinephrine stores.

 Low dopamine dosages (0.5-5 μg/kg/min) stimulate
dopaminergic receptors, medium dosages (5-10 μg/kg/min)
stimulate the β receptors, and high dosages (≥10 μg/kg/min)
stimulate the α receptors.
Gomella TL, Cunningham MD, Eyal FG and Zenk KE (2004): Neonatology:
Management, Procedures, On-Call Problems, Diseases, and Drugs. 5th ed. Stanford, CT: McGraw-Hill.


 Exogenous dopamine activates receptors in a dose-dependent manner:

1. Low dose dopamine (0.5-2 µg/kg/min) stimulates peripheral
dopamine receptors (DA1 and DA2) and  renal, mesenteric, and
coronary blood flow with little effect on COP.

2. Intermediate dose dopamine (2-6 µg/kg/min) has positive inotropic
and chronotropic effects (β1 and β2).

3. High dose dopamine (6-10 µg/kg/min) stimulates α1 and α2
adrenergic receptors and serotonin receptors, resulting in VC and 
PVR and may  VR.

Wilkins, 6th ed.


 The established dose ranges of 2-20 μg/kg/min have been
derived from studies conducted with healthy adults.

 Interestingly, there are no recorded data regarding
administration of dopamine above 20 μg/kg/min having any
destructive effects on the neonate.
Barrington KJ (2008): Hypotension and shock in the preterm infant. Semin Fetal Neonatal Med;13:16-23.

 Higher dosages of dopamine (>20 μg/kg/min) are avoided
clinically for the theoretical concern of  COP occurring
because of VC.
Roze JC, Tohier C, Maingueneau C, Lefevre M and Mouzard A (1993): Response to dobutamine and
dopamine in the hypotensive very preterm infant. Arch Dis Child;69:59-63.


 There are very serious side effects of dopamine including:

1. Extravasation causes tissue necrosis (infusion site should
be monitored).

2. Ventricular arrhythmia, widened QRS complexes, ectopic

heartbeats

3. Vomiting

4. Hypertension.


 Dopamine receptors are also found in the hypothalamus and the

pituitary.

 If dopamine is administered on a continuous basis, the natural

balance of the hypothalamic–pituitary–adrenal axis disappears in
some patients. This results in  of thyroid hormones leading to
down-regulation of the receptors that dopamine affects. This leads
to dopamine-resistant shock.

 If this occurs, additional pharmacological agents to maintain organ

perfusion should be considered.

Second Tier: Vasoactive Drugs (Dobutamine)

 Unlike dopamine, dobutamine is not an endogenous catecholamine.

 Dobutamine have limited effect on the peripheral vasculature. It has

a greater affinity for the β receptors on the myocardium producing a
stronger left ventricular contraction. This  systemic perfusion
while  only the MAP a negligible amount.

 Dobutamine is often used with dopamine to improve COP in cases

of  myocardial function as its inotropic effects, unlike those of
dopamine, are independent of norepinephrine stores.

Second Tier: Vasoactive Drugs (Dobutamine)

 Adverse effects of dobutamine include
arrhythmias, hypertension, and VD of the capillary
in cutaneous tissue.

 Neonates may become excessively tachycardic during

dobutamine therapy; a reduction in dosage is usually
all that is required.

Second Tier: Vasoactive Drugs (Epinephrine)

 Epinephrine as a pharmacological agent  both BP and COP
by stimulating the α and β receptors.

 Like dopamine, animal studies have shown that when
epinephrine is administered at a low dose VD occurs together
with a positive inotropic action. The VC was not seen until
higher dosages.

 These data have been applied to neonatal medicine with
limited human studies.


 In clinical practice, low dose epinephrine stimulates

the β receptors causing a positive inotropic effect.

 An elevation in BP may be not seen until higher

doses which stimulate the α receptors in the

peripheral vasculature.


 Epinephrine is widely used in neonatal resuscitation

and BP management, but there have been concerns

regarding its safety concerning the peripheral VC, in

particular of the renal vasculature.

 So, it is not a first-line drug in newborns.


 Some infants who respond poorly to dopamine or

dobutamine will respond to a constant infusion of
epinephrine at a starting dose of 0.05-0.1 μg/kg/min and
can be  rapidly as needed while dopamine infusion rates
are .

 Conditions with peripheral VD involved in the circulatory

collapse, as in septic shock, may respond to epinephrine.


 Epinephrine is an effective adjunct therapy to

dopamine because cardiac norepinephrine stores are
readily depleted with prolonged and higher rate
dopamine infusions.

 Simultaneous infusions of epinephrine and
dopamine  BP and UOP in preterm neonates in a
state of shock.

Second Tier: Vasoactive Drugs (Norepinephrine)

 Norepinephrine use is limited because of its
prominent VC activity, which raises concerns about:

1. Possible ischemia

2.  Afterload

3.  Myocardial oxygen demand

4.  RBF and UOP

Dose in neonates: 20-100 nanograms (base)/kg/min IVI adjusted
according to response; max. 1 μg (base)/kg/min. BNFC 2010-11

Second Tier: Vasoactive Drugs (Milrinone)

 This phosphodiesterase III inhibitors possesses inotropic

and vasodilating properties.

 Although a major complication of their use is
hypotension, they have been used in conjunction with
other inotropic agents such as dopamine or dobutamine
in patients who have chronic CHF or septic shock in
which VC of some vascular beds is significant.

Third Tier: Steroids

 Previously therapeutic doses of vasopressor agents

may become ineffective with neonates requiring

higher doses to maintain organ perfusion

“vasopressor-resistant shock”.

Third Tier: Steroids

 Vasopressor-resistant shock has 2 etiologies:

1. Natural down-regulation of androgenic receptors with

the administration of exogenous catecholamines.

2. Neonate’s inherent adrenal insufficiency (especially

preterms) that causes a naive cortisol stress response.

Third Tier: Steroids (Glucocorticoids)

 Hydrocortisone dosage for refractory hypotension:

- 1 mg/kg/dose.

- If efficacy is noted, the dose can be repeated Q8-
12h for 2-3 days, especially if low serum cortisol
levels are documented before hydrocortisone
treatment.
Wilkins, 6th ed.


 Hydrocortisone, the synthetic version of cortisol,

compensates for the neonate’s relative state of
adrenal insufficiency.

 After administering hydrocortisone, nongenomic
and genomic responses occur.


 The immediate response (nongenomic) occur 1-2
hours after drug administration.

 Nongenomic effects assist the vasculature in 3 ways:

1. Promote hormone availability

2. Alter calcium accessibility

3. Prohibit further circulatory compromise


 Hydrocortisone promotes hormone availability
(more catecholamines available at receptor) by:

1.  Catecholamine metabolism

2. Inhibit the reuptake of catecholamines by the

sympathetic nervous system.


 During the shock state, intracellular calcium is depleted

because of  cellular metabolism.

 After 1-2 hours of hydrocortisone
administration, intracellular calcium is replenished.

 This  the threshold for the action potential, allowing for

improved myocardial contractility.


 Steroids also blunt the effects of local vasodilators, such

as nitric oxide, to prevent further circulatory
compromise.

 After nongenomic effects occur, an improvement in the

MABP is noticed. However, the patient will still require a
high doses of vasopressors to maintain organ perfusion.


 The prolonged (genomic) response occurs 8-12 hours
after hydrocortisone administration.

 It is the induction of new receptor protein synthesis
(upregulation of the adrenergic receptors).

 After this effect occurs, the vasoactive agents can be
titrated back to the initial rate before the neonate
experiences vasopressor-resistant shock.


 A double-blinded control trial results showed that

patients who were given prophylactic hydrocortisone 5
days postnatally required fewer rounds of volume
expanders and received lower dosages of vasopressors.

 These cardiovascular effects were not associated with

adverse effects of steroids such as hyperglycemia and risk
of infection.
Ng PC, Lee CH, Bnur FL, et al. (2006): A double-blind, randomized, controlled study of a “stress dose” of
hydrocortisone for rescue treatment of refractory hypotension in preterm infants. Pediatrics;117:367-375


 While these findings look promising, a recent

Cochrane Review was unable to comment on the
safety and efficacy of steroid administration in the
hypotensive neonate because of a lack of associated
research.

Subhedar NV, Duffy K and Ibrahim H (2007): Corticosteriods for treating hypotension in preterm infants.
Cochrane Database Syst Rev;(1):CD003662. http://www. cochrane.org/reviews/en/ab003662.html.

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