INTRODUCTION — Shock is a dynamic and unstable pathophysiologic state characterized by inadequate tissue perfusion. Although the effects of inadequate perfusion are reversible initially, prolonged hypoperfusion and tissue hypoxia can disrupt critical biochemical processes, which, if not addressed, result in cell death, end-organ failure, and, possibly, death.
The classification and underlying mechanisms of neonatal shock are the same as those seen in pediatric and adult shock. However, the etiology, clinical manifestations, and initial management of neonatal shock differ somewhat from shock in other populations. (See "Initial evaluation of shock in children" and "Definition, classification, etiology, and pathophysiology of shock in adults".)
The management of neonatal shock will be reviewed here. The etiology, clinical presentation, and evaluation of neonatal shock and the management of asymptomatic hypotension in extremely preterm neonates are discussed separately. (See "Neonatal shock: Etiology, clinical manifestations, and evaluation" and "Assessment and management of low blood pressure in extremely preterm infants".)
DEFINITION — Shock, or circulatory failure, is defined as a physiologic state characterized by tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization. It is manifested by physical findings of tissue hypoperfusion (eg, cold extremities, acrocyanosis, and poor capillary refill), tachycardia, and metabolic acidosis. Shock is often initially reversible, but must be recognized and treated immediately to prevent progression to irreversible organ dysfunction.
The causes of neonatal shock are classified into four pathophysiologic mechanisms (table 1):
However, neonatal shock may be the result of more than one of these processes (multifactorial shock). When the underlying mechanism is unclear or unknown, the term "undifferentiated shock" is used. (See "Neonatal shock: Etiology, clinical manifestations, and evaluation", section on 'Etiologic classification'.)
It is important to recognize that hypotension, which is commonly used to define shock states in adults, is generally a late finding of shock in neonates. Of note, blood pressure (BP) values vary considerably depending on gestational age (GA) and postnatal age (figure 1), particularly for extremely preterm (EPT) infants born <28 weeks GA (figure 2). As such, defining hypotension in this population is challenging . The definition of hypotension in EPT infants is discussed in greater detail separately. (See "Assessment and management of low blood pressure in extremely preterm infants", section on 'Definitions'.)
INITIAL STABILIZATION — Successful management of neonatal shock requires rapid intervention to restore perfusion regardless of the underlying etiology . During the initial stabilization, evaluation to determine the etiology should occur concomitantly in order to best direct subsequent therapy (algorithm 1).
Respiratory support — The infant's airway and respiratory status should be assessed and stabilized, including administration of supplemental oxygen and/or mechanical ventilation. Neonates in shock often require endotracheal intubation and mechanical ventilation due to respiratory distress and/or apnea. (See "Overview of mechanical ventilation in neonates".)
Vascular access — Vascular access should be established and blood samples obtained for initial testing. If feasible, a central line should be placed for frequent blood drawing, durable vascular access, and administration of vasoactive agents. Arterial access for invasive BP monitoring should also be considered, though this is not always necessary and placement of peripheral arterial lines can be challenging in neonates with poor perfusion. (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies", section on 'Umbilical vein access'.)
Ongoing diagnostic evaluation — A focused diagnostic evaluation is performed concomitantly with the resuscitation, including:
●Brief review of the history
●Focused physical examination
●Basic laboratory tests (electrolytes, blood gas, complete blood count, lactate, blood culture, renal and liver function tests, and type and cross)
●Chest radiograph if respiratory symptoms are present
The diagnostic evaluation is discussed in greater detail separately. (See "Neonatal shock: Etiology, clinical manifestations, and evaluation", section on 'Diagnostic evaluation'.)
Fluid resuscitation — An initial intravenous (IV) fluid bolus of isotonic crystalloid (eg, normal saline or Ringer's lactate) is appropriate for most neonates presenting with shock. Normal saline is the most commonly administered isotonic fluid in neonates .
The volume of fluid and rate of administration vary depending on the suspected underlying etiology and the gestational age:
●Hypovolemic shock – Infants with hypovolemic shock due to acute blood loss generally require a large amount of fluid given fairly quickly. We generally start with 20 mL/kg of normal saline over 15 minutes. Additional isotonic crystalloid and/or blood transfusion may be necessary, as discussed below. (See 'Assess need for further fluid resuscitation' below and 'Acute blood loss' below.)
●Septic/distributive shock – For neonates with suspected septic or distributive shock, we suggest an initial fluid bolus of 10 to 20 mL/kg of isotonic crystalloid. In our center, we typically start with 20 mL/kg of normal saline given over 15 to 30 minutes. Other centers may begin with smaller boluses (eg, 5 to 10 mL/kg) and/or administer the bolus more slowly. (See 'Assess need for further fluid resuscitation' below.)
●Cardiogenic shock – Fluid bolus may not improve perfusion in patients with cardiogenic shock and in some cases may cause clinical deterioration. (See 'Cardiac disease' below.)
●Undifferentiated shock – For neonates in whom the etiology of shock is uncertain, it is reasonable to administer an initial fluid bolus of 10 to 20 mL/kg and monitor carefully for signs of fluid responsiveness (ie, improved perfusion) or clinical deterioration. (See 'Monitoring' below and 'Assess need for further fluid resuscitation' below.)
●Caution in extremely preterm infants – Fluid boluses should be administered cautiously in extremely preterm infants (gestational age <28 weeks) as rapid fluid administration exceeding 30 ml/kg is associated with an increased risk of intraventricular hemorrhage and death in this population [4-6]. (See "Germinal matrix hemorrhage and intraventricular hemorrhage (GMH-IVH) in the newborn: Pathogenesis, clinical presentation, and diagnosis", section on 'Additional risk factors'.)
Further fluid resuscitation is generally dependent on the type of shock and is discussed below. (See 'Assess need for further fluid resuscitation' below.)
Empiric antimicrobial therapy — Prompt administration of empiric IV antibiotics is appropriate for all neonates presenting with shock after blood cultures are obtained because sepsis is the most common cause of neonatal shock. If there is clinical suspicion for herpes simplex virus (HSV) infection, the empiric antimicrobial regimen should include acyclovir.
●Antibiotic therapy – Pending culture results, the empiric antibiotic regimen should include agents active against organisms that most commonly cause neonatal sepsis (group B streptococcus and Escherichia coli). The combination of ampicillin and gentamicin provides appropriate empiric coverage for these organisms until culture results are available. Local antibiotic resistance patterns should also be considered. Empiric regimens used in term infants are summarized in the table (table 2). Treatment of neonatal sepsis in term and preterm infants is discussed in greater detail separately. (See "Management and outcome of sepsis in term and late preterm neonates", section on 'Initial empiric therapy' and "Treatment and prevention of bacterial sepsis in preterm infants <34 weeks gestation", section on 'Empiric antibiotic therapy'.)
●Antiviral therapy – Disseminated HSV is another common cause of neonatal shock. When there is clinical suspicion for neonatal HSV infection, empiric acyclovir therapy should be administered after appropriate viral testing is performed. The evaluation and treatment of neonatal HSV infection are discussed separately. (See "Neonatal herpes simplex virus infection: Clinical features and diagnosis", section on 'Evaluation and diagnosis' and "Neonatal herpes simplex virus infection: Management and prevention", section on 'Initial antiviral therapy'.)
Other interventions — Other physiologic disturbances may occur in neonates with shock, and if present, should be promptly corrected. These may include:
●Abnormal glucose levels – Glucose levels should be monitored and both hyper- or hypoglycemia should be corrected. (See "Management and outcome of neonatal hypoglycemia" and "Neonatal hyperglycemia", section on 'Management'.)
●Hypothermia. (See "Neonatal resuscitation in the delivery room", section on 'Temperature control'.)
●Electrolyte disturbances. (See "Fluid and electrolyte therapy in newborns".)
●Thrombocytopenia. (See "Neonatal thrombocytopenia: Clinical manifestations, evaluation, and management", section on 'Management'.)
●Coagulopathy. (See "Disseminated intravascular coagulation in infants and children", section on 'Management'.)
●Tension pneumothorax. (See "Pulmonary air leak in the newborn", section on 'Thoracentesis'.)
ONGOING GOAL-DIRECTED THERAPY — After the initial stabilization, ongoing management may include (algorithm 1):
●Ongoing assessment of fluid status and administration of additional fluid boluses as needed (see 'Assess need for further fluid resuscitation' below)
●Administration of vasoactive medications to support cardiac output (CO) and/or improve vascular tone (see 'Vasoactive agents' below)
●Administration of hydrocortisone in neonates with refractory shock and/or suspected adrenal insufficiency (see 'Hydrocortisone' below)
●Interventions targeting the suspected underlying cause (see 'Interventions for suspected etiologies' below)
Goals — The goal of the initial stabilization and ongoing management is to restore tissue perfusion. This is generally based on targeting improvements in physiologic parameters. However, some physiologic indicators may be less reliable in neonates due to the relative immaturity of the cardiovascular and nervous systems, technical challenges with invasive monitoring, and challenges of establishing intravenous (IV) access and obtaining blood samples in compromised neonates.
Nevertheless, we utilize the following physiological indicators to establish the goals of therapy and to monitor response to therapeutic interventions:
●Improvement in heart rate (HR):
•Decrease in HR for patients who are tachycardic (HR >180 beats per minute)
•Increase in HR for patients who are bradycardic (HR <90 beats per minute)
●Improvement in peripheral perfusion:
•Improving color and warmth of distal extremities
•Decreasing time for capillary refill
●Increase in blood pressure (BP) for neonates with hypotension (figure 2 and figure 1). The goal is to increase the BP to values observed before the onset of shock at a rate of 5 to 10 mmHg over several hours. A greater accelerated rate of rise in BP in preterm infants is associated with an increased risk of intraventricular hemorrhage (IVH). (See "Germinal matrix hemorrhage and intraventricular hemorrhage (GMH-IVH) in the newborn: Pathogenesis, clinical presentation, and diagnosis".)
●Resolution of metabolic acidosis – Evidence of resolving metabolic acidosis based on point-of-care testing as follows:
•Increase in blood pH
•Increase in serum/plasma bicarbonate level
•Decrease in serum/plasma lactate
●Improvement in neurologic status – Increased neurologic activity based on increased movement including facial expression (grimace), which is either spontaneous or in response to stimulation.
Although we use these specific parameters, it is important to recognize that they are evaluated together to provide an assessment of the infant's global condition. So for example, if we reach the BP goal but there are persistent signs of poor perfusion and elevated lactate levels, it is reasonable to assume that the chosen BP goal is not adequate and further intervention is warranted.
Similarly, escalation of intervention is not necessary, even when the BP goal has not been attained but the infant seems to be improving based on the other parameters (normalization of lactate levels and improved perfusion and neurologic examination).
Monitoring — The management of neonatal shock requires close monitoring and observation of the following parameters to assess the hemodynamic status of the neonate:
●Continuous HR and pulse oximetry monitoring.
●Frequent BP monitoring (either continuously via an arterial line or non-invasive cuff measurements every 15 to 30 minutes).
●Clinical observation and assessment every one to two hours to evaluate changes in perfusion.
●Blood gas monitoring every three to four hours.
●Urine output recorded at least every four hours.
●Electrolyte levels, complete blood counts, and coagulation studies measured several times per day.
The physiologic targets listed above (see 'Goals' above) should be assessed before and after each intervention to guide further management. In some cases, the infant's response to specific interventions may be helpful in identifying the underlying etiology (eg, clinical deterioration after fluid resuscitation may point to a primary cardiac etiology).
Since BP is not a reliable indicator of perfusion of critical organs (particularly the brain) in neonates, near-infrared spectroscopy (NIRS) has been proposed as a potentially more informative tool for monitoring perfusion [7-10]. NIRS measures blood flow and oxygenation to specific vital organs including the brain, gastrointestinal tract, and kidneys. Some studies have suggested that NIRS may be a useful tool for perioperative monitoring in neonates undergoing surgery for congenital heart disease (CHD) [11,12]. NIRS has also been used to monitor perfusion in preterm infants in the immediate postnatal period [7,8]. However, reliable data on its use for infants with neonatal shock are limited and insufficient. As a result, additional studies are needed before NIRS can be recommended for routine clinical use.
Assess need for further fluid resuscitation — Following the initial stabilization, ongoing assessment of the patient's volume status determines whether additional fluid boluses should be given. The response to initial fluid administration may vary depending on the underlying mechanism of shock (eg, hypovolemic, distributive, cardiogenic, or obstructive). (See "Neonatal shock: Etiology, clinical manifestations, and evaluation", section on 'Etiologic classification'.)
●Patients with hypovolemic and distributive shock generally respond well to fluid administration unless there is concomitant cardiac dysfunction. Additional fluid boluses are often required, which are given as 10 to 20 mL/kg of isotonic crystalloid solutions (eg, normal saline or Ringer's lactate) administered over 15 to 20 minutes. Normal saline is the most commonly administered isotonic fluid in neonates .
The patient's clinical response should be reassessed after each bolus (see 'Monitoring' above). Additional fluid should be given until the goals of therapy are reached or signs of fluid overload develop (eg, rales, worsening respiratory distress, increasing ventilator requirements, and hepatomegaly).
•In patients with distributive shock (eg, septic shock), 20 to 30 mL/kg of isotonic fluid is typically adequate for restoring intravascular blood volume. If the neonate has ongoing signs of shock despite adequate volume expansion, vasopressor therapy should be initiated (see 'Vasoactive agents' below). Excessive fluid administration (>30 mL/kg) in preterm infants is associated with an increased risk of death and IVH [4-6]. (See "Germinal matrix hemorrhage and intraventricular hemorrhage (GMH-IVH) in the newborn: Pathogenesis, clinical presentation, and diagnosis".)
•In patients with hypovolemic shock, greater volumes of isotonic fluid and/or blood products may be needed before there is a clear improvement in hemodynamic status. (See 'Acute blood loss' below.)
●In patients with cardiogenic shock, fluid boluses may not improve perfusion. Volume expansion may in fact cause the neonate to deteriorate due to fluid overload (eg, rales, worsening respiratory distress, increasing ventilator requirements, and hepatomegaly) . In these patients, additional fluid therapy should be avoided. When a cardiac etiology of shock is suspected, prompt echocardiography is essential to assess cardiac function and identify the underlying etiology. Prostaglandin E1 therapy should be initiated (even prior to echocardiography results) if there is strong clinical concern for ductal-dependent CHD (table 3). (See 'Cardiac disease' below and "Diagnosis and initial management of cyanotic heart disease in the newborn", section on 'Prostaglandin E1'.)
●In patients with obstructive shock, volume expansion helps to maintain CO by improving preload. However, therapy should focus on urgent correction of the underlying cause (eg, needle or chest tube thoracostomy for tension pneumothorax or pericardiocentesis for cardiac tamponade) as the neonate's hemodynamic status is unlikely to improve if the cause of the obstruction is not addressed. (See "Pulmonary air leak in the newborn", section on 'Management'.)
Vasoactive agents — Vasoactive agents are used to support neonates with distributive shock who have not improved with initial fluid resuscitation and those with cardiogenic shock who have ongoing ventricular dysfunction despite addressing reversible causes (eg, hypoxia, arrhythmia, hypothermia). Vasopressor therapy has little role in the management of patients with purely hemorrhagic or hypovolemic shock and may be harmful in this setting.
Commonly used vasoactive agents include dopamine, epinephrine, dobutamine, and milrinone. For neonates with distributive shock, we generally prefer dopamine based on greater clinical experience and familiarity with its use. There is less experience with epinephrine, and its pharmacologic properties are less well understood in neonates compared with older patients. The available clinical trial data suggest that dopamine and epinephrine have comparable efficacy, though epinephrine may be associated with more tachycardia and hyperglycemia [14,15]. The pharmacologic properties of these agents and their use in older children and adults are discussed in greater detail separately. (See "Use of vasopressors and inotropes" and "Initial management of shock in children", section on 'Vasoactive agents'.)
The pharmacokinetics of the various vasopressor agents are more variable in neonates compared with older patients and it is challenging to accurately predict the effects of these medications on CO, HR, and systemic vascular resistance (SVR).
●Dopamine – Dopamine is commonly used as a first line agent for both distributive and cardiogenic shock because its effects are both inotropic (ie, it increases CO, which is the predominant effect at doses of 5 to 10 mcg/kg per min) and vasoconstrictive (ie, it increases SVR, which is the predominant effect at doses >10 mcg/kg per min). Dopamine is infused beginning at a rate of 5 mcg/kg per min with titration up to a maximum of 15 mcg/kg per min based on the infant's clinical response. Careful titration is necessary because the response to the drug and its clearance can be unpredictable in neonates [14,16-19]. Some studies suggest dopamine can have a negative impact on CO due to an imbalance in vasopressor/inotrope activity [16-18]. Limited data suggest gestational and postnatal ages have little effect on dopamine pharmacokinetics . In addition, plasma dopamine concentration cannot be predicted accurately from the dopamine infusion rate. Dopamine clearance is reduced in patients with renal or hepatic failure.
●Epinephrine – Epinephrine is a potent inotrope and at higher doses increases SVR. It is most commonly used as a second-line agent for distributive shock or as a first-line inotrope for severe cardiogenic shock. There are conflicting data on whether it is associated with more transient adverse effects compared with dopamine [14,15]. Epinephrine is started at a rate of 0.05 mcg/kg/min and titrated up in increments of 0.01 mcg/kg/min based on response to a maximum of 1 mcg/kg per min based on the infant's clinical response.
●Dobutamine – Dobutamine is an inotrope that increases CO via improved myocardial contractility and increased HR. Dobutamine is an appropriate first-line agent for cardiogenic shock because of its inotropic properties. The impact of dobutamine on BP is highly variable in neonates, as it may increase BP, lower BP, or have little effect on BP [19,21]. In neonates, drug clearance is variable  and dobutamine appears to have a greater ability to increase CO compared with dopamine [23-25]. Dobutamine infusion begins at a rate of 5 mcg/kg per min with titration up to a maximum of 20 mcg/kg per min based on the infant's clinical response.
●Milrinone – Milrinone is a phosphodiesterase enzyme inhibitor that has inotropic and vasodilatory effects (ie, it increases CO and reduces SVR). Its use in neonatal shock is generally limited to neonates with confirmed cardiac disease and it should only be given in consultation with a pediatric cardiologist after obtaining an echocardiogram. There is limited dosing information available for neonates. The response to this agent is unpredictable in neonates and it frequently causes hypotension [26,27]. (See "Heart failure in children: Management", section on 'Milrinone'.)
Hydrocortisone — For neonates with distributive or cardiogenic shock that is refractory to fluid resuscitation and vasopressor therapy, we suggest administering hydrocortisone [28,29].
For infants with known or suspected adrenal insufficiency based on clinical findings (eg, ambiguous genitalia), hydrocortisone should be administered at an earlier stage in the management, if possible.
Hydrocortisone is given at an initial dose of 1 mg/kg IV. If there is a clinical response (rise in BP, weaning of vasopressors, and overall clinical improvement) within six to eight hours, it is generally continued at a dose of 0.5 to 1 mg/kg IV every eight hours. Hydrocortisone should be discontinued or weaned as the patient's condition improves, ideally within five days. (See 'Suspected adrenal insufficiency' below.)
This practice is supported by observational studies and a few small randomized trials that suggest hydrocortisone may reduce the need for vasopressor therapy and shorten the duration of shock [28,30]. A reduction in mortality or long-term outcome has not been demonstrated.
Interventions for suspected etiologies
Cardiac disease — Cardiac disease may be suspected on the basis of any of the following:
●Physical findings (eg, murmur, gallop, weak or absent femoral pulses)
●Cyanosis that does not improve with administration of 100 percent oxygen
●Differential in pre- and postductal oxygen saturation
●Clinical deterioration with fluid administration
●Abnormal rhythm on cardiac monitor
●Abnormal chest radiograph (eg, cardiomegaly, pulmonary edema)
If a cardiac etiology is suspected, additional interventions depend on the nature of the suspected cardiac problem (structural versus arrhythmia). Treatment decisions should generally be made in consultation with a pediatric cardiologist.
If there is strong clinical suspicion for ductal-dependent congenital heart disease (CHD) (table 3), prompt administration of prostaglandin E1 (alprostadil) is warranted. The typical starting dose is 0.01 mcg/kg per minute IV. Deterioration of the clinical status after starting prostaglandin E1 usually indicates the presence of rare congenital cardiac defects associated with pulmonary venous or left atrial obstruction. Echocardiography should be performed as soon as is possible to assess cardiac anatomy and function. The diagnosis and initial management of suspected ductal-dependent CHD is discussed in detail separately. (See "Diagnosis and initial management of cyanotic heart disease in the newborn".)
For neonates with arrhythmia:
●Bradycardia – Many preterm infants have transient apneic/bradycardic events that resolve spontaneously or with tactile stimulation or an increase in respiratory support. Neonates with persistent bradycardia should receive epinephrine or atropine (if atrioventricular [AV] block is present) and cardiac compressions according to standard resuscitation algorithms (algorithm 2). Rarely, persistent bradycardia may require subsequent cardiac pacing. A pediatric cardiologist should be consulted promptly if the etiology of bradycardia is thought to be a primary cardiac rhythm disturbance (eg, congenital heart block). (See "Bradycardia in children", section on 'Acute management of patients with poor perfusion' and "Congenital third degree (complete) atrioventricular block", section on 'Treatment'.)
●Supraventricular tachycardia (SVT) – Patients with persistent SVT should be treated with initially with vagal maneuvers, followed by adenosine (0.1 mg/kg/dose via rapid IV injection), or synchronized cardioversion (0.5 to 1 Joules/kg) (algorithm 3). (See "Management of supraventricular tachycardia (SVT) in children", section on 'Unstable patients'.)
●Ventricular tachycardia – Patients with sustained ventricular tachycardia (VT) should undergo synchronized cardioversion (algorithm 3). Urgent consultation with pediatric cardiology is recommended for any neonate with sustained VT. (See "Management and evaluation of wide QRS complex tachycardia in children", section on 'Unstable patient'.)
Septic shock — The mainstays of therapy for septic shock consist of the interventions discussed above (ie, prompt administration of empiric antibiotics [and acyclovir if there is concern for HSV], fluid resuscitation, vasopressor support if shock persists despite fluid administration, and hydrocortisone for shock refractory to fluid resuscitation and vasopressors). (See 'Empiric antimicrobial therapy' above and 'Fluid resuscitation' above and 'Vasoactive agents' above and 'Hydrocortisone' above.)
For patients with persistent or worsening septic shock despite these interventions, additional measures may include the following, which generally should be undertaken in consultation with an infectious disease specialist:
●Broadening the antimicrobial coverage (eg, adding vancomycin if not already part of the empiric regimen, adding meropenem if there is concern for a multidrug-resistant gram-negative organism, and adding coverage for fungal pathogens such as Candida). (See "Treatment of Candida infection in neonates", section on 'Invasive infection' and "Neonatal herpes simplex virus infection: Management and prevention".)
●Addressing any focal sources of infection, including removing a central line if it is suspected to be the source of infection, and evaluating for intra-abdominal pathology (eg, necrotizing enterocolitis, abscess, or malrotation with midgut volvulus), septic joint, osteomyelitis, or endocarditis. (See "Treatment and prevention of bacterial sepsis in preterm infants <34 weeks gestation", section on 'Source control'.)
The management of neonatal sepsis and neonatal HSV are discussed in greater detail separately. (See "Management and outcome of sepsis in term and late preterm neonates" and "Treatment and prevention of bacterial sepsis in preterm infants <34 weeks gestation" and "Neonatal herpes simplex virus infection: Management and prevention".)
Acute blood loss — For neonates with significant blood loss, red blood cell (RBC) transfusion can be life-saving. In life-threatening circumstances, any available RBC product that is compatible with the infant's blood type can be administered. Additional details on RBC transfusion, including indications and selection of products, are provided in a separate topic review. (See "Red blood cell (RBC) transfusions in the neonate".)
In addition to resuscitative measures, the source of bleeding should be identified if it is not readily apparent. Subgaleal hemorrhage usually can be diagnosed clinically but detection of intracranial hemorrhage requires cranial ultrasonography. (See "Neonatal birth injuries", section on 'Subgaleal hemorrhage' and "Germinal matrix hemorrhage and intraventricular hemorrhage (GMH-IVH) in the newborn: Pathogenesis, clinical presentation, and diagnosis", section on 'Cranial ultrasound' and "Neonatal birth injuries".)
Ultrasonography can also detect bleeding into the abdomen or kidney. A positive test for fetal cells in a sample of maternal blood can be indicative of fetomaternal hemorrhage as a cause for hypovolemic shock . (See "Spontaneous massive fetomaternal hemorrhage", section on 'Kleihauer-Betke assay'.)
Suspected adrenal insufficiency — Adrenal insufficiency due to impaired synthesis or release of adrenocortical hormones may cause or contribute to shock.
●Primary adrenal insufficiency (eg, congenital adrenal hyperplasia [CAH]) may be suspected based on the physical finding of ambiguous genitalia and laboratory findings of hyperkalemia, hyponatremia, and hypoglycemia.
●Secondary or relative adrenal insufficiency may be suspected in patients with refractory shock (ie, failure to respond to fluid resuscitation and vasoactive agents).
In both settings, intravenous hydrocortisone is administered. (See 'Hydrocortisone' above.)
CAH is discussed in further detail separately. (See "Clinical manifestations and diagnosis of classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency in infants and children" and "Treatment of classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency in infants and children".)
Undifferentiated shock — In some cases, the underlying etiology remains uncertain. Continued general support including fluid therapy, vasopressor support, and ongoing antimicrobial therapy is provided while further diagnostic evaluation is pursued. In addition, we suggest hydrocortisone for infants who remain refractory to supportive measures. (See 'Assess need for further fluid resuscitation' above and 'Vasoactive agents' above and 'Empiric antimicrobial therapy' above and 'Hydrocortisone' above.)
The patient's status should be reevaluated frequently with clinical assessments and repeat laboratory testing. If physiologic or laboratory abnormalities are identified (eg, fever, hypothermia, electrolyte derangements, hypoglycemia, coagulopathy), they should be addressed promptly since these findings can contribute to the ongoing shock state. (See 'Monitoring' above and 'Other interventions' above.)
Additional evaluation is discussed separately and may include (see "Neonatal shock: Etiology, clinical manifestations, and evaluation", section on 'Additional selective testing'):
●Echocardiography to assess cardiac anatomy and function
●Abdominal imaging to assess for necrotizing enterocolitis
●Cranial ultrasound to assess for intracranial hemorrhage
●Lumbar puncture (if clinical status permits) to assess for meningitis
SEVERE REFRACTORY SHOCK — In some centers, extracorporeal membrane oxygenation (ECMO) may be offered to patients who have ongoing severe shock despite maximal medical management, including aggressive fluid management and inotropic support. Although there is some variability among institutions with ECMO capability, general requirements include the following:
●Birth weight >1800 g.
●Postmenstrual age >34 weeks.
●Reversible lung disease without an anticipated need for prolonged mechanical ventilation.
●No evidence of cyanotic congenital heart disease (CHD), although ECMO may be used in the perioperative period to support neonates with CHD.
●No other conditions that would be considered contraindications to ECMO, including multiple organ system failure; contraindications to full anticoagulation (eg, coagulopathy, grade 2 or greater intracranial hemorrhage); massive cerebral edema; irreversible pulmonary or cardiac disease; or multiple congenital anomalies.
SUMMARY AND RECOMMENDATIONS
●Initial stabilization – Successful management of neonatal shock requires rapid intervention to restore perfusion regardless of the underlying etiology. During the initial stabilization, evaluation to determine the etiology should occur concomitantly in order to best direct subsequent therapy (algorithm 1). Initial stabilization includes (see 'Initial stabilization' above):
•Providing appropriate respiratory support (see "Overview of mechanical ventilation in neonates")
•Obtaining vascular access (see "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies", section on 'Umbilical vein access')
•Ongoing diagnostic evaluation (see "Neonatal shock: Etiology, clinical manifestations, and evaluation", section on 'Diagnostic evaluation')
•Administering a fluid bolus (20 mL/kg isotonic crystalloid over 10 to 15 minutes) (see 'Fluid resuscitation' above)
•Administering empiric antimicrobials (see 'Empiric antimicrobial therapy' above and "Management and outcome of sepsis in term and late preterm neonates", section on 'Initial empiric therapy')
•Addressing any correctable abnormalities noted on the initial evaluation (see 'Other interventions' above)
●Monitoring response to therapy – The neonate should be assessed before and after each intervention to guide further management. In some cases, the infant's response to an intervention may help identify the underlying etiology (eg, clinical deterioration after fluid resuscitation may point to a primary cardiac etiology). The following physiologic indicators are used to monitor the response to therapy (see 'Monitoring' above and 'Goals' above):
•Improvement in heart rate
•Improvement in the quality of central and peripheral pulses
•Improvement of skin perfusion
•Improved acid-base balance (resolving metabolic acidosis, decreasing lactate level)
•Improvement in neurologic status (grimace, spontaneous movement, response to stimulation, presence of normal newborn reflexes)
•Rise in blood pressure if hypotensive
●Ongoing management – After the initial stabilization, ongoing management includes (algorithm 1) (see 'Ongoing goal-directed therapy' above):
•Fluid therapy – The fluid status should be reassessed frequently and additional fluid boluses given as needed until goals of therapy are reached or signs of fluid overload develop. (See 'Assess need for further fluid resuscitation' above.)
•Vasoactive medications – Vasoactive medications are used to support cardiac output and/or improve vascular tone in patients with persistent shock despite adequate fluid resuscitation. For most neonates with distributive shock, we suggest dopamine as the initial vasopressor agent rather than epinephrine (Grade 2C). This is based largely on greater experience with dopamine in this setting. Both agents appear to have comparable efficacy. For patients with cardiogenic shock, dobutamine, dopamine, and epinephrine are all reasonable choices for inotropic support. Milrinone is also a reasonable choice, but it frequently causes hypotension, and therefore it generally should be used in consultation with a cardiologist. (See 'Vasoactive agents' above.)
•Hydrocortisone – For neonates with persistent distributive or cardiogenic shock that is refractory to fluid resuscitation and vasopressor therapy, we suggest administering hydrocortisone (Grade 2C). Hydrocortisone should be administered at an earlier stage in the management if the infant has known or suspected primary adrenal insufficiency based on clinical findings (eg, ambiguous genitalia). (See 'Hydrocortisone' above.)
●Additional interventions – Additional interventions may be warranted depending on the underlying etiology (see 'Interventions for suspected etiologies' above):
•Suspected structural cardiac disease – If there is strong clinical suspicion for ductal-dependent congenital heart disease (CHD) (table 3), prostaglandin E1 (alprostadil) should be started promptly. Echocardiography should be performed as soon as is possible to assess cardiac anatomy and function. (See "Diagnosis and initial management of cyanotic heart disease in the newborn", section on 'Prostaglandin E1'.)
•Arrhythmia – Supraventricular or ventricular tachyarrhythmias associated with acute hemodynamic instability should be converted without delay (algorithm 3). Bradycardia should be treated with epinephrine or atropine according to standard resuscitation algorithms (algorithm 2). A pediatric cardiologist should be consulted promptly if the etiology of bradycardia is thought to be a primary cardiac rhythm disturbance (eg, congenital heart block). (See "Management of supraventricular tachycardia (SVT) in children" and "Management and evaluation of wide QRS complex tachycardia in children" and "Congenital third degree (complete) atrioventricular block".)
•Refractory septic shock ‒ For patients with persistent or worsening septic shock despite administration of empiric antimicrobials, fluid resuscitation, vasopressor support, and hydrocortisone, additional measures may include broadening antimicrobial coverage and addressing any focal source of infection. (See 'Septic shock' above and "Management and outcome of sepsis in term and late preterm neonates" and "Treatment and prevention of bacterial sepsis in preterm infants <34 weeks gestation".)
•Acute blood loss – For neonates with significant blood loss, red blood cell (RBC) transfusion can be life-saving. In life-threatening circumstances, any available RBC product that is compatible with the infant's blood type can be administered. (See "Red blood cell (RBC) transfusions in the neonate".)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Lisa Adcock, MD, who contributed to an earlier version of this topic review.
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10 : Investigation of the Pattern of the Hemodynamic Response as Measured by Functional Near-Infrared Spectroscopy (fNIRS) Studies in Newborns, Less Than a Month Old: A Systematic Review.
11 : Near-infrared spectroscopy: what we know and what we need to know--a systematic review of the congenital heart disease literature.
12 : Perioperative Near-Infrared Spectroscopy Monitoring in Neonates With Congenital Heart Disease: Relationship of Cerebral Tissue Oxygenation Index Variability With Neurodevelopmental Outcome.
14 : Epinephrine versus dopamine in neonatal septic shock: a double-blind randomized controlled trial.
15 : Dopamine versus epinephrine for cardiovascular support in low birth weight infants: analysis of systemic effects and neonatal clinical outcomes.
17 : Randomized trial of dobutamine versus dopamine in preterm infants with low systemic blood flow.
22 : Pharmacokinetic study (phase I-II) of a new dobutamine formulation in preterm infants immediately after birth.
24 : Hemodynamic and metabolic effects of a new pediatric dobutamine formulation in hypoxic newborn pigs.
25 : Randomized, blind trial of dopamine versus dobutamine for treatment of hypotension in preterm infants with respiratory distress syndrome.
26 : Dosing of Milrinone in Preterm Neonates to Prevent Postligation Cardiac Syndrome: Simulation Study Suggests Need for Bolus Infusion.
27 : Randomized trial of milrinone versus placebo for prevention of low systemic blood flow in very preterm infants.
28 : Hemodynamic changes after low-dosage hydrocortisone administration in vasopressor-treated preterm and term neonates.
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