Showing posts with label Shock. Show all posts
Showing posts with label Shock. Show all posts

Management of Shock in Pediatric

Airway and breathing
The resuscitation mantra of Airway, Breathing, Circulation or ‘ABC’ remains the management priority in the shocked child as in any other. Before assessment of the nature or severity of shock can be made, the clinician must ensure that the airway is patent and that the patient is breathing adequately without assistance. If this is not so then appropriate steps should be taken to stabilise the airway and ensure adequate breathing.

Intubation and judicious positive pressure ventilation can benefit the shocked child when significant myocardial dysfunction exists and will reduce oxygen consumption caused by increased work of breathing. High flow oxygen should be administered via a facemask with a reservoir bag to maximise oxygen concentration. The shocked child must not be allowed to become hypoxic by the omission of a simple treatment such as oxygen therapy.

As the airway and breathing are being managed, the following monitoring should take place:
• Pulse oximetry
• 3 lead electrocardiogram monitoring
• Blood pressure

Circulation
The clinician should pay particular attention to:
• Pulse rate, rhythm and volume
• Peripheral skin color, temperature, capillary refill time, rashes
• Respiratory rate and work of breathing
• Signs of cardiac failure
• Neurological state
• Signs of injury that might have caused hemorrhage (limb fracture, abdominal trauma, head trauma)
• Urine output

Whilst relatively uncommon in children, the presence of cardiac dysrhythmia associated with shock will require immediate management. Vascular access should be achieved as quickly as possible. At least one, but preferably two, large-bore venous cannule should be sited. If poor perfusion makes this impossible then intraosseous, central venous (femoral or internal jugular vein) or peripheral venous cutdown are acceptable alternatives. At the time of vascular access appropriate blood samples should be taken:
• Full blood count and film
• Blood cross-match—in hemorrhage; most children with septic shock will require transfusion
• Coagulation screen—particularly in septic shock
• Plasma urea, creatinine and electrolytes
• Serum calcium
• Plasma glucose and lactate
• Blood gas estimation—arterial or central venous gases are most useful
• Blood culture and microbial sensitivities

A bedside blood glucose test should also be performed and hypoglycemia corrected promptly. Once assessment and monitoring have been completed (in the acutely sick child this should take no more than 1–2 minutes), the clinician then moves on to definitive management of the shock state. With reference to the three factors involved in the shocked heart there are three objectives of treatment:
1. Correction of hypovolemia (preload)
2. Optimising the cardiac pump (contractility)
3. Ensuring peripheral distribution of blood (afterload)
Following restoration of circulation, a secondary survey for organ specific signs should be carried out.
Correction of hypovolemia

The objective of volume replacement in shock is to optimise preload. The hypovolemic child should be managed initially with a rapid intravenous infusion of warmed fluid of 20 ml/kg. The approximate weight of a child can be calculated by using the formula:

WEIGH of CHILD (Kg) = 2 (Age in years + 4)


The selection of fluid is a matter of departmental policy and no little controversy in the literature. The author recommends 0.9% saline as the fluid of choice in volume resuscitation except in suspected meningococcemia and septic shock when 4.5% human albumin solution is preferred. This is because albumin offers a more logical approach and a theoretically longer duration of action in the presence of the profound capillary leak that occurs, particularly in meningococcal sepsis. Close attention should be made to the effect of the fluid bolus on heart rate, pulse volume and, to a lesser extent, blood pressure. A lack of or very transient fall in heart rate should be followed by a second similar fluid bolus. Further boluses of 10–20 ml/kg  may be required depending on clinical response. 

Prompt consideration of definitive airway support and intensive care unit admission will be required for these patients as the risk of pulmonary edema is very high. If available, reference to serial blood gas and plasma lactate measurements may aid assessment of progress and invasive monitoring of central venous pressure (CVP) is a marker of preload in the unobstructed heart. A CVP higher than that usually acceptable (i.e. >10mmHg) will be required to optimise cardiac performance in myocardial dysfunction which is universal in septic shock. 

Important management notes
• When hemorrhage is suspected, no more than 40 ml/kg of crystalloid should be given before blood is used as the replacement fluid
• In meningococcemia and septic shock, 4.5% albumin is preferred to crystalloid
• In infants with gastroenteritis, 4.5% albumin should be used after 40 ml/kg crystalloid, and other diagnoses considered, e.g. volvulus, peritonitis
• Children with meningococcal sepsis often require up to and over 100 ml/kg fluid in resuscitation


Optimising the cardiac pump
Inotropic support may be required when shock persists despite significant fluid replacement. This may not apply when hemorrhage is the cause of hypovolemia. In this case surgical management of the bleed will be required whilst the child continues to receive blood as volume replacement. Patients in septic shock commonly demonstrate poor myocardial contractility and concurrent low SVR in the presence of metabolic acidosis and endothelial injury. These children benefit from agents producing strong inotropy and peripheral vasoconstriction. Table below lists commonly used inotropes, their principal actions and therapeutic dose ranges.

Inotropic drug in pediatric shock treatment
Inotropic drugs in pediatric shock treatment


Choice of inotropic agent is not without controversy and is an issue for departmental consideration. Dopamine is widely used as the first line inotrope in the shocked child, followed by epinephrine (adrenaline) if response to dopamine is inadequate. In cases of septic shock, where low SVR is likely, there is logic in choosing first an agent that produces vasoconstriction. Epinephrine (adrenaline) (often in conjunction with norepinephrine (noradrenaline) offers positive inotropy and peripheral vasoconstriction, and its early use in the septic shocked child can be very valuable. The dose of inotrope should be titrated according to clinical response. Once this level of cardiac support has been instituted, the patient is likely to have been intubated and ventilated and requires invasive blood pressure monitoring and definitive intensive care management.


Ensuring peripheral distribution of blood
Afterload can be too great or too low to allow normal delivery of blood to the tissues. In the vasodilated child, such as in sepsis, norepinephrine (noradrenaline) and epinephrine (adrenaline) provide vasoconstriction to improve SVR and reduce maldistribution. In the child with cardiogenic shock, such as in those following cardiac surgery, the afterload is relatively high as the injured heart struggles to pump efficiently. Vasodilators such as sodium nitroprusside can ‘off-load’ ventricular work improving cardiac output. More recently phosphodiesterase inhibitors, such as enoximone and milrinone, are increasingly used, as they provide low-level inotropy in conjunction with vasodilatation to enhance cardiac output.


Specific therapies
Individual problems require action in addition to the general principles of management employed in most cases of shock. The following are for consideration:
• Antimicrobial drugs as clinically indicated, e.g. in meningococcemia or the immunocompromised
• Coagulopathy—correct with fresh frozen plasma or cryoprecipitate 
• Metabolic acidosis—can improve with volume replacement or might require alkalising agents
• Electrolyte disturbances—correct as necessary

Clinical Signs of Shock in Pediatric

Clinical Signs of Shock

Most physical signs are consistent regardless of the origin of shock; there are some exceptions. Table below presents the principal clinical findings in the shocked child.

Physical examination may give clues as to the etiology of shock, which may aid management, e.g.
• meningococcemia              purpuric and petechial rash
• cardiac failure                   gallop rhythm/hepatomegaly
• dehydration                      dry mucous membranes, oliguria, reduced skin turgor
• anaphylaxis                       angioedema, pallor, urticaria, wheeze, stridor



Clinical Signs of Shock in Pediatric

Classification of Shock in Pediatric

Classification of shock

The diagnosis of shock is purely clinical. It is possible to classify shock into physiological categories but in reality there is usually overlap between these in individual patients. Classification may be useful in diagnosis since clinical signs may differ between types, as may treatment. Shock is most commonly classified by the anatomical site of the circulation failure.

1. Hypovolemic Shock
Hypovolemic shock results from a fall in actual circulating volume within the intravascular space. In children there are:
• Common causes
• dehydration, e.g. diarrhea and vomiting
• hemorrhage
• sepsis (due to fluid redistribution secondary to increased capillary permeability)
• Less common
•burns
• peritonitis
Compensatory mechanisms will be employed in response to a fall in circulating volume.
Cardiac output is maintained or augmented by tachycardia and peripheral vasoconstriction, the latter maintaining afterload. Renal perfusion is reduced as blood is diverted to the brain and heart, resulting in activation of the renin-angiotensin system and a subsequent increase in circulating volume by sodium and water reabsorption.

2. Cardiogenic shock
Cardiogenic shock refers to situations where myocardial contractility is compromised resulting in reduced cardiac output and tissue perfusion. It is less common than hypovolemia as the primary etiology in the shocked child but, since reduced perfusion will always eventually affect myocardial function, it is an inevitable consequence wherever shock is prolonged (see Figure 3.1). Causes are as follows:
• heart failure
• cardiac surgery
• intrinsic myocardial disease, e.g. acute viral myocarditis, cardiomyopathy
• drug toxicity
• electrolyte and acid-base disturbances
• dysrhythmias.
Reduction in cardiac output brings about compensatory manoeuvres as with hypovolemia.

3. Obstructive shock 
Obstructive shock describes a scenario where despite adequate contractility the heart is unable to pump out an adequate volume of blood to be oxygenated and/or distributed to the tissues. Causes include:
• obstructive congenital cardiac lesion, e.g. aortic coarctation or critical aortic valve
stenosis
• tension pneumothorax
• cardiac tamponade.

4. Distributive shock
Distributive shock is usually a complication of severe infection. It is the principal pathophysiological process that defines septic shock. In the presence of overwhelming sepsis an unchecked, generalised inflamma-tory response develops. Inflammatory mediators such as TNFα, inter-leukin-1 and lipopolysaccharide endotoxin are produced causing local cell damage particularly to vascular endothelium. The vasoactive effects of these mediators on the endothelium produce variation in vascular tone. Whilst areas of vasoconstriction and vasodilatation may coexist side-by-side, the overall effect is that of peripheral vasodilatation and a fall in systemic vascular resistance (SVR). This means that blood is not distributed efficiently to the tissues despite a state of high cardiac output, which may exist in septic shock. Adults in septic shock secondary to Gram negative bacteremia classically present with this picture where good peripheral perfusion mediated by profound vasodilatation gives rise to the description of ‘warm shock’. In children, however, the more common presentation is that of cold peripheries, skin mottling and prolonged capillary refill time. Causes of distributive shock include:
• Septic
• meningococcemia
• Gram negative bacteremia
• streptococcal infection (group B streptococcus in neonates, pneumococcus in older children)
• Non-septic
• anaphylaxis
• neurogenic, e.g. following transection of the spinal cord
• drugs, e.g. vasodilators or anesthetics

5. Dissociative shock
Dissociative shock occurs when there is inadequate oxygen capacity. It occurs in:
• profound anemia
• methemoglobinemia
• carbon monoxide poisoning

Shock in Pediatric

Shock is most simply conceptualised as failure of the circulation to provide adequate delivery of oxygen and essential nutrients to the tissues to ensure normal cell respiration. The process leading to this state may be single or multifactorial. In the management of sick and injured children, the emphasis lies in swift recognition of shock followed by rapid assessment of the nature of the circulatory failure. The latter is essential because avoidance of significant morbidity and mortality relies on the clinician’s ability to determine the origin(s) of the shock accurately and initiate appropriate and specific management.

At a cellular level inadequate oxygen delivery leads to lactic acid formation and the development of metabolic acidosis. Up to a point the body compensates for this by redistributing blood flow away from non-essential tissues (e.g. mesenteric circulation, skin) to the vital organs (e.g. brain and heart). This state of compensated shock is completed by increased extraction of oxygen from the blood by these essential organs to maintain oxygen delivery. Uncompensated shock develops when despite these mechanisms the pathological insult makes it impossible for the body’s vital organs to overcome the inadequacy of oxygen delivery. Untreated, uncompensated shock will inevitably lead to a spiralling deterioration. An inflammatory cascade ensues at the endothelium causing cellular tissue damage. If prolonged, this damage becomes irreversible and indeed restoration of adequate circulation at this stage may lead to reperfusion injury, itself exacerbating the damage. Multi-organ failure will follow, which in many cases will be unrecoverable. However, compensated and early, uncompensated shock are treatable and so this chapter focuses on the clinician’s recognition, assessment and initial management of shock in the Pediatric Emergency Department.

Heart Condition During Shock

Shock can be thought of in terms of three key elements that affect the heart’s ability to provide an adequate circulation, namely preload, contractility and afterload.

Preload
Preload refers to the degree of tension placed upon the cardiac muscle as it begins to contract. It is usually considered to be the end-diastolic pressure at the completion of ventricular filling. A sufficient degree of stretch to the myocardium is required to produce a level of contraction as governed by the Frank-Starling mechanism. This stretch is produced by venous return, itself inherently linked to actual circulating volume. A fall in circulating volume will reduce venous return, myocardial stretch, force of myocardial contraction and cardiac output.

Contractility
The force generated during ventricular contraction defines ventricular contractility. Contractility is maximised in a neutral homeostatic environment when myocardial oxygen delivery is adequate, acidosis absent, electrolytes in balance, etc. Improvement in contractility increases cardiac output through improved stroke volume.

Afterload
Afterload may be thought of as the resistance against the heart as it exerts its force during contraction. It is actually the pressure created in the artery leading from the ventricle during ventricular systole. Whilst it is true that too high an afterload would result in a reduction in the output by the ventricle, too low an afterload itself poses significant problems since adequate organ perfusion relies on a finely balanced relationship between preload, contractility and afterload.