Syncope in Pediatric

Syncope
A syncopal attack is brief, usually with sudden loss of consciousness and muscle tone caused by cerebral ischemia or inadequate oxygen or glucose to the brain.

Features

• It usually lasts only a few seconds
• The child limp and unresponsive
• Tonic—clonic movements can occur with prolonged unconsciousness
• The patient is back to normal on awakening

Cause

There are several causes, including:
• Vasovagal (fainting)
• Orthostatic or postural hypotension
• Cardiac
• structural (e.g. critical aortic stenosis, tetralogy of Fallot, atrial myxoma etc.)
• arrhythmia (e.g. prolonged QT, AV block, sick sinus syndrome)
• Respiratory (e.g. cough, hyperventilating, breath holding)
• Metabolic (e.g. anemia, hypoglycemia, hysteria etc.)

Management

A history of the surrounding events is important. Orthostatic hypotension usually occurs on standing suddenly. Vasovagal collapse is usually associated with environmental or emotional stresses. Structural cardiac lesion is more likely if the syncope is exertional. 

The patient should be examined for cardiac anomaly (e.g. murmur, heaves etc). Investigations should include an ECG to look for dysrythmias, short/abnormal PR interval (e.g. Wolff-Parkinson-White syndrome) or prolonged QT syndrome.

If unconsciousness lasts more than a few seconds and the patient is not fully awake immediately after the event, then consider seizures as a cause. The patient may need an EEG to clarify this issue. Hysterical syncope generally occurs in front of an audience, patients do not hurt themselves and there is associated moaning or nonrhythmical jerking.

Follow up
All patients who have unexplained syncope should be reviewed in outpatients.

Supraventricular Tachycardia in Pediatric

Supraventricular tachycardia will usually present with signs of congestive cardiac failure or shock, but will also depend on the age of the child. Sinus tachycardia can be up to about 200 beats per minute. Supraventricular tachycardia (SVT) is usually above 220 beats per minute.

Supraventricular Tachycardia in Pediatric


Assessment

Symptoms
Infants usually present with pallor, dyspnea and poor feeding. Older children have palpitations and chest discomfort.

Signs
In SVT there is a regular tachycardia with a heart rate usually 180–300 per minute. Hypotension might be present but is often compensated early on in presentation. Heart failure with hepatomegaly with gallop rhythm occurs, especially in infants. Consult cardiology urgently if tachycardia is broad complex or irregular.


Management and Treatment
The child must be monitored with continuous ECG trace and frequent measurements of blood pressure. The options for treatment are listed below.
• If necessary apply oxygen 10 liter/min by facemask
• If child is shocked (i.e. hypotensive, poor peripheral perfusion, impaired mental state) proceed to direct current cardioversion (see below)
• If child is not shocked treat with intravenous adenosine

Shocked child
If the child is shocked, then direct current cardioversion is needed. You must:
• Call ICU. Ensure experienced staff and full resuscitative measures are present
• Ensure child is on oxygen, and has intravenous access
• Administer diazepam intravenously if there is any chance of awareness
• DC revert using a synchronised shock of 0.5 J/kg. If this is unsuccessful, increase
dose to 1 J/kg and then to 2 J/kg if still unsuccessful
• An unsynchronised shock is necessary for ventricular fibrillation or polymorphic ventricular tachycardia

Stable child
If the child is stable, vasovagal maneuvers and adenosine should be tried:
• Vagal maneuvers: use the Valsalva maneuver if child old enough, the gag or icepack/iced water for infants (apply to face for a maximum of 30 seconds). Do not use eyeball pressure.
• Intravenous adenosine
• Insert cannula into a large proximal peripheral vein (the cubital fossa is ideal) with a 3-way tap attached
• Draw up starting dose of adenosine 50 µg/kg. If necessary dilute to 1 ml with
normal saline
• Draw up 10 ml saline flush
• Turn on the ECG trace recorder
• Administer adenosine as a rapid i.v. push followed by the saline flush
• Repeat procedure at 2-minute intervals, until tachycardia terminated, increasing the dose of adenosine by 50 µg/kg to a total dose of 300 µgµg/kg for infants of less than 1 month, and to a total dose of 500 µg/kg1 to children between 1 month and 12
years.
• Perform 12-lead ECG postreversion

The recorded strip at the time of conversion to sinus rhythm should be inspected and saved, for concealed pre-excitation may only be revealed during the first few beats after conversion to sinus rhythm. After a patient has been reverted, a 12-lead ECG should be performed to look for pre-excitation and other abnormalities. Rapid re-initiation of tachycardia is not uncommon, mostly because of premature atrial contractions stimulated by the adenosine. If this occurs consider trying adenosine again. Side effects including flushing and chest tightness or discomfort are not uncommon but they are usually brief and transient. Rarely atrial fibrillation or prolonged pauses may occur. Adenosine is contraindicated in adenosine—deaminase deficiency (rare immune deficiency) and patients taking dipyridamole (Persantin). Care is required in asthma, as it may cause bronchospasm. If these measures fail to revert the SVT, consult a cardiology specialist.


Disposition

A follow-up plan should be made in consultation with cardiology. Some children may be started on beta blockers. There may be an underlying conduction abnormality such as Wolff-Parkinson-White syndrome.


Source pict: http://www.medscape.org/

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