pediatric trauma

Management principles of pediatric trauma patients

Management principles of pediatric trauma patients are similar to those of adults, but modified according to the age group of the child. Children are not just small adults. Their unique, developing psychologic, anatomic, and physiologic characteristics pose special challenges to anesthesiologists and the entire trauma care team. Optimal management of the pediatric trauma patient depends on adequate knowledge and

understanding of these unique characteristics.

INITIAL ASSESSMENT AND MANAGEMENT

Primary Survey

The main goal of the primary survey is to rapidly find all potentially life-threatening injuries to prioritize management for efficient resuscitation and achieve hemodynamic stability. This requires immediate assessment of the “ABCDEs” of the Advanced Trauma Life Support (ATLS) protocol and constant reevaluation of the adequacy of resuscitation strategies.

Airway with C-Spine Control

Evaluation of the airway in an injured child can be complex. Injury to the airway or nearby structures may distort normal anatomy and render mask ventilation and tracheal intubation difficult.Preexisting conditions thatmay complicate emergency

airway management include congenital abnormalities, such as micrognathia (mandibular hypoplasia), macroglossia, and cleft palate and the presence of obstructive sleep apnea with or without obesity.

Inspection of the airway includes the face, mouth, mandible, nose, and neck. Look for edema, foreign bodies, secretions, blood, loose or missing teeth, and fractures of the jaw, mandible, and cervical spine. Any trauma victim, especially one with a closed-head injury, is presumed, until proved otherwise, to have cervical spine (C-spine) injury and a full stomach.

C-spine precautions

should be maintained and techniques that minimize the risk of pulmonary aspiration should be taken at all times.

Healthy neonates and young infants have large heads, including prominent occiputs relative to body size, so that, in the supine position, the infant neck is naturally flexed on the chest and the supine infant headmay be flexed on the neck]. This has several important implications.

The natural head and neck flexion of the obtunded or sedated young infant often results in significant airway obstruction that may be relieved by gently lifting the chin up and forward (anteriorly) to slightly extend the head on the neck. Otherwise, an

oral airway can be inserted with no relative movement of head and neck. In suspected C-spine injury, a more neutral, straight head and neck position should be achieved by placing a blanket or pad under the supine infant or young child’s torso.

Neonatesandyounginfants areobligate nose breathers until three to five months of age so that any secretions or blood in their relatively narrow nasal passages can lead to airway obstruction.

The larynx in infantsandchildren ismore cephalad, approximately at the level of the C3–C4 vertebrae in infants compared with the C5–C6 level in adults. This may give the impression that the infant larynx is more anterior during direct laryngoscopy.

The length of the trachea is only 4–5 cm in infants and approximately 7 cm by 18 months of age, so right mainstem intubation or ETT dislodgement can occur with correspondingly small movements of the infant’s head. extubation.When choosing the appropriately sized ETT, keep in mind that in children less than 5 years old, the narrowest part of the upper airway is at the level of the cricoid cartilage, not at the glottis, as in adults. The size of the ETT appropriate for the patient’s age may

be estimated by comparing the tube size with that of the infant or child’s fifth finger, or by using the formula: ETT tube size (diameter in mm) = 4 + (1/4) age .

An air leak around the ETT at 15–20 cmH2Opressure and easy passage of the tube into the trachea clinically suggests that the ETT size is appropriate. The following formula may be used as a guide to determine the appropriate depth of the ETT placement (in centimeters from lips to tip of ETT) for children older than 2 years: 13 + (1/2) age); for under 1 year old: 8 + weight in kilograms [20].

The appropriate depth of ETT insertion may also be approximated bymultiplying the internal diameter (millimeters) of the ETT by 3.

Indications for Endotracheal Intubation

a. Loss of consciousness or altered level of consciousness with inability to protect the airway

b. Inability to maintain patency of airway or clear secretions

c. Provide positive pressure ventilation and adequate oxygenation

d. Significant burn with airway injury.

Ø Anaesthesia for Fetoscopy

Ø By: Dr. Nesrine El-Refai

Ø Professor of Anesthesia

Ø Cairo University

Ø Objectives

Ø Introduction.

Ø Techniques of fetal intervention.

Ø General idea about Fetoscopy.

Ø Anesthetic considerations.

Ø Future of fetoscopy.

Ø Anesthetic complications.

Ø Kasr-Aini  experience.

Ø Introduction

Ø Anesthesia for fetal surgery involves coordination between the surgical and anesthetic teams.

Ø It is important to understand the maternal, fetal and placental issues to tailor the anesthetic to the surgical plan.

Ø Anesthetic risks for the parturient during nonobstetric surgery include fetal asphyxia , fetal and maternal cardiovascular depression from anesthetics and uterocaval compression, and potential teratogenicity of anesthetic drugs and preterm labor/delivery .

Ø However, fetal surgery also involves repair of the fetal or placental anomaly, and the fetus is usually critically ill, such that survival without the surgery is unlikely.

Ø Factors influencing anesthetic management for fetoscopic surgery include fetal cardiovascular status, history of uterine activity, and location of the placenta relative to the amniotic membranes and umbilical cord.

Ø Cordocentesis and IUT - History

Ø 1963 - First intraperitoneal transfusion (Liley)

Ø 1974 - Fetoscopy to obtain fetal samples (Hobbins,       et al)

Ø 1981 - Fetoscopic transfusion (Rodeck, et al)

Ø 1982 - First ultrasound guided IUT (Bang, Bock &                Troll)

Ø 1983 - First large study of IUT - 66 cases (Daffos, et     al)

Ø

Neonatal Anesthesia

Ain Shams Journal of Anesthesiology                                         Vol 4-1; Jan 2011

Neonatal Anesthesia 
Hany M. El-Zahaby, MD
Department of Anesthesia, Intensive Care and Pain Management, Faculty of
Medicine, Ain Shams University, Cairo, Egypt.
Safe and effective neonatal anesthesia is one of the most challenging tasks presented to anesthesiologists. Knowledge of  the neonate's unique features, great manual skills and continuous practice are required for the
anesthesiologist to perform such task.
Neonatal Physiology Related to Anesthesia
Nociceptive System and Stress Response
The central nervous system is incompletely developed at birth. However, studies in preterm and term
neonates reported a fully competent neuroendocrine stress reaction in response to surgical stimulation.
Neonatal pain is capable of producing a "pain memory" as a result of plasticity changes within the central
nervous system or a psychological process.
 This confirms that a nonanalgesic technique practice is no longer acceptable.  The potential incompletely developed autoregulation of cerebral blood flow together with fragile infant's cerebral blood vessels
are important factors in the development of intraventricular hemorrhage.
 The spinal cord extends to a lower segment of the spine in neonates than in older children and adults. The volume of cerebrospinal fluid and the spinal surface area are proportionally larger in neonates, whereas the amount of myelination is less than in older children and adults.
These factors explain the increased amount of local anesthetics (mg/kg) required for a successful spinal
anesthetic in infants.   Hyperoxia has been associated with retinopathy of prematurity (ROP).
 However, ROP has been reported in full-term infants, in preterm infants never exposed to greater than ambient oxygen, may affect retina of one eye only, and even in infants with congenital cyanotic heart disease who has low oxygen tension in their blood.

pediatric nerve blocks

•Introduction

•Equipment

•Local Anesthetics

•Nerve Localization Methods

•Head & Neck Blocks

•Upper Extremity Blocks

•Nerve Block At The Wrist

•Lower Extremity Blockade

•Trunk Blocks

•Summary





IntroductionThe use of peripheral nerve blocks has been regaining significant popularity in the daily practice of most anesthesiologists. Despite the trend towards increase in the use of regional anesthesia and nerve blocks in adults, peripheral nerve blocks in children remain underutilized. Common reasons include the concern of neurologic complications and the lack of technical skills required for successful use of peripheral nerve blocks. Although performance of PNBs in anesthetized adults is often debated, such practice is well accepted in pediatric patients. A large prospective database collected in France demonstrated no increased incidence of complications when regional anesthesia, particularly when peripheral nerve blocks were performed under general anesthesia.1 The incidence of regional anesthesia related complications in one study was less than 0.9/1000 anesthetic procedures performed. When used with skill, the success and complications of performance of peripheral nerve blocks in children should not be significantly different from those in the adults. In addition, the equipment used for PNBs in children is similar to that used in adults (see Chapter 17). Although most peripheral nerve blocks are performed in an operating room environment, the use of regional anesthesia in children extends to an emergency department 2 as well as in an intensive care unit setting.3;4 The key to success of peripheral nerve blockade in children is the proper knowledge of the anatomy, pharmacology, equipment used for regional anesthesia and effective use of pre-procedure sedation and analgesia.

paediatric DKA

Diabetic ketoacidosis (DKA) can occur with both types 1 and 2 diabetes mellitus, and is the leading cause of morbidity and mortality in children with diabetes. Unlike the adult population, paediatric mortality is mainly due to the development of cerebral oedema. This article will review the pathophysiology and complications of paediatric DKA and discuss the principles behind current treatment strategies. PathophysiologyIncidenceThe incidence of DKA is generally higher for type 1 diabetes, both at presentation and in the setting of established disease. Studies from Europe and the USA have estimated an incidence of DKA at first diabetic presentation of 15–70% for type 1 diabetes (with patients under 5 yr of age being at highest risk), and 5–25% for type 2. It is thought that the wide variation in incidence within both sub-types is influenced by the availability of healthcare and frequency of diabetes in a given population. In established type 1 diabetes, the risk of DKA is 1–10% per patient per year, with a considerably lower incidence in type 2 diabetes.AetiologyDKA is the result of an absolute or relative lack of insulin in combination with the effects of increased levels of counter-regulatory hormones, including catecholamines, glucagon, cortisol, and growth hormone. Absolute insulin deficiency is observed in newly diagnosed type 1 diabetes and in insulin-treated diabetics where insulin is omitted. A relative insulin deficiency results in patients who have some circulating insulin; however, levels of the catabolic counter-regulatory hormones are increased in response to various stress conditions such as obesity, trauma, sepsis, and gastrointestinal illness, and outweigh the anabolic effects of any insulin present. It is the resulting accelerated catabolic state that gives rise to the classical picture of DKA with: hyperglycaemia, hyperketonaemia, and hyperosmolality. Hyperglycaemia is due to impaired peripheral uptake of glucose with increased hepatic gluconeogenesis and glycogenolysis, whereas ketonaemia occurs secondary to increased lipolysis; both contribute to the ensuing hyperosmolar state. The resultant osmotic diuresis leads to dehydration and loss of total body electrolytes; if this is severe, the glomerular filtration rate will decrease, exacerbating the hyperosmolar state through inability to excrete glucose and ketones. This is further compounded by release of counter-regulatory stress hormones. The metabolic acidosis at DKA presentation is almost exclusively ketonaemic; lactic acidosis is uncommon, unless DKA has been triggered by a secondary phenomenon, such as sepsis.However, with treatment the aetiology of the acidosis may change, with hyperchloraemia (secondary to resuscitation/rehydration fluid), becoming predominant.The pathophysiology of DKA is summarized in Figure 1. [Image] Fig. 1 Pathophysiology of DKA (reprinted from Diabetes Care®, Vol. 29, 2006; 1150–9 with permission from The American Diabetes Association). Copyright © 2006 American Diabetes Association. DiagnosisThe diagnosis of diabetes mellitus is often delayed in younger children (particularly infants); this is because the classic ‘adult’ triad of polyuria, polydipsia, and weight loss is frequently absent. This may partially explain the increased severity of first presentation of DKA in this age group.The biochemical criteria for the diagnosis of DKA are as follows:

hyperglycaemia (blood glucose >11 mmol litre−1); venous pH <7.3 or bicarbonate <15 mmol litre−1; ketonaemia. Euglycaemic ketoacidosis is rarely seen, but can be present in children who are partially treated or who have had minimal carbohydrate intake.

Severity is classified as follows: SeverityVenous pHPlasma bicarbonate (mmol litre−1) Mild7.2–7.310–15 Moderate7.1–7.25–10 Severe<7.1<5 Several risk factors related to age and severity at presentation have been associated with the development of cerebral oedema and death; these are elaborated in ‘Mortality and cerebral oedema’. ManagementThe management considerations for paediatric DKA are broadly similar to those for adults, namely:

exogenous insulin; i.v. fluid therapy; replacement of electrolytes. However, several important differences between adult and paediatric DKA exist, which may impact on treatment:

paediatric DKA often presents with greater severity; children are more prone to the development of cerebral oedema; development of cerebral oedema may, in part, be exacerbated by treatment. General considerationsABC approachGive oxygen. Failure to adequately protect the airway due to drowsiness is an ominous sign and likely due to cerebral oedema. Drowsiness should be treated urgently with i.v. osmotherapy (either hypertonic saline, 3% at 3–5 ml kg−1 over 10 min, or mannitol 0.5 g kg−1), in conjunction with standard airway positioning manoeuvres. If the patient is in extremis, tracheal intubation may be required; however, hyperventilation should be avoided, regardless of the patient's spontaneous Paco2. A nasogastric tube should be inserted to reduce the risk of pulmonary aspiration of stomach contents. Ensure secure peripheral i.v. access with two cannulae. The decision to give a fluid bolus should be based upon objective signs of inadequate intravascular volume: extreme tachycardia, hypotension and elevated blood lactate (>3 mmol litre−1). Capillary refill alone is an inadequate sign in this setting. Fluid boluses should be given with caution, and in 10 ml kg−1 aliquots only (see ‘Fluid therapy’). Assess the level of consciousnessCerebral oedema can occur at presentation, but may initially produce minimal changes to the sensorium.Marcin and colleagues have published a neurological symptom score which is quick to perform, reproducible, and corresponds to discrete intervals of the Glasgow coma score (Table 1). This score can be used as an early warning sign of cerebral oedema. Any signs of cerebral oedema must be treated promptly and aggressively. View this table:

Table 1 Neurological symptom score to grade severity of cerebral oedema (adapted from Wolfsdorf and colleagues) Weight of the patientThis is essential for calculating fluid therapy and drug dosing.Give antibiotics if febrileAn increased white blood cell count is often seen in DKA without infection;2 however, if the child is febrile, it is sensible to commence broad-spectrum antibiotics empirically after taking cultures. Specific considerationsInsulin therapyInsulin is essential in switching off lipolysis and ketogenesis. Physiological studies suggest that low-dose insulin (0.1 unit kg−1 h−1) achieves steady-state plasma levels of 100–200 µU ml−1 within 60 min.2 These plasma levels are sufficient to overcome insulin resistance, inhibiting lipolysis and ketone production while exerting near maximal effects on gluconeogenesis suppression and peripheral glucose uptake. I.V. bolus doses of insulin at the start of therapy are unnecessary and may increase the risk of developing cerebral oedema, possibly due to activation of membrane Na+/H+ exchangers leading to increased intracellular Na+ with associated osmotic fluid shifts.7 Recent guidelines have suggested avoiding insulin boluses, and delaying commencement of insulin infusion until after 1–2 h of fluid therapy.Fluid therapyThe goals of fluid therapy are two-fold: (i) to resuscitate, if intravascular volume is inadequate (see ‘ABC approach’) and (ii) to replace fluid deficit secondary to dehydration. Fluid resuscitationShock with haemodynamic compromise is uncommon in DKA and judicious use of fluid boluses is advised. When fluid boluses are required to restore intravascular volume (i.e. in the tachycardic, hypotensive patient), the current recommendation is to use saline 0.9%, 10–20 ml kg−1 given in the first 1–2 h, repeated as necessary. Our own experience and current practice is based upon a restrictive view, aiming to give a maximum bolus of 20 ml kg−1 in the first 4 h, and if the patient remains hypotensive, then early consideration is given to commencing inotropes. Ongoing signs of intravascular deficit should raise the suspicion of sepsis. RehydrationAlways rehydrate over a minimum of 48 h. Replacement fluid comprises normal maintenance plus estimated dehydration. Never give hypotonic solutions as they may increase the risk of cerebral oedema; thus standard therapy should comprise saline 0.9%, with added glucose (5–10%) when the plasma glucose decreases to ∼15 mmol litre−1. Urinary losses should not be included routinely in the calculation for fluid replacement. The clinical assessment of dehydration in children with DKA is inaccurate when using standard clinical assessment tools such as capillary refill time, skin turgor, sunken eyes, sunken fontanelle, and dry mucus membranes; thus a recent pre-morbid weight (if available) may be helpful. A recent prospective study of children presenting to an emergency department with DKA yielded a median calculated measure of dehydration of ∼9%; it therefore seems reasonable to assume 10% dehydration for children presenting with severe DKA, and 5% for those with moderate severity (see ‘Diagnosis’). ElectrolytesDKA is associated with major perturbations in plasma electrolytes; primarily sodium, potassium, and phosphate.SodiumIn health, sodium is the most important extracellular cation influencing intracellular volume. Several factors in DKA may cause an apparent lowering of the plasma sodium, making it an unreliable estimator of both intracellular volume and the degree of extracellular volume contraction.3 First, total body sodium may be depleted in tandem with water loss as a consequence of the osmotic diuresis secondary to hyperglycaemia and ketonaemia. Secondly, the increased concentration of extracellular glucose (due to insulin deficiency) produces an osmotic movement of water from the cells, leading to a pseudohyponatraemia. The measured sodium will thus invariably increase as plasma glucose decreases with fluid and insulin therapy; however, this can occur in the face of dramatic decreases in effective osmolality (primarily due to glucose no longer being an extracellular osmole). Thus, it is mandatory to calculate the corrected sodium to provide a more accurate estimate of changes in effective osmolality. [Image] The importance of maintaining an adequate effective osmolality during DKA treatment was underlined by Hoorn and colleagues,7 who demonstrated that cerebral oedema is less likely to occur when the reduction in effective osmolality is minimized, either via smaller decreases in plasma glucose or via larger increases in plasma sodium. Our local protocol utilizes changes in corrected sodium as the trigger for adjustments in fluid volume (http://www.strs.nhs.uk/). PotassiumTotal body potassium deficits in children presenting with DKA are estimated at between 3 and 6 mmol kg−1, mostly from intracellular stores. The serum potassium levels may be normal, increased, or decreased, but this is simply a reflection of how long the DKA process has been continuing for before treatment is commenced. There are several causes of potassium loss including insulin deficiency, metabolic acidosis, vomiting, losses due to an osmotic diuresis and secondary hyperaldosteronism as a result of volume depletion.Potassium replacement is required in all patients; however, if the serum potassium is >5.5 mmol litre−1, defer giving potassium until it begins to decrease or you have a documented urine output. Once treatment with insulin is started, the serum potassium concentration can decrease abruptly. PhosphateIntracellular phosphate depletion also occurs in DKA. Clinically significant hypophosphataemia, however, tends to occur only when the resumption of food intake is prolonged beyond 24 h.3 Studies have not shown phosphate replacement to be beneficial. In addition, i.v. phosphate administration can induce hypocalcaemia; however, this may be considered in cases of muscular weakness. Metabolic acidosis and anion gapAppropriate monitoring of acid–base status during DKA treatment is essential. A primary goal of therapy is resolution of ketoacidosis; this can only be quantified directly by measurement of blood ketones (which is now possible at the bedside)9 or indirectly via calculation of the anion gap. [Image] In clinical practice, however, ketoacidotic resolution is commonly inferred via blood gas analysis using pH and base deficit. A major limitation of this approach is that confounding factors (notably hyperchloraemia secondary to fluid therapy) may supervene during treatment, attenuating the resolution of metabolic acidosis. A recent study in severe DKA showed that metabolic acidosis persisted 20 h after commencement of treatment (mean pH 7.31, base deficit 10 mmol litre−1), despite resolution of ketoacidosis. Over the same time period, the relative contribution of chloride to the base deficit increased from 2% to 98%. MonitoringThe management of DKA requires frequent monitoring of both the clinical status of the patient and physiochemical changes that occur during treatment. In addition to the routine observation chart documenting vital signs and neurological status hourly, it is helpful to have a flow chart to record all electrolyte and blood gas results over each 24 h period. An example is given in Figure 2. [Image] View larger version:

Mortality and cerebral oedemaCerebral oedema occurs in up to 1% of all paediatric DKA episodes with two-thirds of cases presenting within the first 6–7 h after treatment has started. Cerebral oedema is the most common cause of mortality in children with DKA, accounting for 60–90% of all paediatric DKA deaths. Other causes of mortality include hypokalaemia and hyperkalaemia (with associated arrhythmias), sepsis (including mucormycosis), aspiration pneumonia, acute pancreatitis, intracranial venous thrombosis, and rhabdomyolysis.The aetiology of cerebral oedema is poorly understood, although there are likely to be multiple processes involved with vasogenic, osmotic, and ischaemic mechanisms being implicated. There are several risk factors associated with the development of cerebral oedema, including:

younger age; newly diagnosed diabetes; longer duration of symptoms; raised serum urea; initial pH <7.1; extreme hypocapnia (Pco2 <2 kPa) at presentation; hypocapnia in association with mechanical ventilation; >40 ml kg−1 total fluid given in first 4 h; bicarbonate therapy; an attenuated increase, or a decrease in corrected plasma sodium during treatment; bolus insulin therapy. Cerebral oedema is a clinical diagnosis with varying signs and symptoms including alteration in neurological status, headache, cranial nerve palsies, bradycardia, and hypertension. This can be subtle, and may have a worse prognosis if diagnosed later after presentation.6

If cerebral oedema is suspected then treatment should begin immediately using either hypertonic saline (saline 3%, 3–5 ml kg−1) or mannitol (0.5 g kg−1=2.5 ml kg−1 of 20% solution) while arranging for a computed tomography scan. This should be repeated until a clinical improvement in neurological status is seen (this may require achievement of plasma sodium levels of 150–158 mmol litre−1).7We recommend hypertonic saline as the preferred osmotherapy, for several reasons:

Plasma sodium is the most important variable influencing effective osmolality, and hence intracellular volume in DKA (after insulin therapy has commenced); it is also easily measurable (particularly out-of-hours) in all hospital laboratories. Hypernatraemia (150–158 mmol litre−1) is effective at both avoiding and reversing the clinical manifestations of cerebral oedema; this appears most pronounced in patients who demonstrate the largest decreases in plasma glucose.7 Mannitol induces an osmotic diuresis and is rapidly excreted, meaning that its effect may be short-lived. In addition, rapid swings in osmolality may be more harmful. Lastly, plasma corrected sodium can now no longer be used as an estimate of effective osmolality, owing to the presence of another osmole (mannitol). SummaryDKA is a life-threatening condition that requires specific management and monitoring to be instituted early if serious morbidity and mortality are to be avoided. Full treatment guidelines can be found at the websites by following the link: http://www.strs.nhs.uk/ or alternatively http://www.ispad.org/.

pediatric assessment

hi colleagues, if any of you like me get intimidated by getting involved in the perioperative management  of a child then I advice you to attend the PALS course as I did this week.
it gives you a new prospective in preoperative evaluation of pediatric patients or more sprcifically a sick child in PICU or presenting for emergency surgery.
here I like to share you some of the valuble points on
systematic approach to pediatric assessment
general assessment
the general assessment is a visual and auditory assessment of the child general appearance during the first few seconds of encounter. the pediatric assessment triangle(PAT) is a reminder to evaluate the appearance, work of breathing, and circulation.
if you recognize a life threatening condition at any time, immediately begin life-saving interventions and activate the emergency response system(ERS).
life threatening conditions are:
Airway                               complete or severe airway obstruction
Breathing                            apnea, significant work of breathing, bradypnea
Circulation                          no pilse, poor perfusion, hypottension, bradycardia
Disability                            unresposiveness, depressed consioueness
Exposure                           significant hypothermia, bleeding, petechiae(septic shoch),
                                         abdominal distention(acute abdome
interventions
if you recognize a life threatening condition, begin life-saving interventions. examles of these interventions are:

• support ABC
• provide supplemental O2 100%
• provide assessted ventilation(bag mask- ET intubation)
• start cardiac and respiratory monitoring
• estabilish IV/IO acess
• give a bolus of isotonic crystalloid
• obtain laboratory studies
• administer drugs
• provide electrical therapy 

 if the general assessment dose nor reveal a life threatening condition requiring immediate intervention, proceed with the primary assessment.

primary assessment
the primary assessment is a rapid hands on ABCDE evaluation of cardiopulmonary and neurologic function.
this assessment includes vitalsigns and oygen saturation by pulse oxymetry.
Airway: assess patent or not, maintainable or not.
Breathing: 

1.  respiratory rate
2. respiratory effort
3. tidal volume
4. airway and lung sounds
5. oxygen saturation

Circulation: evaluation is 2 parts
1- cardiovascular function

• skin colour and temperature
• heart rate and rhyth
• peripheral and central ulse
• blood pressure

2-end organ function:

• brain perfusion(mental status)
• skin perfusion
• renal perfusion

Disability: assess the child level of consiousness by

• AVPU pediatric response scale
• GCS
• pupilary responses

Exposure: expose the child to assess

• signs of truama
• rashes
• core temperature

after you finish primary assessment you should be able to categorize the clinical condition of the child into respiratory or circulatory
respiratory problems can be furthue categorized by severity into respiratory distress or respiratory failure.
circulatory problems can be furthur categorized by severity into comensated shock or hypotensive shock.
the clinical condition can be also a combination of respiratory and circulatory problems.

now you can proceed to the secondry assessment for more specific diagnosis.
secondry assessment
the secondry assessment consists of a focused medical history using the SAMPLE mnemonic, a thorough physical examination and a review of vital signs.
SAMPLE stands for:

• Signs and Symptoms
• Allergies
• Medications
• Past medical history
• Last meal
• Events leading to presentation

physical examination should go systematicaly from head to toe.
now you finished the secondry assessment, you should be able to provide more specific diagnosis by type.
respiratory problem can be caused by

• upper airway obstruction
• lower airway obstruction
• lung tissue diseases
• disordered control of breathing

circulatory problem can be caused by

• hypotensive shock
• obstructive shock
• distributive shock
• cardiogenic shock

after you reach a specific diagnosis, you should decide appropiate management for the clinical condition.
tertiary assessment
the tertiary assessment includes laboratory, radiological and other advanced tests to help esabilsh the child physiologic ondition and diagnosis.
pay attention that the term tertiary dosenot mean these tests are performed third. the timing of these tests is dictated by the clinical situation.
for example if during your secondary you recognize a hypotensive shock due to hemorrhage you should request now blood typing and cross match, and so on.

Anesthetic considerations for Pediatric Chest Trauma

Anesthetic considerations for Pediatric Chest Trauma


ANESTHETIC CONSIDERATIONS FOR PEDIATRIC CHEST TRAUMA
Hala samir El Mohamady, MD
Dept. of Anesthesiology, Intensive Dare, and Pain management, Faculty of Medicine, Ain Shams University
Abstract
Thoracic trauma is a major cause of morbidity and mortality in children.
The anesthesiologist needs to be prepared to manage such pediatric patient who may have severe multisystem injuries
with underlying respiratory derangements, ongoing blood loss, and cardiac dysfunction.
Many principles used in adult patients can be applied in pediatric patients; however the unique anatomy and physiology
of children must always be remembered.
For pediatric patients timely resuscitation and optimal care to avoid secondary injury is a considerable challenge for any
anesthesiologists.
Prevention of childhood injury remains the cornerstone of reducing the number of children who present for posttraumatic
surgical intervention. Beyond prevention, the next best step is the accurate diagnosis and treatment of
traumatic injury. Anesthesiologists contribute to this step by providing timely resuscitation and optimal care to avoid
secondary injury.
Introduction
Blunt and penetrating chest trauma is a major cause of
morbidity and mortality in children. Most pediatric
cases are caused by blunt trauma while penetrating
trauma is more common in adolescent boys.
Fortunately, children have an extremely compliant
body that may absorb considerable force and energy
with minimal external signs of injury. Conversely,
external signs of injury or rib fractures are an indicator
of significant potential soft tissue damage (1, 2). Young
children are less mineralized and more pliable, and
they tend to bend, but not break. Significant
intrathoracic injuries often occur without rib fractures;
however, the risk of mortality increases with the
number of ribs fractured (3) .Also Mortality from chest
trauma increases with the presence of abdominal (20%)
or head injury (35%) (4).
Evaluation and Management
Airway
Just as in the adult, the initial assessment should
concentrate on the A, B, C's (airway, breathing, and
circulation). It is important to remember the differences
in the pediatric airway, which include a large occiput,
large tongue, anterior larynx;
floppy, stiff Q-shaped epiglottis, and short trachea.
Unlike the adult, the cricoid is the narrowest part of
airway and so intubated patients should have a leak
around the endotracheal tube (ETT). The large tongue
and floppy epiglottis can contribute to airway
obstruction in an unconscious child. Appropriate jaw
thrust can lift the tongue off the back of the pharynx
and minimize airway compromise. A shoulder roll may
be required to place the head in an optimal position for
intubation; however, the presence of possible cervical
spine injury may preclude its use (5).
Any child that presents with respiratory compromise
should immediately receive supplemental oxygen with
continuous oxygen saturation monitoring. A changing
or altered mental status may indicate a closed head
injury, or severe hypovolemia.
Intubation should be considered in any child who is
combative, unconscious, or obtunded, to maintain
cerebral oxygenation and perfusion and to help
decrease the risk of secondary brain injury.
Infants and neonates are obligate nose breathers, so
occluded nasal passages from maxillofacial, neck, or
head trauma may prevent them from breathing
effectively.
Oral intubation is preferable to nasal intubation
because it is easier, faster, and less likely to result in
bleeding. Up to 50% of all pediatric trauma patients
will have brain trauma, including possible basilar skull
fracture. The cervical spine must always be protected
and the neck collar should remain in place until the
physician is absolutely sure there is no neck injury. Inline
stabilization (not traction) should be applied while
the patient is being intubated to prevent further spinal
cord injury (6). All pediatric trauma patients should be
considered at risk for aspiration particularly one with
thoracic injuries, rapid sequence induction with cricoid
pressure should be used until the airway is secured.
Cricoid pressure may destabilize an unstable neck in a
small child or infant and should be applied carefully by
experienced personnel. The ideal ETT should have a
leak at pressure <20-25 cm H20 if patient has normal
lungs. In patients with severe pulmonary trauma, a
larger ETT or cuffed ETT will facilitate ventilation. In
these patients, a leak at pressure 25-30 cm H20 will
maximize ventilation without increasing the risk of
developing subglottic stenosis (5).
Breathing
The trachea can be easily compressed; nasal flaring,
use of accessory muscles, and a "rocking boat" pattern
Ain Shams Journal of Anesthesiology Vol 2; Jan 2009
41
may indicate tracheal obstruction. The obstruction may
need to be relieved by intubation. Very rarely,
percutaneous cricothyrotomy or tracheotomy may be
required. Infants and small children are much more
dependent on diaphragmatic movement for respiration.
Anything that decreases the efficacy of diaphragmatic
motion will interfere with adequate breathing in these
patients (e.g. abdominal trauma and incorrectly
performed bag and mask ventilation. A nasogastric
tube should be expeditiously placed to deflate the
stomach.
The mediastinum in young children is very mobile and,
in the presence of a pneumothorax or hemothorax, can
easily allow compression of the heart and great vessels,
leading to a tension pneumothorax. Treatment for
pneumothorax is decompression with either a needle
placed at the mid-clavicular line of the second
intercostal space or placement of a chest tube (7).
Circulation
A change in blood pressure (BP) occurs only after there
is a 30% to 40% decrease in estimated blood volume
(EBV); therefore, BP is not a very good measure of
circulatory status. On the other hand, hypotension
indicates significant blood loss.
A systolic blood pressure of 90 mmHg or less in a child
is considered a predictive indicator of major trauma (8).
Early signs of hypovolemia include persistent
tachycardia, delayed capillary refill, and diminished
pulse pressure. Central pulses should be strong. An
absent or decreased radial pulse indicates
approximately a 10% reduction in intravascular
volume. Weakened axillary or femoral pulses signify a
loss of about 15%. It is important to calculate estimated
blood volume as soon as possible (Table 1).
Balanced salt solution (lactated Ringers or normal
saline 20 mL/kg) is most commonly used for volume
resuscitation. If there is minimal or no response to this
bolus, then an additional 2 boluses can be given while
preparations are being made to transfuse blood. The
initial dose of blood is 10 mL/kg of packed red blood
cells.
Table 1: Estimated Blood Volume in Children (2)
neonate -90 mL/kg
infant - 80 mL/kg
child -70 mL/kg
Estimated wt = (age x 2) +10
Intravenous access can often be difficult to establish in
a small child. It may be necessary to cut down on the
saphenous vein or place an intraosseous line. Femoral
lines are usually the easiest and least risky central lines
to place in these situations. The presence of a cervical
collar or possible neck injury may prevent access to the
internal jugular or subclavian vein (8).
Central Nervous System
The presence of head trauma in a patient with chest
trauma is a significant predictor of mortality. The
Glasgow Coma Scale (GCS) is not reliable in children
under 1 year of age because spontaneous motor
movements after CHI are common, which can
artificially elevate the, GCS also children may not be
able to cooperate and follow commands because of
their age or level of anxiety (9).
Specific Injuries
Pulmonary Contusion
pulmonary contusion (or lung contusion) is the most
frequent injury caused by chest trauma. It is usually
caused by blunt trauma but also explosions or a shock
wave associated with penetrating trauma can cause
lung contusion (10, 11).
Pathophysiology
Pulmonary contusion results in bleeding and fluid
leakage into lung tissue, which can become stiffened
and lose its normal elasticity. The water content of the
lung increases over the first 72 hours after injury,
potentially leading to frank pulmonary edema in more
serious cases. As a result of these and other
pathological processes, pulmonary contusion
progresses over time and can cause hypoxia. The larger
the area of the injury, the more severe respiratory
compromise will be (12).
Ventilation/perfusion mismatch
Normally, the ratio of ventilation to perfusion is about
one-to-one; the volume of air entering the alveoli
(ventilation) is about equal to that of blood in the
capillaries around them (perfusion). This ratio is
reduced in pulmonary contusion; fluid-filled alveoli
cannot fill with air, oxygen does not fully saturate the
hemoglobin, and the blood leaves the lung without
being fully oxygenated. Insufficient inflation of the
lungs, which can result from inadequate mechanical
ventilation or an associated injury such as flail chest,
can also contribute to the ventilation/perfusion
mismatch. So the mismatch between ventilation and
perfusion grows, blood oxygen saturation is reduced
(13). Pulmonary hypoxic vasoconstriction, in which
blood vessels near the hypoxic alveoli constrict in
response to the lowered oxygen levels, can occur in
pulmonary contusion. The vascular resistance increases
in the contused part of the lung, leading to a decrease
in the amount of blood that flows into it (14), directing
blood to better-ventilated areas. Although reducing
blood flow to the unventilated alveoli is a way to
compensate for the fact that blood passing unventilated
alveoli is not oxygenated, the oxygenation of the blood
remains lower than normal. If it is severe enough, the
hypoxemia resulting from fluid in the alveoli cannot be
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42

corrected just by giving supplemental oxygen; this
problem is the cause of a large portion of the fatalities
that result from trauma (13) .
Management
No treatment is known to speed the healing of a
pulmonary contusion; the main care is supportive (14)
Attempts are made to discover injuries accompanying
the contusion to prevent additional injury, and to
provide supportive care while waiting for the contusion
to heal (19). Monitoring, including keeping track of fluid
balance, respiratory function, and oxygen saturation
using pulse oximetry is also required as the patient's
condition may progressively worsen. Monitoring for
complications such as pneumonia and acute respiratory
distress syndrome is of critical importance (15).
Treatment aims to prevent respiratory failure and to
ensure adequate blood oxygenation (16) . The child with
mild pulmonary contusions may not need more than
good pain control, supplemental oxygen, observation,
pulmonary toilet, and early mobilization (17). More
severe injuries will be progressively more difficult to
treat. The presence of intrapulmonary shunts and
decreased compliance may necessitate mechanical
ventilation and positive end-expiratory pressure
(PEEP) (17). Overhydration can exacerbate edema and
worsen oxygenation; hypovolemia can produce
hypoperfusion and increase the risk of multiorgan
failure. So maintenance of euvolemia is important.
Inotropic agents may be required in patients with
severe pulmonary contusion. The administration of
steroids in these patients can increase the risk of
pneumonia(18).When the contusion does not respond to
other treatments, extracorporeal membranous
oxygenation may be used, pumping blood from the
body into a machine that oxygenates it and removes
carbon dioxide prior to pumping it back in(19).
Rib Fractures
Rib fractures are present in approximately one third of
children who present with thoracic trauma. The
presence of rib fracture should alert the physician to the
possibility of other significant thoracic and
extrathoracic injuries. The severity of other injuries
increased with the number of ribs fractured, as did the
mortality. All children with at least 4 fractured ribs had
other injuries. Treatment consists of maximizing
oxygenation and ventilation as necessary, treatment of
associated injuries, and ensuring good analgesia.
Intravenous opioids, patient-controlled analgesia, or
epidural analgesia can all be effective. The technique
selected will depend on the patient's underlying
condition and age (20).
Airway Obstruction
Maxillofacial trauma or laryngotracheal injury can lead
to airway obstruction. Patients may present with
hoarseness, stridor, subcutaneous emphysema, or
intercostals or sternal retractions. Injuries to the great
vessels in the neck can result in an expanding
hematoma that may compromise the airway.
Management includes jaw thrust, clearing of debris
from the oropharynx, intubation as necessary and
rarely, a cricothyrotomy or tracheostomy (21, 17) .
Pneumothorax
Pneumothorax is the most common immediately or
potentially life-threatening thoracic injury in a child.
Children higher rate of oxygen consumption and
smaller functional residual capacity makes them more
susceptible to hypoxia. The highly mobile and
compliant mediastinum in children allows the
mediastinal contents to shift to the contralateral side,
which can compromise blood return and cardiac output
so decompression of the tension pneumothorax is life
saving.
Definitive treatment is with a chest tube. The
pneumothorax may be stable until positive pressure
ventilation is instituted. Any patient who becomes
hypoxic and/or hypotensive after institution of positive
pressure ventilation, should be considered to have a
tension pneumothorax until proven otherwise.
Persistent air leak after the placement of appropriate
chest tubes may indicate a tracheobronchial tree injury.
One-lung ventilation is often necessary and can be
tricky in a small, unstable patient when operative repair
is needed (7).
Hemothorax
Pulmonary hematoma or massive hemorrhage is rare
unless accompanied by laceration to a vessel as their
lung has high levels of tissue thromboplastin and low
circulatory pressure, thereby limiting bleeding from
parenchymal injuries.
Unexplained hypotension, or chest tube output that is
initially greater than 15 mL/kg or continued bleeding
of 2-3 mL/kg/hr consider hemothorax and chest
exploration may be needed(22).
Traumatic Aortic Rupture
Injury to the great vessels has been shown to increase
mortality to more than 50%. Diagnosis of aortic rupture
is made by history and aortography. Tracheal deviation
to the right, and unequal blood pressures in the arms
may be signs of aortic rupture. On chest radiograph, a
widened mediastinum, abnormal contour of the aortic
knob, nasogastric tube deviation to the right,
depression of the left main bronchus, left hemothorax
may indicate aortic rupture necessitating urgent
exploration (23).
Flail Chest
Immediate treatment consists of applying pressure to
the flail segment to reduce chest wall instability and
minimize circulatory and ventilatory impairment. Most
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43
children will require internal stabilization with
endotracheal intubation and mechanical ventilation.
Fluid restriction after initial resuscitation and insurance
of adequate gas exchange will minimize complications
(24) .
Myocardial Contusion and Other Cardiac Injuries
Cardiac trauma in children is relatively uncommon.
The severity of injury can vary from cardiac
concussion, which has no histologic manifestations and
is transient, to myocardial muscle or valve rupture.
These children will usually be unstable and mortality is
high (24, 25). The most common ECG abnormalities
included persistent sinus tachycardia, ST-T wave
abnormalities, conduction abnormalities, and
premature ventricular contractions (26).
Cardiac Tamponade
Cardiac tamponade is much more common with
penetrating injuries. The classic finding of Beck's triad
(muffled heart tones, increased central venous pressure,
decreased blood pressure) may be difficult to
appreciate in the small, hypovolemic child. Most
penetrating cardiac injuries will present with
hemopericardium and tamponade. Treatment is with
pericardiocentesis (7).
Anesthetic Management
Approximately 20% will require operative intervention
because of abdominal injuries, which may be
associated with massive blood loss (27).
A patient that is not already intubated, should undergo
a rapid sequence induction with cricoid pressure.
Children can desaturate much more quickly than
adults, so a modified rapid sequence induction is often
preferable. Cricoid pressure will need to be applied
carefully in the child with an unstable neck. Most of
these patients will be volume depleted and resuscitation
will be ongoing.
Induction agents that do not decrease blood pressure or
heart rate should be chosen. Ketamine or etomidate are
good choices, although small doses of thiopental or
propofol can be used in more stable patients,
particularly if they have an associated head injury (28) .
Standard monitors should be applied. Pulse oximetry
may be difficult to obtain in a small, cold
vasoconstricted patient; therefore, it is prudent to use
multiple probes in several locations. Respiratory
variation in the waveform of the pulse oximeter may
indicate hypovolemia. Bradycardia usually indicates
hypoxia, ischemia, acidosis, or hypothermia and should
be rapidly corrected. Persistent tachycardia can signify
hypovolemia and acute blood loss. End tidal carbon
dioxide (ETCO2) is less accurate in smaller patients
because they have a relatively higher dead space to
tidal volume ratio than adults. Hypovolemic patients
will have even more dead space, and patients with
thoracic injuries may have increased shunting as well.
A low ETC02 may reflect low cardiac output, because
there is less blood flow to lungs (29).
At least 2 intravenous (IV) catheters should be placed,
preferably one above and one below the diaphragm,
and blood obtained for crossmatch.
If there is difficulty obtaining peripheral IV access, a
central venous or intraosseous catheter can be placed.
Femoral venous catheters are often the easiest to get
access to, have easy landmarks and the lowest
complication rate. A subclavian catheter should always
be placed on the side of the suspected injury, especially
if there is already a chest tube on that side. Maintaining
body temperature with radiant warming lights, warm
fluids, or a forced air warmer is critical. Hypothermia
and vasoconstriction can increase coagulopathy and
bleeding, adversely affecting perfusion. Small children
have a large body surface area to mass, and
temperature control can be exceptionally difficult.
Actively warm patients if they arrive cold. The only
exception is in patients with severe closed head injury,
in whom mild hypothermia is preferred. Rewarming
may lead to increased acidosis (rewarming shock).
Invasive blood pressure monitoring will be important
and can be challenging to place. It may be necessary to
cut down on the radial artery, or to place the catheter in
the femoral, axillary, dorsalis pedis, or post tibial
arteries.
The presence of significant hypovolemia can cause
hypoperfusion and metabolic acidosis. Once
resuscitation has started, perfusion may occur to
previously underperfused areas, causing washout of
acid, vasodilatation, decreased cardiac output, and
continuing hypotension. Metabolic acidosis usually
improves with fluid resuscitation. However, in patients
with severe trauma, the acidosis may need to be treated
with sodium bicarbonate, as long as ventilation is
adequate. The Dose of bicarbonate is wt (kg) x 0.15 x
base deficit. However, since many of these patients
will have a base deficit of more than 10 mEq/L, 2 x
weight is a good starting dose.
The fluids most often used in resuscitation in children
are balanced salt solution (lactated Ringers or
Plasmalyte) or albumin.
Blood should be available and the child should be
transfused for the same indications as in adults.
Consider administration of fresh frozen plasma (FFP)
and platelets after the equivalent of 1 to 2 estimated
blood volumes have been transfused. FFP has the
highest citrate content per unit. Citrate binds with
calcium, so severe hypocalcemia may develop (citrate
intoxication) especially if FFP is administered rapidly.
Citrate toxicity is treated with calcium chloride (CaCl2)
10 mg/kg or calcium gluconate 30 mg/kg.
Hyperkalemia can occur as a result of massive blood
transfusion. One-week-old blood contains 5 mEq/L
potassium; while three-week-old blood, has 22 mEq/L
potassium. In a small child, this amount of potassium
may be significant. Treatment is with CaCl2 10 mg/kg,
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44

hyperventilation, and bicarbonate. If hyperkalemia
persists then glucose (0.5 gm/kg) and insulin (1
unit/5gms glucose) can be administered (7).
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