Ghai Essential Pediatrics8th

tion andslowconduction throughthemyocardium. Exces­ sive vagal stimulation, raised intracranial pressure or brainstem compression may cause bradycardia. Sinus bradycardia, sinus node arrest with junctional or idio­ ventricular rhythm and AV blocks are the usual preter­ minal rhythms observed in infants and children. All slow rhythms resulting in hemodynamic instability require immediate treatment. Epinephrine is a useful drug in treating symptomatic bradycardia unless due to heart blockorvagalovertone.Forbradycardiaduetovagalover­ tone, atropine is the drug of choice. If no effect is observed after ventilation and oxygenation, continuous infusion of epinephrine or dopamine should be considered.

Thisisastateofelectricalactivity observed on a monitor or ECG in absence of detectable cardiac activity. This is often the preterminal state prece­ ding asystole representing the electrical activity of a hypoxic and acidotic myocardium. Occasionally, the state may be due to sudden impairment of cardiac output, with normal ECG rhythm and increased or rapidly decreasing heart rate. Pulses or other evidence of cardiac output are absent and child appears lifeless, as in electromechanical dissociation. The reversible causes of electromechanical dissociationareseverehypovolemia,hypoxia,hypothermia, hyperkalemia, tension pneumothorax, toxins and drugs, pericardialtamponadeandpulmonarythromboembolism.

Defibrillation. Defibrillation is the asynchronous depolari­ zation of a critical mass of myocardium that successfully terminates ventricularfibrillation or pulseless ventricular tachycardia. It is successful in cases of sudden onset fibril­ lation along with oxygenated normothermic myocardium without significant acidosis. Small paddles are used in infants and children weighing less than 10 kg. Larger size defibrillatorpaddles, i.e. 8to 10cmindiameter, arerecom­ mendedinchildrenweighingmorethan 10kg to maximize the current flow. One paddle is placed over the right side of the upper chest and the other one over the apex of the heart (to the left of the nipple over the left lower ribs).

Theoptimalelectricalenergydosefordefibrillationisnot conclusively established in children, but varies from 2 to 4 J/kg. If this is unsuccessful, higher energy dose should beused. SingleshockstrategyfollowedbyimmediateCPR (beginning with chest compressions) is recommended for children with out-of-hospital or in-hospital ventricular fibrillation or pulseless ventricular tachycardia. After 5 cycles ofCPR,therhythmischeckedtolookforreversion to sinus rhythm. Simultaneous correction of hypoxia, aci­ dosis and hypothermia is necessary. After failure of 3 attempts,atrialofdefibrillationisrepeatedafteradminis­ tering epinephrine and CPR for 30 to 60 seconds. After the fourth failed defibrillation, the use of amiodarone (5 mg/ kgbolus)or lidocaine (1 mg/kg) followed bydefibrillation with 4 J/kg is recommended.

Pediatric Critical Care -

Suggested Reading

2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommen­ dations; part 10: Pediatric Basic and Advanced Life Support. Cirwlation 2010;122:S466-515

SHOCK

Shock is an acute syndrome that occurs because of cardiovascular dysfunction and inability of circulatory system toprovideadequateoxygen and nutrientsto meet the metabolic demands of vital organs. Shock can be classified as: (i) hypovolemic; (ii) distributive (septic, anaphylactic, drug toxicity, neurogenic); (iii) cardiogenic (congenital heart disease, ischemic heart disease, cardio­ myopathy, tamponade or arrhythmias); (iv) obstructive (pulmonary embolism); and (v) due to miscellaneous causes (pancreatitis, heat stroke or adrenal insufficiency).

Pathophysiology

The body has several regulatory systems that maintain adequate perfusion to vital vascular beds.

Baroreceptors. Reduction in mean arterialpressure orpulse pressure results in decreased stimulation of carotid sinus andaortic archbaroreceptorswhich leads tovasoconstric­ tion byinhibition of vasomotor center. Vasoconstriction is severe in skeletal muscles, splanchnic and cutaneous vas­ cularbeds whereas flowis preserved in cerebral, coronary and renal circulation due to autoregulation.

Chemoreceptors. Hypotension causes reduced perfusion, localtissue hypoxiaand acidosisleading tofiring of signals from chemoreceptors. Increased signals from these recep­ tors cause respiratory stimulation, increased vasocons­ triction and cardiac function.

Humoral receptors. Release of epinephrine and norepine­ phrine from adrenal medulla and systemic adrenergic nerve endings causes vasoconstriction and inotropic and chronotropic effects.Releaseof vasopressin from the pos­ terior pituitary leads to vasoconstriction and water reabsorption.

Renin-angiotensin-aldosterone system. Reducedrenalperfusion stimulates release of renin from the juxtaglomerular cells of kidney. Renin enhancesconversion of angiotensinogen toangiotensinI,whichissubsequentlyconvertedtoangio­ tensin II by angiotensin converting enzyme. Angiotensin II is a potent vasoconstrictor and also stimulates release of aldosterone, enhancing renal sodium reabsorption.

Diagnosis

Diagnosis of shock at an early stage and appropriate managementmayimprovetheoutcome.Themanagement ofachildwithclassicfeaturesofshock, includinglethargy, ashen graycolor, tachypnea, cold extremitieswithdimini­ shedperipheral pulses andhypotension, is difficult. Early diagnosis of shock requires ahigh degree ofsuspicion and

knowledge of conditions that predispose to shock. Childrenwhohavefever,anidentifiablesourceofinfection or hypovolemia due to any cause are at increased risk of developingshock. Signsofearlyshockincludetachycardia, mild tachypnea, prolonged capillary refill (>2-3 sec), orthostatic change in blood pressure or pulse and mild irritability. Table 27.7 summarizes the features of various stages of shock. Unexplained tachycardia may be the earliest indicator of shock. Decreased tissue perfusion can be identified by changes in body temperature (i.e. cold extremities)anddecreasedcapillaryrefill (rateofrefillafter firm pressure over soft tissues or nail bed for 5 seconds). Narrowing of pulse pressure is an early finding of shock dueto reduction insystolicbloodpressureand mild incre­ ase in diastolic blood pressure. Early septic shock reveals increased peripheral pulses, warm and overperfused extremities, widened pulse pressure and hyperdynamic precordium.

Ifthestate of shockcontinues, thecompensatorymecha­ nismsarenotenoughtomaintainthemetabolicneedsofthe tissues. The cellular ischemia and inflammatory mediators released affect the microcirculation to compromise the functioning of brain, kidney and heart. Increase in tachy­ pnea duetometabolicacidosisleadstoreduction inPaCO2 and respiratory alkalosis. Skin shows features of reduced capillaryrefillandmottling. Hypotensionand oliguriasets in with hypothermia. Mental changes in the form of agitation, confusion, stupor and finally coma may occur.

Clues in the history that suggest hypovolemic shock include (i) fluid losses due to diarrhea, vomiting, blood loss, profuse and prolonged sweating, or polyuria or a combination of these; and (ii) decreased intake due to vomiting, poor appetite or fluid deprivation. Physical examination shows dry mucous membranes, absence of tearsand decreased urine output. Others features arepoor perfusion, delayed capillary refill, diminished peripheral pulses and poor color. The central venous pressure is usually low. Laboratory investigations show elevated blood urea and to a lesserextent creatinine, elevated uric acid levels and small cardiac silhouette on chest X-ray.

Patients with cardiogenic shock show presence of a murmur, extra heart sounds (S3, gallop), elevated JVP, hepatomegaly or friction rub. Central venous pressure is usually elevated. Chest X-ray film may show a large silhouette and pulmonary edema.

Thetriad offever,tachypneaand tachycardia iscommon in benign infections in children. Septic shock is suspected if, in addition to these, there are features such as altered mentation, prolonged capillary refill of >2 seconds (cold shock) or flush capillary refill (warm shock), diminished or bounding peripheral pulses, or decreased urine output of <1 ml/kg/hr. Hypotension is a relatively late finding in septic shock.

Monitoring

Monitoring of patients who are in shock or impending shockis done to detect the alteration in physiologic status and intervene at the earliest. Clinical parameters to be monitored are pulse rate and volume, respiratoryrate and pattern, temperature, skin color, blood pressure, senso­ rium, urine output, ECG and pulse oximetry. Metabolic parameterstobemonitoredarebloodglucose,electrolytes and arterial blood gases. Invasive pressure monitoring shouldbedonewhereverpossiblebymeasurement ofcen­ tral venous pressure and by pulmonary arterial cathe­ terization using a Swan-Ganz catheter.

Treatment

Therapy essentially depends on the type of shock. In hypovolemic shock, replacement of intravascular volume by isotonic intravenous fluid is the mainstay of therapy. Cardiogenic shock usually requires inotropic support. In some cases of cardiogenic shock, reduction of afterload by use of vasodilators may be beneficial.

Fluid Therapy

Vascular access. A largebore intravenouscannula on cathe­ ter should be placed in a large vein like femoral vein. In older children and adolescents, cannulation of internal jugular, externaljugular, subclavian veins can be consi­ dered.

If there is undue delay in establishing central or peri­ pheral venous access, intraosseous access should be considered in an emergency setting (see Chapter 28).

Choice offluids and bloodproducts. Thefirstchoiceoffluidfor acuteresuscitation isnormalsalineorRingerlactate. Large volumes of fluid for acute stabilization have not been shown to increase the rate of acute respiratory distress syndrome or cerebral edema in children. Crystalloids are the fluid of choice in the acute phase but if the fluid

requirementishigh,colloids(dextran,gelatin,5%albumin) may be used. Experience with starch, hypertonic saline or hyperoncotic albumin is limited in pediatric practice. Packed RBC should be given at 10 ml/kg to maintain hematocrit at 33%.

Volume offluids. Fluid infusion is best started with boluses of 20 ml/kg titrated with clinical parameters of cardiac output like heart rate, capillary refill, sensorium. The ideal first fluid should be normal saline or Ringer lactate and infused rapidly over 5-10 min. If no significant improve­ ment is noticed, repeat boluses of 20 ml/kg should be given. Large volume fluid deficits may require 40 to 60 ml/kg and maximum up to 200 ml/kg for replenishing the deficit. The patients who do not respond to rapid boluses of 40-60 ml/kg in first hour of therapy are labeled as fluid refractory shock and should be given inotropic support. Such patients require invasive monitoring and need intubation and mechanical ventilation.

Vasoactive Drugs

Vasopressortherapy. Dopamineisacceptedastheinotropeof choiceforshockwithhighoutputandlowsystemicvascular resistance in both newborns and children (Table 27.8). Dopamineincreasescardiacoutputatdosesof5-10µg/kg/ min.Thevasoconstrictoreffectofdopamineisevidentatdoses above15µg/kg/mindueto release ofnorepinephrinefrom sympathetic vesicles which may not be well developed in infantsbelow6 months.Administeringdopaminein'renal' doses (2-5 µg/kg/min) does not have a role in preventing ortreatingacutekidneyinjury.Patientswithshockrefractory to dopamine may respond to norepinephrine or high doses of epinephrine. Some intensivists use low dose nor­ epinephrine as the firstlineagent for warm hyperdynamic shock. The dose of vasopressors used can be titrated to perfusionpressureorsystemicvascularresistancethatensures optimum urine output and creatinine clearance.

Inotropic therapy. After initial fluid resuscitation, myocar­ dial contractility should be augmented to improve the cardiac output to meet the metabolic demand and cate­ cholamines are the most useful drugs for this effect (Table 27.9). Dobutamine and mid-dose dopamine are first line inotropic agents in adults, but children may be less responsive. Epinephrine infusion is useful in cases of dopamine or dobutamine refractory shock. Low dose epinephrine may be used as first linechoice for cold hypo­ dynamic shock, i.e. low cardiac output states.

In children remaining normotensive with low output state and high vascularresistance despite epinephrine and vasodilator, use of type ill phosphodiesterase inhibitors should be considered. These agents increase cyclic AMP and potentiate the areceptor stimulating effect on cardiac vascular tissue. These drugs should be discontinued at the first sign of tachyarrhythmia, hypotension or diminished systemic vascular resistance.Hypotensioncanbeovercome by stopping epinephrineandstartingnorepinephrine which acts by stimulating a receptor activity.

Vasodilator therapy. Vasodilators are of use in pediatric patients remaining in hypodynamic with high systemic vascular resistance shock despite fluid and inotropic support (Table 27.8). Figure 27.5 outlines the plan of management of a child with septic shock.

Acid-base and Metabolic Parameters

Therapy with sodium bicarbonate rarely maintains the arterialpHiftheperfusionandventilationarenotoptimized. So, it should be considered as a temporary and immediate therapy to improve the myocardial function, only when the pH is less than 7.2. Improved circulation and oxygenation improves the acid-base homeostasis. Hypoglycemia and hypocalcemia should be rapidly diagnosed and corrected along with attempt to prevent recurrence.

Antibiotic Administration

Appropriateantibioticsshouldbe administered topatients in septic shock. The choice of antibiotics depends on the focus ofinfectionand the most likelypathogen. If no focus is obvious, the patient is given antibiotics that cover both gram negative and gram positive bacterial infections (e.g. third generation cephalosporin and vancomycin). Pus collections should be drained.

Steroids

Therapy with corticosteroids is recommended in patients with catecholamine-resistant shock and suspected or proven adrenal insufficiency. Other therapies that have

been used anecdotally include naloxone hydrochloride (blocks endorphin effect), methylene blue (inhibits nitric oxide release), activated protein C and extracorporeal membrane oxygenation.

Suggested Reading

Carcillo JA, Fields AL. Task Force of the American College of Critical Care Medicine, Society of Critical Care Medicine. Clinical practice parameters forhemodynamicsupportof pediatric andneonatalpatients in septic shock. Crit Care Med 2002;30:1365-78

Tabbutt S. Heart failure in pediatric septic shock: utilizing inotropic support. Crit Care Med 2001;29(10 Suppl):S231-6

Zingarelli B. Shock and reperfusion injury. In: Nichols DG (Ed.): Roger's Textbook of Pediatric Intensive Care, 4th edn. Lippincott Williams & Wilkins: Philadelphia 2008;252-65

MECHANICAL VENTILATION

Principles

Themaintenanceofnormalgasexchange dependson ade­ quate oxygenation and ventilation. Oxygenation depends onthefractionof02 (Fi02) andtheextentofventilation-per­ fusionmismatch. IncreasingtheFi02 increasesthealveolar P02 (Pa02) andtherebythearterialP02 (Pa02). Ventilation­ perfusion mismatch is usually due to atelectasis or poorly ventilated alveolar units, which act as right to left shunts. Theseunitscanberecruitedby increasingthemeanairway pressure (MAP), which reduces mismatch and increases theendexpiratoryvolume,therebyimprovinglungcomp­ liance. MAP depends on the peak inspiratory pressure (PIP),positiveendexpiratorypressure(PEEP),inspiratory time (Ti), expiratorytime (Te) andthe characteristicsofthe waveform (k).

PaC02 depends on CO2 production and the alveolar ventilation.

Alveolar ventilation = [Tidal volume (VT)- dead space volume (V0)]x respiratory frequency (f)

The PaC02 can be altered by regulating VT and frequency. Efforts should be made to minimize the dead space during mechanical ventilation. Tidal volume (VT) depends on the difference between PIP and PEEP, airway resistance, compliance, and inspiratory time (Ti).

Indications

The indications for mechanical ventilation are listed in Table 27.10.

Modes

Mechanical ventilators can deliver four different types of breaths: mandatory, assisted, supported, or spontaneous, or a combination of these.

Mandatory or Controlled Ventilation

In controlled ventilation, all breaths are triggered, limited and cycled by the ventilator. This mode is used when the

Table 27.10: Indications for mechanical ventilation

Establishedorimminentrespiratoryfailuredueto (i)pulmonary disease and (ii) hypoventilation or apnea caused by central nervous system pathology

Impaired ventilation due to neuromuscular diseases or chest wall trauma

Postresuscitation for circulatory arrest

To reduce the work of breathing in circulatory shock

For hyperventilation to reduce raised intracranial pressure Prophylactic indication: During and after surgery

Pediatric Critical Care -

patient's ventilatory drive is limited or absent and during neuromuscular blockade by drugs.

Pressure controlventilation. The ventilator deliverspositive pressure up to a predetermined pressure above PEEP at a set frequency during preset inspiratory time. The tidal volume delivered depends on the lung compliance. This mode is preferred in newborns and young infants.

Volume control ventilation. In this mode, a preset tidal volume is delivered during the set inspiratory time and a set frequency. In contrast to pressure control ventilation, afixedtidalvolumeandminuteventilationaremaintained. However, in newborns and young infants, the tidal volume required is small. In this scenario, the losses in the ventilator circuit significantly reduce the effective volumedeliveredtothelungsleadingto ineffective venti­ lation, hence the pressure controlled mode is preferred.

Pressure regulated volume control ventilation. This mode combines the features of volume and pressure control modes. It uses decelerating inspiratory flow waveform to delivera settidal volume duringthe selected Ti and at set frequency. The advantage of this mode over volume control is that ventilation occurs at lower pressures, thereby reducing barotrauma.

Assisted Ventilation

Assisted ventilation is identical to the controlled modes except that the patient's inspiratory effort triggers the ventilator to deliver the breath using preselected limit and cycle variables, i.e. the ventilator completes patient triggered breathing efforts. Assisted ventilation thus reduces patient efforts and optimizes comfort. These modes are often used during weaning.

Assist control ventilation (ACV). In this mode of mechanical ventilation, the ventilatorprovides a presetVT or pressure in response to every patient-initiated breath. If the patient fails to initiate a breath within a preselected time period, the ventilator delivers the VT or pressure at the pre­ determined frequency. Since every inspiratory effort detected by the machine results in a mechanical breath, hyperventilation and respiratory alkalosis may occur.

Synchronized intermittent mandatory ventilation (SIMV). In this mode, mechanical breaths are delivered at a preset frequency, but the machine tries to deliver these breaths in response to the patient's spontaneous inspiratory efforts. For example, if a SIMV frequency of 20/minute is chosen, a breath is due every 3 seconds. If the machine detects patient's inspiratory effort during a small time windowwhenthebreathisdue, itsynchronizesthebreath. If no such effort is detected during the time window, the machine delivers the breath on its own. In between the mandatorybreaths,thepatientcanbreathespontaneously. There is no risk of hyperventilation even if patient is

breathing rapidly because only the set SIMV frequency willbedelivered. Whilethismodehasconventionallybeen used as a weaning mode, this mode can be used as a starting mode.

Supported Ventilation

Supported ventilation is defined as breaths that are triggered by the patient, limited by the ventilator and cycled by the patient. In pressure support ventilation, the patient triggers the ventilator to deliver a flow of gas sufficienttomeetthepatient'sdemandswhilethepressure in the circuit increases because of closure of the expiratory valve. Inspiration isterminated when the inspiratory flow decreases to a percentage of its initial peak value. This modedecreasesinspiratorywork and abolishesdiaphrag­ matic muscle fatigue and enables weaning.

Adjusting Settings on Mechanical Ventilation

Patient age andweight, thespecific disease and the under­ lying pathophysiology are important parameters consi­ dered when ventilator settings are adjusted. The choice of initial settings is summarized in Table 27.11. Higher PEEP may be required in ARDS.

While a patient is receiving mechanical ventilation, clinical assessment includes evaluation of chest move­ ments/expansion, air entry, breath sounds and the color of the skin. Pulse oximetry is a useful adjunct. The patient ventilator interaction should be evaluated carefully and efforts aremadetoimprove synchronization.Aftera short time of stabilization, blood gases are measured and necessary adjustments made.

Weaning from VenHlatlon

Weaning is the process of discontinuation of mechanical ventilation. As the child's condition improves, the need for ventilatory support decreases. Decreasing support earlier than indicated imposes greater work of breathing whichwoulddelayextubation. Discontinuation ofmecha­ nical ventilation can be considered when: (i) the child is hemodynarnically stable and neurologically improved; (ii) underlying disease and its complications have improved; (iii) ventilator support is minimal compared withthe patient'sspontaneousbreathing;and (iv) the Fi02

is low (.$.0.4).

During weaning, the ventilator's contribution to total ventilation is gradually reduced, as the patients' share is increased. Usually during SIMV (preferable) mode or by reducing the frequency of pressure controlled breaths. This goes on until no or minimal ventilator breaths are used.

NUTRITION IN CRITICALLY ILL CHILDREN

A critically ill child is prone to develop malnutrition. Decreased intake and accelerated demands of severe illness due to stress results in increase in resting energy

Table 27.11: Guidelines for initiating positive pressure ventilation

Maintenance of adequate oxygenation

Set Fi02 at 1.0

Keep peak end expiratory pressure (PEEP) at 3 cm H20 or higher as required by underlying lung disease

Assess for signs of adequate oxygenation (e.g. color, pulse oximetry) and circulatory status

Measure Pa02; decrease Fi02 while maintaining Pa02 70-80 mm Hg. In restrictive disease (low compliance, low functional residual capacity), increase PEEP to achieve Pa02 >70 mm Hg at Fi02 <0.6

Providing adequate alveolar ventilation

Set respiratory rate at physiologic norm for age Select tidal volume (Vr) of 5-6 ml/kg

Keep peak inspiratory pressure (PIP) at about 15-20 cm Hp for normal lungs, 20-25 cm H20 for moderate pulmonary disease and at 25-30 cm H20 for severe disease

Begin ventilation with the ratio of inspiratory to expiratory time (I:E) at 1:2, keeping the inspiratory time initially at 0.4-0.5 seconds in young infants and higher for older children In obstructive disease, use longer expiratory time and avoid prolonged inspiratory time

Assess chest expansion and breath sounds to determine adequacy of ventilation

Measure PaC02; adjust Yr, PIP or rate to maintain PaC02 between 35 and 45 mm Hg

expenditure, proteolysis, gluconeogenesis, urinary nitro­ gen loss, glucoseintolerance and resistance to insulin. In sick children, reduced nutrition intake is an important factor determiningoutcome. It isessentialto provide ade­ quate nutrition early in course of severe illness in order to improve the outcomes.

Tworoutesare availablefor administration ofnutrients, enteralandparenteral. Iftheintestinesarefunctioning,the enteral route is preferred, since it is safer and more cost effective thanparenteralnutrition.Enteralnutritionhelps in maintaining the gut barrier, preserves the indigenous flora andpreventsovergrowth of the pathogens, reducing the risk of bacteremia and pneumonia. Enteral feeding prevents gut mucosa} atrophy, so thatresumption of oral feeds is easier duringrecovery.

While a milk based feed is simple, various commercial formulae are available to supplement nutrition. The ele­ mentalformulaecontaincarbohydratesasoligosaccharides, maltodextrins or hydrolyzed corn starch; nitrogen as peptides or free amino acid and lipids as various oils or medium-chain triglycerides. Special formulae are also available,e.g.lowlactoseorlactosefreediets. Itisimportant to start with 10-15 ml/kg/day of feeds and increase by 10-15 ml/kg/day till target calories are achieved. Enteral feedsmaybedelivereddirectlyintothestomachbynasal/ oral routes. Small-bowel feedings are useful in cases of gastroparesis. Supplementation of vitamins and minerals is best done by enteralroute.

Common conditions where enteral feeding is contra­ indicated are severe gastrointestinal hemorrhage, recent gastrointestinal surgery and intestinal obstruction. Complicationsofenteral feedingareintolerance,misplace­ ment of the feeding tube, esophagitis and esophageal ulceration.Gastroesophagealrefluxmayleadtopulmonary aspiration. Diarrhea may occur because of hyperosmolar formulae, infection or malabsorption.

Parenteral nutrition refers to the delivery of all the nutrientsdirectlyintothebloodstream, throughamino acid mixtures, lipids, glucose and trace mineral and vitamins. These may be infused into a peripheral or central vein.The use of peripheral veins is limited by the osmolality of infusate (should be <700 mOsm/kg).Thus, for delivery of adequate calories, central venous access is essential.

For infants,thegoalforcalories isabout 100cal/kg/day. Glucose infusions are started at a rate of about 5-6 mg/ kg/minute and increased gradually; insulin may be used if there is hyperglycemia. Amino acids are begun at 1 g/ kg/day; then increased over 2-3 days to 2.5 g/kg/day. Lipids are infused at 0.5 g/kg on day 1 and increased to 2-2.5 g/kg/day over 4-5 days. Appropriate combination can be achieved by considering fluid requirements.Trace elements and vitamin preparations are added.Use ofTPN requires regular monitoring blood glucose thrice a day; serum electrolytes and urea twice a week; and serum chemistry, triglyceridesandcomplete blood counts once a week.Weightisrecordeddaily;otheranthropometricmea­ surements recorded once a week. Complications include catheter related infections, liver dysfunction, hyperglyce­ mia, hyperlipidemia, acidosis and electrolyte imbalances.

The use of enteral formulae supplemented with irnmunonutrientshasbeen demonstrated tomodulate gut function, inflammatory and immune responses. Agents used for irnmunonutrition include glutamine, arginine, 0>3 fatty acids, nucleotides, taurine, cysteine, certain com­ plex carbohydrates and probiotic bacteria.Use ofirnmuno­ nutritionmight reducemorbidity and the risk of infectious complications in critically ill patients.

Suggested Reading

Biolo G, Grimble G, Preiser JC, et al. Metabolic basis of nutrition in intensive care unit patients. Intensive Care Med 2002;28:1512-20

deCarvalho WB,Leite HP.Nutritionalsupportinthe criticallyill child. In: Nichols DG, ed. Roger's Textbook of Pediatric Intensive Care, 4th edn. Lippincott Williams & Wilkins, Philadelphia 2008;1500-15

SEDATION, ANALGESIA AND PARALYSIS

The management of acute pain and anxiety in children undergoing therapeutic and diagnostic procedures has improved substantially.The goal of sedation is safe and effective control of pain and anxiety so as to allow neces­ sary procedures to be performed and to provide appro­ priate amnesia or decreased awareness.

The state of sedation varies from conscious sedation to deep sedation to general anesthesia. Inconscious sedation,

Pediatric Critical Care -

the consciousness is depressed but the protective airway reflexes are maintained and the child can respond appro­ priately to verbal command or physical stimulation. Deep sedationrefers to amedicallycontrolledstate of depressed consciousness from which the child is not easily aroused. This is accompanied by partial or complete loss of protec­ tive reflexes and the child cannot respond purposefully to physical stimulation or verbal commands.

Monitoring isveryimportant duringsedation.Thechild's face, mouth and movement of chest wall must be conti­ nuously observed. Vital signs should be measured before and after administration of the drugs, on completion of the procedure, duringrecovery and at completion of recovery. ECG monitoring and pulse oximetry are useful adjuncts. The sedation and procedure room should have all the equipment for airwaymanagementand essential drugs for resuscitation.

Table 27.12 summarizes the details of commonly used drugs for sedation and analgesia.Table 27.13 lists various clinical scenarios requiring sedation or analgesia. For children undergoing mechanical ventilation, continuous infusion of midazolam or diazepam may be used for better control of ventilation. In addition, intermittent doses or continuous infusion of fentanyl or morphinemay be used for pain control.

Neuromuscular Blocking Drugs

The use of neuromuscular blocking drugs is common in intensivecareunits.Succinylcholineistheonly depolarizing muscle relaxant available. Nondepolarizing drugs include pancuronium, atracurium, vecuronium and rocuronium. Short-term indications for use of these drugs are to: (i) facilitateairway instrumentation; and (ii) facilitate invasive procedures; while longterm use is required (i) to facilitate mechanical ventilation, overcome patient-ventilation asynchrony and allow ventilation at high settings; (ii) for reduction of work of breathing and metabolic demands; (iii) for treatment of agitation unresponsive to maximum sedation and analgesia; (iv) to treat tetanus; and (v) to facilitate treatment ofstatusepilepticus, undercontinuous EEG monitoring.

Children receiving neuromuscular blocking drugs should be monitoredvery carefully, particularly for posi­ tion of artificial airway and adequate ventilation. Any child who requires paralysis should be sedated.

Suggested Reading

Krauss B, Steven SM. Sedation and analgesia for procedures in children, N Engl J Med 2000;342:938-45

Young C, Knudsen N, Hilton A, Reves JG. Sedation in intensive care unit. Crit Care Med 2000;28:854-66

NOSOCOMIAL INFECTIONS IN PICU

Nosocomial or hospital acquired infections are infections that occur during hospitalization and are not present or

IM intramuscular; IV intravenous; PO per orally

Table 27.13: Common indications and strategy for sedation and analgesia

Duration of action, min

60-120

4-6 hr

45-60

60-120

10

30-60

15-60

15-150

incubating at admission. These also include infections that appear to have been acquired in hospital but do not manifest until after discharge. Hence, all infections diagnosed 48 hr after admission until 72 hr after discharge are considered nosocomial.

Nosocomial infections are a significant problem in PICUs. The increased risk of infection results from the severity of underlying disease, frequent invasive inter­ ventions and the use of devices that bypass natural barriers

to infection. The estimated rates vary between 10 and 20 per 1000 patient days or 6-10% of all admissions. Primary bloodstream infections account for 25-30% of nosocomial infections; other common infections include, pneumonia (20-25%) and urinary tract infection (15-20%). Usual pathogens include S. aureus, coagulase negative staphy­ lococci, E. coli, P. aeruginosa, Klebseilla spp., enterococci and Candida. The overall mortality attributed to nosocomial infections is about 10%.

The risk of nosocomial infections is increased in propor­ tion to the severity of illness, the level of invasive moni­ toring, the indiscriminate use of antimicrobial agents and the nature of diagnostic procedures. The duration of stay in an ICU is an important determinant of nosocomial infection. Theuseof invasive devices (endotracheal tubes, intravascularcatheters,urinarycatheters)hasanimportant roleincausationofbloodstreaminfections,pneumoniaand urinarytractinfections. Occasionally, theenvironmentmay be the source of organisms causing life-threatening noso­ comial infections, e.g. aspergillosis in immunocompro­ mised individuals.

Strategies to Prevent Nosocomial Infections

Well-directed infection control activities can reduce the nosocomial infectionratesby up to 50%. Each PICUshould have an infection control program aimed at reducing the incidence of nosocomial infections. A team of health professionals should ensure implementation ofthe policies and compliance on part of the PICU team.

The importance of hand washing and hand disinfection is well proven. Appropriate hand washing should be followed by drying with disposable paper or cloth towel. Hygienic hand rubs are increasingly used. Rubbing of 3-5 ml of a fast acting preparation (n-propanol, isopropanol, ethanol and chlorhexidine diacetate) is an effective substitute to hand washing.

In addition to the specific measures mentioned earlier for prevention of specific nosocomial infections, proper sterilization or disinfection of various medical items is mandatory. Aseptic precautions should be followed whenever an invasive procedure is being carried out. Nutrition should be maintained; enteral nutrition is preferred to parenteral nutrition. Appropriate and rational prescription of antibiotics is essential to prevent emer­ gence ofresistant strains. There should be constantsurveil­ lance and periodic review of the antibiotic policies and prescriptions. Education of staff about various infection control practices and procedure-specificguidelines has an important role in reducing the incidence of infections.

Surveillance for nosocomial infections is an essential element of any infection control program. This provides data foridentifyinginfectedpatients, determining the sites of infection and identifying risk factors that contribute to nosocomial infections. Control measures can be evaluated objectively if the surveillance is good.

Specific Measures to Prevent Infections

Nosocomial pneumonias. The colonization of upper airway by pathogenic microbes and thereby, the risk of noso­ comial pneumonias, can be reduced by compliance to hospital infection control policies and effective hand washing by healthcarepersonnel.The use of antacids and H2 blockers raises gastric pH and facilitates gastric microbial colonization. When indicated, sucralfate may

Pediatric Critical Care -

be preferred for prophylaxis against gastric bleeding. Selective decontamination of the gut using tobramycin, gentamycin,polymyxin and nystatinis notrecommended.

Contaminated respiratorytherapy equipment has been implicatedinnosocomialpneumonias.Resuscitationbags, ventilator tubings and nebulizers should be disinfected. Only sterile fluids should be nebulized or used in humi­ difiers. Care should be taken to prevent contamination during suctioning. Ventilator circuit tubings should be changed every48 hr. Positioning with head end elevation reduces the riskof aspiration and nosocomial pneumonias.

Bloodstream infections. The chief factors associated with development of catheter-related bloodstream infections are: (i) breach in sterility of technique of insertion and maintenance of the catheter; (ii) administration of paren­ teral lipid solutions through the intravenous catheter; (iii) increased number of 'break-ins' into the catheter and/or intravenous tubings; and (iv) the presence of infection elsewhere in the body.

The following measures help in reducing catheter­ related infections: (i) preferring catheter insertion into the subclavian, basilic or cephalic vein instead of femoral or internaljugular vein; (ii)usingmaximalaseptic precautions during catheter insertion; (iii) use of mupirocin ointment (reduces the risk of bacterial colonization but increases colonization rate of fungi); (iv) use of cotton gauze rather than transparent dressing; (v) insertion of catheter by an experienced physician; (vi) avoiding the use of TPN catheters for infusions other thanTPN; and (vii) provision of adequate staff for management of patients with central venous catheters.

Urinary tract infections. The need for catheterization must be strictly evaluated. Strict asepsis should be maintained duringinsertion of thecatheterusingsterilegloves, drapes and localantiseptics.Closed drainageshould be maintained with the collection tubing and bag kept below the level of the patient's bladder. The system must be handled and manipulated as infrequently as possible. The urinary catheter should be replaced by closed condom drainage, whenever possible. While antibiotic prophylaxis does reduce the frequency of infections, it is not universally recommended as it selects multidrug resistant strains.

Suggested Reading

Lodha R, Natchu UCM, Nanda M, Kabra SK. Nosocomial infections in pediatric intensive care units. Indian J Pediatr 2001;68:1063-70

Richards MJ, Edwards JR, Culver DH, Gaynes RP, and the National Nosocornial Infection Surveillance System. Nosocomial infections in pediatric intensive care units in the United States. Pediatrics 1999;103:e39

TRANSFUSIONS

Blood

The common indications for red cell transfusion in children are listed in Table 27.14.

Table 27.14: Common indications for red cell transfusion Infants

Hematocrit ::;20% and asymptomatic with reticulocytes <100,000/mm3

Hematocrit ::;30% and any of the following: Oxygen requirement >35%

Requiring mechanical ventilation or continuous positive airway pressure

Significant apnea or bradycardia

Heart rate>180/min or respiratory rate >80/min persisting for >24 hr

Weightgain <10g/day over 4 days while on 100 Cal/kg/day

Children

Hemoglobin ::;4g/dl (hematocrit ::;12%), irrespective of the clinical condition

Hemoglobin 4-6 g/dl (hematocrit 13-18%) with hypoxia, acidosis or impaired consciousness

Anemia with features of cardiac decompensation Hyperparasitemia (>20%) during malaria

Transfusion for acute blood loss. If the patient with acute blood loss is not stabilized after 2 boluses of 20 ml/kg of isotonic crystalloids, it is likely that the loss exceeds 30% of blood volume; hence such patients should receive transfusion with fresh blood.

Transfusion for chronic anemia. Children with chronic ane­ mia usually tolerate hemoglobin levels as low as 4 g/dl. It is important to identify the underlying cause of anemia andtreat it appropriately. Standard rules regarding choice of blood group should be followed. For red cell trans­ fusion, the choices are based on the principle that the recipient plasma must not contain antibodies corres­ ponding to donor A and/or B antigens. For plasma and platelet transfusion, donorplasmamust not contain A/B antibodies corresponding to recipient A or B antigens. Patients who are RhD antigen positive may receive RhD positive or negative RBCs but patients who are RhD negative should receive only RhD negative RBCs.

Quantityoftransfusion. The quantityofblood administered depends on the donor hematocrit, pretransfusion hemo­ globin level and patient'sweight. If the hemoglobin level is above 5 g/dl and packed red cells (hematocrit 0.7-0.75) are used, a transfusion of 10 ml/kg usually raises hemo­ globin level by 2.5 g/dl. If anemia has developed slowly andhemoglobinlevelisbelow5 g/dl,redcellstransfusion should be given slowly or in small quantities to avoid precipitating cardiac failure from circulatory overload.

Massive transfusion. The replacement of blood loss equivalent to or greater than the patients total blood volume withstoredblood in less than 24 hr (70 ml/kg) in adults and 80-90 ml/kg children/infants constitutes massive transfusion.

Platelets

The need for platelet transfusion depends on the platelet count, bleeding tendency, underlying etiology and

interventions like invasive procedures or surgery (Table 27.15). Platelet concentrates are usually prepared from whole blood donation and less commonly by apheresis. Usually, each unit (bag) of platelets contain about 5.5 x 1010 platelets, 50 ml plasma, trace to 0.5 ml of red cells and varying number of leukocytes (up to 108). Units of platelet collected by apheresis contain 3 x 1011 platelets, approximately 250-300 ml plasma, trace to 5 ml of RBCs and 106 - 109 leukocytes.These units can be stored for up to 5 days at 20-24°C.

Plasma

Plasma is prepared from a whole blood donation by centrifugation or can be collected using automated apheresis techniques. When prepared from whole blood donations, each unit contains 150-250 ml of plasma and, immediately following collection, approximately 1 unit/ ml of each of the coagulation factors. Coagulation factors V and VIII are heat-labile and not stable in plasma stored at l-6°C. After24hrofdonation,theplasmacontains<15% of factor V and VIII. Plasma frozen within 8hr of donation contains at least 0.7 U/ml of factor VIII and is called fresh frozen plasma (FFP). FFP may be stored for 12 months at temperature at or below -18°C. The use of FFP is limited to the treatment or prevention of clinically significant bleeding due to deficiency of one or more plasma coagu­ lation factors. The indications for FFP transfusion are listed in the Table 27.16.

Dosage and administration. Compatibility tests are not necessarybeforeplasma transfusionandit isonlyessential that the plasma is ABO compatible with the recipient's red cells. The Rh group need not be considered unless where large volumes of FFP are required. FFP is thawed in a water bath at 30-70°C or in a microwave designed for

this purpose. The dose of FFP depends on the clinical situation and the underlying disease. If used at a dose

Table 27.15: Indications for transfusion of platelets

Platelet count <10 x 109/1 due to any cause

Plateletcount <20 x 109/1 andbone marrowinfiltration, severe mucositis, disseminated intravascular coagulation or anticoagulant therapy

Platelet count <30-40 x 109/1 and disseminated intravascular coagulation

Platelet count <50----60 x 109/1 and major surgical intervention

Table 27.16: Indications for transfusion of fresh frozen plasma

Anticoagulant overdose

Severe liver disease with prolonged prothrombin time or bleeding tendency

Disseminated intravascular coagulation Massive or large volume transfusion

Isolated congenital coagulation factor deficiency, e.g. hemophilia A or B