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Critical Care Pediatrics

David Johnson, M.D.

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Importance of Early Recognition of System

Failure

# Outcomes in pediatric cardiopulmonary arrest are generally

poorer than in adults.

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Projected Impending Existing Failure

• Respiratory Failure

• Circulatory Failure

• CNS Failure

• Organ Failure

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Respiratory Failure

## Inadequate oxygenation and CO excretion2

## Respiratory distress is not always present

Respiratory failure causes most of thecardiopulmonary arrests and involves most of thecritical pediatric arrests. The respiratory systemneeds to maintain oxygenation and excrete carbondioxide. Hypoxemia may be occult. It takes ahigh degree of hypoxemia before the respiratorycenter is stimulated to generate the kind ofventilatory response that will identify clinically.So there are some babies whose oxygen saturationis in the low 90’s or the high 80’s who may haveno symptoms as a result of the hypoxemia. Andtherefore we try to keep a high index of suspicionfor respiratory disease and for hypoxemia, espe-cially in young infants.

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Causes of Airway Obstruction

## Congenital Lesions

# Acquired Lesions

# Infections

• Epiglottitis

• Laryngotracheobronchitis (croup)

• Retropharyngeal Abscess

• Bacterial Tracheitis

Now when we talk about respiratory failure Ithink it makes sense to start with the upper airwayand then work our way down through the respira-tory tree to the alveoli. An airway obstruction canbe caused by any number of different lesions.Congenital lesions are numerous. Take for in-stance a call to the delivery room. The child hassevere respiratory distress, which may be causedby bilateral commingled atresia. Newborn infantsare almost exclusively obligate nose-breathers,and, therefore, bilateral choanal atresia would bean example of a congenital lesion that wouldcause upper airway obstruction. There are variousacquired lesions. They could be mass lesions orinfections lesions, which cause inflammatoryconditions that obstruct the airway.

There’s always a lot of focus on epiglottitis.We’ve seen one case of epiglottitis in our emer-gency department that treats 50,000 kids a year.One case of epiglottitis in the last four years. Butas a model for upper airway obstruction I think allthat you learned about epiglottitis pertains to otherinflammatory conditions.

Laryngotracheobronchitis, or croup, is a muchmore common cause of upper airway obstruction.On rare occasions viral laryngotracheobronchitiscan be life-threatening. And in those cases theymay need critical care intervention to maintain theairway. Steroids or epinephrine may be requiredto reduce the inflammatory obstruction of theupper airway.

This is a child who comes in with difficulty swal-lowing and fever. He demonstrates a fever andswelling of the pharyngeal soft tissues, consistentwith a retropharyngeal abscess. Retropharyngealabscesses usually occur in younger childrenbecause of lymphatic drainage. Older kids withperforating injuries also can develop soft tissueinfections which in some cases can obstruct theupper airway.

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Causes of Acquired Airway Obstruction

## Neurologic Dysfunction - loss of pharyngeal tone

# Trauma

# Foreign Body Aspiration

# Mass Lesion

Airway obstruction can also be caused by a loss ofthe pharyngeal tone. There is a very complex,integrated neural network by which on the start ofinspiration the upper airway dilates and therebykeeps the airway patent for expired air. If theintegrated neural network of dilation of the upperairway on inspiration is not functioning, themandibular soft tissue will fall back on the poste-rior pharynx, leading to airway obstruction.Neurologic problems can cause loss of pharyngealtone and airway obstruction from a number ofcauses. Occasionally there is acute onset, instanta-neous onset of severe respiratory distress fromforeign body aspiration in the upper airway. It ismore common for foreign bodies to lodge in thelower airways, in which case the presentation maybe a little less dramatic. And certainly when youhear a child has instantaneous onset of severerespiratory distress, it’s a foreign body in a centralarea.

Mass lesions tend to develop and lead to a chronic,progressive upper airway obstruction. Sometimesthe signs or symptoms can be pushed backwardsto the past few weeks. In think one example ofthat is adenoid-tonsil hypertrophy where nighttimeairway obstruction can be reported by parents.

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Management of Airway Obstruction

## Positioning

• Head Tilt

• Chin Lift

- Lifts base of tongue off posterior pharyngeal wall

• Clear Secretions

## Bag-Valve-Mask Ventilation

• Self-inflating bags

• Anesthesia bags

# Intubation

• Suction

• Oxygen

• Bag-Valve-Mask

• Laryngoscope

• Blades

- Straight

- Curved

- Endotracheal Tubes: 16 + age (yrs)4

Now, what do we do for a child who has upperairway obstruction? Responding to any emergencywe want to immediately open the airway andmaintain airway patency even before an artificialairway is inserted. In the delivery room and in theemergency departments and in severely ill chil-dren who show up in the office, you want toposition the child in an optimal way, and that canbe either by tipping the head back or pulling thetongue forward, or both. This helps to move thetongue off the posterior pharynx. A small move-ment, like positioning a child in the manner inwhich the shoulders are elevated, can make a bigdifference in terms of the ability of that child tomaintain a patent airway. You want to clear anysecretions with suction, and we want to use bag-valve-mask ventilation if necessary.

Children who have severe airway obstruction,more severe with respiratory distress and respira-tory failure, may require intubation. Intubation issomething that should be done in as controlled amanner as is possible. If you are not working in ahospital and there are more experienced intubatorsin the building, I think it makes sense to get themost experienced person there when possible.You want to have suction, oxygen available, andbag and masked ventilation available. It takessome time to properly put in an endotracheal tube.So you want the functional residual capacity ofthe child, that reservoir of oxygen in their lungsthat maintains oxygenation despite a period ofapnea or inadequate ventilation, you want theFRC to be full of 100% oxygen. You want to pre-oxygenate with bag-valve-masks. You want tomake sure the laryngoscope works before youbegin intubation.

Now there are different blade types. Most pediatri-cians like myself, are more comfortable with astraight blade. In older children, the curved bladesin some ways are easier, where the curved blade isreplacing the vallecula in the elevation becausethe epiglottis is somewhat rigid. It lifts up and liftsoff the pressure on the trachea at intubation.

In the 16+ age in years, half a tube and a half sizesmaller and a half size larger for routine or emer-gent intubation. If the child has signs of airwayobstruction, especially in the case of somethinglike epiglottitis or perhaps croup, you may want tohave a tube a whole size smaller or even one anda half sizes smaller, recognizing that there may bea narrowed area, making the predicted tube sizetoo large.

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Causes of Lower Pulmonary Disease and

Respiratory Failure

## Bronchiolitis

# Asthma

# Pneumonia

# Acute Respiratory Distress Syndrome

# Aspiration/Near Drowning

Now as we move down the respiratory tree, thereare a number of other causes of respiratory failure.And most of the causes of respiratory failure, bothupper and lower, are more common in younginfants. In fact if you look at all cardiopulmonaryarrests, infants far outnumber any other age range.And so treat all these conditions, certainlybronchiolitis and asthma and cardiacs, with greatcaution.

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Respiratory Pump Dysfunction

# The chest wall is much more compliant in infants

# Paradoxical respirations or thoracoabdominal asynchrony occurs when

airway resistance becomes increased

In addition to the problems with the respiratorytree and the alveoli, critically ill children mayhave problems with their respiratory pump, thebellows of their chest. The chest wall, especiallyin younger infants, is so compliant that there areproblems when there is high airway resistance.And so with upper or lower obstruction, often wehave to ventilate the child with very highintrathoracic pressures to entrain air into thelungs. And if the chest wall itself is very pliant,you may have paradoxical respirations.

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Chest Trauma

## Chest trauma is most commonly cause is by a blunt mechanism, such

as a motor vehicle accident.

# Chest trauma is usually associated with other injuries.

# Chest trauma isore likely to injure both intrathoracic and abdominal

organs.

Chest trauma. Most chest trauma in children isblunt trauma. And again, because of the compli-ance of the chest wall, force is more likely to betransmitted to the internal organs. And the goodnews is that the compliant chest wall seldomresults in fractured ribs. Fracturing a younginfant’s ribs takes considerable force, but internalinjuries to the thorax are more common becausethe chest wall doesn’t serve to protect the thoraxas well.

There is an intrathoracic component to the abdom-inal structures, so the liver and the spleen arereally tucked up into the thorax. After chesttrauma in a small patient, one needs to be con-cerned injuries to abdominal structures that arewithin the thorax. Pulmonary contusion is one ofthe more common, significant chest injuries thatoccur. It occurs frequently without rib fractures,again because of the compliance of the chest wall.Occasionally there will be tachypnea orhypoxemia without a definite abnormality onchest exam. Perhaps there are decreased breathsounds. The chest x-ray may lag behind theseclinical findings, so we need a high index ofsuspicion of pulmonary contusion in a young childwho had suffered blunt trauma to the chest. Inaddition to pulmonary contusion, occasionallythere will be rib fractures. Most rib fractures inyoung infants are inflicted. Fracture of the lowerribs are often associated with abdominal visceralinjuries. And occasionally there are so many ribfractures that the bellows function of the chest isdisrupted. With multiple rib fractures, which isquite common in young infants, you may have aproblem with bellows function.

Pneumothoraces are not that common, especiallyin very young children. As children get older theybecome somewhat more common. They mayoccur without a rib fracture, but it must be ex-cluded in patients with significant chest trauma.Tension pneumothorax develops because of thetension, and shifts the mediastinum over. There isrespiratory failure associated with living off onedepressed lung and there is also a circulatoryfailure associated with the obstruction of thesuperior and inferior vena cava and inflow to theheart. So the tension physiology needs to berelieved as soon as possible. If there’s tension inthe thorax, a chest tube or a needle should beplaced in the chest.

Hemothoraces are uncommon in younger kids.Often shock is the presenting sign, rather thanrespiratory failure from blood loss.

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Chest Injuries

## Pulmonary Contusion

• Chest wall findings may be absent

• Tachypnea, asymmetric breath sounds, and hypoxemia may be

present

• Symptoms and radiographic changes may be delayed

Cardiac injuries are quite rare. In children weseldom see clinically significant cardiac contu-sions, but they can occur. Commotio Cordis orcardiac concussion. I like to think of it as ananalogies to what we used to do with adult arrestswas deliver a precordial thump. With a precordialthump, more than an amp of electrical energy isdischarged to the heart. In the fibrillation situa-tion, a precordial thump may defibrillate thepatient. It works probably infrequently, but thereare anecdotal reports of it working. Similarly aprecordial thump say from a pitched baseball thathits right on the sternum, may deliver a smallelectrical burst of energy which can trigger fibril-lation and sudden death in young children. And sothe story of a child being hit by a baseball in thechest, dropping unconscious and dying fromimmediate fibrillation after trauma, is what wecall Commotio Cordis, and it is probably by asimilar mechanism.

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Rib Fractures

## Rib fractures in infants are usually intentionally inflicted by another

person

# Severe intrathoracic injury may occur without rib fractures

# Fractures of the lower ribs are often associated with abdominal visceral

injuries

# Multiple fractures can cause a flail chest, resulting in ineffective

respiratory mechanics

Chest trauma causes problems with bellowsfunction. Obviously children with neuromusculardisease can have respiratory failure. Children withsimple hypoventilation need to have assistedventilation, obviously, or they will arrest. Andchildren with spinal cord injuries or any of theseother conditions may have a central cause of theirhypoventilation.

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Pneumothorax

## Most occur occurs in the absence of a rib fracture

# Untreated tension pneumothorax may be rapidly fatal

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Hemothorax

# Hemothorax is usually caused by penetrating trauma

# Shock usually occurs before respiratory failure

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Cardiac Injuries

## Cardiac injuries are rare

• Commotio cordis

• Cardiac contusion

Circulatory failure. Children do not have a lot ofinotropic reserve. Their cardiac output increasesmostly through an increase in the heart rate. Andso when children have circulatory failure, tachy-cardia is the most reliable symptom to look for.Although absence of tachycardia doesn’t abso-lutely exclude the possibility of circulatory failure.Shock can be compensated or uncompensated.And clearly children who present with shock andlow blood pressure do very poorly. So our role inemergency medicine or critical care is to identifykids with shock before blood pressure drops. Weneed to identify shock early, looking for tachycar-dia and decreased perfusion of the skin. That’scapillary refill, color and temperature of theperipheral extremities. Altered sensorium anddecreased urine output is obviously critical in achild with projected, impending or existing circu-latory failure.

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Neuromuscular Respiratory Muscle Failure

## Central Hypoventilation

# Spinal Cord Injury

# Tetanus

# Poliomyelitis

# Guillain Barre

# Myasthenia Gravis

# Botulism

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Circulatory Failure

## Cardiac Output is rate dependent in infants

# Compensated vs. uncompensated shock

• Recognize shock before blood pressure drops

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Clinical Manifestations of Circulatory Failure

# Tachycardia

# Decreased perfusion of skin (temperature, color, capillary refill)

# Altered sensorium

# Decreased urine output

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Vascular Access

# Peripheral

# Central

# Intraosseous

# Endotracheal

Much more fluid can go through 18 gauge IV anda 20 gauge IV, over a given period of time.Similarly the length is also of importance, so verylong central lines, even if they are large bore, havesome added resistance by virtue of their length. Solarger IV’s are better for rapid fluid administra-tion. We know now, and this is not new, is that thebone marrow can be used for vascular accesswhen the peripheral veins are difficult to get, andspinal needles, or hypodermic needle or a bonemarrow needle preferably placed in the bonemarrow very rapidly gains access to the centralcirculation. Fluid or medication administered tothe bone marrow is more like administering it to acentral line than to a peripheral line. Even a childwith no arms and legs can have vascular access byputting a bone marrow needle in the iliac region ofthe hip.

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Causes of Circulatory Failure

# Inadequate Blood Volume - Hypovolemic Shock

• Dehydration

• Hemorrhage

• Third Spacing

# Inadequate Pump Function - Cardiogenic Shock

• Cardiomyopathy

• Dysrhythmia

• Tamponade

# Inadequate Vascular Resistance - Distributive Shock

• Drug Overdose

• Toxic Shock

• Septic Shock

Circulatory failure takes many forms,hypovolemia and in particular, dehydration issomething we deal with on a daily basis. There isa lot of overlap between an ill-appearing child anddry child. Certain tenting of abdominal skin hasbeen used for a sign. In addition to hypovolemia,cardiogenic shock, as appears in cardiomyopathy,a rhythm disturbance or tamponade, are alsocauses of cardiogenic shock. This is a child with alarge heart and some fluffy infiltrates in the begin-ning of congestive heart failure.

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Septic Shock

# Early "warm" shock is caused by decreased vascular resistance from

cytokine release

# Late "cold" shock is caused by hypovolemia from capillary leak,

acidosis, myocardial depression

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Central Nervous System Failure

## Asphyxia

# Trauma

# Toxic/Metabolic

# Status Epilepticus

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Head Trauma

## Primary vs. Secondary Injury

# Outcome is usually related to concurrent hypoxemia hypercapnia,

duration and degree of coma (Glasgow Coma Scale)

Head trauma causes primary injury that occursinstantaneously and then a secondary injury.Secondary injury after head trauma occurs fromswelling and poor perfusion and poor airwaymanagement. The outcome in many cases isdelayed swelling, hypoxemia, hypercapnia. Thisis just taken from one study showing head traumaplus hypotension, hypoxemia, hypercapnia. Thesehave a very high mortality rate. Head traumaalone would seem to have a much lower mortalityrate. Physiology of head trauma is important.Intracranial volume is a constant so anything thatincreases in the brain, something else has todecrease or the pressure will go up dramatically.And perfusion of the brain is really a differencebetween a arterial pressure and the intracranialpressure. All increases in intracranial pressuretherefore reduce cerebral perfusion pressure. Butthe arterial reductions can also reduce cerebralperfusion factor. So injured children need tomaintain the arterial pressure and do it because itminimizes the intracranial pressure.

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Head Trauma

## Pathophysiology

• Intracranial volume is constant

• Intracranial compliance curve is exponential

• Cerebral Perfusion Pressure = Mean arterial pressure - ICP

• Edema peaks 48 - 72 hrs after injury

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Head Trauma

## Signs and Symptoms of Brain Injury

• History of loss of consciousness

• Retrograde amnesia

• Prolonged vomiting

• Subtle alterations in consciousness are important

• Glasgow Coma Score

• Herniation/Brainstem reflexes

Any child with a loss of consciousness we willobtain a CT-scan. We are not talking about acouple of seconds of being dazed and confused,but a true loss of consciousness, which actually isquite, quite significant. Other signs of concussionare defined here. And we certainly, on the severelyhead injured children, look for signs ofherniation.

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Brainstem Reflexes

## Pupillary Response

# Oculocephalic Reflex (Doll's eyes)

• Positive if eyes lag behind movement of the head

# Oculovestibular Reflex (cold calorics)

• Positive if cold water causes sustained deviation of eyes toward

the irrigated ear

The herniation that is most importantly identifiedis uncal herniation where the third nerve getsdepressed. You look for a pupillary response.Once we have cleared the neck we look for anoculocephalic or doll’s eyes reflex. And when wetalk about doll’s eyes we are talking about anormal child, if the brain stem is intact, the eyeswill stay in position as the head moves and so theeyes will match the plane of the movement of thehead. And a child who has a nonfunctioning brainstem, the eyes will be painted on the face and theywill move with the turning of the head. So doll’seyes is positive if the eyes move relative to thehead as opposed to staying fixed in position. Andthen a squirt of cold water in the ear should causethe eyes to deviate towards the cold water in asustained fashion and occasionally have a fastphase away.

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Head Trauma Management

## Airway management is crucial

# Treat elevated intracranial pressure before Cushing's Triad or uncal

herniation occur

# Elevate head

# Hyperventilate to maintain a pCO of 25-30 mmHg2

# Mannitol - osmotic diuretic

Airway management in head injuries is crucial.You want to treat intracranial pressure beforeCushing’s Triad--hypotension, bradycardia--occurs and we want to prevent uncal herniationwhenever possible. Elevate the head, hyperventi-late between pCO 25 and 30. Extreme hyperven-2

tilation causes too much vasoconstriction and thatcan cause poor perfusion in the brain.

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Organ Failure

## Renal Failure

• Prerenal

• Intrarenal

• Postrenal

# Hepatic Failure

• Causes

- Infectious (viral)

- Toxic (acetaminophen, iron)

- Ischemic

Organ failure. When you are dealing with kidneyfailure, the patient usually can get critical, an youwant to decide whether it’s prerenal, which ischaracterized usually by hypervolemia and highratio of BUN to creatinine. Intrarenal where theremay have been an ischemic insult. Postrenalfailure can usually be defined through an imagingstudy.

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Signs and Symptoms of Hepatic Failure

## Protracted vomiting

• Behavior change - euphoria, belligerence, confusion

• Bruising

• Edema, Ascites

• Asterixis

• Coma. The depth of encephalopathy correlates with the severity of

hepatic failure

For liver failure, the causes include viral hepati-tis, toxic conditions, especially acetaminophen andiron. And as part of a toxic ischemic event. It’simportant to recognize that this type of failure canhave a solo presentation of vomiting and a solopresentation of unusual behavior change. Otherfindings include easy bruisability, edema andascites. Asterixis occurs in the severe phase,which is the flapping of the hands and coma.Often the severity of the failure, as related to thedepth of encephalopathy, correlates with theseverity of the hepatic failure and is somewhatrelated to the height of the pneumonia.

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Hepatic Failure

## Laboratory Tests

• The height of the transaminase elevation does not corellate with

severity of disease

• Elevated conjugated and unconjugated bilirubin, prolonged

prothrombin time and decreased albumin are indicators of liver

dysfunction

• Decreasing transaminases with increasing bilirubin and PT suggest

liver failure

• Increased arterial ammonia correlates with hepatic coma

Recognize that high transaminase is liver en-zymes. They are not truly liver function tests;these are enzymes that leak from the hepatocytes.So very high transaminase levels doesn’t neces-sarily correlate with very severe disease. We getworried with the pre-liver function tests. The waythey function is to conjugate bilirubin and synthe-size various proteins. When we see elevatedconjugated and unconjugated bilirubin, prolongedcoagulation times and low albumin, which reallyreflects liver synthesis function. Arterial ammoniaresults are very reasonable for documenting theseverity of the hepatic coma.