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Management of Emergency Pediatrics Made Easy®

Management of Emergency Pediatrics Made Easy® S Letha

Professor and Head, Department of Pediatrics Government Medical College Kottayam, Kerala India

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi • Ahmedabad • Bengaluru • Chennai • Hyderabad • Kochi • Kolkata • Lucknow • Mumbai • Nagpur

Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3 EMCA House, 23/23B Ansari Road, Daryaganj, New Delhi 110002,lndia Phones: +91-11-23272143, +91-11-23272703, + 91-11-23262021 +91-11-23245672, Rel: +91-11-32558559, Fax:+91-11-23276490, +91-11-23245683 e.mail: jaypeebrothers.com, Visit our website: www.jaypeebrothers.com Branches q 2/8, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380015, Phones: +91-79-26926233. Rel: +91-79-32988717 Fax: +91-79-26927094, e-malI: [email protected] q 202 Batavia Chambers, 8 Kumaro Krupa Road, Kumara Park East Bengaluru 560001, Phones: +91-80-22265971, +91-80-22382956, 91-80-22372664, Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected] q 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897 Rel: +91-44-32972089, Fax: +91-44-28193231 e-mail: [email protected] q 4-2-1067/1-3, lst Floor, Balaji Building, Ramkote Cross Road, Hyderabad 500095, Phones: +91-40-66610020, +91-40-24758498 ReI: +91-4O-32940929 Fax:+91-40-24758499 e-mail: [email protected] q No. 41/3098, B & B1, Kuruvi Building, S t. Vincent Road Kochi 682 018, Kerala, Phones: +91-484-4036109, +91-484-2395739, +91-484-2395740 e-mail: [email protected] q I-A Indian Mirror Street, Wellington Square Kolkata 700013, Phones: +91-33-22651926, +91-33-22275404 +91-33-22276415, Rel: +91-33-32901926, Fax: +91.J3.22656075 e-mail: [email protected] q Lekhraj Market III, B-2, Sector-4, Faizobad Rood, lndira Nagar , Lucknow 226016, Phones: 0522-3040553,3040554 e-mai: [email protected] q 106 Amit Industrial Estate, 61 Dr SS Rao Road. Near MGM Hospital, Parel Mumbai 400012, Phones: +91-22-24124863, +91-22-24104532, ReI: +91-22-32926896, Fax: +91-22-24160828 e-maiI: [email protected] q “KAMALPUSHPA” 38, Reshimbag, Opp. Mohota Science College, Umred Road Nagpur 440 009 (MS), Phone: ReI: +91-712-3245220, Fax: +91-712+2704275 e-maiI: [email protected] Management of Emergency Pediatrics Made Easy ® ©2008,Jaypee Brothers Medical Publishers All rights reserved. No part of this publication and CD ROM should be reproduced, stored in a retrieval system, or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the author and the publisher. This book has been published in good faith that the material provided author is original. Every effort is made to ensure accuracy of material, but the publisher , printer and author will not be held responsible for any inadvertent error(s). In case of any dispute, all legal matters are to be settled under Delhi jurisdiction only . First Edition:2008 ISBN 978-81-8448-282-9 Typeset at JPBMP typesetting unit Printed at Rajkamal Electronic Press, B-35/9, G.T. Karnal Road, Delhi-33

To My beloved husband R Sadasivan who was my encouragement and inspiration throughout this endeavor

PREFACE Prompt recognition and appropriate management of a critically ill child improves the quality of life. It prevents morbidity as well as mortality. To identify a critically ill child is the most important aspect of critical care management. After identifying the sick child, a protocol oriented management done by a team of trained personals is the next step in the management of such a child.This book is intended to help the young doctors in managing the common pediatric emergencies in a simple way . Lack of sophisticated instruments, costly equipments and drugs are often compensated to a great extent by the sincerity and dedication of the health personals and constant and careful personal monitoring. I express my sincere gratitude to all my teachers and my students, my tiny patients and their parents who all inspired me for putting in such an effort. My thanks are due to Mr KVVarkey, Royal DTPCentre, Gandhinagar, Kottayam for all the help he has rendered tome. Lastly but of most importance, I would like to thank Mis Jaypee Brothers Medical Publishers (P) Ltd, New Delhi for their help extended to me for publishing this book. S Letha

CONTENTS 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

How to Identify a Sick Child? .................................. 1 Pediatric Cardiopulmonary Resuscitation ................ 9 Vascular Access....................................................... 25 Oxygen Therapy ..................................................... 35 IV Fluid Therapy ..................................................... 51 ABG Analysis ......................................................... 69 Mechanical Ventilation ........................................... 81 Management of Shock in Children ......................... 95 Status Epilepticus .................................................. 101 Coma ..................................................................... 107 Acute Respiratory Failure ...................................... 111 Acute Severe Asthma ............................................. 115 Hepatic Failure ...................................................... 121 Acute Renal Failure .............................................. 129 Diabetic Ketoacidosis ........................................... 135 Cardiac Emergencies ............................................ 141 Hypertensive Emergencies ................................... 153 Blood and Blood Component Therapy ................. 157 Envenomation ....................................................... 163 Poisoning in Children ........................................... 171 Index ...................................................................... 183

CHAPTER 1

How to Identify a Sick Child?

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MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

Identifying a sick child is the first step in the management of a critically ill child. Often the young doctor finds it difficult to recognize a child who needs immediate, emergency management. A sick child or critically ill child is one who is in vital compromise, having serious respiratory, cardiovascular or neurological illness who may have to face mortality if not treated promptly. Timely and appropriate emergency care will help save the life. He has to be assessed rapidly through a step- wise approach-golden hour concept. The golden hour is aptly termed as ‘golden’ because it is this critical duration which is vital for saving the child. Rapid cardiopulmonary assessment is indicated if the child is having the following features. a. Tachypnea RR >60/mt b. Tachycardia >180 in under 5 years >160 over 5 years. c. Bradycardia <80 in under 5 years <60 over 5 years d. Increased work of breathing e. Cyanosis f. Diminished level of consciousness g. Seizures h. Fever i. Petechiae j. Trauma k. Burns Very simple assessment of overall illness is by using the pediatric assessment triangle Appearance

Circulation

Breathing

HOW TO IDENTIFY A SICK CHILD?

3

Appearance This denotes the neurological status of the child which is determined by the oxygen and blood supply to the brain which in turn is dependent on the cardiopulmonary function and structural integrity of the brain. Alertness See if baby is alert, active, or lethargic, confused or comatose. The consciousness can be roughly assessed by the AVPU scale. A—Awake V—Verbal-response to voice P—Pain-response to pain U—Unresponsive Modified Glasgow scale also can be used for the rapid assesment of critical function. Glasgow Coma Scale Eye opening Spontaneous To voice To pain None

Total points 5 4 3 2 1

Verbal Response Total Points 5 Older children Oriented

5

Confused Inappropriate Incomprehensible None

4 3 2 1

Infants Appropriate words, smiles, fixes, follows Consolable crying Persistently irritable Restless, agitated None

5 4 3 2 1

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Motor Response Total Points 6 Obeys 6 Localizes pain 5 Withdraws 4 Flexion 3 Extension 2 None 1 GCS of 8 or less carry bad prognosis and need aggressive management. Distractibility and Consolability By the parent is a useful observation. The most sick child does not regard even the mother. Eye Contact Absence of eye contact even to mother is a grave sign. Speach/cry Identify the reason for cry and observe whether it is normal or not. The quality of the cry also is important. Weak, shrill or whimpering cry shows that the child is very sick. Motor Activity Assess whether it is normal or not. Pupil Size May be abnormal depending on the cerebral perfusion and pressures. Unequal pupils are seen in raised intracranial pressure.


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Breathing Respiratory rate is very important in the assessment of a critically ill child. Tachypnea is an early sign of respiratory distress whereas bradypnea is an omnious sign. Respiratory Rate NB 40-60 mt.

1-5 yr 26-22

>5 yr 22-20

>18 yr 18

Upper limit of RR is: Newborns 60/mt Infants 50/mt Children 40/mt Effortless or quiet tachypnea is seen in shock, cardiac disease, acidosis, etc. A slow or irregular respiration in an acutely ill child is an omnious sign. Work of Breathing Increased work of breathing is evidenced by working of the accessory muscles of respiration like intercostals, and sternocleidomastoids. There may be intercostal, subcostal and suprasternal retractions, nasal flaring, grunting and head bobbing indicating respiratory distress and potential respiratory failure. Child with impending respiratory failure will be having tachycardia, which when severe produces bradycardia. Hypoxia leads to catecholamine release producing pallor of skin progressing to central cyanosis as hypoxia worsens. Hypoxia and hypercarbia alters the level of consciousness. Oxygen saturation can be assessed by pulse oximetry which is very useful for the early detection of hypoxia.

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CIRCULATION Pulse and Heart Rate Tachycardia is a very sensitive indicator of inadequate oxygen delivery and the first response to circulatory failure. Bradycardia in an acutely ill child is an omnious sign. Normal heart rates in children

Tachycardia

Bradycardia

Newborns Infants Children

>160/mt >150/mt >120/mt

<100/mt <80/mt <60/mt

120-160/mt 100-120/mt 80-120/mt

Pulse Volume Pulse volume is low during the early phase of circulatory failure because of the peripheral vascular constriction, as a compensatory mechanism to the vital organs. When circulatory failure is established the peripheral pulses will not be palpable. In early septic shock there is low systemic vascular resistance and so there can be bounding pulse during the early phase of warm shock. Pulse Pressure As cardiac output decreases pulse volume reduces and the pulse pressure narrows and pulse became thready. As cardiac output increases in warm septic shock and anaphylactic shock pulse pressure widens and pulses become bounding. Blood Pressure In early compensated shock BP is normal. Hypotension develops when the compensatory mechanisms fail. Low BP is an indicator of late, decompensated shock.


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BP in Children Normal Newborn 1 yr 2-10 yr >10 yr

Minimum acceptable level of systolic BP. 60 mmHg 70 mmHg 70+(age+2) mmHg 90 mmHg

Skin Perfusion Skin perfusion can be assessed by temperature, color and capillary filling time. Temperature Hands and feet become cold as cardiac output falls. Color Skin appears pale, cyanozed or mottled due to the decreased perfusion to skin. Capillary Filling Time The capillary blood flow is reduced in shock. The normal capillary filling time is 2-3 seconds. Prolonged CFT is a useful sign in shock. But capillary filling time can be prolonged in rising fever and exposure to cold ambient temperature also. Organ Perfusion Poor organ perfusion occurs when shock progresses. Cerebral hypoperfusion results in altered sensorium. Renal hypoperfusion results in decreased urine output. Ischemia of gut can produce GI hemorrhage.

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So, with the help of the pediatric assessment triangle the status of the critically ill child can be characterized as: 1. Stable 2. Respiratory distress—Respiratory failure 3. Cardiovascular failure—Compensated or decompensated shock 4. Disturbed neurological status. If the child is not stable the initial management should be aimed at stabilizing the child in an agressive manner by maintaining the Airway Breathing and Circulation. Monitoring is very important in the management of a critically ill child. Being aware about the age specific emergencies and current epidemics will help in the management of critically ill children. All children brought to the hospital should be thouroughly assessed for their critical nature, stabilized within no time to be followed by definitive management for specific management of the underlying condition. Periodic reassessment is also very important to detect the progress or deterioration. Last but not of least importance is the management of the worried parents and relatives. They should be explained about the condition of the child and the doctor should have the empathetic attitude.

CHAPTER 2

Pediatric Cardiopulmonary Resuscitation

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The relevance and community participation of pediatric cardiopulmonary resuscitation is often a neglected part of our training. Many children develop cardiopulmonary arrest outside the hospital and BLS training is to be offered to all expectant parents, parents of young babies and highrisk children and also to those who are entrusted with care of children like nursery teachers, school teachers, day care personnel, etc. The content of such BLS courses should include the preventive strategies, training in BLS techniques, access to EMS system which are to be developed in our country. Cardiopulmonary arrest in children is different from that of adults. Primary cardiac arrest in young children is very rare. More commonly it results from low oxygen level secondary to respiratory difficulty or arrest. The outcome of respiratory arrest alone is best with a prompt resuscitation followed by aggressive ALS. Pediatric cardiopulmonary arrest can occur in newborn to adolescence and the causes differ in different age groups. CAUSES IN INFANCY BEYOND NEWBORNS 1. 2. 3. 4. 5. 6. 7. 8. 9.

Injuries ALTE (Acute life-threatening events) SIDS (Sudden infant death syndrome) Respiratory diseases Airway obstruction–FB aspiration Smoke inhalation Submersion Sepsis Neurological diseases

PEDIATRIC CARDIOPULMONARY RESUSCITATION

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Beyond Infancy Accidents and injuries are the leading causes for cardiopulmonary arrest. Airway obstruction leading to asphyxia is a major cause of death and disability in children. It can be due to a foreign body or edema due to infection. Poisoning through accidental ingestion is most common in 1-4 years age group. The basic steps of CPR are the same in an infant, child or adult. It includes the sequential assessment and motor skills designed to support or restore effective ventilation and circulation to the person in respiratory or cardiorespiratory arrest. The steps are: 1. Determine responsiveness This helps in assessing the presence and extent of injury and determine the consciousness. This is done by tapping the child and speaking loudly to elicit a response. The victim should not be shaken or moved unnecessarily if spinal cord injury is suspected because such handling may aggravate the injury. If child is unresponsive but breathing or struggling to breathe he should be transported to an advanced life support facility. Once unresponsiveness has been determined the lone rescuer should shout for help and then provide BLS to the child. 2. Position of the victim In order to provide an effective CPR the victim must be lying on his or her back on a firm flat surface. Sometimes, it is mandatory to move the child from a dangerous

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location (e.g. in a burning building). Great care must be taken while moving the child particularly if there is evidence of trauma. The cervical spine should be immobilized and the head and the body must be held as a unit and the head and neck firmly supported so that the head does not roll, twist or tilt. 3. Open the airway Relaxation of the muscles and passive posterior displacement of the tongue may lead to airway obstruction in the unconscious victim. Opening of the airway is essential for effective ventilation. Head Tilt—Chin Lift Place one hand on the child’s forehead and tilt the head gently back into a neutral position. The neck is slightly extended. Place the fingers not the thumb, of the other hand under the bony part of ther lower jaw at the chin, and lift the mandible upward and outward. Be careful not to close the mouth or push the soft tissues under the chin which may obstruct the airway. Jaw Thrust Safest method when neck or cervical spine injury is suspected because it can be done without extending the neck. Place two or three fingers under each side of the lower jaw at it’s angle and lift the jaw upward and outward. If jaw thrust alone does not open the airway, slight head tilt may be added in patients with no evidence of cervical spine injury. Whenever head or neck injury is suspected the cervical spine must be completely stabilized


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when airway is opened. This can be accomplished by a combined jaw thrust and spinal immobilization maneuver using only the amount of manual control necessary to prevent cranial cervical motion by pressing over the forehead by the thumbs of the rescuer. If two rescuers are present, the first rescuer can open the airway with jaw thrust maneuver and the second can immobilize the neck in the neutral position. Breathing After airway is opened the rescuer should determine if the baby is breathing or not. He can look for the movement of chest, listen for the exhaled air, feel for the exhaled air flow at the mouth. If the victim is breathing effectively he can be placed in the recovery position. The victim should not be moved if there is suspicion of trauma or if he needs rescue breaths and CPR. Recovery Position Victim is moved on to his side moving his head, shoulders and torso simultaneously. The leg not in contact with the ground may be bent and the knee moved forward to stabilize the victim. Rescue Breathing Rescue breaths are the single most important manuever in assisting a non-breathing child victim. If a mask with a one-way valve or other infection control barrier is readily available it can be used. However, ventilation should not be delayed while such a device is located.

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If the victim is an infant place the mouth of the rescuer over the infant’s nose and mouth creating a seal. In a large infant or older child, make a mouth-to-mouth seal and pinch the victim’s nose tightly with the thumb and forefinger of the hand maintaining head tilt. First inhale deeply and then seal the mouth and nose or mouth as required depending on the age of the baby. Give two slow breaths (1 to 1½ seconds per breath) to the victim pausing after the first breath to a take a deep breath. The volume and pressure of the rescue breaths should be sufficient to cause the chest to rise. The breaths should be delivered slowly. Slow breaths will allow delivery of an adequate volume of air and ensure effective lung and chest expansion. Taking a pause in between the breaths maximizes the oxygen content and minimizes carbon dioxide content in the delivered breaths. If air enters freely and chest rises the airway is clear. If not, either the airway is obstructed or more breath volume or pressure is necessary. So the rescuer should reattempt opening the airway and re-attempt ventilation. If there is no suspicion of neck or spine injury, the rescuer should move the victim’s head into several positions of neck extension until a position of optimal airway patency results in effective rescue breathing. If rescue breathing fails to produce chest expansion after several attempts, a foreign body airway obstruction is to be suspected and the necessary maneuvers are to be done to remove the foreign body. Rescue breathing especially if done rapidly may cause gastric distension. Excessive gastric distension can interfere with ventilation and so if a second rescuer is


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there, he can apply cricoid pressure to displace trachea posteriorly compressing the esophagus against the vertebral column to prevent gastric distension and reduce the likelihood of regurgitation. In a single rescuer, delivering the rescue breaths slowly will prevent gastric distension. Circulation Once the airway is opened and two rescue breathes have been provided, the rescuer should determine the need for chest compression. Pulse Check If cardiac contractions are ineffective or absent, there will not be a palpable pulse. In infants, since the carotid artery is difficult to palpate due to the short and chubby neck the brachial artery palpation is recommended with the thumb on the outside of arm, the index and middle fingers are gently pressed over the brachial artery to feel the pulse. In children the carotid artery on the side of the neck is the most acceptable central artery to palpate. To feel the carotid artery, locate the victim’s thyroid cartilage with two or three fingers of one hand while maintaining head tilt with the other hand. Slide the fingers onto the groove on the side of the neck closer to the rescuer, between the trachea and sternocleidomastoid muscle. If pulse is present but spontaneous breathing absent, provide rescue breathing alone at a rate of 20 breaths per minute (Once in every 3 seconds) till spontaneous breathing resumes. If not able to resume spontaneous breathing child needs emergency medical care services.

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If pulse is not palpable or heart rate is less than 60 and signs of poor systemic perfusion are present child needs chest compressions. Chest compressions are serial rhythmic compressions of chest to facilitate oxygen containing blood to be circulated to vital organs like heart, lungs and brain until advanced life support can be provided. To achieve optimal chest compressions, the child should be supine on a hard, flat surface. For an infant the hard surface may be the rescurer’s hand or palm itself. Chest Compressions in the Infant 1. Use one hand to maintain the infant’s head position (unless the hand is under the child’s back). 2. Use the other hand to compress the chest. Place the index finger of the hand on the sternum just below the level of the infant’s nipples. Place the middle finger on the sternum adjacent to the index finger. Sternal compression is done approximately the width of one finger below the level of nipples. Compression to the xiphoid process is to be avoided since it may damage the liver, stomach or spleen. 3. Using two or three fingers, compress the sternum approximately one-third to one-half the depth of the chest. This will correspond to a depth of about ½ to 1 inch. The rate of compression should be at least 100 times/minute. Compressions should be co-ordinated with ventilation in a 5:1 ratio with pauses for ventilation. The number of compressions will actually be at least 80/minute.


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4. At the end of the each compression, pressure should be released without removing fingers from the chest. A smooth compression relaxation rhythm without jerky movements should be developed with equal time for compression and relaxation. When the victim resumes effective breathing he may be placed in the recovery position. Chest Compression in the Child For the purposes of BLS, 1 to 8 years old are considered as child. If the child is large or more than 8 years chest compression should be provided as for adults. 1. Use one hand to maintain child’s head position. 2. Using fingers of the other hand the lower margins of the victim’s rib cage is traced on the side near to the rescuer. Reach the notch where the sternum and ribs meet. 3. Place the heel of the hand over the lower half of the sternum between the nipple line and the notch, avoiding the xiphoid process. The long axis of the heel should be over the long axis of the sternum. 4. Compress the chest as already mentioned as in the infant to 1/3 to 1/2 of the depth. If the victim resumes effective breathing, place him in the recovery position. If not, he needs emergency care services. Foreign Body Airway Obstruction Foreign body airway obstruction should be suspected in infants and children with sudden onset of respiratory distress associated with coughing, gagging, stridor or wheezing. Attempts to clear the airway should be

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MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY Summary of BLS in Infant Child and Adult 0-1 yr

1-8 yr

>8 yr

Determine responsiveness shake and shout tapping and speaking loudly

Yes

Yes

Yes

Call for help

Yes

Yes

Yes

Position the victim

Yes

Yes

Yes

Look, listen and feel for breath

Yes

Yes

Yes

Open the airway

Yes

Yes

Yes

Rescue breaths

Yes

Yes

Yes

Check pulse

Brachial

Carotid

Carotid

Activate EMS

Yes

Yes

Yes

Locate the position of chest compression

Lower sternum

Lower sternum

Lower sternum

Compression with

2 fingers

heel of one hand

heel of two hands

Compression depth

½-1” 1-1½” 1½ to 2” (1/3 or 1/2 (1/3 to 1/2 (1/3 to 1/2 of total depth) of total depth) of total depth)

Compression/ minute

at least 100

100

80-100

Compression ventilation ratio

5:1

5:1

5:1

considered when foreign body aspiration is witnessed or strongly suspected or when airway remains obstructed during attempts to provide rescue breathing. Relief of airway obstruction should be attempted only if signs of complete obstruction is observed.


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In Infants—Back Blows and Chest Thrusts (Figs 2.1 and 2.2) 1. Hold the infant face down resting of on the forearm of the rescuer. Support the infant’s head by firmly holding the jaw. Rest the forearm on the thigh to support the infant. The infant’s head should be lower than the trunk. 2. Deliver up to 5 back blows forcefully between the infants shoulder blades using heel of the hands.

Fig. 2.1: Back blows

Fig. 2.2: Chest thrusts

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3. After delivering the blows, place the free hand on the infants back, holding the infants head. Thus one hand supporting the back, other hand supporting the head, neck and jaw the baby is turned to the supine position draped on the thigh. The infant’s head should be lower than the trunk. 4. Give up to five quick downward chest thrusts in the same location as in the manner of chest compression. If the infant is large or rescuer’s hands are small, the infant may be placed on the lap with head lower than the trunk. After the five back blows, infant is turned as a unit to the supine position and five chest thrusts are given. All these steps are repeated until the object is expelled or the infant losses conciousness. If the infant losses consciousness open the airway using a tongue jaw lift and remove the foregin body if it is seen and attempt rescue breathing and relief of airway obstruction. Tongue Jaw Lift Grasp both the tongue and lower jaw between the thumb and finger and lift. This action draws the tongue away from the back of the throat and may itself partially relieve the obstruction and if a foreign body is seen it can be removed. THE CHILD—THE HEIMLICH MANEUVER Victim Conscious 1. Stand behind the victim with arms directly under the victim’s axilla encircling the victim’s torso.


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Fig. 2.3: Abdominal thrusts

2. Place the thumb side of one first against the victim’s abdomen in the midline slightly above the navel and below the xiphoid process. 3. Grasp the fist with the other hand and exert a series of quick upward thrusts. Each thrust should be a separate distinct movement intended to relieve the obstruction. Continue the abdominal thrusts till the foreign body is expelled or the patient losses conciousness (Fig. 2.3). Unconscious Child Place the child supine. If the loss of consciousness is witnessed and foreign body aspiration is suspected open the airway with a tongue jaw tilt and remove the object if it

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is seen. Attempt rescue breathing. If ventilation is unsuccessful try re-position of head and re-attempt ventilation. If ventilation is unsuccessful go through the following steps. Kneel beside the victim or straddle the victim’s hips. Place the heel of one hand on the child’s abdomen in the midline, below the xiphoid process and above the navel place the other hand on top of the first and press with both hands in to the abdomen with a quick upward thrust. Perform a series of five thrusts. Each thrust should be a separate and distinct movement. Open the airway and with tongue jaw tilt, if the foreign body is seen, remove it. If not repeat the steps till foreign body is expelled and ventilation is successful (Fig. 2.4). Advanced Life Support ALS is done as a continuation of BLS which is initiated immediately and then the victim is to be transferred to a facility that can care for them appropriately.

Fig. 2.4: Head tilt-chin-lift maneuver


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Fig. 2.5: Recovery position

Respiratory—Airway and Ventilation Respiratory problems are common resulting in cardiopulmonary arrest and if respiratory failure is promptly treated intact survival of the child is likely. If not it may progress to cardiac arrest and the prognosis is poor. Most important is to anticipate and recognize respiratory problems and to support the child. Alert children with respiratory distress should be allowed to remain in a position of comfort to them, preferably with their parents and airway equipment with oxygen should be introduced in a non-threatening manner. If the child is uncomfortable with one method of oxygen support, alternative methods are to be tried. If the child is somnolent or unconscious see that the airway is not obstructed by neck flexion, relaxation of the jaw, posterior displacement of the tongue and collapse of the hypopharynx. If necessary, airway is to be cleared off secretions, mucous or blood (Fig. 2.5).

CHAPTER 3

Vascular Access

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Establishment of a vascular access is highly essential in the emergency care setting. It helps in successful resuscitation because infusion of the fluids and drugs are possible through it. Endotracheal tube may help in administering some drugs used in resuscitation but intravenous or intraosseous access is preferred for administration of fluids and drugs. Venous Access Peripheral venepuncture provides a satisfactory route if it can be achieved within a few minutes. It can be performed in veins of arm, hand, leg and foot. But cannulation of small veins may be difficult when patient is in shock or cardiopulmonary arrest. In such circumstances, large veins are to be tried like femoral or jugular. Cannulation of scalp veins are less desirable because the catheters in these veins may infiltrate when fliuds and medications are infused rapidly and forcefully and may interfere with control of the airway and ventilation. Intraosseous route is a reliable alternative to venipuncture in infants and children who are in shock if peripheral venous access is not achieved within a few seconds. The proximal tibia is the preferred site of intraosseous puncture. The main contraindication is the presence of fracture in the bone chosen or proximal to it. During CPR intraosseous route is to be tried if a venous access is not achieved within 3 attempts or within 90 seconds whichever comes first. Since the tibial marrow is more difficult to cannulate as age advances, in children older than 6 years, percutaneous central venous access or saphenous vein cut down should be established if reliable venous access cannot be obtained within first 90 seconds

VASCULAR ACCESS

27

of resuscitation. The preferred site of venous access remains the largest vein that can be rapidly accessed without interfering with CPR. Intraosseous Cannulation (Fig. 3.1) Complications following intraosseous infusion are reported in fewer than 1% of patients. But when they occur they are often more serious and so intraosseous cannulation is done in the treatment of critically ill infants and children only as a temporary measure until other venous access sites become available.

Fig. 3.1: Intraosseous cannulation

Devices Two types are available, specially designed intraosseous infusion needles and Jamshidi type bone marrow aspiration needles. In an emergency short wide gauge spinal needles with internal stylets can be used if no alternatives are available. All commonly used drugs during resuscitation, crystalloids, colloids and blood can be given through intraosseous route. The drugs administered should be followed by a sterile saline flush of at least 5 ml to ensure that the drug is delivered to the central circulation. The complications reported include tibial fracture, compartment syndrome, skin necrosis and osteomyelitis.

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Site The flat anterolateral surface of the tibia approximately 1-3 cm below the tibial tuberosity is the preferred site. Insertion of the needle is successful if the following conditions are present: • A sudden decrease in resistance occurs as the needle passes through the cortex to the marrow cavity. • The needle remain up wright without support. • Marrow can be aspirated into a syringe but this is not consistantly achieved. • Fluid flows freely through the needle without evidence of subcutaneous infiltration. If the cannulation is blocked it can be replaced with a second needle provided no infiltration. If evidence of infiltration occur a second attempt on the other tibia is to be tried. Central Venous Cannulation This enables delivery of the infusate directly into the central circulation and delivery of medications at or near their site of action. It allows monitoring of central venous pressure during post-resuscitation stabilization. In addition, there is little risk of infiltration of drugs. Complications of the procedure include local and systemic infections, venous or arterial bleeding, arterial cannulation, thrombosis, phlebitis, pulmonary thromboembolism, hydrothorax, hemothorax, cardiac tamponade, arrhythmias, air embolism and catheter fragment embolism. The incidence of the complications depends on the site, experience of the clinician and clinical condition of the patient. Since complications are more in pediatric age group central

VASCULAR ACCESS

29

venous cannulations are done only if the benefits outweigh the risks. Devices and Techniques Though the needle catheters can be used, great care must always be exercised during placement of a through the needle catheter because the catheter tip can be sheared off by the sharp needle. If any resistance is encountered during catheter advancement the catheter should not be withdrawn through the needle. Instead, the entire assembly should be withdrawn as a unit to prevent catheter shearing and potential fragment embolism. Modified Seldinger’s Technique for Insertion of Catheters and Introducing Sheaths Pressure monitoring catheters are catheters of relatively low compliance that allow measurement of central venous or intracardiac pressure. A catheter introducing sheath consists of a dilator within a large bore sheath. Once the catheter-introducer is placed in to a central vein, the dilator is removed and the sheath may be used for fluid infusin or to guide the insertion of a central venous catheter. The Seldinger’s (Guidewire) technique is especially useful for establishing vascular access in children. This technique allow the introduction of catheters into the venous circulation after the initial venous entry using a small gauge, thin walled needle or an over the needle catheter. Once the free flow of blood is achieved through the needle or catheter a guidewire is threaded through the needle or catheter into the vessel and the small gauge needle or catheter is withdrawn over the guidewire while

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the guidewire is held in place. A large catheter or a catheter introducing sheath is then passed over the guidewire into the vessel and the guidewire is withdrawn. If the catheter introducing sheath is used both the sheath and the dilator are then removed simultaneously, leaving the sheath in the large vein. Sites—Femoral Vein Femoral vein is used most frequently during emergency because it is relatively easy to access with lower rates of complications. Leg is restrained with slight external rotation. The femoral artery is identified by palpation of the femoral artery. If pulses are absent, the mid point of anterior superior iliac spine and the symphysis pubis is taken. After scrubbing, cleansing and anesthetizing the skin flush the needle, syringe system and catheter with sterile saline. The thin walled needle or over the needle catheter is introduced one finger’s breadth below the inguinal ligament just medial to the femoral artery. Gentle pressure is applied with an attached 3 ml syringe and slowly the needle is advanced with direction towards umbilicus at 45° angle. Once a free flow of blood is achieved the syringe is disconnected and a guidewire is advanced through the needle during a positive pressure breath or spontaneous exhalation. Remove the needle over the guidewire leaving the guidewire in position. Then pass a catheter or catheter introducing sheath over the wire. Advance the catheter in to the inferior vena cava to the right atrium. The guidewire may then be removed. Secure the catheter or introducer in place with suture material or tape and attach the infusion set. A sterile occlusive dressing is applied to the catheter insertion site.

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31

A chest radiograph is taken to verify that the catheter tip is correctly placed at the inferior vena cava right atrial junction. After introducing the needle if no free flow of blood through the needle occur, with gentle aspiration slowly withdraw the needle and syringe so that it may unkink a vessel which has become kinked during the entry. External Jugular Vein External jugular vein is actually a peripheral vein with an excellent portal to the central venous circulation. It is tried when other peripheral venous access is unsuccessful. Not preferred much in CPR because it requires extension and rotation of neck. Child is restrained in 30° head down (Trendlenberg) position with the head turned away from the side to be punctured, right side is preferred for better access. After cleansing and anesthetising the skin, the saline flushed needle is used to puncture the skin slightly distal to or to one side of the visible external jugular vein with a 16 or 18 gauge needle to facilitate entry of the catheter through the skin. Do not enter the vein with the needle. Temporarily occlude the vein just above the angle of the mandible by applying gentle pressure with the tip of the long finger of the non-dominant hand to mimic the effect of a tourniquet. Stretch the skin over the vein just below the angle of the mandible using thumb of the nondominant hand to immobilize the vein after allowing it to distend fully. If peripheral cannulation desired, insert a short length over the needle catheter. If central venous cannulation is desired, insert a long length through the needle catheter or catheter-over-guidewire and proceed as for any central venous cannulation.

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Arterial Access Arterial catheters are extremely useful for patient monitoring, for monitoring blood pressure and blood sampling. But their use is associated with complications including local and systemic infection, air or particulate embolization, thrombosis of artery with associated ischemia and growth failure in the affected limb. Sites Radial, brachial, axillary, femoral, dorsalis pedis and posterior tibial arteries can be used but radial and femoral arteries are the preferred sites of cannulation. Technique—Radial Artery Collateral circulation to the hand may be evaluated before radial artery cannulation is done with modified Allen’s test or Doppler flow evaluation. Regardless of the method of evaluation of collateral flow before cannulation, it is imperative that hand circulation is closely monitored following radial artery catheterization. If any evidence of hand ischemia is observed, the catheter should be removed. Cannulation of radial artery is done as follows. Hand is dorsiflexed at wrist 45° to 60° and secure both the hand and the lower forearm to a board. Dorsiflexion is maintained by a roll of gauze placed behind the wrist. Tape the hand down, leaving all fingers exposed so that perfusion of the hand can be assessed. Thumb may be taped aside to prevent movement during attempts at arterial cannulation. Radial pulse is located. After sterile precautions, anesthetize the skin with 1% lidocaine. Puncture the skin at the site of maximal pulsation with a 20 gauge

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33

needle. Advance a 20-24 gauge heparin flushed catheter at 30° angle and advance till the blood appears in the hub. Two techniques are frequently used. Pass the catheter and the needle through the artery to transfix it. Withdraw the catheter very slowly until there is a free flow of blood. Advance the catheter slowly through the lumen of the artery. Puncture only the anterior wall of the artery, advance the catheter slowly until blood appears in the needle. Lower the needle carefully to a 30° angle. Ascertain that blood flow is continuing and advance the catheter slowly over the needle into the lumen of the artery. Remove the needle and attach the catheter to a T connector to permit continuous infusion of heparinized saline 1-5 units/ml. Apply sterile dressing and tape the puncture site. Remove the gauze roll and secure the wrist in a neutral position. Label the arterial line so as to prevent accidental administration of drugs through it. Catheter should be removed immediately if any evidence of ischemia is developing and microvascular surgeon is to be consulted. Modified Allen’s Test Compress or clench the child’s hand several times. Elevate the hand above the heart and compress or clench the hand tightly. Occlude both ulnar and radial artery and lower the hand to the level of heart open the hand but do not hyperextend the fingers. Release pressure over the ulnar artery. If color returns to hand within 6 seconds while radial artery is occluded, the Allen’s test is negative and radial catheterization can be done because the flow through ulnar artery and palmar arch is adequate when the radial artery is occluded.

CHAPTER 4

Oxygen Therapy

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Oxygen therapy is very important in the management of critically ill children. Oxygen is a drug which is to be used judiciously. Patients on oxygen needs close monitoring. Reduced oxygen content of blood is hypoxemia and impaired oxygen utilization is hypoxia. If spontaneous ventilation is effective oxygen may be administered via a number of delivery systems determined by the child’s clinical status and desired concentration of oxygen. OXYGEN DELIVERY SYSTEMS The oxygen delivery systems can be of two types. Low Flow Systems The low flow system provides an FiO2 that varies with the patient’s inspiratory flow. Here the room air is entrained. The low flow system is often insufficient to meet all inspiratory flow requirements. They can provide an oxygen concentration of 23 to 90% although not reliably. High Flow Systems The high flow system provides a specific FiO2 at flows that meet or exceed patient’s inspiratory requirements. Oxygen Mask The simple oxygen mask is a low flow device that delivers 35-60% oxygen with a flow rate of 6-10 l/minute. The inspired oxygen concentration can be increased only modestly (up to 60%) because the inspiratory entrainment of room air occurs through exhalation ports in the sides of the mask and between mask and the face. Oxygen concentration delivered to the patient will be reduced if the

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patient’s spontaneous inspiratory flow requirement is high, the mask is loose or the oxygen flow into the mask is low. A minimum oxygen flow of 6 l/min must be used to maintain an increased inspired oxygen concentration and prevent rebreathing of exhaled carbon dioxide. Partial Rebreathing Mask (Fig. 4.1) Consists of a simple face mask with a reservoir bag. It reliably provides an inspired oxygen concentration of 5060%. During exhalation the first third of the exhaled gases flows into the reservoir bag and combines with fresh oxygen. Since the initial portion of the exhaled gas remains in the upper airway and is not involved in respiratory gas exchange during prior breath it remains oxygen rich. During inspiration the patient draws gas predominantly from the fresh oxygen inflow and from the reservoir bag, so entrainment of room air through the exhalation port is minimized. Rebreathing of exhaled carbon dioxide from the mask is prevented if the oxygen flow rate into the bag is consistently maintained above the patients minute ventilation. If the oxygen flow rate is sufficient and the mask fit secure, the reservoir bag will not empty completely

Fig. 4.1: Partial rebreathing mask

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during inspiration. An oxygen flow rate of 10-12 l/min generally is required. Non-rebreathing Mask Consists of a face mask and reservoir bag with the following additions. 1. A valve is incorporated into the exhalation port to prevent entrainment of room air during inspiration. 2. A valve is placed between the reservior bag and the mask to prevent flow of exhaled gas into the bag. On inspiration the patient draws 100% oxygen flow. Oxygen flow into the mask is adjusted to prevent collapse of the bag. An inspired oxygen concentration of 95% can be achieved with an oxygen flow of 10-12 l/min and the use of a well sealed mask. Venturi Mask This is designed to reliably and predicably provide controlled low to moderate (25-60%) inspired oxygen concentrations. Venturi valves deliver air oxygen mixture at high flow rates the ratio of which will not varry at any point of time and thus fixed FiO2 is delivered to the patient. They are advantageous because humidification may not be necessary as a much greater air flow than oxygen is there resulting in the delivery of essentially room air humidity. Moreover it is economical and cheap. Face Tent (Fig. 4.2) A face tent or face shield is a high flow soft plastic ‘bucket’ often better tolerated by children than a face mask. Even with a high oxygen flow (10-15 l/min) stable inspired

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Fig. 4.2: Face tent

oxygen concentration greater than 40% cannot be reliably provided. An advantage of the face tent is that it permits access to the face (e.g. suctioning) without interrupting the oxygen flow. Oxygen Hood (Fig. 4.3) An oxygen hood is a clear plastic shell that encompasses the patients head. It is well tolerated by infants, allows easy access to the chest, trunk and extremities, permits control

Fig. 4.3: Oxygen hood

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of inspired oxygen concentration, temperature and humidity. A gas flow rate equal to or greater than 10-12 l/mt maintains an inspired oxygen concentration of 80-90%. The hood is usually not large enough to be used for more than 1 year old. Oxygen Tent It is a clear plastic shell that encloses the child’s upper body. It can be used to deliver more than 50% oxygen with high flows but cannot reliably provide a stable inspired oxygen concentration. Room air is entered into the tent whenever the tent is entered and the inspired oxygen concentration falls. The tent limits access to the patient when humidified oxygen is used the mist limits observation of the patient. In practice it does not provide greater than 30% concentration of inspired oxygen. Nasal Cannula Simple low flow oxygen delivery device suitable for infants and children who require only minimal amounts of supplemental oxygen. The cannula contains two short plastic prongs arising from a hollow face piece. The prongs are inserted into the anterior nares and oxygen is delivered into the nasopharynx. The inspired oxygen concentration cannot be reliably be determined because it is influenced by other factors including nasal resistance, oropharyngeal resistance, inspiratory flow rate, and tidal volume. A high oxygen flow rate (>4 l/min) irritates the nasopharynx and may not appreciably improve humidified oxygen.

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Nasal Catheter It is a flexible, lubricated catheter with multiple holes in the distal 2 cm. The catheter through one nostril is advanced into the pharynx behind the uvula. This method is discouraged because it has no advantage over the nasal cannula and it may cause trauma to adenoids, gastric distension if inadvertently placed in the esophagus. AIRWAYS Oropharyngeal Airway It consists of a flange, a short bite block segment and a carved body made of plastic. The carved body is designed to fit over the back of the tongue to hold it and the soft hypopharyngeal structures away from the posterior pharyngeal wall. This is indicated in an unconcious infant or child if the procedures to open the airway fail to provide and maintain a clear airway. Airway sizes differ from 4-10 cm in length. (Guedel’s sizes 0000-4). The proper size is estimated by placing the oropharyngeal airway next to the face with the flange at the corner of the mouth, the tip of the airway should reach the angle of the jaw. It is not of correct size whether large or small will result in airway obstruction. Nasopharyngeal Airway It is a soft rubber or plastic tube that provides a conduit for airflow between the nares and posterior pharyngeal wall. They are available in sizes 12F to 36F. 12F corresponds approximately to the size of 3 mm endotracheal tube and will generally fit to a newborn baby. The outside

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airway diameter should not be so large as to cause sustained blanching of alae nasi. The proper length is approximately equal to the distance from the tip of the nose to the tragus of the ear. Management of Respiratory Failure or Arrest As soon as respiratory failure or inadequate ventilation is identified clinically or by blood gas analysis, rapid initiation of assisted ventilation is the only appropriate therapy. BAG- VALVE-MASK VENTILATION Ventilation Face Mask A ventilation mask consists of a rubber or plastic body, a standardized 15-22 mm connecting port and a rim or face seal. Ideally the face mask should be transparent, permitting the rescuer to observe the color of the child’s lips and condensation on the mask (indicating exhalation) and to detect regurgitation (Figs 4.4 and 4.5). They are available in variable sizes. The proper mask size is selected to provide an air-tight seal. The mask should extend from the bridge of the nose to the cleft of the chin, enveloping the nose and mouth but avoiding compression of the eyes. An airtight seal is essential for an effective ventilation. Two hands must be used to provide bag-valve-mask ventilation. The mask is held on the face with one hand as a head tilt chin lift maneuver is performed. The other hand compresses the ventilation bag. In infants and toddlers, the jaw is supported with the base of the middle or ring finger. In older children the fingertips of the third, fourth and fifth fingers are placed on the ramus of the mandible to the hold the jaw forward and extend the head.

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Fig. 4.4: Bag and mask ventilation

Fig. 4.5: Proper area of the face for mask application

This creates a one handed jaw thrust maneuver. When two rescuers are available one uses both hands to open the airway and make an airtight mask to face seal while the second rescuer compresses the ventilation bag. A neutral sniffing position without hyperextension of the head is usually appropriate for infants and toddlers. Children older than 2 years may require some anterior

44


displacement of the cervical spine to obtain optimal airway patency. This may be achieved by placing a folded towel under the neck and head. If the child demonstrates spontaneous ventilatory effort and partial airway obstruction application of 5-10 cm H2O continuous positive pressure (CPAP) via a face mask may maintain adequate airway patency and oxygenation without the need for assisted ventilation. This requires a tight mask fit and a breathing circuit capable of delivering CPAP. Gastric inflation in an unconcious child can be minimized by applying cricoid pressure (Sellick maneuver). This occludes the proximal esophagus by displacing the cricoid cartilage posteriorly, the esophagus is compressed between the cricoid ring and the cervical spine. Cricoid pressure is applied by the second rescuer using a finger tip in infants and the thumb and index finger in children. Excessive pressure must be avoided because it may produce tracheal compression and obstruction in infants. Self Inflating Bag-valve Ventilation Devices Self inflating bag-valve device with a face mask provides a rapid means of ventilating a patient in an emergency. The bag recoil allows the self inflating bag to refill independent of inflow from a gas source. During inflation the gas intake valve opens, entraining room air or supplemental oxygen if a fresh oxygen inflow reservoir is provided. During bag compression the gas intake valve closes and a second valve opens to permit gas flow to the patient. During patient exhalation, the bag outlet valve

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(non-breathing valve) closes and the patient’s exhaled gases are vented to the atmosphere to prevent rebreathing and retension of carbon dioxide. A self inflating bag-valve device delivers room air (21% oxygen) unless supplemental oxygen is provided. At an oxygen inflow of 10 l/min, pediatric self inflating valves without oxygen reservoirs deliver 30-80% oxygen to the patients. Reservoir equipped bag-valve device can provide oxygen concentration of 60-95%. Before initiating ventilation the flow of oxygen to the bag is to be confirmed by listening to the sound of oxygen flow. Many self inflating bags are equipped with a pressure limited pop off valve set at 35-45 cm H2O to prevent barotrauma. Bags used for resuscitation should have no pop off valve or one that is easily occluded since pressures required for ventilation during CPR may exceed the pop off limit, particularly during bag-valve-mask ventilation. The bag-valve device must be appropriate to patient size and condition. When assisted ventilation is provided the administered tidal volume should be approximately 10-15 ml/kg. Neonatal size (250 ml) are usually inadequate to support effective tidal volume and even in infants it should have a minimum of 450 ml. CPAP It is a simple way of improving the oxygenation in patients with normal ventilatory activity. CPAP improves oxygenation by 1. Increasing the FRC and thus reducing the work of breathing.

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2. Increasing static compliance of lungs. Recruiting the alveoli for gas exchange. 3. Improving ventilation perfusion relationship. CPAP can be given Without intubation a. Nasal prongs b. Nasopharyngeal catheters c. Tightly fitting mask With intubation a. With ventilator b. Without ventilator CPAP partially obstruct the expiratory flow and thus prevent the complete collapse of lung at the end of expiration. Simple devices can be made from a bottle with a glass tube immersed in it for the intended depth to deliver the desired CPAP. Patient is weaned from CPAP at a point when the patient maintains adequate saturation on FiO2 of 30%. Then the CPAP is reduced slowly. Endotracheal Airway Ventilation via an endotracheal tube is the most effective and reliable method of assisted ventilation. Endotracheal Tube The basic design of the endotracheal tube is standardized. The connector fits into the tube at the proximal end with a standard 15 mm outside diameter permitting connection to the mechanical ventilator circuit, bag-valve-mask device or anesthesia devices. The tube body has a standard

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curvature with markings that allows determination of the depth of insertion. The distal tip has a bevelled edge and in murphy type there is a hole just opposite the bevelled edge- the murphy’s eye. This allows ventilation even when the bevelled edge is blocked. A vocal cord marker may also be present at the level of glottic opening to endure that the tip of the tube is in the mid tracheal position. Cuffed endotracheal tubes are used in children older than 8-10 years and adults. The normal anatomic narrowing at the level of the cricoid cartilage provides a functional cuff in children younger than 8 years. Size of the Endotracheal Tube 3-3.5 mm internal diameter - newborns. 4 mm - 1year 5 mm - 2 years Above 2 years Age (yr) Endotracheal tube = +4 4 or the size of the 5th finger of the baby, roughly. Depth of Insertion (alveolar edge to mid trachea) Older than 2 years of age. Age (yr) + 12 2 Another calculation is by using the internal diameter of the tube. Depth of insertion is internal diameter × 3 in cm. Oral intubation is preferred in emergency as it is easier to insert.

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Preparation and Technique of Intubation Before intubation, ventilation should be provided by bagvalve-mask device using 100% of oxygen. Monitoring of heart rate and oxygen saturation by pulse oximetry should be performed because ventilation may be interrupted during intubation. Intubation attempts should be brief and if longer than 30 seconds patient may be provided ventilatory support with bag and mask. Intubation should be done with direct laryngoscopic examination. Heart rate is to be continuously monitored during the procedure. In the incidence of reflux bradyarrhythmia atropine 0.02mg/kg may be given IV during intubation in a spontaneously breathing child. However in an emergency, intubation should be done without atropine in order to avoid delay in intubation. Continuous evaluation of oxygen saturation monitoring is important if the heart rate response to hypoxemia has been blunted with atropine. The laryngoscope handle is held in the left hand, and the blade is inserted into the mouth in midline following the natural contour of the pharynx to the base of the tongue. Once the tip of the blade is at the base of the tongue and the epiglottis is visualized, the proximal end of the blade is moved to the right side of the mouth sweeping the tongue toward the middle. Alternatively the blade may be inserted in the right side of the mouth to the base of the tongue. Once the epiglottis is visualized, the proximal end of the blade and the handle are swept to the midline. This movement toward the midline provides a channel in the right third of the mouth through which the endotracheal tube will be passed while direct visualization of the laryngeal structures is maintained.

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Either a curved or straight blade may be used for intubation of children. The tip of the curved blade is inserted into the vallecula to displace the tongue anteriorly. With the straight blade, the tip of the blade is used to lift the epiglottis and visualize the glottic opening. The tip should rest beyond the vallecula. Then traction is exerted upward in the direction of the long axis of the handle to displace the base of the tongue and the epiglottis anteriorly exposing the glottis. To avoid visual obstruction of the glottic opening, by the endotracheal tube, the ETT is inserted from the right corner of mouth not down the barrel of the lanyngoscope blade. In this way the rescuer will be able to see the ETT as it passes through the glottic opening. It will be helpful if an assistant can displace the corner of the mouth to the right so as to enable the visualization of the passage of ETT through the glottic opening. Application of pressure at the cricoid also can facilitate visualization of glottic opening. The black glottic marker of the ETT is placed at the level of the vocal cord so that the tip of ETT is in mid tracheal position. Immediately after intubation, the position of the ETT is clinically assessed by observation of chest movements and auscultation of the chest. If not in the right position tube is to be removed, patient is stabilized with bag and mask ventilation and then intubation is re-attempted. After intubation, the ETT should be secured to the patient’s face to prevent unintentional extubation. Before ETT is taped, correct position is confirmed once again. The distance marker at the lips should be noted to allow detection of unintentional extubation.

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Complications Associated with Endotracheal Intubation During the intubation procedure • • • • • • •

Vomiting with possible aspiration Trauma - laryngeal, pharyngeal, tracheal and dental Bradycardia caused by vagal stimulation Hypoxemia caused by delay in procedure Cardiac arrhythmias Right mainstem intubation Esophageal intubation

While the Tube is in Place • • • • • • • • • •

Tube malposition—too high, too low Right mainstem intubation Laryngeal or tracheal erosion, necrosis Pharyngeal edema Mouth lip or nares pressure sore development Inadequate ventilation or oxygenation as a result of tube obstruction or kinking Loss of cuff integrity Self extubation Aspiration Sinusitis/otitis media.

CHAPTER 5

IV Fluid Therapy

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Proper maintenance of fluid and electrolytes is very important in the supportive care of critically ill children. Even when they don’t have any changes in fluid and electrolytes they may have to be supported with the maintenance therapy for a few days in the intensive care setting. Maintenance of Water The total body water content in an average adult or adolescent is about 60% of body weight and in a newborn it is as high as 80% of body weight. The total body water is distributed in the body in two major compartments, the extracellular fluid and the intracellular fluid. Two-third is in the intracellular compartment and 1/ 3 is in extracellular compartment. ICF is rich in potassium and ECF is rich in sodium. The maintenance fluid therapy has to take into consideration the insensible fluid loss which is usually lost through skin, respiratory tract and kidneys. The basic principles of parenteral fluid therapy were laid by Holliday and Segar in 1957. It should contain 5% dextrose to minimize the endogenous breakdown of proteins and fats thus preventing formation of ketones. It should also contain sodium and potassium (3 mEq/kg/ day and 2 mEq/kg/day respectively). Maintenance Fluid and Electrolytes Body wt Water Na K Glucose 0-10 kg 100 ml/kg/day 3 mEq/kg/day 2 mEq/100 ml 5 gm/100 ml 11-20 kg

1000 ml + 50 ml/kg 20 ml/kg for each kg above 20 kg 1500 + 20 ml/kg

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Rate of Fluid Infusion 1000 ml in 24 hrs. Roughly 40 ml/hr or 4 ml/kg/hr. For microdrop set 1ml = 60 micro drops and conventional IV set. 1ml - 15 drops. Maintenance fluid has to be modified in certain clinical situations. Increased Requirement 1. 2. 3. 4. 5.

Radiant warmer (20 ml/kg/day) Phototherapy (20 ml/kg/day) Fever 10-15% for each 1° C above normal Tachypnea Bypassing upper airways

Decreased Requirement 1. Increased ambient humidity 2. Humidification of inhaled gases. Most of the commercially available maintenance fluids are approximately 1/6th saline having 25 mEq/1000 ml. There is an increasing concern over development of hyponatremia especially in older age groups. Administration of parenteral fluids has its own deleterious effects on health and so as far as possible enteral fluids are to be preferred and IV fluid therapy should be as short period as possible and those on IV fluids should be closely monitored. Younger babies need more careful monitoring.

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IV FLUIDS IN SPECIFIC SITUATIONS Acute Diarrheal Disease IV fluids are indicated only if the child is having: 1. Severe dehydration 2. Severe purging - purging more than 3 times/hour or if fluid lost is >15ml/kg stools 3. Persistent vomiting - more than 3 times/hour 4. Abdominal distension 5. Associated illnesses 6. Severe dyselectrolytemia Fluid preferred is Ringer’s lactate or 1/2 Darrow solution. If both are not available N. saline may be used. Amount of fluids for a chlid with severe dehydration: 30 ml/kg 70 ml/kg <12 months 1 hour 5 hours >12 months 1/2 hours 21/2 hours DYSELECTROLYTEMIAS Hyponatremia Commonest electrolyte disturbance in critically ill children. It is defined as S. sodium less than 135 mEq/L. Causes Can be due to loss of sodium (hypovolemia). Renal Losses Diuretics Recovering ATN Congenital adrenal hyperplasia Adrenal insufficiency

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Hypoaldosteronism Bartter’s syndrome Extrarenal Gastrointestinal- ADD Excessive sweating Gain of Water (Hypervolemic hyponatremia) Nephrotic syndrome Cirrhosis liver CCF ARF, CRF Gain of Water (Euvolemic hyponatremia) Pain, stress, anxiety, drugs Hypothyroidism, Cortisol deficiency , SIADH. Pseudohyponatremia Methodology dependent artifact when serum sodium is estimated by flame emission spectrometry which measures sodium in total serum. When the serum solids are increased as in hyperlipidemia or hyperproteinemia the serum sodium appear low. When serum sodium is measured by ion specific electrode, measurements are made directly in the fluid compartment of serum which gives the correct measurement of sodium. Factitious Hyponatremia Presence of osmotically active particles (e.g. glucose) rises the serum osmolality and so water is drawn from ICF to ECF and thence the S. sodium becomes low.

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In pseudohyponatremia the serum osmolality is normal. In factitious hyponatremia the serum osmolality is high. In other causes, hyponatremia is associated with hypoosmolality. Symptoms of hyponatremia are non-specific and may simulate a primary neurologic disorder. A high index of suspicion is necessary to detect hyponatremia in a critically ill child. Differential diagnosis of hyponatremia can be done by estimating the urine sodium. Hypovolemic U Na <20 mEq Extrarenal

U Na>20 Renal CAH

Euvolemic

Hypervolemic

U Na >20 Drugs Hypothyroidism Glucocorticoiddeficiency Pain SIADH

U Na <20 N syndrome Cirrhosis CCF U Na >20 ARF CRF

Treatment Whatever be the type or cause of hyponatremia serum sodium above 130 mEq/L is usually asymptomatic and no treatment is necessary. When serum sodium falls rapidly to 125 mEq/L or less cerebral edema can occur and CNS symptoms can occur. The child is to be treated with hypertonic saline, 3% NaCl 10-12 ml/kg over a period of 2-4 hours (1 ml NaCl= 0.5 mEq Na). Once the acute symptoms are controlled further correction is done gradually over a period of 48 hours. The sodium required is calculated as per the formula. 0.6 × body weight × (135 – measured serum sodium) 135 is the expected serum Na

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This should be given over 48 hours. Serum sodium is to be increased at a rate 0.5 mEq/L per hour or not more than 12 mEq/day Hypovolemic Hyponatremia Hypovolemia is corrected with the bolus of 20 ml normal saline. After the serum sodium concentration has been corrected to approximately to 125 mEq/L the rest of the deficit should be corrected slowly in 18 to 36 hours. The fluid to be given is determined on the basis of water deficit. The water deficit is decided by the weight loss or by assessing the level of dehydration by the clinical signs. 10% dehydration in a 10 kg child would mean a water deficit of 1000 ml. Hypervolemic Hyponatremia Occurs due to water gain and in fact total body sodium is high despite the low serum sodium. Administration of sodium may worsen edema and may result in fluid overload. The treatment would consists of fluid restriction. Fluids given should be less than the total amount of insensible water loss and urine output. The fluid excess can be calculated as follows. TBW × (1– measured sodium/expected sodium) Fluid restriction will slowly correct the hyponatremia. In addition, furosemide if given will correct the hyponatremia more rapidly. Euvolemic Hyponatremia Most common condition is SIADH. Restrict the fluids to insensible water losses. Fluid replacement is done with

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isotonic saline. Furosemide is administered to improve free water clearance. If serum sodium is less than 120 mEq/ L and accompanied by CNS symptoms, administration of 3% NaCl is given. In slowly developing hyponatremia CNS cells adapt to the hypotonic milleu. The cells do so by extruding osmotically active particles and lowering the intracellular osmolarity. If the serum sodium level is corrected rapidly, the ECF tonicity becomes normal but since Na cannot enter the cells the ICF is unable to increase its tonicity rapidly. This osmotically challenged cells undergo osmotic demyelination and can result in psuedobulbar palsy, quadriparesis and even death. The changes in autopsy or MRI are seen as central pontine myelinolysis. Therefore unless symptomatic, hyponatremia should be corrected gradually, not more than 12 mEq/L day. Hypernatremia Serum sodium level above 150 mEq/L is hypernatremia. It is rare compared to hyponatremia. It is often due to increased free water loss or due to a true gain in sodium. Often occurs in infants with ADD especially when they are offered high solute containing fluids like inappropriately prepared ORS, salted kanji water or when large amounts of fluids are given IV as Ringer’s lactate. Extremely premature babies who have large insensible water losses through immature skin can develop hypernatremia. Exclusively breast fed infants when there is lactation failure or in hot weather can develop hypernatremia. Central or nephrogenic diabetes insipidus can result in excessive water loss and result in hypernatremia.

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Accidental or intentional salt poisoning, sea water drowning, administration of hypertonic saline or sodium bicarbonate are other causes. Marked thirst and irritability inappropriate for other signs of dehydration are the characteristic features in infancy. Other CNS symptoms can follow. The cause of hypernatremia can be made out by clinical evaluation with specific attention to the volume status, urine output, urine osmolality and specific gravity. S. sodium >150 mEq/L with dehydration Urine output >3 ml/kg/hour Urine output decreased Sp gravity < 1005 Sp gravity >1020 Urine osmolality < 200 Diarrhea Diabetes Insipidus VLBW Lactation failure S. sodium >150 mEq/L with overhydration Urine output normal or high Urine Na high Salt poisoning Excess hypertonic saline or soda bicarb Treatment The more common problem is hypovolemic hypernatremia or hypernatremic dehydration which is due to free water deficit. Correction should be done by slow rehydration. The fluid deficit should be corrected in 48 hours or longer. The volume of fluid to be given is 2 × maintenance fluid + calculated deficit to be given equally spread over 48 hours. No fluid bolus unless the child is in shock. The free water deficit can be calculated as:

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Free water deficit = 0.6 × Wt × (S. sodium – expected sodium) – 1 l This deficit is pure water. In diarrhea there will be sodium losses also. So the total free water deficit can be calculated and the rest of the fluid can be given as isotonic saline. Since the total sodium lost is very little the total calculated fluid can be given as 0.2 N saline also. The rate of fall of sodium should not be not more than 0.5 mEq/ L/hr or not more than 12 mEq/L/day. A sudden fall in S. sodium is to be avoided as this can result in several complications. If the serum sodium is lowered rapidly, the serum osmolality, and tonicity gets lowered rapidly. To protect the cell from shrinkage cells generate idiogenic osmoles to maintain osmotic equilibrium. During correction of hypernatremia the cells are unable to dissipate these idiogenic osmoles rapidly. As the intracellular osmolality is high water moves to the cells leading to cerebral edema, which can result in seizures, respiratory and pupillary irregularities and even death. This may even necessitate infusion of 3% NaCl to prevent rapid fall in serum sodium. Rapid correction of hypernatremia again result in extrapontine myelinolysis as evidenced by MRI. Hyperglycemia is frequently encountered in hypernatremic dehydration as the high serum sodium has an inhibitory effect on insulin secretion. Insulin should not be given as this will worsen cerebral edema. Glucose in IV fluids can be reduced to 2.5% or patient is allowed free water orally by nasogastric tube as hourly instalment to prevent worsening of hyperglycemia. In polyuric children with DI the concentration of fluid administered should not exceed 0.2 DNS. The total fluid for 24 hours should include.

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Maintenance fluid + 1/2 deficit + hourly replacement of urinary losses. The deficit can be given as free water orally or by nasogastric tube as infusion or hourly instalment. Central D1 needs vasopressin as specific therapy. When the response to vasopressin occurs (Urine output < 2ml/kg/ hour) the administration of hypotonic fluids should be limited to prevent hyponatremia. Hypokalemia is defined as serum potassium of < 3.5 mEq/L. Can occur in. PEM GI losses in diarrhea or vomiting Ketonuria RTA Bartter’s syndrome Steroid therapy In these conditions, total body potassium also is low. Hypokalemia without decrease in body potassium can occur due to transcellular shift of potassium as in Administration of glucose Insulin Catecholamines Bicarbonate Clinical history along with analysis of urine potassium, acid base balance and urine chloride gives the right diagnosis.

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Urine K < 20 mEq/L Low Bicarbonate—Diarrhea High Bicarbonate—Vomiting Urine K > 20 mEq/L Low Bicarbonate—RTA Urine K > 20 mEq/L, Urine Cl < 10 mEq/L Vomiting Urine K > 20 mEq/L, Urine Cl > 10 mEq/L Diuretics Bartter’s syndrome Mg depletion, Extreme K depletion Treatment Hypokalemia need to be corrected slowly, orally if feasible. If given IV it should be diluted and given with fluids, upto 40 mEq/L. Up to 80 mEq/L can be given if required under continuous ECG monitoring in ICU set up. One ml KCl yields 2 mEq of potassium. Rapid correction may be necessitated in severe hypokalemia resulting in cardiac arrhythmias, bradycardia, slow respiration and severe muscular weakness where 0.5 to 1 mEq/kg can be given suitably diluted over 1 hour with continuous ECG monitoring. Should never be given as a bolus. Persistent hypokalemia should arouse suspicion of hypomagnesemia. In co-existant hypocalcemia and acidosis correction should be deferred since bicarbonate can still lower serum potassium and administration of calcium can precipitate cardiotoxicity.

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Hyperkalemia Defined as serum potassium more than 5 mEq/L. Causes Often renal as kidney is the main route of excretion of potassium- Renal failure. Drugs like ACE inhibitors Aldosterone antagonists Adrenal insufficiency Transcellular shifts of potassium from ICF → ECF occurs in acidosis, β blockers Crush injuries, burns Spurious hyperkalemia occur during excessive pressure of tissues during the collection of blood. Mild hyperkalemia K level is < 6.5 mEq/L No ECG changes. Moderate K levels 6.5 mEq/L ECG changes -peaking of T waves. Severe K levels >8 mEq/L or regardless of plasma K levels ECG shows. Widened QRS complexes, flattenig of p waves or ventricular arrhythmias. Treatment Measures aims at: Shift of potassium into cells Antogonism of effects of potassium Removal of potassium from body. 1. Sodium bicarbonate 2 mEq/kg IV diluted and as a rapid push in 3 to 5 minutes

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2. Calcium gluconate 10% 0.5 to 1 ml/kg IV as a rapid push over 3 to 5 minutes 3. Glucose 0.5 to 1 gm/kg IV over 30 minutes accompanied by regular insulin 0.1 to 0.2 u/kg 4. Na/K cation exchanger orally or as a retention enema over 30 to 45 minues. Finally, if these measures fail or because of accompanying renal failure, peritonial or hemodialysis must be instituted. Hypocalcemia Defined as total serum calcium less than 8.5 mg/dl in children, less than 8 mg/dl in term neonates and less than 7 mg/dl in pre term babies. Cause of hypocalcemia varry with age. In children the causes are: Vitamin D deficiency Pancreatitis Hypoalbuminemia Hungry bone syndrome Alkalosis Hypophophatasia Hypoparathyroidism Renal failure Malabsorption syndrome Treatment Asymptomatic hypocalcemia is treated with oral Ca. 100200 mg/kg/day of elemental Ca as calcium gluconate or carbonate. Vitamin D supplements may be required in patients with renal disease and vitamin D deficiency states. In critically ill patients IV calcium is given as 10% calcium gluconate in a dose of 1-2ml/kg IV over 3-5 minute upto a total of 10 ml with cardiac monitoring. Calcium gluconate contains 9.8 mg/ml or 0.45 mEq/ml of elemental

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calcium. Calcium chloride 10% contains 27mg/ml and so is more irritating to the veins. The bolus can be followed by 100-200 mg/kg of IV calcium gluconate infusions over 24 hours in children. If magnesium is low, 50% magnesium sulfate may be given as 0.1 - 0.2 ml/kg IM every 12-24 hours as needed. Hypercalcemia Defined as S. calcium levels >12mg/dl. It is rare as compared to hypocalcemia. Causes Varry with age and in infants and children the causes are Vitamin D excess. Primary hyperparathyroidism Idiopathic infantile hypercalcemia William’s syndrome Severe autosomal recessive hyperphosphatasia Thiazide diuretics Treatment Primary line of treatment is to augment urinary losses of calcium by saline diuresis coupled with IV furosemide. 1.5- 2 times the maintenance fluid requirement is given with close monitoring of S. electrolytes and urine output. If serum calcium is greater than 14 mg/dl calcitonin 2-4 units/kg every 6-12 hours may be used. Biphosphonates such as pamidronates at 0.5 to 1 mg/kg/dose over 4-5 hours can be tried but rarely used in children. In severe hypercalcemia dialysis is life-saving.

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Hypomagnesemia Defined as serum Mg < 1.8 mEq/L. Causes Diarrhea, nasogastric suction IBD ↑ Renal losses with drugs like Thiazides Loop diuretics Aminoglycosides Amphoterecin B Poorly controlled diabetes, recovery of diabetic ketoacidosis. Treatment If mild and asymptomatic oral replacement with 10-20 mg/ kg/day of elemental magnesium in 3-4 divided doses is enough. In symptomatic hypomagnesemia IV magnesium can be given 1 mEq/kg over 2-6 hours on day 1 followed by 0.5 mEq/kg over 2-4 hours for next 3 days. 50% Mg SO4 contains 4 mEq per ml (48 mg). The total replacement recquired would be about 4 mEq/kg. Careful monitoring of electrolytes and blood pressure is required during IV magnesium infusion due to the chance of developing hypotension, hypocalcemia and hypermagnesemia. Hypermagnesemia Is defined as serum magnesium levels above 2.5 mEq/L.

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Causes Patients in renal failure with excessive intake of Mg. Trauma, shock, burns. Initial dehyrated phase of DKA. Treatment IV calcium gluconate 1 ml/kg diluted is given slowly with cardiac monitoring to antagonize the effects of Mg at the cardiac membrane and neuromuscular level. When urine output is good, saline diuresis can be given. Non Mg containing enemas or cathartics may be given to enhance GI clearance. In hypermagnesemia with S. Mg >8 mEq/L dialysis is indicated and also in any patient with cardiovascular or neuromuscular effects of hypernagnesemia, irrespective of the serum level.

CHAPTER 6

ABG Analysis

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Knowledge of blood gas analysis is essential in critical care management. Analysis is normally performed in the blood obtained from the peripheral artery. Radial artery is the commonly used one. After the Allen’s test, radial artery is punctured and 2-3 ml of blood is taken in a 5 cc syringe that is coated on the inside with 1:1000 solution of heparin. 0.05 ml of heparin is enough anticoagulant for 1 ml blood and up to 0.1 ml for 1 ml of blood shall not interefere with the blood gas values. It is to be immediately immersed in ice to prevent the continued gas consumption of the blood cells which can alter the values. The syringe to be used should be made of glass since the air bubbles adhering to the sides of the plastic syringe may increase the value of oxygen. Heparin has high H+ ion concentration and so the values can get altered if the amount of heparic used is more. Values Obtained pH—represents a measure of the overall acid-base balance. PCO2—represents arterial CO2 levels and thus gives a measure of the ventilatory status. PO2—represents the oxygen tension in the arterial blood and gives the oxygenation status. HCO 3—Base excess or deficit indicate the metabolic component of acid-base status. Normal Status pH PCO2 PO2 Saturation

Arterial 7.4 40 mmHg 97 mmHg 97%

Venous 7.37 45 mmHg 40 mmHg 75%

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>7.45 Alkalosis <7.35 Acidosis pH PCO 2 PO2 Hypoxemia Mild Moderate Severe

Normal 7.3-7.4 30-50 mmHg >80 mmHg

range 7.35-7.45 35-45 mmHg

60-80 mmHg 40-60 mmHg <40 mmHg

What are the steps in analyzing the values? 1. What is the overall acid-base status given by pHacidosis or alkalosis? 2. What is the ventilatory status given by the PCO2 and oxygenation status given by PO2? 3. What is the metabolic status given by HCO3? 4. What is the problem?. Acute? Compensated? Uncompensated? Partially Compensated? Simple? Mixed? Chronic? The primary alteration can be four types: 1. Acidosis 2. Alkalosis Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis Mixed disorders are those where there are more than one primary disorder. A normal expected compensation in a primary disorder does not make it a mixed disorder. What is physiological compensation respiratory acidosis? In ventilatory failure respiratory acidosis occurs and there is an increase in PCO2 due to inadequate CO2 wash out.

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This is buffered initially by non bicarbonate buffers like proteins in ECF and phosphate, hemoglobin and lactate in the cells. If hypercapnea is sustained the renal compensatory mechanism comes in to play resulting in. 1. Excretion and secretion of H+ ions. 2. Formation and excretion of ammonium ions. 3. Retension of bicarbonate ions and excretion of chloride ions. An increase in bicarbonate is approximately the same as the decrease in serum chloride and so there is no change in anion gap. Additionally, respiratory acidosis causes a shift of electrolytes leading to a rise of serum potassium concentration. This hyperkalemia may increase to toxic levels to produce cardiac toxicity. Many patients with respiratory acidosis may over compensate leading to metabolic alkalosis associated with hypokalemia which a may warrant therapy with potassium chloride Examples pH 7.25 PCO2 58 mmHg HCO3 25 mEq/L There is obvious acidemia, PCO2 levels are ↑, but bicarbonate is still low. Impression Simple respiratory acidosis with inadequate time for compensation or have a renal pathology. The compensatory mechanisms take time to be effective. Respiratory responses occur rapidly, 50% in 6 hours and 100% in 16 hours. Renal mechanisms are slower and renal acid excretion is still

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slower compared to base excretion. 50% of base excretion occurs in 8 hours and 100% in 24 hours whereas in renal acid excretion 50% occurs in 36 hours and 100% occur in 72 hours. Renal compensation for respiratory alkalosis occurs faster than for respiratory acidosis. In the presence of a single acid-base disorder even after compensation has occured pH will still be in the direction of the primary disorder. A physiological compensation never over compensates. So in such a case either the data is wrong or it is a second primary acid-base disorder. Example pH PCO2 HCO3

7.23 58 mmHg 17 mEq/L

Here the pH is acidic. There is CO2 retention. But instead of expected high HCO3 there is low HCO3. Impression: Mixed respiratory and metabolic acidosis. There are certain rules for compensation by which we can predict certain values and interpret the results. Rule No I An acute change in PCO2 of 10 mmHg is associated with an increase or decrease of pH by 0.08 units. This is by considering the normal pH as 7.4 and normal PCO2 as 40 mmHg. If the predicted pH is equal to the measured pH it is respiratory in origin. If the measured pH is greater than the predicted pH there is associated metabolic alkalosis also and if less than the predicted value there is associated metabolic acidosis.

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Example pH 7.26 50 mmHg PCO2 Predicted pH for PCO2 of 50 is 7.32 but the actual pH is 7.26 (less than expected). There is a deficit of 0.06 units which is indicative of metabolic acidosis combined with respiratory acidosis. Rule No II Helps us to estimate the magnitude of the metabolic component. It says that the pH change of 0.06 units is as a result of a base change of 0.67 mEq/L. So the base deficit can be calculated by multiplying the difference with 0.67. So 0.06 × 0.67 is roughly 4 mEq/L. Rule No III Helps in calculating the total base deficit. It is based on the fact that HCO 3 is located in the extracellular compartment which consists of 30% of body weight. So the total base deficit is calculated by. Base deficit (mEq/L) × wt × 0.3 in kg. 10 kg Child4 × 10 × 0.3 = 12 mEq. Only half the calculated dose is to be given in 2-3 hours Due to the detrimental effects encountered with bicarbonate therapy (tetany, cardiac arrhythmias, intraventricular hemorrhage in newborn) base deficit is not corrected until the serum bicarbonate value is < 10 mEq /L or the pH is <7.2 unless there is cardiopulmonary instability. In chronic acid-base disturbances the appropriate compensation occurs and in long standing metabolic

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acidosis the normal expected degree of respiratory compensation can be recognized by inspection of the last 2 digits of pH and PCO2. If the two digits are close, the respiratory response is adequate. pH expected PCO2 7.25 25 7.3 30 7.35 35 In case of metabolic acidosis next thing to be done is to look for the anion gap. Anion gap = [Na + K] – [Cl + HCO3] Normal is 8-16 mEq/L This represents the unmeasured anions which, along with bicarbonate and chloride counter balance the positive charges of Na and K. Increased Anion Gap Acidosis Diabetic Ketoacidosis Lactic acidosis Inborn errors of metabolism Renal failure Poisoning-alcohol, ethylene glycol, paraldehyde, salicylates. Normal Anion Gap Acidosis Renal tubular acidosis Carbonic anhydrase inhibitor Chronic diarrhea. How to determine whether there is coexistence of other metabolic disturbances with an anion gap acidosis? To find out this one has to determine if there is an increase in anion gap and whether there is additional

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variation in HCO3 existing. If no other metabolic disturbance exists the following calculation should result in 24 mEq/L. Corrected HCO3= Measured HCO3 + (Anion gap – 12) If corrected HCO3 varries above or below 24 there is a mixed or complex metabolic disturbance. To be more specific, if the corrected HCO3 is more than 24 a metabolic alkalosis coexists and if the corrected HCO3 is less than 24 a non-anion gap acidosis coexists. E.g.: Corrected HCO3 = 10 + (26 – 12) 10 + 14 = 24 There is only anion gap metabolic acidosis. The Practical Approach to Rapid Analysis of ABG 1. Look at pH

< 7.35 Acidosis > 7.45 Alkalosis Normal pH does not rule out an ABG disorder 2. Look at bicarbonate. Is it normal? If bicarbonate is responsible for the pH change, the pH will change in the direction of the change in bicarbonate. 3. Look at PCO2. Is it normal? If CO2 is responsible for the change in pH then the pH will change in the opposite direction of the change in PCO2. Increase in PCO2 will decrease pH and vice versa. 4. Now look for the compensation Metabolic acidosis PCO2=1.5 × [HCO3] + 8 + 2 Metabolic alkalosis PCO2 increases by 7 mmHg for each 10 mEq/L increase in the serum HCO3

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Respiratory acidosis: HCO3 increase by 1 for each acute 10 mmHg increase in PCO2 Chronic HCO3 increases by 3.5 for each 10 mmHg increase in PCO2 Respiratory alkalosis: HCO3 falls by 2 for each acute 10 mmHg decrease in PCO2 Chronic HCO3 falls by 4 for each 10 mmHg decrease in PCO2 Another method for looking for compensation is Metabolic acidosis Expected PCO2 = last 2 digits of pH (If pH is 7.22 expected PCO2 is 22) Metabolic alkalosis PCO2 = rise of 6 mm per 10 mEq rise in Bicarbonate. Respiratory acidosis Acute: For every rise of PCO2 by 10 mmHg pH fall by 0.08 Chronic: For every rise in PCO2 by 10 mmHg pH fall by 0.03. Respiratory alkalosis Acute: For every fall in PCO2 by 10 mmHg pH rise by 0.08 Chronic: For every fall in PCO2 by 10 mmHg pH rise by 0.03. Look for mixed disturbance pH is normal and Bicarbonate is high (Metabolic alkalosis + Respiratory acidosis)

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Bicarbonate is low (Metabolic acidosis + Respiratory alkalosis). Bicarbonate is low and anion gap is high (Metabolic acidosis + Metabolic alkalosis). Bicarbonate is low and pH acidic (Chronic respiratory acidosis + Respiratory alkalosis). Bicarbonate is normal and pH in alkalemic range (Metabolic alkalosis + Metabolic acidosis) pH is acidic, PCO2 ↑, Bicarbonate ↓ (Respiratory acidosis + Metabolic acidosis) pH is alkalemic PCO2↓ Bicarbonate↑ (Respiratory alkalosis + Metabolic alkalosis) In presence of predominent involvement of two systems, often coupled with therapeutic intervention the patient may present with acid-base disturbances both respiratory and metabolic (e.g. respiratory acidosis and metabolic acidosis). Additive disturbances are proven to be more fatal compared to counter balancing ones (e.g. respiratory acidosis with metabolic alkalosis). Treatment Respiratory Acidosis Maintenance of ventilation and hemodynamic status is the mainstay of treatment. Correction of the specific underlying disorder also is essential. Alkali therapy is not indicated unless the patient has severe hyperkalemia and ventricular fibrillation. Chronic respiratory acidosis per se does not require specific therapy but hypoxemia must always be treated. If chronic respiratory acidosis is over compensated then metabolic alkalosis may occur and in such situation patient may be treated with potassium chloride.

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Respiratory Alkalosis Most common cause is functional hyperventilation. Other causes are Gram –ve sepsis, salicylate intoxication, asphyxiants and cerebral diseases with involvement of respiratory centre producing hyperventilation. Treatment is to correct the underlying disorder. In hyperventilation rebreathing into a bag will usually terminate the attack. Metabolic Acidosis Look for anion gap. Wide anion gap means addition of an acid load. Bicarbonate therpy is given when pH is < 7.2 after ensuring good perfusion and ventilation. Metabolic Alkalosis Classified according to urinary chloride. Low urinary chloride (<10 mEq/L) “Chloride responsive” Hypovolemic Diuretic therapy Nasogastric suction Vomiting Secretory diarrhea High urinary chloride (> 20 mEq/L) normo or hypervolemic Bartter’s syndrome, Cushing’s syndrome Hyperaldosteronism, Potassium depletion Alkali administration Treat the underlying cause first and correct by normal saline if indicated.

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Anion Gap and Acidosis Increased anion gap acidosis DKA Lactic acidosis In born error of metabolism Renal Failure

Normal anion gap RTA CA inhibitor therapy Chronic Diarrhea

Wide Anion Gap Mnemonic (MUDPILES’, KUSMAL, MULIPAK) Methanol, uremia, DKA, paraldehyde, infections, lactic acidosis (from different causes), ethylene glycol, salicylates. Normal Anion Gap HCO3 loss – diarrhea, small bowel damage, ureteroenterostomies, proximal RTA ↓ HCO3 regeneration- distal RTA, hyperkalemic RTA, CRF, adrenal insufficiency Commonly used mnemonic ACCURED Acid infusion, compensated respiratory alkalosis, CA inhibitor, RTA, Ureteral divertion, Extra-alimentation, hyperalimentation and diarrhea.

CHAPTER 7

Mechanical Ventilation

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Normal ventilation occurs when chest expands to create a negative intrathoracic pressure. Air is then drawn in to the lungs. Expiration is passive due to elastic recoil of lung which expells air out. Intermittent negative pressure ventilation (INPV) is the method which mimics physiological ventilation. But this cannot be used in clinical situations due to the cumbersome equipment and difficulty in nursing the patient. The method which is used in clinical situations is intermittent positive pressure ventilation (IPPV). In IPPV inspiration is accomplished by applying a positive pressure to the upper airway to drive in air into the lungs. Expiration is passive. So the airway pressure (Paw) is positive and the mean intrathoracic pressure during IPPV is greatly increased leading to adverse side effects on the cardiovascular system and barotrauma on the airways and lungs. Though unphysiological IPPV has become popular because of it’s ease of clinical application. Artificial Airways Artificial ventilation for any length of time mandates the use of artificial airways. This is to make the ventilation optimal and also to protect the lung from the danger of aspiration. Two types of artificial airways are used. Endotracheal Tubes Endotracheal tubes are made of non irritant tissue compatible materials like polyvinyl chloride (PVC), e.g. portex tubes. They can be passed through oral or nasal route. Nasotracheal is used for prolonged use. For children upto 8 years uncuffed tubes are used. For children above

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8 years cuffed tubes with low pressure baloon are used. In younger children the narrowest portion of the airway is below the vocal cords at the level of the nondistensible cricoid cartilage and the larynx is funnel shaped and so there is no necessity of a cuffed endotracheal tube. Though there can be problems like dislodgement of the tube, difficulty in removing the secretions, subglottic stenosis, etc. with proper care they can be used for 7-10 days. Tracheostomy When the need for artificial airway exceeds for more than 7-10 days tracheostomy is resorted to. Tracheostomy is done as an elective procedure. Removal of the secretions is easy through the tracheostomy tube and dislodgement can be managed easily. MECHANICAL VENTILATOR Basic System The driving force in a ventilator is contributed by either compressed air or oxygen or both. A compressor giving 50-75 pounds/sq inch is used (PSI). The concentration of oxygen and air can be adjusted by the blender to the required concentration (FiO2). A flow meter regulates the flow between air and oxygen. The use of artificial airways bypasses the natural humidifier, the nose. Breathing dry air will lead to decreased mucociliary activity, encrustation of secretions and infection. So ventilators are equipped with efficient humidifier to provide water vapour. The inspiratory limb has a pop off valve set at 5070 cm of H2O pressure as a safety measure for the patient.

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The humidifier present in the inspiratory limb humidifies air to a temperature close to body temperature (37oC). The inspiratory limb has a bacterial fitter to sterilize the inspiratory air given to the patient. Pressure gauges are there to measure the mean airway pressure (MAP) and peak inspiratory pressure (PIP) and peak end expiratory pressure (PEEP). Finally, an expiratory valve is added to the system. When the valve is open a continuous flow will occur through the system preventing CO2 accumulation in the tubing. When this valve is closed the pressure will increase in ventilator tubing and patient’s airway until desired pressure level is attained. The ventilator is cycled by the opening and closing of the expiratory valve. Present ventilators are driven by electrical power. The controls and alarms are electronically operated. A piston and bellows is classically used to drive in air into the lungs. Mechanical ventilators always use atmospheric air to ventilate the lungs. Oxygen is used only if it is indicated by patient’s condition and laboratory data. The aim of ventilation is to achieve satisfactory PaO2 using minimum oxygen. PEDIATRIC VENTILATORS ARE MAINLY OF TWO TYPES Pressure Limited Ventilators Pressure limited ventilators deliver gas at a predetermined flow rate until a preset pressure is reached, regardless of tidal volume delivered. This is generally simple and cheap but less versatile. Pressure limited ventilators are extensively used in NICUs for the following reasons. 1. Simplicity of design, low cost and easy operation


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2. Peak inspiratory pressure (PIP) the key parameter related to barotrauma and bronchopulmonary dysplasia can be controlled directly. Disadvantage The tidal volume depends on the compliance of the lungs. Hence, there is likelihood of hypoventilation when lungs are less compliant and hyperventilation when they are more compliant. Volume Limited Ventilators The ventilator delivers a preset tidal volume over a given inspiratory time regardless of the pressure generated. Advantage Because of the constant tidal volume there is no hypo- or hyperventilation with change in compliance. Disadvantages 1. Not ideal for newborns. Tidal volume in neonates being small may be lost in the ventilator circuit. Since uncuffed endotracheal tubes are being used an unknown amount of preset volume may leak from the airway. 2. As the tidal volume is constant the normally compliant areas tend to get preferentially ventilated. The atelectatic areas which require higher opening pressure continue to remain unventilated. 3. The design is complicated, the cost is high and operation is more difficult.

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Other types are also there Time limited- Inspiration ends with a preset time. Flow limited - Inspiration ends when the flow has reached a critical level. Mixed cycling can occur when two or more independent parameters are considered. High frequency ventilators—the ventilators are capable of cycling at a rate of >150 per minute. TYPES OF VENTILATION Controlled Mechanical Ventilation When the ventilator completely take over the ventilatory function of the patient it is termed Controlled Mechanical Ventilation (CMV). This is easy in a completely apneic patient but in others to facilitate controlled mechanical ventilation, sedatives and neuromuscular blocking drugs will have to be used. So in many instances CMV cannot ensure a normal PaO2 and PaCO2 and cannot improve gas exchange. And also to ease transition from mechanical to spontaneous ventilation other types of ventilatory modes are used. Constant Distending Pressure (CDP) It is often seen that mechanically ventilated patients show a gradual decline in PaO2 in spite of increased FiO2. An FiO2 of more than 0.5 (inspired oxygen concentration of 50%) is dangerous. This reduction in PaO2 is due to a gradual closure of distal airways leading to decrease in FRC. It has been shown that if a positive pressure is applied to the airway during expiration or throughout the respiratory cycle this pressure will be transmitted to the


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distal airways to keep them open leading to an increase in FRC which improve PaO2. Two types of CDP can be used. CPAP, continuous positive airway pressure is used in spontaneously breathing patients who are usually not intubated. This is generally given by various means namely nasal prongs, naso pharyngeal prongs or endotracheal tubes. It is supplied on to a spontaneously breathing neonate to produce a functional residual capacity at the end of each expiration. It is the fundamental management to be instituted on atelectatic disease. Indications for CPAP 1. 2. 3. 4. 5. 6. 7.

Respiratory distress syndrome with FiO2 < 0.4 Meconium Aspiration Syndrome Apnea of prematurity Weaning patients from mechanical assistance As adjunct to intermittent positive pressure ventilation Sleep apnea Bronchomalacia.

CPAP is a simple device which contains 3 parts a. A circuit for continuous flow of gases (oxygen and air) b. Air oxygen blender to deliver appropriate oxygen c. Patient device. Positive end Expiratory Pressure (PEEP) PEEP is used along with IPPV. PEEP can be gradually increased till a satisfactory PaO2 is obtained. PEEP 0-2 cm of H2O —low 4-7 cm of H2O—medium—standard > 8 cm of H2O—high unusual

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Intermittent Mandatory Ventilation In IMV the machine is presenting a certain frequency of breaths per minute. Patient breathes spontaneously but the ventilator provides mandatory breaths at rate set by the operator. Sometimes the spontaneous breaths and mechanical breaths may not coincide and this can lead to inefficiency or fighting with the ventilator. Hence adequate sedation is required to overcome this. Synchronized Intermittent Mandatory Ventilation (SIMV) In this mode the mechanically delivered breaths are synchronized to the onset of spontaneous breaths of the patient. It allows the patient to breathe spontaneously between mechanical breaths. SIMV may be either pressure controlled or volume controlled. At set intervals the ventilator’s timing circuit becomes activated and if the patient initiates a breath in the expected time the ventilator delivers a mandatory breath. If no spontaneous breath occur in the expected time, the ventilator delivers a mandatory breath at a fixed time. In pressure support mode spontaneous breaths by the patient is allowed. The ventilator assists a predetermined amount of airway pressure above the set PEEP. Here fighting with the ventilator is absent. This mode is useful in a spontaneously breathing child. Assist Control Mode of Ventilation This modality involves the delivery of a synchronized mechanical breath each time a spontaneous breath is taken by the patient (assist) or the delivery of a mechanical breath


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at a regular rate in the event that the patient fails to take a spontaneous breath (control). In assist control mode of ventilation and SIMV there is synchrony between the patient’s and ventilated breath and the need for sedation is minimal. Pressure Support Ventilation In many situations baby has poor muscle power to sustain effective spontaneous ventilation. For these patients during transition from CMV to complete spontaneous respiration support can be provided by PSV. The patient is allowed to breathe spontaneously and each inspiration is supported by the ventilator. The support is gradually decreased allowing the patients system to be on it’s own. Mechanical ventilation is indicated in different clinical set ups where there can be a normal lung or an abnormal lung. The abnormal lung can either with a decreased lung compliance or increased airway resistance or both. Compliance means the unit change in volume for a given change in pressure. Airway resistance is the resisting force to expiration. Diseases with Decreased Lung Compliance Various diseases like AIDS, atelectasis, pneumonia, pulmonary edema and pulmonary hemorrhage have decreased lung compliance. In all these diseases FRC is reduced as terminal air spaces are flooded or collapsed owing to the presence of abnormal fluid in the alveoli or atelectasis due to lack of sufactant. Intrapulmonary shunt is increased as blood is flowing through poorly ventilated lung tissues. So the aim of mechanical ventilation is to

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decrease the intrapulmonary shunt by improving FRC by increasing mean airway pressure in order to recruit more atelectatic areas of lungs. This can be achieved by higher PEEPs although higher PIPs also can increase mean airway pressure. Decreased compliance requires a higher pressure gradient or a higher rate of respiration. If neither the pressure nor the rate is increased to compensate for the decreased compliance, hypercarbia will result. Diseases with Increased Resistance Resistance is increased in diseases that decrease the caliber of the airway lumen by edema, spasm or obstructing material. Because the airways decrease in caliber during exhalation increase in resistance affects expiratory flow more than inspiratory flow. The diseases in which the airway resistance is increased include asthma, bronchiolitis, bronchopulmonary dysplasia, smoke inhalation and cystic fibrosis. These diseases with increased airway resistance are often accompained by both increased intrapulmonary shunt and dead space ventilation. Shunt occurs because of the impedance of gas flow to the lungs. Dead space ventilation occurs if the increasing resistance lead to gas trapping in areas of lung that contain hyperinflated alveoli. These hyperinflated alveoli exert pressure on the surrounding tissues and it results in reduction in pulmonary capillary blood flow. The increases in both shunt and dead space produce significant hypoxemia and hypercarbia. Increased resistance requires higher pressure for the gas to reach the terminal air sacs. Therefore if volume controlled ventilation is used, an increase in PIP is required to deliver a given VT. If pressure


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controlled ventilation is used, tidal volume is lower than in a normal lung at the same pressure. Increased resistance may result in significant increase in time constant. A longer time constant is necessary. If the ventilator frequency is too high gas trapping can occur as the ventilator cycles back into inspiration before the lung has had sufficient time to empty. More and more gas is trapped leading to lung hyperinflation a predisposition to pneumothorax and chronic barotrauma and reduction in compliance. Initial Setting of Ventilator The initial settings are different for normal lung and diseased lung. Normal Lung Volume controlled ventilation Respiratory Rate Ventilator frequency may be slightly lower than the normal respiratory rate. Tidal Volume Set higher than a healthy patient’s VT 5-7 ml/kg. Pressure controlled ventilation An initial PIP of 20-25 cm of H2O is sufficient to move an adequate VT but this must be immediately assessed by observation of chest expansion and measurement of VT. Lung with Decreased Compliance Mean airway pressure need to be higher. A higher PEEP is necessary. PEEP is titrated in an attempt to provide

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adequate oxygenation at an FiO2 less than 0.6. If volume controlled ventilation is used the PIP may be much greater than in normal lungs and clinicians should pay attention to pressure alarms. If pressure controlled ventilators are used the initial PIP may exceed 30 cm of H2O. The VT has to be monitored closely. Significant hypoxemia results from these diseases and it is customory to start with FiO2 of 100% and then reduce. The ventilator frequency may be set higher than normal. A common inspiratory time is 0.8-1 second. Diseases with Increased Resistance Ventilator frequency may need to be set as low as 12-16 breaths per minute. PEEP is to be minimized to minimum 2-3 cm of H2O to reduce the risk of gas trapping. Tachycardia is the earliest sign of too much PEEP. Fall in blood pressure and metabolic acidosis are late signs of excessive PEEP. Increasing CO2 is also a sign of excessive PEEP. Inspiratory Time Inspiratory time is an important aspect in controlling MAP and hence oxygenation. Inspiratory time is to be individualized on the understanding of the time constant of that lung. Time constant TC= C × R (C, the lung compliance and R the airway resistance). In conditions where the lung compliance is reduced like HMD the TC is extremely short and so the complete emptying of alveoli can be effected by a longer inspiration time (IE ratio of 1:1). In MAS where the airway resistance in high the TC is long and the IE ratio would be in the region of 1:1.8 to 1:2.5


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depending on the oxygenation. This well help in producing sufficient expiration and hence less air trapping. Control of CO2 Elimination CO2 elimination is simple when compared to the complex process of oxygenation. The CO2 elimination depends on minute ventilation MV= TV × RR(tidal volume and respiratory rate). The tidal volume is related to PIP. Monitoring Close monitoring of the system as well as the patient is very important. Patient Clinical 1. 2. 3. 4. 5. 6.

Colour-pink Adequate chest expansion Absence of chest retraction Adequate air entry Prompt capillary filling Blood pressure

Pulse Oximetry Oxygen saturation (SaO2) to be kept between 88-95%. ABG PaO2 50-80 mmHg PaCO2 35-45 mmHg (chronic cases upto 60 mmHg) pH 7.35-7.45

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System Needs monitoring for set parameters and alarms. Weaning Gradual reduction of ventilatory support after the recovery stage has reached. In 70-80% cases no weaning may be required, e.g. upper airway obstruction. In severe lung disease and neuromuscular disease weaning is required. It is not necessary that a complete resolution of the disease process has occured when you start weaning. The pace is more important than the method. The modes used are. Pressure support , volume support, proportional assist, volume assured pressure support, mandatory minute ventilation, CPAP or T piece trials, PSV and SIMV of which SIMV may take a longer period of weaning time. Extubation Exiteria 1. Primary cause should be resolving (not necessarily resolved). 2. Reasonbly free of secretions. 3. Should be able to protect the airway. 4. Should have enough muscle strength to generate good cough. 5. Should not be on high cardiovascular support.

CHAPTER 8

Management of Shock in Children

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Shock is an acute state of circulatory dysfunction resulting in failure to deliver sufficient amounts of oxygen and nutrients to meet the tissue metabolic demands. If prolonged it will result in multiorgan failure and death. Pathophysiologically it can be divided into three phases: 1. Compensated: Blood is maldistributed so that the vital organ function is maintained. 2. Uncompensated: Microvascular perfusion is compromised resulting in reduction of circulating volume. 3. Irreversible: Inadequate perfusion of vital organs leading to irrepairable damage. Shock can be classified into four functional categories. Hypovolemic Shock Most common cause in children is hypovolemia due to loss of fluid and electrolytes as in diarrhea, bleeding and acute blood loss, relative loss as in anaphylaxis or sepsis. Cardiogenic Shock Occur in cardiac conditions like myocarditis, cardiomyopathy or dysrrhythmias. Obstructive Shock Occur in aotic or mitral stenosis, pulmonory embolism or cardiac tamponade. Distributive Shock Occur in sepsis, neurogenic or anaphylaxis.

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Dissociative Shock Occur in heat stroke, carbon monoxide or cyanide poisoning. Symptoms: Early symptoms are sinus tachycardia, giddiness, irritability, apprehension, delayed capillary refill, decreased urine output. Late Signs Altered mental status like lethargy and coma, hypotension, anuria, mottled skin, acidotic breathing, cold extremities, hypotonia, ↓ DTR, chyne stokes breathing. Management Whatever be the cause the first thing is to assess Airway, Breathing and Circulation (ABC) Hypovolemic Shock There is fluid or blood loss producing low preload leading to decreased stroke volume and decreased cardiac output. Compensation occurs with increase in heart rate and systemic vascular resistance. Mainstay of therapy is administration of fluid and treatment of the specific cause for fluid or blood loss. If blood loss is the cause replacement therapy is necessary with measures to arrest bleeding. Rapid fluid replacement to expand the intravascular volume is the most important step in the management of shock Which fluid? Colloids or crystalloids? Many studies and many meta-analysis has shown that both are equally good and in usual clinical set up normal

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saline is the first choice. In dehydration and shock due to acute diarrhea Ringer’s lactate is the fluid of choice. In hypovolemic shock the initial resuscitation usually is about 20-30 ml/kg as the first bolus and repeated if necessary. It can be as much as 200 ml/kg during the first 4-6 hours. Patients who do not respond to initial fluid boluses should be considered for invasive hemodynamic monitoring. It usually does not occur in diarrhea or external blood loss. Constant and continuous monitoring is needed to reassess perfusion, urine output and vital signs. Septic Shock Classically described as warm shock and cold shock but such chronologic differentiation may not be possible in a given patient. Often the children are commonly seen in cold septic shock. In warm shock there is bounding pulses, tachycardia, tachypnea, wide pulse pressure, increased cardiac output, mixed venous saturation, decreased systemic vascular resistance, hypocarbia, elevated lactate and hyperglycemia. In late shock there is cyanosis, cold clammy skin, rapid thready pulses, shallow respiration, decreased mixed venous saturation, decreased cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leak, metabolic acidosis, hypoxia, coagulopathy and hypoglycemia. Monitoring is very important in assessing the clinical improvement.

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Steps in Management of Shock Assess ABC. Secure the airway. Start oxygen with mask or cannula. Oxygen supply is optimized by maintaining the oxygen saturation. If adequate ventilation and oxygenation cannot be achieved endotracheal intubation and mechanical ventilation should be initiated. Mechanical ventilation minimize the work of breathing, reduces the oxygen consumption and improves oxygenation. Early respiratory support will help patients with severe shock and also children with cardiogenic shock complicated with pulmonary edema. Secure IV line- peripheral, intraosseous or central whichever is feasible. Saline is infused 20-40 ml/kg in 20-40 minutes, followed by 20 ml/kg in 20 minutes. Hydrocortisone 1 mg/kg IV statum and 8 hourly. In warm shock- (wide pulse pressure > 40 mmHg) Nor adrenaline can be given 0.2 mcg/kg/minute (maximum of 1 mcg/kg/minute). In cold shock, continue IV fluids 20-40 ml kg and start on dopamine 10 mcg /kg/minute. Use fluids to keep the CVP 10-15 mmHg. With the above measures if the child is not improving, Diastolic BP <30 mm of Hg in <8 years and < 40 mmHg in > 8 years if contractility is poor, calcium gluconate is given (10% 0.4 ml/kg/hour). If contractility is still poor add adrenaline 0.01mcg/kg/minute. If > 0.5 mcg/kg/minute is needed child needs ECMO, respiratory support and plasma filtration. If contractility is acceptable, injection vasopressin is given in the dose of 0.001 mcg/kg/minute.

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Ventilatory support may be needed with minimum FiO2 to maintain SaO2 to >90%, PEEP as needed. Ventilate to keep pH >7.3 but minimum PCO2 (35 mmHg and peak expiratory pressure 35 cm of H2O. If pH is 7.1 and base deficit >10 mmol/L consider bicarbonate IV over 1 hour. On ventilatory support, and is on ionotrope if lactate is >4 mmol/ L plasma filtration may be tried.

CHAPTER 9

Status Epilepticus

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Status epilepticus is referred as seizures persisting for more than 30 minutes or two or more seizures occuring consecutively without an intervening period of full recovery of conciousness. It is estimated that 20-30 minutes is the duration necessary to cause injury to central nervous system. Majority of seizures resolves spontaneously within a few minutes time. A child is who is still having convulsion on arrival in to the emergency department may be considered to have status, since they usually continue to have convulsions until he receives active treatment. And if a child needs a second dose of anticonvulsant for the control of seizure also deserves special care treatment in the emergency department. STEPS IN MANAGEMENT The most important step is the provision of proper oxygenation and ventilation. So the airway and breathing is assessed and supported by: a. Positioning of the head and mandible to keep the airway patent. b. Suction with a large bore suction catheter to remove oropharyngeal secretions. c. 100% oxygen is provided with a non rebreathing mask. d. If feasible, an oropharyrngeal airway is introduced. May not be feasible if there is clenching of the jaws during the convulsion. e. The stomach is decompressed with a nasogastric tube to prevent vomiting and aspiration. f. If the patient is not breathing, bag and mask ventilation is to be tried. g. If the patient is not ventilating due to convulsion and becoming cyanosed, the airway is secured using an

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orotracheal intubation. A high dose of midozolam and a short acting neuromuscular blocking drug may be required. h. Though mentioned last, the most important aspect of management is the control of seizure. Airway compromise is not a contraindication for anticonvulsant therapy but may be a necessity for assisted ventilation. Seizure control is to be done as quickly as possible. Circulation and vascular access is very important for seizure control and also for other supportive measures. Intravenous access is to be tried and if not possible in a child with shock, it can be given through the intraosseous route. If not in shock, but difficult to get an IV line, drugs can be tried, rectally or intramuscularly (Midazolam). In hypovolemia fluid correction is to be done with saline bolus. If not in shock give only 2/3 of the maintenance fluid. Hypoglycemia can cause severe disruption of autoregulation of cerebral blood flow. If hypoglycemia is documented or if it is not possible to measure blood glucose, a bolus of 2 ml/kg of 25% dextrose may be given intravenously. Anticonvulsants During drug administration, attention should be paid to the possibility of apnea or hypoventilation. This complication may be due to the effect of anticonvulsant drugs or due to seizure activity itself. So be prepared for assisted ventilation. Benzodiazepine is the drug of choice as the first line drug. Apnea is not a contraindication provided the airway

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and breathing are simultaneously looked after. Diazepam is the most commonly used one and it controls the seizure in 1 minute. Lorazepam controls the seizure in 3 minutes and has a longer duration of action of about 12-24 hours and has less respiratory depression than diazepam. Inj diazepam 0.2 mg/kg/IV slowly upto a maximum of 10 mg/dose. OR Inj Lorazepam 0.05 mg to 0.1mg/kg upto a maximum of 4 mg/dose, slow IV infusion with a rate of 2 mg/minute. If diazepam is given, the effect will be lasting only for 30 minutes and so even when the seizure is controlled there is the chance of recurrence and so phenytoin may be given to prevent recurrence. A second dose of benzodiazepine is required after 5-10 minutes if the seizures are not controlled. IV midazolam has no advantage over diazepam or lorazepam. But if an IV access is not available, it can be given intramuscularly and can control the seizure. After the two doses of benzodiazepines if seizures are not controlled IV phenytoin is the second line drug except in newborns and febrile status. Phenytoin is infused in normal saline in the dose of 15-20 mg/kg as a bolus dose at the rate of 1mg/kg/minute. The action is expected within 10-30 minutes. Rapid infusion can produce hypotension, bradycardia, dysarrhythmia and asystole. If convulsions are not controlled, 5mg/kg increments can be given up to a maximum of 30mg/kg. If the patient is already on phenytoin the loading dose of the drug is to be avoided. Phenobarbital is highly effective and the drug of choice as a second line drug in febrile and neonatal status epilepticus. The drug is given in the dose of 20 mg/kg as

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infusion at the rate of 1-2 mg/kg/minute. The effect occurs within 10-20 minutes. Phenobarbital can be given as bolus dose even when the child was already on maintenance dose of the drug. The disadvantages are depression of mental status, respiratory depression and hypotension especially when administered after benzodiazepines. Fosphenytoin is a drug which liberates phenytoin when metabolized. It can be given IM or IV. It has a faster action also. The dose is 15 mg phenytoin equivalent/kg at a rate of 3 mg/kg/minute (1 mg phenytoin is equivalent to 1.5 mg of fosphenytoin). Valproate IV infusion 25 mg/kg at rate of 3-6 mg/kg/ minute can also be given. Rectal administration of anticonvulsants are not preferred in status epilepticus because the blood levels can be erratic. Refractory Status Epilepticus Seizures not controlled by the administration of the above said drugs within a period of 60-90 minutes have been defined as refractory status epilepticus. General anesthesia and assisted ventilation is the ideal management for refractory status epilepticus if feasible. If not, midazolam can be given, as IV bolus 0.15mg/ kg followed by a continuous infusion of 1mg/kg/minute. Increase in increments of 1 mg/kg/minute every 15 minutes until the seizures are controlled. Maximum rate of infusion is 10mg/kg/minute. OR Propofol 3 mg/kg/minute bolus followed by 1-1.5 mg /kg/hour infusion.

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OR Thiopental 30 mg/kg bolus followed by infusion at a rate of 5 mg/kg/hour. Lidocaine 3 mg/kg IV bolus not faster than 25 mg/ minute followed by infusion at a rate of 5-10 mg/kg/hour may be useful when refractive to other drugs. Early Status 0-30 minutes Drug used is benzodiazipines Stage of established status 30-60 minutes Drugs added are phenobarbital, phenytoin/ fosphenytoin followed by valproate infusion Stage of refractory status >30-60 minutes Drugs used are Midazolam, thiopental or propofol infusion These drugs are given in sufficient doses to maintain a burst suppression pattern of EEG. Treatment of specific causes if present should be paid attention to, like infections, trauma, cerebral edema, dyselectrolytemia, hypertensive encephalopathy, drug toxicity etc. Investigations Blood is to be collected for glucose, S. electrolytes- Na, K, bicarb, Ca, Mg, RFT, LFT, ABG and hematogical parameters. Vitals are to be monitored every half hourly, especially while on continuous infusion of drugs. The cardiac monitoring is very important while on infusion therapy with phenytoin or lidocaine. Respiratory depression is a risk with benzodiazepines especially when combined with other drugs.

CHAPTER 10

Coma

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A child presenting with altered consciousness is one of the most difficult problem in pediatric critical care management. The causes of coma can differ and the specific management also. But the primary management is the same. The causes of coma in a child 1. Infection Meningitis Encephalitis Cerebral malaria 2. Drugs and poisons 3. Trauma 4. Vascular-intracranial hemorrhage, thrombosis embolism 5. Epilepsy 6. Hypertensive Encephalopathy 7. Tumors 8. Hypoxic ischemic encephalopathy 9. DKA 10. Malignant hypothermia 11. Hypoglycemia MANAGEMENT The prime consideration is to assess the airway, breathing and circulation. This is to be followed by a quick history and systemic examination both general and CNS examination. Bleeding-bruising and hematomas Purpura, petechiae, mucosal bleed Fever, seizures, meningeal signs Focal seizures and focal neurological signs Abnormal smell

Trauma Bleeding diathesis, e.g. ITP Meningitis Focal intracerebral pathology. Hepatic failure, Metabolic error

COMA

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Temperature, pulse, blood pressure, respiration are to be recorded correctly and sometimes the diagnotic clue is evident from them. Examination of the pupils, eyes, and motor system also may give clue towards the aetiology of diagnosis. LAB EVALUATION Blood CBC, coagulation screen, blood smear, blood sugar, RFT, LFT, S. electrolytes, Calcium, Magnesium, ABG, urine for sugar, ketone bodies. X-RAY, ECG, EEG, CT SCAN, CSF ANALYSIS S. ammonia, Lactate, Pyruvate in suspected metabolic diseases. TREATMENT Start IV fluids Normal saline bolus if in shock Two-third maintenance if suspecting raised ICP Give a dose of 10% dextrose if hypoglycemia is suspected Gastric lavage in suspicion of poisoning Antipyretics/anticonvulsants Anti edema measures. Care of eyes, skin and bladder is very important in a comatose child.

CHAPTER 11

Acute Respiratory Failure

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Respiratory system fails to meet the oxygen demand of the body and/or remove carbon dioxide from pulmonary circulation. Failure of optimal gas exchange in lung results in hypoxemia and hypercarbia. Respiratory failure exists when the arterial CO2 tension (PaCO2) is greater than 50 mmHg and/or the arterial O2 tension (PaO2) is less than 50 mmHg. But the laboratory values alone cannot be considered in clinical set up. Because there are exceptions like. 1. PaO2 may be normal if a patient with respiratory failure is breathing increased concentration of oxygen (high FiO2). 2. PaCO 2 is increased in patients with right to left intracardiac shunt despite having normal respiratory function. 3. PaCO2 may be increased in patients with chronic metabolic alkalosis as a compensatory mechanism in spite of child having no respiratory failure. Failure of ventilation and failure of arterial oxygenation can occur individually but often both coexist. Ventilation is the exchange of respiratory gases between the atmosphere and lungs and minute ventilation is the volume of air exchanged in one minute. VE is divided into two components- alveolar ventilation (VA) which participates in gas exchange and dead space ventilation (VD) which does not. Because the body’s CO2 production (VCO2) is eliminated by VA the partial pressure of CO2 in the alveoli (PA CO2) is approximately equal to VCO2 divided by VA. PA CO2 = VCO2/VA This is known as alveolar ventilation equation and it states that the PaCO2 (Which is equal to PA CO2 because

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the CO2 in the alveoli and the pulmonary capillary blood is in equillibrium across the alveolar capillary membrane) is directly proportional to the body’s CO2 production (V CO2) and inversely proportional to alveolar ventilation (VA). So hypercapnia occurs when VCO2 increases when VA does not VA decreases when VCO2 does not VD increases without a concomitant rise in VA Causes for hypercapnia Decrease in VA - hypoventilation Increased VCO2 Increased VD. Hypoventilation can occur in 1. CNS Causes: Brainstem disease CNS depression due to narcotics, anesthetics or intracranial hypertension resulting in irregular breathing or shallow breathing. 2. Respiratory muscle weakness Poliomyelitis GBS 3. Severe metabolic derangement as in hypokalemia, hypophosphatemia, poor nutrition, diminished vital capacity and total lung capacity 4. Abnormal lung mechanics leading to the secondary event of respiratory muscle fatigue as a result of airway obstruction or restrictive lung disease.

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Increased CO2 Production (VCO2) Occur due to: (1) fever, (2) severe burns, (3) hyper alimentation with high concentration of dextrose. In patients with respiratory disease and minimal respiratory reserve will go in for hypercapnia and acidosis. Increased VD occurs in 1. Air trapping and overdistension as in asthma. 2. Loss of pulmonary capillary area as in vasculitis or pulmonary embolism. 3. Respiratory diseases in presence of a large number of gas exchange units with high ventilation/perfusion ratios. Effects of High Arterial CO2 Tension For each 1 mm of acute rise in PaCO2 the pH increase by approximately 0.01. Plasma bicarbonate remain stable for a few hours after a PaCO2 change. An acute rise of 10 mm of PaCO2 change the pH to 7.4 to 7.3. This causes severe depression of cardiac function and may trigger lethal arrhythmias. The rising PaCO2 also dilates cerebral blood vessels and increased cerebral flow causes restlessness, confusion or lethargy. This necessitates immediate action, intubation, mechanical ventilation and specific treatment for the cause of increased CO2 production. Failure of Arterial Oxygenation 1. Low oxygen in the inspired air, e.g. high altitude. 2. Hypoventilation, alveolar hypoventilation causes hypoxemia because less oxygen is available for gas exchange. Increase in PaCO2 will cause decrease in PA O2 and it will produce decreased PaO2.

CHAPTER 12

Acute Severe Asthma

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Any child with wheezing the first line management offered is β agonists either by MDI or nebulization. Salbutamol 0.15 mg/kg repeated at 20 minutes interval for 3 doses and if child is not improving, fits in with the diagnosis of acute severe asthma. If inhaled salbutamol is not available, terbutaline 0.01 mg/kg s/c or adrenaline 0.01mg/kg of 1:1000 solution s/c is administered and repeated every 20 minutes for 3 doses. Beta agonists are contraindicated in congestive cardiac failure and tachycardia (HR>180/mt in < 1year old and HR>160/mt in >1year). Dose of Salbutamol Respiratory Solution for Nebulization > 20 Kg 1 ml in 3 ml N saline < 20 Kg 0.5 ml in 3 ml N saline Oxygen Therapy Child should be given oxygen with the help of oxygen hood, mask or cannula whichever is comfortable for the child at a flow rate of 2-3 l/minute so that the oxygen saturation is maintained at 90-95%. Ipratropium Bromide Salbutamol nebulization is combined with ipratropium in the dose of 0.5 ml in <1 year. Steroids Steroid is the life-saving drug in acute severe asthma. It can be either methyl prednisolone intravenously, 2 mg/ kg statum followed by 1mg/kg every 6 hourly or

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hydrocortisone 10 mg/kg statum followed by 5 mg/kg every 6 hourly or prednisolone 1-2 mg/kg orally in 2-3 divided doses. IV Fluid IV fluid therapy is important in acute severe asthma. Ideally the fluid offered should be 1-1.5 of maintenance fluid. Child should be monitored frequently for assessment of deteriorating respiratory functions, dyselectrolytemias and air leak syndrome. If the child is not improving with the above mentioned initial treatment, diagnosis is to be reconfirmed. X-rays and ABG to be done if at all it was done earlier. Oxygen flow is to be checked. Clinical monitoring can be done by the pulmonary score index. Score

Respiratory rate < 6 yrs > 6 yrs

Wheezing

Sternomastoid activity

0 1

< 30 31-45

< 20 21-35

2

46-60

36-50

3

> 60

> 50

None Terminal expiration with stethoscope Entire expiration with stethoscope Inspiration and expiration without stethoscope

No apparent activity Questionable increase Apparent increase Maximal activity

0-3 mild. 4-6 moderate > 6 severe

If no wheezing (silent chest) the score is 3 If the score is >6 ICU management is necessary.

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Oxygenation can be assessed by pulse oximeter. Dyselectolytemia is to be checked. Most common problem is hypokalemia. So IV fluids should contain potassium. If the Child is Improving Nebulized salbutamol can be continued hourly or 2 hourly till the improvement is consistent and then the interval can be increased every 4 hourly. Ipratropium is continued every 4 hourly Steroids—Hydrocortisone or methyl prednisolone continued 6 hourly. Children usually improve in 24 hours. After 48 hours the drug interval can be increased and changed to oral medication as per the clinical judgement. If Child is Not Improving by the Initial Treatment Terbutaline IV infusion should be started 10 mcg/kg bolus followed by continuous infusion at a rate of 0.4-0.6 mcg/ kg/minute under cardiac monitoring. The rate of infusion can be increased by 0.2 mcg/kgminute every 15 minutes, to a maximum of 3-6 mcg/kg/minute. If the child is not improving with the maximum doses of terbutaline, aminophylline infusion should be tried. When aminophylline is started, the dose of IV terbutaline can be reduced to 50%. The dose of aminophylline is is 5-10 mg/kg in N saline to be infused statum followed by 0.5-1 mg/kg/hour infusion. If the child is not improving with aminophylline infusion also, magnesium sulphate can be given 20-40 mg/kg (maximun 2 gm) in 30 ml N Saline over 30 minutes. The drug can be repeated after 6 hours.

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Heliox the mixture of oxygen and helium if available can be given to improve oxygenation. If child is not responding, general anesthesia with halothane and supported ventilation is the last resort. Indications for Mechanical Ventilation 1. Failure of maximum pharmacologic therapy 2. Cyanosis and hypoxia not relieved by oxygen- PaO2 < 60% 3. PaCO2 >50 or rising by 5 mm Hg/hour. 4. Deteriorating mental state 5. Pneumothorax or pneumo mediastinum Mechanical ventilation may be given with ketamine and midazolam or fentanyl IV infusion. Paralysis with vacuronium if required. When the child is better and discharged from ICU, long term management is to be decided. Persistent asthma should be offered preventor therapy. In a child who was on local steroids, rescue steroids are to be advised during an episode of acute asthma. If a child with mild intermittent asthma develops acute asthma, he should be given rescue steroids for about 2-3 days. Oral prednisolone 2mg/kg in 2-3 divided doses to be started at the onset of an acute episode. When the child improves and able to do, PEFR should be measured with the Wrights peak flow meter. This will help in assessing the asthma severity and will help in further management. But this is often possible only in an older child 5-6 years and above. When clinical improvement is sustained for 4-6 hours drugs can be discontinued as “last in -first out” principle.

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Omit MgSO4 if used. Then omit aminophylline infusion in next 24 hours. Then omit terbutaline infusion. Then ipratropium nebulization in next 24-48 hours. Reduce β agonist 2-4 hourly, 4-6 hourly and then orally thrice a day. Replace any steroid with oral steriod twice or thrice a day. There are centers using MgSO4 as the drug which is used next to beta agonist inhalation steroids and ipratropium before terbutaline infusion and aminophylline which is actually the new recommendation but the the author’s experience is with the other regimen. Discharge Criteria Pulmonory score < 3, slept well at night, comfortable, feeding well and no need of nebulization β agonist as sos basis. On discharge, beta agonist can be given 6-8 hourly for 3-7 days Rescue steroids for 3-7 days Review or initiate long term preventor strategy.

CHAPTER 13

Hepatic Failure

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Acute hepatic failure is one of the most challenging problems in pediatric critical care. Fulminant hepatic failure is defined as a potentially reversible condition, the consequence of severe liver injury with an onset of encephalopathy within 8 weeks after the appearance of the first symptom and in the absence of preexisting liver disease. The main features of acute hepatic failure are: 1. Hepatic encephalopathy 2. Coagulopathy 3. Metabolic changes 4. Acid-base disturbances 5. Electrolyte disturbances 6. Infections 7. Haemodynamic changes 8. Renal failure 9. Respiratory problems 10. Ascites Encephalopathy The West Haven criteria for semiquantitative grading of mental state is acceptable and is based on the level of conciousness, intellectual function and behavior. Grade 1 Trivial lack of awareness Shortened attention span Grade 2 Inappropriate behavior Lethargy or apathy Disorientation to time and space. Grade 3 Somnolence to semistupor or confusion Grade 4 Coma

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Very often the first two stages are missed and child is received in the ICU in grade 3 or 4 encephalopathy and the routine monitoring of a coma child with Glasgow coma scale is an additional useful clinical parameter. The early clinical signs of cerebral edema are subtle and include changes in pupillary response, bradycardia, hypertension and hyperventilation. Changes in muscle tone, myoclonus, seizures and decerebrate rigidity are signs of irreversible brain damage leading on to respiratory failure and death. Simple procedures like mouth care or endotracheal suction may precipitate a surge in intracerebral pressure. ICP monitoring is indicated in grades 3 and 4 of encephalopathy but not feasible everywhere. Since CT or MRI are not sensitive enough to pick up the changes even in presence of a high ICP, invasive monitoring with placement of sensors in intraventricular, subarachnoid or epidural spaces needed but they are not easily available in many centers in our country and hazardous also. As in any other critical care situation maintenance of ABC is the first and foremost step. Placement of a central venous line, an arterial line, an indwelling urinary catheter and a nasogastric tube should be done. An orotracheal tube is to be placed if encephalopathy is grade 3 or 4. Management of Cerebral Edema 1. Head of the patient may be elevated to 10-20 degrees. 2. Avoid factors which may increase ICP such as sensory stimulae. 3. Hydration - give IV fluids 75% of the maintenance

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4. Mannitol -20% in the dose of 0.5-1 gm/kg over 10-20 minutes. Can be repeated every 6 hours. 5. If mannitol is not useful or in the presence of poor renal perfusion thiopentone can be used. It has antioxidant anticonvulsant activities and will reduce the cerebral metabolic rate. Severe hypotension is an occasional complication which should be agressively managed. Pentobarbital can also be used . 3-5 mg/kg over 15 minutes followed by continuous IV infusion 0.5-2 mg/kg/hour. 6. N. acetyl cysteine may reduce cerebral edema by increasing cerebral blood flow and enhancing tissue oxygen consumption. 100-150 mg/kg/day till INR falls below 2. It also acts as a free radical scavenger. The goal of the therapy is to maintain the ICP to < 20 mmHg (normal is 10 mmHg). Methods to Reduce Serum Ammonia In order to reduce enteric production of nitrogenous toxins protein feeds are to be stopped. Lactulose is an ammonia lowering agent by many different mechanisms. It is administered in a dose of 2 ml/kg with a goal to result in 2-3 semiformed stools per day. Infections Sepsis is the cause of death in 25-50% of acute hepatic failure. The common sites of infections are chest, urinary tract, blood and IV cannula site. Fungal infections are possible after one week of hospital stay. Since systemic staphylococcal infections are common the antibiotics preferred are ampicillin and cloxacillin, ceftriaxone, amoxycillin, metronidazole and vancomycin.

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Unabsorbable antibiotics to decontaminate the bowel is not necessary if on prophylactic systemic antibiotics. When cultures are positive antibiotics can be given accordingly. If no response in 72 hours- amphotericin 1.5 mg/kg/day or fluconozole 3-6 mg/kg/day can be given. L Ornitine, L Aspartate These ammonia lowering agents can be given either orally or as IV infusion. They provide critical substrates for both uregenesis and glutamine synthesis, the key pathways for ammonia detoxification thus lower the serum ammonia level. Fluid and Electrolytes Maintenance fluids with additional dextrose is to be given upto 75% of total maintenance fluid. The urine output is to be maintained at 1ml/kg/hour. If the urine output is less fresh frozen plasma may be given. Dopamine drip 2-5 mcg/kg/minute also may be given. Sodium intake is 0.5-1 mEq //kg/day Potassium intake is 3-6 mEq /kg/day Hyponatremia, hypocalcemia, hypomagnesemia and hypokalemia when present, are to be corrected. Metabolic Problems Hypoglycemia is a common problem. Blood sugar is to be monitored and should be maintained above 70 mg% with 10% dextrose. If hypoglycemia is present, it should be corrected with 50% dextrose. Metabolic acidosis can occur due to tissue hypoxia and hypovolemia which should be corrected with oxygen

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therapy and proper volume replacement. N acetyl cysteine given as a infusion can help in correcting the metabolic acidosis in the dose of 150 mg/kg/24 hours. Coagulopathy Vitamin K can improve the clotting abnormalities in the initial stages but FFP is to be given if there is evidence of bleeding or any invasive procedures are planned.15-20 ml/ kg can be given as an infusion every 6 hourly. Platelet transfusion is given to keep the platelet counts above 50000 . PRC are transfused if Hb is less than 8 gm% which will help in improving tissue oxygenation. Prevention of GI Hemorrhage IV Ranitidine 3 mg/kg/dose 8 hourly. Sucralfate 250-500 mg 4-6 hourly. Proton pump inhibitors also can be used. Vitamin K is to be given IV, 2.5 mg in < 6 months, 5 mg in 6 months -2 yrs, 10 mg in > 2 yrs. Renal Dysfunction Circulating blood volume is to be maintained to prevent pre -renal hypovolemia. If there is hypovolemia as evidenced by low CVP a fluid challenge is given with normal saline 10 ml/kg. If CVP is > 8-10 ml of water, frusemide 1-2 mg/kg is given IV or 0.25mg/kg/hour by infusion. In established renal failure hemodialysis may be required. Ascites Requires only correction of oncotic pressure by 50% albumin.

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Respiratory Problems Elective mechanical ventilation guided by ABG should be initiated in respiratory failure. Nutrition Protein intake to be limited to 1-2 gm/kg per day. Calories should be adequate to maintain the blood glucose at 75 mg%. Management of Seizures Choice of anticonvulsants is very crucial. Phenytoin and gabapentin are relatively safe in hepatic failure. Agitation and Restlessness It is often a problem in a child with hepatic failure. Benzodiazepines are usually avoided because of the respiratory embarassment and deepening of coma. If to be used lorazepam is the better tolerated one. Haloperidol also can be used which is relatively safe. Liver Support Systems The curative treatment may be liver transplant. Other support systems are hemodialysis, hemofiltration, plasma exchange and hemoperfusion. Molecular absorbant recirculating system (MARS) enables albumin bound toxins to be removed by dialysis along with other dialyzable toxins. It comprises a double sided albumin impregnated polysulphone or hollow fiber dialysis membrane in a closed loop dialysis unit.

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Bioartificial Liver Systems They combine biological tissue with non-biological materials. One such system contains human or pig hepatocytes implanted to hollow fiber ultrafiltration catridges. The patient’s blood or plasma circulates through these bioreactors and after clearance of toxic compounds and addition of synthesized products is returned to patients. The two main types are (1) extra corporeal liver assist device (ELAD) and bioartificial liver (BAL). Liver Transplantation Acute hepatic failure is responsible for 11% of pediatric liver transplantation. Orthotopic liver transplant is the treatment of choice whenever there is no potential for recovery. Auxillary liver transplant is desirable for those who have a chance of spontaneous recovery. The survival rate is 70-80% in well recognized centers.

CHAPTER 14

Acute Renal Failure

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Acute renal failure is characterized by inability of the kidneys to maintain body homeostasis and is manifested as reduced urine output with increasing blood urea and serum creatinine level. But 10% renal failures can have good urine output- non oliguric or polyuric ARF. It occurs secondary to sepsis, aminoglycoside toxicity and burns and is a feature of multiorgan dysfunction in PICU setting. The problems usually faced are- hypervolemia, hyponatremia, hyperkalemia and metabolic acidosis. Fluid Management Majority of acute renal failure patients presents with hypervolemia. The preferred route of fluid administration is oral or through nasogastric tube. The parenteral fluid is preferred only if there are gasterointestinal problems. Fluid intake is restricted to insensible water loss on day one and there after insensible fluid loss plus the previous day’s urine output. Insensible fluid loss comes to 30 ml/kg body weight for infants. 20 ml/kg body weight for older children 10 ml/kg weight for adolescents and adults. OR 400ml/m2 BSA per day If any other abnormal fluid loss is there, e.g. vomiting or loose stools that also is to be replaced. If fluid therpy offered is ideal the body weight is either steady or child losses around 0.5% of previous day’s weight. If there is hypovolemia, in addition to the above said fluids extra fluids to correct dehydration is to given.

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If child is hypervolemic and edematous, fluids are to be restricted and if hypervolemia persists furosemide 2-4 mg/kg IV can be given. Since they need first class protein the preferred oral fluids is usally milk or curd. If IV fluids are planned the maintenance fluid to be given is 5% dextrose. If child is grossly acidotic. 5 mEq of soda bicarbonate per 100 ml of fluid may be added and if the child is non acidotic 3 mEq/ 100 ml may be given. If child is having hypokalemia 4 mEq of potassium per 100 ml of fluid is added to the maintenance fluid. In normokalemia or hyperkalemia no potassium is to be added. Daily estimation of serum electrolytes will decide about the addition or substraction of electrolytes. Fluid loss and hypovolemia is to be corrected with normal saline or Ringer’s lactate as in any other child. In addition to the signs and symptoms of hypovolemia elevation in blood urea disproportionate to serum creatinine also shows hypovolemia and dehydration. In acute renal failure with edema say in AGN with failure often there is dilutional hyponatremia which does not necessitate sodium correction. But children with tubulointerstitial disorders, post obstructive release diuresis, recovering ATN and chronic renal failure normal sodium requirement is to be given on a daily basis. If on IV fluids 0.45% saline can be given. Hyperkalemia is often a problem in ARF. It should be anticipated and tried to delay it by avoiding potassium in diet, discontinuation of ACE inhibitors and potassium sparing diuretics, avoiding antibiotics containing high potassium salt, rapid control of infection, debridement of necrotic tissues and control of hemolysis.

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Potassium is to be given only in the presence of hypokalemia or in a child who is losing potassium. Tender coconut water, orange and other fruits are to be given initially. Later it can be given as potassium salts orally or rarely as IV potassium only if there is severe hypokalemia. Hypovolemia Can occur in renal disease due to indiscriminatory use of diuretics and restriction of salts and fluids. Child with oliguric renal failure can present with hypervolemia and non oliguric renal failure can present with euvolemia. Children with hypovolemia should get 20 ml/kg of normal saline over 1 hour and if no improvement, another 3 more similar doses can be given if CVP monitoring is available and two more doses if no CVP monitoring is available. If CVP monitoring is not available the patient should be carefully monitored for assessment of pulse volume, pulse rate, liver size, onset of hypertension and basal crepitations. If euvolemia is attained and urine output is inadequate, diuretic therapy can be given with 2 mg/kg body weight of furosemide intravenously. If no diuresis occur even after IV furosemide with an elevated CVP or clinical evidence of hypervolemia child is to be restricted of fluids and dialysis or continuous renal replacement therapy is indicated. Problems of vascular leak is a common problem in PICU where a child presents with volume overload but with decreased effective circulating blood volume. This is because of the vascular leakage, fluid shift from the intravascular compartment to the extravascular compartment. More fluids are needed to maintain the

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intravascular volume for renal and tissue perfusion but will aggravate the clinical features of fluid overload. This can occur in sepsis, dengue shock syndrome, leptospirosis, burns, snake envenomation and hypoalbuminemic conditions. If renal functions are adequate, diuretics can be given as continuous infusion 0.0 4mg/kg per hour. If renal function is inadequate, where in diuresis is not possible, peritoneal or hemodialysis is needed to maintain the fluid balance.

CHAPTER 15

Diabetic Ketoacidosis

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It is a usual medical emergency in a child who is known to have Diabetes Mellitus. It may be the first presentation of Diabetes Mellitus in a child. The clinical presentation is characterized by dehydration and acidosis. Detailed history may sometimes yield the presence of polydypsia and polyuria. Dehydration and hyperglycemia should be treated with caution as rapid treatment may result in cerebral edema. As in any sick child stabilization of the child, ABC is the first and the most important step. DKA Blood glucose > 300 mg/dl Acidosis pH arterial < 7.3, serum bicarbonate < 15 mEq/L Glucosuria (+++ to ++++) Ketonuria (+++ to ++++) Severe DKA Moderate DKA Mild DKA

Blood pH <7.1 pH 7.1 - 7.2 pH >7.2

S. bicarbonate <5 mEq/L S. bicarbionate 5-10 mEq/L S. bicarbonate 10-15 mEq/L

Hydration Assess the level of dehydration. Usually it is around 10%. IV fluids first started is either normal saline or Ringer’s lactate. 15-20 ml/kg is given in the first hour to expand the intravascular volume. If peripheral circulation is not improving (CRT>3 seconds) a second bolus can be given. If the child is still in shock colloids (e.g. Albumin) can be given. The rest of the deficit fluid and the calculated maintenance fluid for the next 24 hours should be given during next 23 hour.

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IV fluids for a 30 kg child with 10% dehydration is as follows. Ist hour 15 ml/kg (450 ml) of 0.9% saline or Ringer’s lactate as IV bolus. 2nd hour and subsequently 85 ml × 30 + 1750– 450 = 167 ml 23 hr hr as 0.45% saline with 10 mEq/L potassium phosphate and 20 mEq/L potassium acetate. Instead of potassium phosphate and potassium acetate, potassium chloride can be used 20 mEq/L Ongoing losses are to be corrected. Dehydration should be assessed clinically and fluids to be calculated accordingly. Potassium phosphate is advised to replace phosphate. Though phosphate depletion shifts the oxygen dissociation curve to left this defect is neutralized in untreated DKA by acidosis. Thus phosphate depletion does not appear to be mandatory. If it is given, serum calcium is to be monitored. In severe dehydration often there is associated hypokalemia. It is not wise to wait for the serum potassium report. ECG can help. In lead 2 if there is a flat T wave it is the evidence for hypokalemia and potassium can be given even if the child has not passed urine. Five percent dextrose is added to the fluids when the blood glucose approaches 250 mg/dl. It can be 5% dextrose saline so that the insulin infusion can be continued without risk of hypoglycemia till the acidosis is corrected. Bicarbonate is not to be given because it may over correct acidosis and produce true alkalosis, hypernatremia and severe hypokalemia. Should be used only in emergency

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situations with (a) severe hypokalemia (b) cardiovascular instability with pH < 7.2, shock or renal failure (e) blood pH is less than 7. Though serum bicarbonate is low, true deficit is not present because ketoacids and lactate are metabolized to bicarbonate during therapy. Insulin Therapy Continuous low dose insulin is the method of choice. A loading dose of 0.1 unit per kg body weight is given as and when IV fluids are started. This is followed by an infusion of 0.1 units/kg/hour (50 units of regular insulin is added to 500 ml of normal saline and 50-60 ml is run off to fill up the tubings). The infusion is then started with the infusion pump. If blood glucose does not fall by 50-100 mg/dl per hour in 2-3 hours the insulin dose is doubled. When blood glucose reaches 250 mg/dl 5% glucose is added to the fluid. IV fluid should not be discontinued till acidosis is corrected. (PH > 7.3, S bicarbonate>18 mEq/L). The insulin dose can be reduced to 0.05 unit/kg/hour or 0.025 unit/ kg/hour depending on the blood glucose level till acidosis is corrected, child is alert and oral feeds are tolerated. The subcutaneous insulin can be started. The dose is 1 unit/ kg/day divided 6 hourly. Half an hour before the insulin infusion has to be stopped, a subcutaneous dose of regular insulin 0.25 units/kg is to be given. Following this, a regimen of regular and intermediate acting insulin in two or more daily doses can be started. Oral feeds can be started as soon as the patient is conscious, has no vomiting or abdominal distension, has

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normal bowel sounds and willing to eat. This usually takes about 4-12 hours after initiation of therapy. Initially clear fluids are offered, then soft solids and finally full diet. Oral potassium may have to be continued for a few days if the serum potassium is low. Investigations Blood - CBC, Glucose, S electrolytes, ABG, S phosphates, Creatinine and Osmolatily. Serum osmolality can be calculated by the following equation. Serum Na + K × 2 + glucose + BUN Urine - Glucose, acetone, culture and sensitivity ECG for changes due to hypokalemia -flattening of T waves (> 2 div), appearance of U waves and QRS widening. Screening for sepsis-blood culture, urine culture Follow-up Blood glucose hourly to 2 hourly bedside till child is stable and free of acidosis. Serum potassium hourly till stabilized. S sodium, pH, Bicarbonate, Osmolality 2, 6, 10, 24 hours. Fallacies in Biochemical Tests in DKA • Hemoglobim and BUN may be elevated due to dehydration • Leucocytosis may be due to ketosis • Creatinine is elevated since the assay also measures aceto acetate • Pseudohyponatremia is common for every 100 mg% rise of glucose so add 1.2 mEq/L to the actual sodium level.

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• Apparent increase in ketone bodies in starting treatment as betahydroxybutyrate which is not detected by the nitroprusside reaction will be converted to acetoacetate and detected in urine. Complications A close monitoring is very essential which includes mental status, vital signs, insulin dose, fluid and electrolytes given, urine output and laboratory parameters like blood glucose, urine ketones, (early transient rise is a good sign) electrolytes and anion gap (narrows with treatment). Hypoglycemia should be corrected with appropriate measures but insulin should not be discontinued suddenly. Most serious complication a child with DKA is cerebral edema. Treatment is difficult and so should be avoided as best as possible. It usually develops in 4-16 hours after starting treatment and must be suspected if sudden neurological deterioration occur after the initial response. The signs include decreasing sensorium, headache, vomiting, disorientation, agitation, deterioration of vital signs, incontinence, pupillary changes, papilledema and seizures. A decreasing heart rate or occasionally tachypnea may be the earliest sign of impending cerebral edema. At the earliest sign, supportive treatment is to be started - IV mannitol and hyperventilation. Symptomatic cerebral edema carries a high level of mortality. Cerebral edema can be avoided by slow rehydration 3648 hours, after the initial circulatory stabilization, avoidance of hypotonic fliuds, avoidence of hypertonic fluids. (infusion of bicarbonate) and avoidance of rapid correction of hyperglycemia.

CHAPTER 16

Cardiac Emergencies

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CONGESTIVE CARDIAC FAILURE Heart failure characterizes the clinical syndrome resulting from the inability of heart to pump blood and oxygen at a rate commensurate with body’s metabolic demands. 80% of CHF occurs in infancy and is a common cardiac emergency in infancy and neonate. The causes of congestive cardiac failure differs in different age groups and in infancy the structural defects of the heart or great vessels is the commonest cause of heart failure. Diagnosis of cardiac failure in neonatal period is quite difficult as a number of non cardiac conditions such as infections, metabolic disturbances, and respiratory problems can have a similar presentation with tachypnea and tachycardia. The clinical manifestations differ based on the age, aetiology of heart disease, specific chambers involved and rate and extent of impairment of cardiac performance Cardiac failure can be insidiously merge into chronic congestic cardiac failure. Neonates and infants with cardiac failure grow slowly because of increased caloric requirement and decreased caloric intake. They feed poorly and feeding time is prolonged. In severe cases babies are unable to suck because of rapid breathing. The respiratory effort is more and breathing is rapid even in resting stage. Since babies cannot suck continuously they cry frequently and excessively and the sleep also is disturbed. They sweat profusely even in cool environment and the head sweating during feeding is very charecteristic. Due to orthopnoea, babies are distressed on

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supine position and comfortable when put on shoulders of the caretakers. Increased pulsations of the precordium may be noticed by some mothers. Edema is not a common complaint in a small baby. Physical Examination The major manifestations in CHF in babies are tachypnea, tachycardia, tender hepatomegaly and cardiac enlargement. Tachycardia may be a cause or effect. A heart rate of 180/minute or more is seen in CHF. But of the heart rate is sustained and more than 220/minute should raise the possibility of SVT. Bounding pulses seen in CHF should lead to the consideration of PDA, AV malformation, Truncus arterosus with truncal value regurgitation and other run off lesions. Ausculation may show systolic murmurs in many of the conditions. Diastolic rumble is common in shunt lesions with pulmonary over circulation. Gallop rhythm is a very suggestive finding in CHF. Auscultation of cranium (Vein of Galen malformation) and abdomen (hepatic AVM) is very important in a newborn or young infant presenting with CHF. Respiratory rate of 60-80/minute is common in CHF. Bilateral rales or ronchi may be heard. Raised jugular venous pulsations is a reliable sign in a child but not in an infant. Cool extremities, decreased peripheral pulses, lowered blood pressure and mottled extremities are signs of impaired peripheral perfusion and cardiogenic shock. Central cyanosis can occur due to impaired gas exchange. In general, intense cyanosis do not occur due to CHF.

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Measurement of BP in all the four limbs is important to rule out aortic obstructive lesion. Investigations Since cardiomegaly is an important sign of CHF, X-ray chest is an essential investigation. Cardiothoracic ratio more than 55% is considered cardiomegaly in infants and neonates. Pulmonary vascular markings are increased in pulmonary overcirculation. ECG is helpful in delineating ventricular hypertrophy, atrial enlargement and rhythm disturbances. A 14 lead ECG with rhythm strip is to be taken. Other laboratory investigations often indicated are blood glucose and serum electrolytes. Septic work up, ABG and metabolic work are sometimes needed. Echocardiography is always needed to assess the structural changes but to be done after stabilizing the child. Causes of CHF in First 2 Hours of Life 1. 2. 3. 4. 5. 6. 7. 8.

Tricuspid regurgitation Pulmonary regurgitation AV fistula Hypoplasia of left heart Endocardial fibroelastosis Birth asphyxia Twin to twin transfusion Paroxysmal tachycardia.

Causes of CHF in Day 1 1. Perinatal asphyxia 2. Severe anemia-Rh incompatibility, severe hemorrhage

CARDIAC EMERGENCIES

3. 4. 5. 6. 7.

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Ebstein’s anomaly Absent pulmonary valve Systemic AV Fistula SVT Neonatal myocarditis

CHF in First Week 1. 2. 3. 4. 5.

Aortic stenosis Hypoplastic left heart syndrome Co-arctation of aorta Interrupted aortic arch Critical pulmonary stenosis. All these presents when the ductus arteriosus closes. 7. TAPVC, 8. Preterms with PDA. Noncardiac 1. Acute renal failure 2. Neonatal hyperthyroidism 3. Adrenal insufficiency CHF—Around 1 Month of Age 1. 2. 3. 4. 5. 6. 7. 8.

Shunt lesions - VSD TGV with VSD Complete AV canal defect PDA AP window Truncus arteriosus Single ventricle ALCAPA

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Treatment Immediate aim of treatment is to improve the contractile performance of myocardium and to remove the excess salt and water. Establishing the IV line is crucial. Oxygen by mask is started immediately. Baby is to be kept warm. Mainstay of drug therapy is ionotropes, diuretics and vasodilators. Ionotropes Digoxin is the preferred ionotrope over the years. Though the role is controversial it remains the mainstay of management in the medical management of CHF. This cardiac glycoside blocks the myocardial cellular sodium - potassium pump. Thus intracellular sodium concentration increases, stimulating the uptake of calcium exchange mechanism. The intracellular calcium concentration allows for more actin and myosin cross bridges to form during activation of the cardiac muscle increasing efficiency of contraction. Digoxin also causes sympathetic withdrawal and relieves tachycardia, diaphoresis and other systemic signs and symptoms of CHF. In addition, digoxin is a good drug for the initial treatment of certain arrhythmias. The dosage schedule is as follows: Patient

total digitizing dose maintenance dose frequency

Newborn Infant Child

30 mcgm/kg 40-50 mcgm/kg 40 mcgm/kg

7.5 mcgm/kg/day 10 mcgm/kg/day 10 mcgm/kg/day

BD BD OD

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Dobutamine and Dopamine These ionotropes are used when baby is not responding to the initial treatment. Dobutamine is the preferred drug due to its predominant beta 1 action and less conspicuous alpha activity. Dose is 5 mcgm per kg per minute and upto 10-15 mcgm/kg/minute. It is the ideal drug when there is cardiac dysfunction with maintained blood pressure. Dobutamine is dissolved in 5% or 10% dextrose started at 5 mcgm/kg/mt infusion tritrated to 10 mcg/kg/mt upto a maximum of 20 mcgm/kg/mt. 1 ampoule 250 mg. Formula for Drug Infusion—Rule of six 1. 6 × wt in mgms of drug to be diluted in 100 ml. 2. 10ml/hour gives 10 mcgm/kg/mt. e.g. 14 kg child needs dobutamine 10 mcgm/kg/hour. 6 × 14 = 84 mgms 84 mgm in 100 ml fluid 10ml/hour = 10mcgm/kg/mt. Dopamine is another ionotrope which has beta 1 and beta 2 activity and also act on dopaminergic receptors in renal vasculature. It increases arterial vascular resistance and could be useful in acute CHF with hypotension. The dose is 5 mcgm/kg/mt titrated upto 15 mcgm/kg/mt. It may increase the pulmonary capillary wedge pressure and can worsen pulmonary congestion and so once BP is stable it may be switched over to dobutamine for continued ionotropic effect. Both can be used together with the advantage of less doses of individual drugs with maximal therapeutic effect. The dose is 5 mcgm/kg/mt. Each catecholamine should be continued for at least 48 hours and then tapered off.

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OTHER PARENTERAL IONOTROPES Amrinone and Milrinone The dose of amrinone is 0.75 mcgm per kg as a bolus dose over 2-3 minutes followed by an IV infusion of 5-10 mcgm/ kg/mt. Repeat bolus doses may be given if clinical response is not adequate, 2-3 doses given 15 minutes apart. It is a proarrhythmic. It can also cause severe diuresis, hypotension and thrombocytopenia. Milrinone is given as a loading dose of 50 mcgm/kg, IV and a maintenance dose of 0.35 - 0.75 mcgm/kg. Diuretics The commonly used diuretic drugs are the loop diuretics - furosemide, thiazides and aldosterone antagonists spiranolactone. Furosemide is the commonly used one and the drug of choice. The dose is 1-3 mg/kg/dose IM, IV or oral, repeated every 8-12 hourly. It is better to start as parenteral doses initially. 0.1mg/kg/hour as infusion also can be given. Aldosterone antagonist, spironolactone is a weak diuretic and is rarely used as an additional diuretic. Vasodilators ACE inhibitors are used in CHF. They augment cardiac pump function by altering the resistance of the peripheral vascular bed. Captopril is the drug of choice. The dose is 0.5 - 3 mgm/kg/day in two to three divided doses. Maximum dose is 4 mg/kg/day. Contraindicated in renal failure. Enalapril and prazocin is not well studied in children.

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Isoprenaline may be used in CHF with very high pulmonary vascular resistance (PPHN) or with low heart rate. Other Supportive Measures IV fluids are necessary since child cannot take enough orally. The fluid recommended is 2/3 of total maintenance fluid. Potassium supplementation is necessary in children on furosemide. Not necessary if the child is on ACE inhibitors. Oxygen therapy is needed till cardiac failure is controlled. Nutrition - Babies with chronic CHF the growth is always affected and they need 150-170 kcal/kg/day to achieve adequate growth. Nasogastric feeding may be required. Supplementation of iron is necessary to avoid anemia. CYANOTIC SPELL Cyanotic spell is one of the common cardiac emergency in an infant. It is due to an increase in impedance of pulmonary blood flow and reduction in systemic vascular resistance. It is classically found in TOF. Can occur in VSD with. pulmonary atresia, tricuspid atresia, and occasionally in TGA. The steps in management are • Oxygen with mask to combat hypoxemia. • Knee chest position to elevate systemic vascular resistance and to reduce right to left shunting and improve pulmonary circulation. • Injection morphine 0.1mg/kg, half the dose IM/SC immediately and rest of the dose once the IV line is

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established. Morphine relaxes the infundibulum and quieten the baby and reduces hyperpnea. • Once IV line is established normal saline is infused to expand the intravascular compartment. • Sodium bicarbonate 2ml/kg is given as a bolus diluted in equal amount of distilled water, to correct acidosis. • Beta blockers, propranalol in a dose of 0.1mg/kg is given. Half the dose is diluted and given immediately and the rest 10 minutes later. 0.5mg/kg may be given 4-6 hourly orally. Esmolol can be given initially as a bolus, 500 mcg/kg IV followed by IV infusion at a rate of 50-200 mcgm /kg/mt. They reduce infundibular spasm, reduce heart rate and increase systemic vascular resistance. • Vasopressors like phenylephrine or methoxamine can be used to increase systemic vascular resistance. Other modalities tried are abdominal compression, packed RBCS transfusion (5ml/kg) and ketamine instead of morphine (0.25 - 1mg/kg IV). Refractory spell may need general anesthesia and mechanical ventilation. Arrhythmias Common arrhythmias in children include SVT (supraventricular tachycardia) VT (Ventricular tachycardia) and bradycardia due to complete heart block. SVT SVT is the most common arrhythmia in children. Majority of them are paroxysmal. It is a narrow QRS tachycardia with a cardiac rate of more than 200/minute with an absent or buried P wave.

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Once diagnosed, hemodynamic compromise is looked for - CCF or hypotension. An ECG of 14 leads with a long lead II should be taken. The drug of choice is adenosine, given as IV boluses at frequent intervals. Each dose is given as a rapid push through a large vein flushed immediately with saline at an interval of 3-4 minutes. The recommended schedule is an follows Dose 1 50 mcgm/kg push 2 100 mcgm/kg push 3 150 mcgm/kg push 4 200 mcgm/kg push 5 250 mcgm/kg push 6 300 mcgm/kg push Usually, SVT breaks at a median dose of 200 mcgm/ kg. The other drugs available are: Amiadarone 3-5 mgm/kg/dose IV bolus administration for 10-20 minutes, followed by 10 mgm/kg/24 hours for 2 days. Diltiazem 0.2 mg/kg IV bolus for 2 minutes 0.3 mg/kg can be repeated after 5-10 minutes. Esmolol 500 mcgm/kg/mt bolus for 4 minutes followed by. 50-200 mcgm/kg/mt infusion.

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Verapamil Can be given in an older child. 0.2 mg/kg IV bolus slowly. In less urgent cases digoxin, oral verapamil and propranalol can be given. In refractory cases DC version may be needed. In a child with no hemodynamic compromise with SVT, vagal maneuvers such as iceberg application to face and carotid massage may be tried but with limited success.

CHAPTER 17

Hypertensive Emergencies

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Hypertensive emergencies exist when blood pressure is markedly elevated for age and signs and symptoms directly attributable to uncontrolled hypertension develops. In these clinical situations the blood pressure elevation is associated with vital organ dysfunction and the bood pressure has to be lowered in minutes to hours using parenteral drugs so as to save the vital organs. Hypertensive emergencies occur with rapid rise in blood pressure because chronic elevations in blood pressure is usually well tolerated as in chronic renal disease and end stage renal failure. Rapid elevation in BP can occur due to stoppage of antihypertensive therapy, inadequate fluid restriction or stopping the dialysis. Hypertensive urgencies are associated with severe hypertension but with no vital organ dysfunction and the reduction need be achieved over hours to days using even oral drugs. The causes for hypertensive emergencies can be renal or nonrenal origin. Renal • • • • • • •

Acute glomerulonephritis. Hemolytic uremic syndrome. Reflux uropathy. Chronic renal failure/end stage renal failure. Renal artery stenosis. Systemic lupus erythematous. Transplant rejection.

Nonrenal • Pheochromocytoma.

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• Volume overload. • Drugs—cyclosporine, erythropoietin, steroids Signs and Symptoms They may present with headache, blurring of vision, scotoma or blindness, lethargy, coma, seizures and abdominal pain. They can present with cardiovascular accidents, congestive cardiac failure or retinopathy. Treatment The goal of treatment is to reduce the BP but without a precipitous fall. The blood pressure is to be lowered by 25% within 6 hours and remainder of BP reduction to normal is to be by 24-36 hours. Too aggressive reduction is not advisable as it may be counterproductive and a precipitous fall may worsen organ damage. Though the parenteral drugs like nitroprusside, labetalol and enalaprilat are effective and are recommended drugs the use of these drugs are limited in our set up because of their toxicity and the lack of careful monitoring they demand. Very good results are obtainable from nifidipine 0.250.5mg/kg/dose oral or sublingual. The onset of action is within minutes and lasts for about 30-60 minutes. Can be repeated once or twice if required. Captopril sublingual in the dose of 0.5mg/kg can be used if there is no renal impairment. In very efficient ICU set up the recommended drugs and dosages are as follows.

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Sodium Nitroprusside is the Drug of Choice It is an extremely potent vasodilator which reduces systemic arterial and venous pressure. It’s action begins within seconds after infusion is started and disappears rapidly when it is discontinued. Because of it’s potent effect, nitroprusside should be administered in an ICU with blood pressure recording every 5-10 minutes. The drug is to be shielded from light to prevent degradation. The metabolic product of sodium nitroprusside is cyanide which is converted to thiocyanate in the liver and almost exclusively removed by the kidneys. And so cyanide poisoning is extremely rare. Nitroglycerin has a similar mechanism of onset and duration of action as nitroprusside. It is preferred to the latter in patients with renal impairment. The dose is 0.5 - 1mcg/kg IV initially titrated to 5-8 mcgm/kg/mt. The effect occurs within seconds. The side effects are sweating, muscle twitching and thiocyanate toxicity. Esmolol 500 mcgm/kg IV in 2-4 minutes followed by an infusion of 100-200 mcgm/kg every 10-20 minutes. Phentolamine 0.1 - 0.2 mg/kg/IV can reduce the BP in a few minutes. The drug can cause tachycardia, headache and flushing.

CHAPTER 18

Blood and Blood Component Therapy

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Transfusion of blood and blood components are indicated in restoring and maintaining the oxygen carrying capacity of blood, circulating blood volume, hemostasis, leukocyte and platelet function. Whole blood transfusion is indicated only for replacement of blood loss after trauma or surgery. In other situations the components needed for the patient only is transfused. Red Cell Concentrate Red cell concentrate is used for symptomatic anemia after an acute blood loss or in chronic anemia secondary to bone marrow suppression. One unit of red cell concentrate is expected to increase the hemoglobin level by 1gm/dl (Hct by 3%) in an average sized adult. The dose recommended for pediatric population is 10-15 ml/kg. Platelet Transfusion Transfusion of platelets is indicated in severe thrombocytopenia (Platelet count less than 10,000/ml). Platelet transfusion may be required prior to an invasive procedure in patients with thrombocytopenia with the count less than 50, 000/ml. The dosage is l unit/10 kg body weight. A baby of 10 kg needs 1 unit and child of 20 kg needs 2 units. The platelet increment after each unit transfused is 5000 to 10, 000 (single or pooled donor). If a single donor unit apherised is used, it contains an equivalent of 6 units, adequate for an average sized adult.

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PLATELET TRANSFUSION—INDICATIONS Non-immune thrombocytopenia 1. Platelet count <20, 000/ml 2. Platelet count <50, 000/ml with bleeding or prior to an invasive procedure or minor surgery 3. Platelet count <100, 000/ml prior to major surgery 4. Platelet count <100, 000/ml with recent intracranial hemorrhage 5. Qualitative platelet defect with bleeding or prior to any invasive procedure or surgery. Immune thrombocytopenic purpur Platelet transfusions are given to tide over the crisis when platelet count is below 20, 000/ml. Neonatal alloimmune thrombocytopenia Either matched antigen negative platelets or irradiated maternal platelets are to be given. If both are not available, routine platelet transfusion can be given in life-threatening bleeds. Thrombocytopenia due to maternal antibodies Platelet transfusions are given only in life-threatening bleeds. Plasma Transfusion Plasma obtained from one unit of whole blood (450 ml) has a volume of 200-220 ml. Plasma is frozen at –80° C and stored at –30° C within 6 hours of collection of blood (FFP). FFP has a shelf-life of one year and has all the labile and stable coagulation factors. Outdated plasma is designated as single donor plasma and it contains only the stable

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coagulation factors. This has a shelf-life of 4 years at 30°C. Plasma transfusion is indicated in • Coagulation factor deficiency - both congenital and acquired • Replacement therapy in congenital antithrombin III deficiency, protein C deficiency and protein S deficiency • Clinical evidence of coagulopathy pending laboratory results • Vitamin K deficiency with coagulopathy • Cheap substitute for albumin infusion, in increasing the serum albumin value in Nephrotic syndrome. The dose of plasma is 10-15 ml/kg. Cryoprecipitate Cryoprecipitate is prepared from one unit of FFP. FFP frozen at – 80° C thawed at 4° C triggers the precipitation of certain protein present in plasma. Each unit of cryoprecipitate contains 80-120 units of factor VIII activity and 150 mg of fibrinogen. It is stored at –30° C and is thawed for transfusion. Once thawed, it should be used within 6 hours. Granulocyte Transfusion May be used as an adjunctive therapy in severe bacterial sepsis. Warning - All components for transfusion should be as close to the room temperature as possible. This is done by placing the components at room temperature for about 30 minutes.

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Flow rates RBC 3-5 ml/kg/hour FFP within 30 minutes if volume dose not exceed 10-15 ml/kg. Platelets within 2 hours Vascular access: Blood transfusion sets should have filters. The standard IV cannulas or scalp vein sets with size ranging from 21-27 gauges can be used.

CHAPTER 19

Envenomation

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Snake Bite Snake bite and envenomation is one of the commonest causes for ICU admissions. Often the snakes are brought to the casualty and will be of help if the snake can be identified to be poisonous or not. The three common poisonous snakes in Kerala are viper, cobra and krait. How to identify them? Vipers Broad belly plates, triangular head, scales with or without pit on the head. Cobras Head is covered with shields. There is a hood and the spectacle mark on the hood. Third shield on the upper jaw extends from the eyes to the nostrils and the fourth one is small and triangular. Krait Central prominent row of shields with bands on the body. When you are in doubt your forensic colleague can help you. The patient care is based on the identification of the signs and symptoms of envenomation. All alleged cases of envenomation are to be admitted and kept in close observation for a minimum of 24 hours. Snake venom is a mixture of about twenty or more components and 90% are proteins. It contains, neurotoxins, myotoxins, cardiotoxins, hemolysins, autacoids, enzymes

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like hyaluronidase and so on. The neurotoxins can cause pre- and post-synaptic block in the myoneural junction to produce flacid paralysis. The endogenous autacoids released by the venom increase the vascular permeability producing fluid loss from intravascular to extravascular compartment. Hypovolemia, hyperalbuminemia, hemo-concentration, serous effusions, facial edema and ARDS result from capillary leak. Tissue necrosis is caused by myotoxin, vascular thrombosis and compartmental syndrome. Bleeding can occur due to DIC, endothelial damage, defibrination and thrombocytopenia. Hypotension is due to vasodilation, myocardial dysfunction and hypovolemia. Hypovolemia is due to vomiting, reduced fluid intake, capillary leak syndrome, bleeding and myocardial dysfunction. Persistent hypotension, hypersensitivity reaction to venom, acute tubular necrosis and direct nephrotoxicity result in acute renal failure. Clinical Features Early symptoms are vomiting, abdominal pain, and regional lymphadenopathy. Pain and sewelling at local site may or may not be evident depending on the type of venom. Severe envenomation is characterized by progressive deterioration of sensorium, myasthenic paralysis, respiratory, circulatory, renal and coagulation failures and ARDS. Viper envenomation is characterized by severe local changes, even leading to gangrene of the limb and hemorrhagic manifestations. Krait envenomation is mainly neuroparalytic and cobra can have neuroparalytic and myocardial toxicity. Pain without bleeding and other local

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changes occur in cobra and krait envenomation, there is too minimal local reaction. Severity of envenomation is influenced by many factors. The severity can be graded as follows: No envenomation Grade 0 Grade I Local swelling, and pain without (mild) progression Grade II Swelling and pain progressive with mild (moderate) systemic and laboratory manifestations Grade III Marked local response, severe systemic (severe) manifestations, significant alteration in laboratory findings The interval between bite, envenomation signs and death are as follows Viper Local changes within 15 mts Lymphadenopathy within 30 mts Serious manifestations and death within 2 hours to 9 days (mean 48 hrs) Cobra Local pain within 5 mts Systemic manifestations and death may occur within 30 mts to 60 hours (Mean 8½ hours) Krait Local pain is not usual. Systemic manifestations and death may occur within 3 hrs to 63 hrs (Mean 18 hours) Investigations Step I

- Hemogram, clotting time, clot retraction, grouping and cross matching

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Step II

- Bleeding time, clotting time, APTT. Platelet count, Peripheral smear, PCV, CXR, Step III - RFT, S electrolytes, ABG, SGOT, CPK, S cholesterol, Fibrinogen, FDP, ECG Clotting time is to be done every 6 hourly. RFT and Electrolytes, other tests for coagulation, clot retraction and FDP are done 12-24 hourly when clinically indicated. Urine is to be measured and urine routine examination is done for albuminuria and microscopic hematuria. Treatment ASV is the specific treatment. Monovalent antivenom is not available in India. 1 ml of ASV available in India is able to neutralize 0.45 mg of krait, 0.6 mg of cobra and 0.6 mg of viper venom. ASV should be administered as early as possible but should be given at any time if signs of envenomation are present. The dose is judged by the degree of envenomation. Since the ASV is horse derived, allergy or anaphylaxis can occur. So all measures to counteract anaphylaxis are to be taken. Parents are to be informed about the risks and benefits and an informed consent is obtained. The lyophilized ASV powder is diluted 5-10 times with normal saline and given as IV infusion. Before starting the infusion an intradermal test is given. In evidence of allergy or if there is history of allergy previously and also in severe envenomation where ASV is a must, each dose of ASV is started under cover of adrenaline (0.01ml/kg 1:1000 soln S/C, Injection chlorphenaramine maleate 0.03 mg/kg IV

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or diphenhydramine/mg/kg IV to reduce the risk of anaphylaxis. If some untoward effects develop the ASV infusion may be stopped and adrenaline and steroids are given. ASV is restarted at a lower rate after adrenaline 2030 mts prior to infusion. The dose of ASV is repeated if signs of envenomation persists, every 6 hourly, often 5-6 vials, till all signs and symptoms disappear. At the end of 6 hours, if CT is normal but the clot retraction is abnormal ASV is to be continued. Dosage Schedule Mild

Local edema Upto ½ of limb Moderate > ½ of limb Systemic signs + CT prolonged Early paralysis

Extensive edema Necrosis/blebs Systemic signs ++, + + + Bleeding, hypotension CT prolonged ARF Tests for allergy.

3-5 vials

5-15 vials followed by 5 vials 6 hrly

Severe -

20 Vials followed by 5 vials 6 hrly

Skin Test ASV 0.01ml of 1:1000 solution in normal saline is injected subcutaneously. Positivity is the appearance of a wheal in 20-30 minutes with or without systemic signs. The test can be false positive in 50% and false negative in 20% of cases.

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Conjunctival Test One drop of 1:100 solution of ASV in normal saline is put into the lower conjunctival sac. If sensitive, conjunctivitis and tears will appear in 10-30 mts. Supportive Therapy In early phase 1-1.5 times maintenance fluid is to be given. Fluid losses are to be replaced accurately. Fluids should be modified based on clinical situations like renal failure, hypotension, administration of blood and blood component therapy. In early phase, proper fluid therapy prevents renal failure. Broad spectrum antibiotics are to be given to prevent infection. The oral cavity of snake can contain G +ve, G –ve and anerobic organisms. Chloromycetin 100 mg/kg/day in 4 divided loses or Ampicillin 200 mg/kg/day in 3 divided doses. is an acceptable first line therapy. Aminoglycosides can be given if indicated with special care being taken with respect to renal status. Tetanus prophylaxis is to be taken when necessary. IV methyl prednisolone 30 mg/kg/day for 3 days may be given in patients with increased capillary permeability. In hypotension CVP is decreased and PCV < 40%—Blood transfusion is indicated. CVP is decreased and PCV normal—N saline is to be infused. CVP is decreased and PCV increased - Albumin or hemocele is the choice.

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CVP is normal and BP decreased - Steroids, IV methyl prednisolone 2 mg/kg/every 6 hours is given. In DIC - if FDP are increased, above 80 mcgm/ml, heparin may be given. In cobra or krait envenomation with neurological involvement IV neostigmine sulphate 0.04 mg/kg/dose is given. every 4 hourly or more frequently if clinical situation warrants, till recovery. IV atropine sulphate 0.01mg/kg/ dose 4 hourly is to be given to counteract the untoward effects. The dose is titrated to get the clinical effects and the interval of administration is increased as the clinical state improves. Most important aspect of treatment is the early and optimum administration of ASV and proper fluid therapy in the early phase. Prognosis is good if ASV is administered within 3 hours after the bite. Better be late than never. ASV is effective upto 21 days after the snakebite. Surgical help may be necessary in for development of compartmental syndrome, amputation of the limb, skin grafting, etc. In myocardial or circulatory failure - dopamine, dobutamine and steroids may be necessary. ARDS - needs mechanical ventilation.

CHAPTER 20

Poisoning in Children

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Poison is defined as a substance which introduced into the body or absorbed by a living organism causes injury or death. Poisoning in young children can often be accidental but in older children and adolescents it can be suicidal also. Small children are more prone because of their ignorance regarding poisonous nature of the object Outcome depends on the time lapsed after the injestion, the dose, the treatment received and how the person reacts to the poison. Any child admitted with unexplained coma, convulsions and altered sensorium, the possibility of poisoning is to be considered and the history and circumstances are to be revaluated. TYPES OF POISONS Household Poisons Drugs and Pharmaceuticals Plant poisons Depending of the action the poisons can be Stimulant poisons Sympathomimetics They produce restlessness, sweating, tachycardia, dilated pupils and flushing. For example, amphetamines, caffeine, cocaine, decongestants, theophyllines. Anticholinergetics They produce warm dry flushed skin, tachycardia, dilated pupils, hyperthermia. For example, datura, belladona alkaloids, mushrooms.

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Hallucinogens LSD and it’s analogues, Marijuana. Withdrawal Syndrome Alcohol, antidepressants, beta blockers, narcotics, sedatives, hypnotics. Depressant Poisons Sympatholytic agents They produce bradycardia, hypotension, bronchoconsriction, sedation and depression For example, adnergic blockers, anti arrhythmics, antihypertensives, Ca channel blockers, digoxin. Cholinergic Agents They produce nausea vomiting, abdominal cramps, diarrhea, involuntary defecation and micturition, sweating, salivation, lacrimation, bronchorrhea, blurred vision and weakness. For example, organophosphorus, organocarbomate, pyridostigmine, etc. Narcotics, sedatives and hypnotic agents Analgesics, antispasmodics, alcohol, babiturates, benzodiazepines GENERAL SIGNS AND SYMPTOMS OF POISONING Skin Pallor, insulin, sympathomimetics, aniline deivatives Cyanosis—morphines, sulpha, CO, drug causing methemoglobinemia, e.g. dapsone.

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Sweating—cholinesterases inhibitors, nicotine, pilocarpine Dry hot skin—datura, belladona alkaloids. Eyes Miosis Cholinesterase inhibitors, barbiturates, nicotine, opium, morphine, para sympathomimetics Mydriosis Cocaine, datura, thallium, cyanosis, sympathomimetics. Blindness Methyl alcohol Blurring of vision Choline esterases, datura, alcohol, ergot. GIT Corrosives, phenol, cresol, mushrooms, digitalis, morphine, choline esterase inhibitors Cocaine, salicylates. CNS Headache Atropine, CO, phenol, benzene, strychnine, cadmium. Convulsion Mushroom, cyanides, salicylates, datura, cocaine, strychnine, cholinesterase inhibitors. Delirium Datura, cocaine, lead, arsenic, gold, ergot, barbiturates.


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Coma Salicylates, mushrooms, cholinesterase inhibitors phenol, CO, cyanates, lead, barbiturates, morphine and nicotines Respiratory Pulmonary edema CO, cyanide, narcotics, salicylates Tachypnea cough and wheezing nicotine. CVS Bradycardia Beta blockers, antiarrythmics, Ca channel blockers, organic phosphates and carbomates, digoxin, odollum. Tachyarrythmia Ventricular Antipsychotics, tricyclic antidepressants heavy metals, lithium, Mg. MANAGEMENT ABC Removal of the Poison Gastric lavage and emesis help in removing the poison from gut. Emesis is not advised in children for fear of aspiration. Gastric lavage can be done in hospitals except when there is a suspicion of corrosives. Inhibiting the absorption of poison Activated charcoal 1gm/kg statum folowed by 0.2 gm/kg/ hour.

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Cathartics not advised in children for fear of dehydration and dyselecrolytemias. Whole body irrigation helps in eliminating the poison not adsorbed by activated charcoal. Polyethylene glycol electrolyte solution orally via nasogastric tube’20-40 ml/ hour until clean effluent occurs. Forced diuresis ionizable drugs can be excreted either in acid or alkaline media, e.g. phenobarbitone, salicylates. Hemodialysis Useful in poisoning with salicylates, methanol, ethylene glycol, theophylline, barbiturates, methotrexate, procainamide, digitalis, chloral hydrate Hemoperfusion Hemoperfusion over activated charcoal resin is done in theophylline, salicylate, paraquat poisoning. ANTIDOTES PHYSICAL ANTIDOTES They impair the absorption of poison For example, demulcents-fats, egg albumin, activated charcoa. CHEMICAL ANTIDOTES They neutralize the effect by forming compounds which are innocuous For example, potassium permanganate — barbiturates Tincture of iodine — heavy metals


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PHYSIOLOGICAL OR PHARMACOLOGICAL ANTIDOTES They act at tissue level counteracting the poison by blockade of receptor stimulation, enzymatic inhibition or reactivation, displacement of poison from tissue binding sites. For example, Naloxone for opiates, atropine for cholinergic agents Pyridoxine for INH Chelating agents for heavy metals Universal antidote Can be used when poison is not known or more than one poison is suspected Powdered charcoal— adsorb alkaloid Milk of magnesia—neutralisation of acids Tannic acid—Precipitation of alkaloids, glucosides, and heavy metals INDIVIDUAL POISONS Kerosine Accidental ingestion of kerosine is very common in children. Often the child aspirate it while drinking, or during the process of vomiting which may be spontaneous or induced by the care taker. Fatal dose is 30 ml. But often the amount taken is very small and the child comes with respiratory symptoms. Treatment is Supportive Gastric lavage is not advised. Oxygen therapy is advocated if necessary. Antibiotics if infection is suspected. Observe for 24 hours since the fatal period is 24 hours.

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Acids Mineral acids are corrosives. They extract water from the tissues and coagulate cellular proteins and form acid albuminates. Hemoglobin is converted to hematin. Local irritation, bleeding and sloughing of mucosa and skin occurs. They damage esophagus and stomach resulting in necrosis and perforation. Management They can be diluted with milk or milk of magnesia. Gastric lavage is contraindicated. Because the child will be unable to swallow IV fluids are to be given. Corticosteroids for 2 weeks are given to decrease the incidence of stricture formation. Prophylactic antibiotics can be given. Supportive therapy for respiratiry distress is to be given. Caustic Potash or Soda They act as corrosives when concentrate and simple irritants when dilute. They are rapidly absorbed from mucous membranes and combine with fat and protein, forming soaps and proteinates. They produce soft deeply penetrating necrotic areas. Emetics and lavage are contraindicated. Weak acids such as lemon or orange juice can be given as diluents for neutralizing the alkali. Dilution with water should not be done.


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Iron Has got 5 stages 30 mts 2 hours characterized by GIT Stage 1 symptoms Stage 2 Apparent recovery 2-6 hours Stage 3 Circulatory failure 12 hours Stage 4 Hepatic necrosis 2-4 days Stage 5 Gasrtic scarring 2-4 weeks When serum iron is >50 mg/dl toxicity manifests. TREATMENT Gastric lavage should be done. X-RAY will confirm the success of the procedure because the iron in GIT can be demonstrated in X-RAY. Chelating Therapy Desferroximine 10-15 mg/kg IV followed by 50 mg/kg every 4 hourly as IM. Maximum dose to be given is 6 gm. When iron is being excreted the urine will be coloured red. The drug is to be continued till the blood level is < 30 mg/dl. ORGANIC CHEMICAL COMPOUNDS Organophosphorus The presently available pesticides come in the group of organocarbamates Baygon, furadan, malathion. The poison can get absorbed through all the routes. They inhibit the enzyme acetyl choline esterase.

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TREATMENT The first step is to remove poison from body. Cleaning the skin will reduce the absorption of poison through the skin. This should be followed by gastric lavage. The treatment of carbamate poisoning is same except that pralidoxim the cholin esterase activator is contraindicated in carbamate poisoning. The drug is atropine which can be given as frequent doses intravenously.as per the clinical judgement. Clinically, the pupil size can decide the dose of atropine. When the pupils are fully dialated then the dose can be reduced. The child with organocarbamate poisoning should not die due to atropine poisoning. PARACETAMOL POISONING The poisoning can be of 4 stages Stage 1 First 24 hours Stage 2 Next 24 hours Stage 3 48-96 hours Stage 4 stage of resolution 4 days -2 weeks Fatal dose is 20-25 gms The drug used in paracetamol poisoning is N-acetyl cysteine orally or through NG tube 140 mg/kg followed by 70 mg/kg 4 hourly for for 17 doses. PLANT POISONS DATURA (ummam in Malayalam) It contains hyocine and hyocyanin They first stimulate the higher centers and then depress Fatal dose is 0.6-1gm (50-75 seeds)


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TREATMENT Stomach wash is to be given The drug to be given is physostigmine. ODOLLUM (OTHALAM in malayalam) It contains many alkaloids producing vomiting diarrhea followed by bradycardia, irregular respiration, collapse and death. TREATMENT Stomach wash Atropine Correction of hyperkalemia JETROPHA CUREAS (Purging nut-Kadalavanakku) Poisonous parts are seeds and juice. The juice can cause burns, blindness, gastritis, diarrhea and vomiting. TREATMENT Stomach wash The rest is symptomatic ARBUS PRECATORIUS (Kunnikkuru) Similar to Viperine snake venom Fatal dose 90-120 mg TREATMENT Symptomatic Anti abrin if available

INDEX A

C

ABG analysis 69 Acute renal failure 129 fluid management 130 hypovolemia 132 Acute respiratory failure 111 Acute severe asthma 115 Airways 41 management of respiratory failure or arrest 42 nasopharyngeal airway 41 oropharyngeal airway 41 Antidotes 176 chemical antidotes 176 physical antidotes 176 Arterial access 32 modified Allen’s test 33 sites 32 technique-radial artery 32 Artificial airways 82

Chest compression in the child 17 Chest compressions in the infant 16 Child-the Heimlich maneuver 20 advanced life support 22 respiratory-airway and ventilation 23 unconscious child 21 victim conscious 20 Circulation 6 blood pressure 6 BP in children 7 capillary filling time 7 organ perfusion 7 pulse and heart rate 6 pulse pressure 6 pulse volume 6 skin perfusion 7 temperature 7 Coma 107 lab evaluation 109 management 108 treatment 109 Congestive cardiac failure 142 investigations 144 physical examination 143 treatment 146 CPAP 45 complications associated with endotracheal intubation 50 during the intubation procedure 50

B Bag-valve-mask ventilation 42 Self-inflating bag-valve ventilation devices 44 ventilation face mask 42 Blood and blood component therapy 157 cryoprecipitate 160 granulocyte transfusion 160 plasma transfusion 159 platelet transfusion 158 red cell concentrate 158

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depth of insertion 47 en endotracheal airway 46 endotracheal tube 46 preparation and technique of intubation 48 size of the cndotrecheal tube 47 Cyanotic spell 149 arrhythmias 150 SVT 150

D Diabetic ketoacidosis 135 hydration 136 insulin therapy 138 complications 140 follow-up 139 investigations 139 Dobutamine and dopamine 147 Dysclectrolytemias 54 causes 54 extrarenal 55 factitious hyponatremia 55 hyponatremia 54 pscudohyponatremia 55 renal losses 54 treatment 56

E Endotracheal tubes 82 Envenomation 163 clinical features 165 investigations 166 treatment 167 Euvolemic hyponatremia 57 External jugular vein 31

F Foreign body airway obstruction 17

H Hepatic failure 121 agitation and restlessness 127 ascites 126 bloartificlal liver systems 128 coagutopathy 126 encephalopathy 122 fluid and electrolytes 125 liver support systems 127 liver trnnsplnntation 128 management of cerebral edema 123 management of seizures 127 metabolic problems 125 methods to reduce serum ammonia 124 nutrition 127 renal dysfunction 126 respiratory problems 127 Hypercalcemia 65 causes 65 treatment 65 Hyperkalemia 63 causes 63 treatment 63 Hypermagnesernia 67 causes 67 treatment 67 Hypematremla 58 Hypertensive emergencies 153 causes 154 nonrenal 154 renal 154 signs and symptoms 155 treatment 155

INDEX

Hypervolemic hyponatremia 57 Hypocalcemia 64 treatment 64 Hypokalemia 61 Hypomagnesemia 66 causes 66 treatment 66 Hypovolemic hyponatremia 57

I Identifying a sick child 2 alertness 3 appearance 3 breathing 5 distractibility and consolability 4 eye contact 4 glasgow coma scale 3 motor activity 4 pupil size 4 respiratory rate 5 speech/cry 4 work of breathing 5 Increased anion gap acidosis 75 Ionotropes 146 IV fluid therapy 51 decreased requirement 53 increased requirement 53 maintenance fluid and electrolytes 52 maintenance of water 52 rate of fluid infusion 53 IV fluids in specific situations 54 acute diarrheal disease 54

M Mechanical ventilator 83 basic system 83 Metabolic acidosis 79 Metabolic alkalosis 79

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N Normal anion gap acidosis 75

O Other parenteral ionotropes 148 amrinone and milrinone 148 diuretics 148 vasodilators 148 Oxygen delivery systems 36 face tent 38 high flow systems 36 low flow systems 36 nasal cannula 40 nasal catheter 41 non-rebreathiug mask 38 oxygen hood 39 oxygen mask 36 oxygen tent 40 partial rebreathing mask 37 venturi mask 38 Oxygen therapy 35

P Pediatric cardiopulmonary resuscitation 9 causes in infancy beyond newborns 10 beyond infancy 11 brea thing 13 circulation 15 head tilt-chin lift 12 jaw thrust 12 pulse check 15 recovery position 13 rescue breathing 13 Pediatric ventilators 84 pressure limited ventilators

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84 disadvantage 85 volume limited ventilators 85 advantages 85 disadvantages 85 Physiological or pharmacological antidotes 177 Plant poisons 180 arbus precatorius 181 treatment 181 datura 180 treatment 180 jetropha cureas 181 treatment 181 odollum 181 treatment 181 Poisoning in children 171 general signs 173 management 175 symptoms 173 types 172 depressant poisons 173 household poisons 172 Practical approach to rapid analysis of ABG 76

R Respiratory acidosis Respiratory alkalosis 79

78

shock 99 Status epilepticus 101 steps in management 102 anticonvulsants 103 investigations 106 refractory status epilepticus 105

T Tracheostomy 83 Types of ventilation 86 assist control mode of ventilation 8 constant distending pressure (COP) 86 controlled mechanical ventilation 86 diseases with decreased lung compliance 89 diseases with increased resistance 90 intermittent mandatory ventilation 88 positive end expiratory pressure (PEEP) 87 pressure support ventilation 89 synchronized intermittent mandatory ventilation (SIMV) 88

V S Shock 96 cardiogenic shock 96 dissociative shock 97 management 97 symptoms 97 distributive shock 96 hypovolemic shock 96,97 obstructive shock 96 septic shock 98 steps in management of

Vascular access 25 central venous cannulation 28 devices 27 devices and techniques 29 intraosseous cannulation 27 modified Seldinger’s technique for insertion of catheters and introducing sheaths 29 venous access 26

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