Pediatric Intensive Care Nurse Handbook -...

Pediatric Intensive Care

Nurse Handbook

2012

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If this book is found please return to:

_____________________________ _____________________________ _____________________________ _____________________________

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This booklet is Dedicated to: The Pediatric Intensive Care Nurse:

The FHFC Critical Care Nurse’s Prayer

Dear Father God, I begin my shift caring for a child. Hear my prayer. Clear my mind of burdens in my personal life. Make me whole in the moment to focus on the needs of this child before me. Bring forth all my knowledge and the knowledge of colleagues in order to provide the most excellent care. Open my eyes to see and my ears to hear all important information. Allow me to speak clearly and be fully understood. Make my choices wise and deliberate. Hold my hand when I am afraid. Love me through the hours ahead. Protect my family while I am here. Guard me on my journey home. Amen

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Original Handbook 2004 by: Terry Cavanaugh, BSN. RNC.CCRN Karen Clawson, RN, CCRN Lisa Dixon RN

Aimee Foreman, BSN, RN Catherine Haskins-Kiefer, BSN RN Kim Kelly, BSN, CCRN Cindy Marshall, BSN, RN

Melinda Mowery, RN Dawn Russell, BSN, RN

Revised Edition 2009 by: Editor: Leigh Ann Mikkleson, BSN, CCRN

Susan Mauer, BSN, CCRN Kristine Janda, BSN, CCRN Charles Brewer, BSN, CPON Marybeth Alderman, BSN, RN

Melissa Carril, BSN, RN Lindsay Anderson, BSN, RN Heloisa Georgiev, RRT-NPS

Revised Edition May 2011 by: Editor: Alicia D. Kane RN

Contributors: Alicia Kleinhans BSN RN CEN CCRN

Nicole Dutcher, RD, LD/N, CSP Catherine Haskins-Kiefer, BSN RN

Karen Clawson, RN, CCRN

Revised Edition September 2012 by: Alicia Kleinhans BSN RN CCRN CEN C-NPT

Disclaimer: This booklet was designed to assist the

PICU Nurse’s clinical knowledge. This booklet will be reviewed annually for content.

Content is NOT protocol. The information contained in this manual

is not intended to replace the policy and procedures (P&P) of Florida Hospital for Children.

Also, refer to Mosby’s Skills online via FHFC intranet.

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Respiratory 6-26

Cardiovascular 27-40

Neurological 41-57

Renal 58-66

Multisystem (Endocrine, Hem/Onc, Sepsis) 67-83

Nutrition 84-88

Line, Drugs, Etc 89-104

Bedside Procedures 105-112

Pain Scales & R.E.S.T.O.R.E. 113-127

TABLE OF CONTENTS

References 128-131

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Respiratory

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Pediatric Respiratory Rates

Attach pulse Ox Correctly

and check for accuracy

often!

AGE RATE Infant (Birth - 1 year) 30-60

Toddler (1-3 yr) 24-40

Preschooler 22-34

School-age 18-30

Adolescent 12-16

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Acute Respiratory Infections

Pneumonia/Aspiration Pneumonia Pneumonia is an infection of the lung caused most often by bacte-ria or viruses. The most likely etiologic agent depends on the age of the patient, how the organism was acquired (community or nosocomial), and the presence of underlying disease. Influenza and RSV are the most common in young children. The presence of compromised host defenses may predispose a patient to pneu-monia such as endotracheal intubation or tracheal aspiration from CNS injury or GER, BPD or CF.

Croup Viral, cold symptoms and fever, edema of vocal cords S&S – stridor, barking cough, symptoms worse at night, in-creased work of breathing, steeple sign Treatment – Cool mist, racemic epi

Epiglottitis

Bacterial (haemophilus influenza B), edema of epiglottis and sur-rounding structures, rapid progression S&S – fever, sore throat, drooling, retractions, sniffing position Treatment – keep child calm, O2 as tolerated, intubation by anes-thesiologist (one shot), cricothyroidotomy if unsuccessful intuba-tion

RSV Premature babies and infants more susceptible, can be life threat-ening S&S – cold-like symptoms, copious, thick upper airway secre-tions, may present with apnea Treatment – Supplemental O2, good pulmonary toilet, nasal suc-

tioning

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BPD

Bronchopulmonary dysplasia is a chronic lung disease occurring in infants born prematurely who have survived respiratory failure. The two most significant risk factors for BPD are extreme prema-turity (<28 weeks gestational age) and hyaline membrane disease. Abnormal development of lung tissue, children continue to grow more alveoli until around two years of age

Symptoms include reduced lung compliance, increased airway resistance, hypercapnia, low to no functional reserve, BPD fits where child becomes cyanotic, hypercapniec and difficult to ven-tilate when crying.

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Pediatric Asthma*

Common Triggers Inhaled allergens Respiratory infections Inhaled respiratory irritants (smoke/cold air) Medications Physical activity Emotional state (anxiety, sudden upset) Hormonal fluctuations

Treatment of Asthma Inhaled Short Acting Beta 2-agonists

- Albuterol Systemic Glucocorticoids

- Prednisolone - Methylpredisolone 1-2mg/kg IV

Smooth muscle relaxant/bronchodilator -Magnesium Sulfate 50mg/kg IV over 30 min IV Bronchodilators (Tx of status asthmaticus)

- Terbutaline - Aminophylline

Supplemental Oxygen - Humidified via nasal cannula or face mask - Maintain O2 Saturation 92% (adjust flow rate PRN)

Asthma Education - Asthma action plan

Adjusting Home Medications

* Refer to Asthma Protocol Treatment Path & Pediatric Drug Book as Reference for dosages Refer to Lexicomp & consult pharmacy staff

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Score 1 2 3

Respiratory Rate

2-3 years 34 35-39 40

4-5 years 30 31-35 36

6-12 years 26 27-30 31

>12 years 23 24-27 28

O2 Sat >95% on room air(RA)

90-95% on RA

<90% on RA or any O2

Auscultation Normal Breath sounds to end

expiration Wheeze only

Expiratory Wheezing

Inspiratory or expiratory

wheezing to deminished

Retractions None or intercostal

Intercostal & Substernal

Intercostal, Substernal, and supra-clavicular

Dyspnea Speaks in sentences, coos and babbles

Speaks in partial

sentences Short cry

Speaks in single words.

short phrases, grunting

The Pediatric Asthma Score (PAS)

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Heliox Therapy Purpose / Description:

Helium’s density is less than Nitrogen’s, so at any given gas flow there is less turbulence. This property of helium can bene-fit patients with airway obstructions by improving gas exchange, lowering airway resistance, and reducing work of breathing.

Indications / Applications of Heliox:

The use of heliox has led to clinical improvement in respiratory distress and reduced work of breathing in a variety of obstruc-tive lesions including: 1. Upper Airway Obstruction:

a. Viral & post-extubation croup b. Anaphylaxis c. Vocal cord paralysis

d. Upper airway masses, including tumors 2. Lower Airway Obstruction

a. Asthma b. COPD c. Brochiolitis d. Bronchopulmonary dysplasia

The effectiveness depends on the concentration of helium:

Best: 80% helium / 20% oxygen Mixtures containing less than 60% helium are too dense to

be clinically beneficial. *Heliox offers no permanent solution to a pathological process. Contraindications: There are no absolute contraindications for heliox. Patients must be able to tolerate the level of oxygenreceived. For example: a 70/30 mix means no matter what form of delivery, your patient will get 70% oxygen

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6 P’s of Rapid Sequence Induction (RSI) & Intubation Preparation– all equipment at the bedside-in working order including:

Oxygen Suction Proper sized ETT laryngoscope and blade with working light CO2 detector any medications drawn up in syringes, flushes, patent IV position patient with a roll

Preoxygenation– give 100% oxygen for 5 minutes via non-rebreather or bag mask Pretreatment– Analgesic and/or sedative Paralysis– Vecuronium (Non-Depolarizing Neuromuscular Blockade Only) Placement-visualize landmarks, through vocal cords, may need to pull side of mouth open, may need cricoids pressure, have suction ready, monitor patient and notify practitioner of decline Post-Intubation-Confirm placement with: improving clinical appearance, Co2 detector, misting in the tube, symmetrical chest rise, no gurgling over epigastrum, bilateral breath sounds, chest x-ray Inhaled Nitric Oxide Purpose/Description:

Inhaled Nitric Oxide (iNO) is a free radical produced by the en-dothelium that relaxes smooth muscle walls. It is a selective pulmonary vasodilator because hemoglobin binds with it easily minimizing the effects in systemic vasculature. iNo improves oxygenation.

Indications/Applications: infants and children in hypoxic respiratory failure in whom conven-tional ventilator therapy fails. An echocardiogram to rule out congenital heart disease is recom-mended. iNO is ordered in PPM (parts per million), usually 20ppm and must be weaned down slowly from 20 to 5 ppm in decrements of 5 ppm every 1 to 2 hours to prevent hypoxia or rebound pulmonary hypertension

Adverse/toxic effects of iNO include methemoglobinemia (secondary to excess nitric oxide concentrations), direct pulmonary injury (attributable to excess levels of nitrogen dioxide), and ambient air contamination

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Some Positive Pressure Ventilation Essentials

Types of Ventilation 1. Pressure controlled Volume delivery is variable as it depends on the

compliance of the patients lungs. Increased level of support. Decreases risk of barotraumas. Pre set amount of pressure, operator set

and delivered by the ventilator. 2. Volume Controlled

Pre set amount of volume, operator set and deliv-

ered by the ventilator. Pressure is variable (dependent upon

compliance of lungs). Increased chance of barotraumas (pressure

will increase in order to deliver the set volume). 3. APV (Adaptive pressure ventilation)

Volume is selected based on patient’s weight. Operator sets a max amount of pressure (pop off)

allowed for the target volume Ventilator will automatically deliver the lowest

amount of pressure needed in order to deliver the target volume

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4. SIMV In SIMV (Synchronized Intermittent Mandatory Ventila-

tion), operator sets a mandatory (mechanical) rate. Patient is allowed to breath spontaneously between the

mandatory breaths with the aid of pressure support. Spontaneous and mechanical breaths are synchronized

(patient comfort) 5. CMV

In CMV (Controlled Mandatory Ventilation), every effort from the patient to breath is assisted from the ventilator. The rate acts more like a pacemaker. Every breath ends up being a mechanical breath.

PEEP Delivery of positive end expiratory pressure in order to keep alveoli from completely collapsing at end of expiration. PRESSURE SUPPORT Supports each spontaneous breath with supplemental

flow to achieve a pre set pressure

Overcomes airway resistance caused by the ETT

Helps to increase patient’s spontaneous volumes

Decreases work of breathing

Should be set to achieve 3-5 mls of pt’s IBW

Do not overload the Hering-Breuer Reflex by Over-bagging

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A/C P– A/C

Volume Controlled Mandatory Breaths

Pressure Controlled Mandatory Breaths

Variable Pressure Set I-time

Variable Volume Set I-time

Every Breath is fully Supported

Every Breath is fully Supported

Patient receives set Volume w/ every breath

Patient receives set Pressure w/ every breath

APV / CMV APV / SIMV

Rate functions as a BUR (Back up Rate)

SIMV rate is an actual Rate

Every breath is guaranteed the target volume

SIMV breaths are guaran-teed the target volume

I-Time set for every breath I-Time set for SIMV rate vari-able IT for spontaneous RR

No Pressure Support Pressure support for Spontaneous breaths

Ventilator Support

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SIMV P-SIMV

Breaths that are volume controlled

Breaths that are pressure controlled

Set volume delivery (set VT for SIMV breaths)

Variable Volume

Pressure support for spontaneous breaths

Pressure support for spontaneous breaths

Variable Pressure Set Pressure

Set Rate and Set I-Time Set Rate and Set I-Time

Volume Ventilation Pressure Ventilation

Rate or Frequency (Breaths per Minute)

Rate or Frequency (Breaths per Minute)

Tidal Volume (liters or milliliters)

Pressure Control or PIP (Term varies depend on

ventilator in use) (cm H2O)

PEEP (cm H2O) PEEP (cm H2O)

Pressure Support (cm H2O) Pressure Support (cm H2O)

FiO2 or (O2 lpm on some home vents)

FiO2 or O2 lpm

Ventilator Values the Nurse must Know

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High Frequency Oscillatory Ventilation (HFOV) is a type of mechanical ventilation that employs very high respiratory rates (>150 breaths per minute) and very small tidal volumes. High fre-quency ventilation is thought to reduce ventilator-associated lung injury (VALI), especially in the context of ARDS and acute lung injury.

Goal of High Frequency Open lungs strategy and move gas in and out with very small volumes (smaller than deadspace). Active inhalation and active exhalation; piston moves air forwards and pushes air out. Clinical Management Use in-line suction catheter if suction is needed Avoid disconnection from the ventilator in order to avoid de recruit-

ment of the lungs Only suction if secretions are visible in the tube or if chest wiggle is

noted to have decreased

Name Responsible for

MAP (Mean Airway Pressure)

Open lung strategy Oxygenation

Amplitude/Power/Delta P

Chest wiggle ventilation– CO2 elimi-nation

Hertz/Frequency 1 Hz = 60 breaths Breaths per minute

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Ventilator Acquired Pneumonia

Definition: Onset of pneumonia at least 48 hrs. after intubation

Is second most common healthcare associated infection

In PICU, VAP increases number of days child spends on a mechanical ventilator, increases length of stay by an average of 8.7 days, and increases hospital costs by $51,157

Occurs in 3-10% of ventilated patients Mortality may exceed 10%

Risk Factors Prolonged intubation

Enteral feeding due to increased risk of aspiration

Paralytic agents or heavy sedation (decreases cough reflex)

Age extremes (very young or old)

Use of PEEP

Underlying illness

Transporting out of unit

Prevention Daily paralytic Holidays

HOB up 30-45 degrees to decrease risk of pulmonary aspiration

Avoid gastric over-distention

Avoid unplanned extubation and re-intubations

Use cuffed ETT and inline suction; only use saline lavage if abso-lutely neccessary

Good oral care with an antiseptic solution

Change vent circuit only when visibly soiled or malfunctioning

Prevent condensate in tubing from entering lower respiratory tract

Good hand hygiene

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Blood Gas Analysis/ABG Normal Values

Respiratory component Metabolic component

pH 7.35 – 7.45 CO2 35 – 45 PO2 80 – 100 HCO3 22 – 28 Base + or -2 Sat 95% - 100%

Respiratory Acidosis

pH < 7.35 CO2 > 35 HCO3 Normal

Respiratory Alkalosis

pH >7.45 CO2 < 35 HCO3 Normal

Mixed Acidosis

pH < 7.35 CO2 > 45 HCO3 < 22

Metabolic Acidosis

pH < 7.35 CO2 Normal HCO3 < 22

Metabolic Alkalosis

pH >7.45 CO2 Normal HCO3 > 28

Normal VBG

pH 7.31 – 7.41 CO2 42 – 51 PO2 35 – 49 HCO3 18 – 26 Base + or -2

Normal CBG

pH 7.35 – 7.45 CO2 35 - 45 PO2 40 - 60 HCO3 18 - 26 Base + or -2

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R espiratory O pposite M etabolic E qual

1. The first step in analyzing ABGs is to look at the pH. If blood pH falls below 7.35 it is acidic. If pH raises above 7.45, it is alkalotic. If it falls into the normal range, note what side of 7.4 it falls. Lower than 7.4 is normal/acidic, higher than 7.4 is normal/alkalotic.

2. The second step is to examine the pCO2. Normal pCO2 levels are 35-45mmHg. Below 35 is alkalotic, above 45 is acidic.

3. The third step is to look at the HCO3 level. A normal HCO3 level is 22-26 mEq/L. If the HCO3 is below 22, the patient is acidotic. If the HCO3 is above 26, the patient is alkalotic.

4. Next match either the pCO2 or the HCO3 with the pH to deter mine the acid-base disorder. For example, if the pH is acidotic, and the CO2 is acidotic, then the acid- base disturbance is being caused by the respiratory system. It is respire- tory acidosis. However, if the pH is alkalotic and the HCO3 is alkalotic, the acid-base disturbance is being caused by the metabolic (or renal) system. Then it is metabolic alkalosis.

5. Does either the CO2 or HCO3 go in the opposite direction of the pH? If so, there is compensation by that system. Example, the pH is acidotic, the CO2 is acidotic, and the HCO3 is alkalotic. The CO2 matches the pH making the primary acid-base disorder respiratory acidosis. The HCO3 is opposite of the pH and would be evidence of compensation from the metabolic system. 6. Finally, evaluate the PaO2 and O2 sat. If they are below limits there is evidence of hypoxemia.

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Chest Tubes Room Preparation

2 Suction Setups 1extra suction tubing 2 Kelly Clamps Xeroform gauze (some physician do not use!)

Foam Tape (Only to tape suction tubing connection) Large Transparent Dressing (Tegaderm) Atrium Dry (Infant/Peds max volume is 200ml)

For older child Adult Atrium Dry

Chest Tube Placement Signed Consent Universal Protocol Sedation As Ordered All equipment

Equipment Needed Thoracotomy or Thoracentesis Tray Thalquick OR Trocar Chest Tubes Atrium Drainage System (Adult/NEO as needed) 2 Kelly Clamps with rubber tips Xeroform Gauze/Tegaderm Sterile Gloves, Gown, Towels Sutures (3.0 silk) Suction should be set at 80 mmHg or higher

Double Suction with tubing and connectors in pt room

For an instructional video visit the following website: http://www.atriummed.com/ and click to the education area drainage

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Chest Tube Assessment STOP S = Site Check for subcutaneous air Bilateral breath sounds Dressing free of drainage and occlusive

T =Tubing Should be secured to chest to prevent pulling No dependent loops Should not be clamped All connections secured and taped

O = Output Monitor drainage (if greater than 50ml/hr call MD) Continuous bubbling in the bottom of the water seal air leak monitor

can confirm a persistent air leak Water seal is a window to the pleural space (see below) Air leak meter (1-5) provides a way to “measure the leak over time

—getting better or worse.

P = Patient Water seal chamber (WSC) @ 2cm (add Sterile water PRN) Drainage in tube & WSC should fluctuate as pt inhales/exhales To confirm that your patient’s catheter is patent, turn suction off

and check for oscillation of the patient pressure float ball in the water seal column coinciding with patient respiration

Water Seal Chamber

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Notes

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Notes

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Notes

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Cardiovascular

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Cardiogenic Shock Cardiogenic shock is a major, and frequently fatal, complication of a variety of acute and chronic disorders that impair the ability of the heart to maintain adequate tissue perfusion The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Hemody-namic criteria for cardiogenic shock are sustained hypotension (systolic blood pressure <90 mm Hg for at least 30 min) and a re-duced cardiac index (<2.2 L/min/m2) in the presence of elevated pul-monary capillary occlusion pressure (>15 mm Hg). Disorders that can result in the acute deterioration of cardiac func-tion and can lead to cardiogenic shock include MI or myocardial ischemia, acute myocarditis, sustained arrhythmia, acute valvular catastrophe, and decompensation of end-stage cardiomyopathy .

Systemic perfusion is compromised by decreased cardiac output, with tissue hypoperfusion intensifying anaerobic metabolism and instigating the formation of lactic acid, which further deteriorates the systolic performance of the myocardium. All forms of shock are characterized by inadequate perfusion to meet the metabolic de-mands of the tissues. Treatment: Initial management includes airway stabilization and fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Correction of electrolyte and acid-base abnormalities, such as hypokalemia, hypomagnesemia, and acidosis, are essential Patients with MI or acute coronary syndrome are given aspirin and heparin

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Cardiomyopathies Cardiomyopathies are conditions in which the normal muscular function of the myocardium has been altered by specific or multiple etiologies, with varying degrees of physiologic compensation for that malfunction. Cardiomyopathies have multiple etiologies but all cardiomyopathies eventually lead to decreased cardiac output (CHF) for different reasons.

Hypertrophic Hypertrophic cardiomyopathy (HCM) is associated with thickening of the heart muscle, most commonly at the septum between the ven-tricles, below the aortic valve. This leads to stiffening of the walls of the heart and abnormal aortic and mitral heart valve function, both of which may impede normal blood flow out of the heart. Hypertrophic cardiomyopathy is a genetic disorder Treatment of HCM depends on whether there is narrowing in the outflow tract; how the heart is functioning; and if arrhythmias are present. Treatment is aimed at preventing symptoms and complica-tions and includes surgeries and medications: Surgeries: Left ventricular myomectomy, mitral valve replacement, pacemaker, Implantable cardioverter defibrillator (ICD), catheter septal ablation Medications: Beta blockers (lopressor), antiarrhythmics (Amiodarone, inderal, etc), Calcium channel blockers (Verapamil), Natriuretic peptides (Natrecor)

Dilated Dilated cardiomyopathy (DCM) is a condition in which the heart's ability to pump blood is decreased because the left ventricle, is enlarged and weakened; this causes a decreased ejection fraction. In some cases, it prevents the heart from relaxing and filling with blood as it should. Over time, it can affect the other heart chambers as well. The enlargement of the remaining heart chambers is primarily due to left ventricular failure, but it may be secondary to the primary cardiomyopathic process.

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At the CNS level, decreased cardiac output with resultant reductions in organ perfusion results in neurohormonal activation, including stimulation of adrenergic nervous system and the renin angiotensin aldosterone system. Unfortunately, initially compensatory mecha-nisms ultimately lead to further disease progression. Viral myocarditis is an important entity within the category of infec-

tious dilated cardiomyopathy. Viral myocarditis can produce variable degrees of illness, ranging from focal disease to diffuse pancarditis involving myocardium, pericardium, and valve structures. Viral myocarditis is usually a self-limited, acute-to-subacute disease of the heart muscle that most often leads to the dilated type of cardiomyopathy Treatment of DCM is aimed at correcting the cause of the condition wherever possible. Another major goal is to decrease the heart size and decrease hormones in the bloodstream that enlarge the heart and ultimately lead to worsened symptoms. Medications include ACE inhibitors, Beta blockers, Aldosterone antagonist (Spironolactone), Cardiac Glycosides (Digoxin), Diuretics, Antiarrhythmics, Vasodila-tors, Angiotensin II receptor blockers (Diovan), Inotropes (Milrinone), Anticoagulants, Human BNP (Natrecor)

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Restrictive Restrictive cardiomyopathy (RCM) is a rare disease of the myocar-dium and is the least-encountered form of cardiomyopathy (5%) RCM is a myocardial disease characterized by restrictive filling and reduced diastolic volume of either or both ventricles with normal or near-normal systolic function and wall thickness. Patients typically have diastolic heart failure, meaning systolic func-tion is normal, but the left ventricle has increased diastolic stiffness (reduced compliance) and cannot fill adequately at normal diastolic pressures, leading to a reduction in cardiac output due to reduced left ventricular filling volume. When pressure tracings are taken at this point, they show a characteristic diastolic dip and a plateau or a square-root sign. Some patients may have complete heart block due to fibrosis encasing the sinoatrial or the atrioventricular nodes RCM is caused by various etiologies including: heart muscle disease (Loeffler endomyocarditis), post heart transplant, malignancy, idio-pathic, amyloidosis, etc Treatment current therapy consists predominately of low-dose diu-retics to lower the preload. Small initial doses should be adminis-tered to avoid hypotension because these patients are frequently ex-tremely sensitive to alterations in left ventricular volume.

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VASOACTIVE AND CARDIAC DRUGS

Adenosine Slows conduction through AV node, depresses SA node automaticity. Used to convert SVT

Amiodarone Anitarrhythmic agent that inhibits adrenergic stimulation. Decreases AV conduction and sinus node function: has vasodilatory and negative inotropic effects.

Digoxin Inhibits Na/K+ ATPase, providing calcium for con-tractile proteins of cardiac muscle. Used for ven-tricular failure, tachyarrhythmias

Dobutamine Acts on Beta1 receptors, positive inotrope (Increases contractility), increases coronary blood flow, and HR. Used to improve cardiac output.

Dopamine Low doses act on dopaminergic receptors causing selective vasodilatation of renal and mesenteric vessels Middle range doses act on Beta1 receptors caus-ing positive inotropy High doses acts on alpha1 receptors to constrict blood vessels and thus increase cardiac output. Used for hypotension, improve perfusion.

Epinephrine Catecholamine- reacts with both α- and β-adrenoreceptors Low doses- beta2 receptors, can cause vasodila-tation and bronchodilation High dose– alpha1 receptors, causes vasocon-striction Used for cardiac arrest, hypotension, acute asthma attacks, low cardiac output and anaphylaxis.

Milrinone Acts on both Beta1 and Beta2 receptors. Positive inotropic effect. Causes relaxation of vascular muscle and vasodilatation of end capillaries

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Norepinephrine Catecholamine, affects both alpha1 and be-ta1 adrenergic receptors in cardiac tissue, causing constriction of blood vessels, in-creased contractility of the heart, and in-creased coronary blood flow. Used for hy-potension

Procainamide

Vasopressin Endogenous hormone released by the pituitary in response to increases in plasma osmolarity or as a baroreflex in response to decreased blood pressure and or blood volume. Causes vasoconstriction. Used for hypotension, diabetes insipidus.

Receptors

Alpha α1 in smooth muscle of vasculature (constricts)

α2 in brain (pre-synaptic axons)

Beta β1 in heart and kidneys β2 in lungs and smooth muscle of vasculature (relaxes) β3 in fat cells Dopaminergic 5 subtypes; Located throughout the body including: Pulmonary artery, renal nephron, smooth muscle of most organ vascu-lature

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AGE LOW HIGH Infant (Birth - 1 yr) 100 160

Toddler (1-3 yr) 90 150

Preschooler 80 140

School-age 70 120

Adolescent 60 100

Age Average Normal Range

Newborn 80/46 96/62 - 64/30

1-11 months 80/60 118/70 - 60/50

1 year 96/66 126/91 - 66/41

2 years 99/64 124/89 - 74/39

3 years 100/65 125/88 - 75/42

4 years 99/65 119/85 - 79/45

5-6 years 94/55 108/64 - 80/46

6-7 years 100/56 115/64 - 85/48

8-9 years 105/57 121/66 - 89/48

10-11 years 107/57 123/66 - 91/48

Pediatric Pulse Rates

Pediatric Blood

Pressure

35

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diti

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eatm

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36

Shock State

HR

BP CVP PCWP PAP COCI

SVR

Hypovolemic ↑ ↓ ↓ ↔/↓ ↓ ↓ ↑ Cardiogenic ↑ ↔/↑ ↔/↑ ↑ ↑ ↓ ↔/↑

Septic ↑ ↓ ↔/↓ ↔ ↔ ↑ ↓ Neurogenic ↓ ↓ ↔ ↔ ↔ ↓ ↓

Anaphylactic ↑

↓

↔/↑ then ↓

↔

↔

↓

↑

Hemodynamics in Shock States

How cardiogenic shock leads to cardiomyopathy and pulmonary edema

37

Dru

gs

CO

HR

MA

P SV

R PV

R PC

WP

CVP

Dob

utam

ine

↑ ↑

↔

↓ ↓

↓ ↓

(< 6

mcg

) D

opam

ine

(> 6

mcg

)

↑ ↑

↑

↑ ↑

↑↑

↑ ↑↑ ↔

↑ ↑ ↑↑

↑ ↑↑

Epin

ephr

ine

↑ ↑

↑ ↑↑

↑

↑ ↑

(< 5

0mcg

) N

itro

glyc

erin

(>

50m

cg)

↔

↑ ↔

↑ ↔

↓

↔

↓ ↔

↓ ↓

↓ ↓

↓

Nip

ride

↑

↑ ↓

↓↓

↓ ↓

↓

Levo

phed

(nor

epi)

↑ ↔

↑

↑↑

↑ ↑

↑

Milr

inon

e ↑

↔/↑

↔

↓↓

↓

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CV D

rug

Effe

cts

on H

emod

ynam

ics

38

Cardiac Conduction System SinoAtrial (SA) node is pacemaker Action potential is generated through sodium potassium pump Electrical signal travels fro SA node across atria to AtrioVentricular (AV) node-> Through Bundle of HIS-> Left and Right Bundle branches-> Purkinje fibers eliciting ventricle to contract

Reading EKGs EKG strips should be printed and interpreted at minimum of once per shift or any change noted.

Measurements should include: rate, PR interval, QRS Name rhythm Sign your name Pay attention to ST segment (elevation or depression and T wave (peaked or inverted.

39

Notes

____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

40

Notes

____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

41

Neurology

42

Your brain uses 20% of the oxygen that enters your blood-stream. The brain only makes up about 2% of our body mass, yet consumes more oxygen than any other organ in the body, making it extremely susceptible to damage related to oxygen deprivation. The brain itself cannot feel pain. While the brain might be the pain center when you cut your finger or burn yourself, the brain itself does not have pain receptors and cannot feel pain. 80% of the brain is water.

The cranial vault is the space in the skull occupied by the brain; it contains brain tissue, blood and CSF Monroe Kellie Doctrine- A change in one part means that the other parts must change, otherwise intracranial pressure will rise. The body will auto-regulate to a point by decreas-ing production of CSF and low-ering blood pressure.

43

The Cerebrum has two hemispheres (left and right) four lobes, four ventricles filled with CSF, the corpus callosum connects the hemispheres The hypothalamus, thalamus and pituitary gland are important hormone production centers in the cerebrum.

The cerebellum (Latin for little brain) plays an important role in motor control. The cerebel-lum does not initiate move-ment, but it contributes to coor-dination, precision, and accu-rate timing. The Meninges-Both the spinal cord and brain are covered in three continuous sheets of connective tissue, dura mater, arachnoid, pia mater

45

Tips for Treating Increased ICP

Edema causing increased ICP from trauma usu-ally peaks at 48-72 hours

Keep the HOB elevated at 30 degrees

Keep head midline to promote CSF and Blood flow and drainage

Quiet environment/ minimal stimulation

Sedation– ensure adequate sedation

BP support-may need to give vasopressors

Medications:

Mannitol

3% Saline

Pentobarb

46

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

ADH is secreted without a physiologic stimulus Can occur with injury or inflammation to the pituitary gland as

occurs with meningitis or trauma ADH increases the permeability of the renal collecting ducts

to water , free water is retained, urine volume is reduced and urine concentrations increased

1. Increased urine Osmolality 2. Increased urine sodium concentration 3. Decreased serum Osmolality 4. Decreased sodium concentration

Clinical Signs: Lethargy Stupor Seizure Coma Urine output decreased

Lab Values Low serum Osmolality <250 Increased extracellular fluid volume Excessive water retention by kidneys Decreased sodium <135 Urine Osmolality >286 Urine Sodium >25

Treatment Restrict fluid 30-70% maintenance, Serum sodium should

rise in response to fluid restriction Loop diuretics may be used to assist in the excretion of free

water in cases of serve hyponatremia

47

Comparison of DI vs SIADH

DI SIADH Serum Sodium >145 meq/l < 135 meq/l

Urine Sodium < 30 meq/l > 30 meq/l

Serum Osmolality

> 300 mOsm/kg

< 280 mOsm/kg

Urine Specific Gravity

< 1.005 > 1.020

Urine Output High Low

Central Venous Pressure

Low

High

Weight Decreased Increased

48

Diabetes Insipidus

Result of decreased production of vasopressin Can occur in patients with head injuries, CNS inflammation,

and hemorrhage Must always be looking for DI in post-op neurology patients ADH is not synthesized therefore the renal collection ducts

are impermeable to water, free water is not absorbed from the collecting tubules, large amounts of water are lost in the urine, intravascular volume depletes, and hemoconcentration develops

1. Intravascular volume lost 2. Increased aldosterone production 3. Increased sodium retention 4. Increased serum sodium 5. Increased serum Osmolality 6. Decreased urine specific gravity < 1.005 7. Decreased urine Osmolality

Clinical Signs: Polyuria Polydipsia Increased urine output Dehydration

Lab Values Increased serum Osmolality >286 Urine specific gravity <1.005 Increased sodium >145 Dehydration

Treatment Support intravascular volume Replace urinary output and losses of electrolytes Administer ADH (Vasopressin or DDAVP)

49

Neurological Monitoring

Why is MAP important (It reflects the hemodynamic perfusion pressure of the

vital organs MAP (mean arterial pressure): (2 X DBP) + SBP

3

Newborn 0.7-1.5 mmHg

Infants 1.5-6 mmHg

Children 3.0-7.5 mmHg

Adult Less than 10 mmHg

Normal ICP for different age groups

Clinical formulas for calculation of SBP and MAP (mm Hg) in normal children are as follows:

SBP (5th percentile at 50th height percentile) = 2 x age in years + 65 MAP (5th percentile at 50th height percentile) = 1.5 x age in years + 40 MAP (50th percentile at 50th height percentile) = 1.5 x age in years + 55

50

Intracranial Pressure Monitoring Helpful Hints

The Foramen Monroe or lateral ventricles are used as the zero reference point

Anatomic location of the zero reference point is usually between the external auditory meatus and the outer canthus of the eye

Normal CSF flow is usually 3 to 5ml/hr in an infant, 5 to 10ml/hr in a toddler or child and 10 to 15ml/hr in an adolescent

CSF should be clear and colorless If your patient’s CSF drainage has stopped, lower the collec-

tion bag until you see some drainage, to verify patency of the system

Cerebral perfusion pressure (CPP) is calculated by the following equation:

CPP = MAP - ICP Normal CCP in the neonate is unknown The child’s CPP should be greater than 60 mmHg

A physician’s order is required to clamp/unclamp an EVD Monitor the patient with an EVD for S/S of increased ICP

Headache Vomiting Irritability Lethargy ↓ LOC Nuchal rigidity Bulging Anterior Fontanel

51

Various Drain Tip Placements

Troubleshooting EVD’s Stopcock OPEN to Drain: NOTE check all stopcocks after zero Position drainage unit HIGHER than the pt ICP (mmHg) ICP measurement accurate when the stopcock CLOSED to drain Check for patency: lower drainage chamber below patient’s head ICP Waveform: should be crisp and correspond to changes in

heart rhythm. A flat waveform suggests that the catheter is not patent

To ensure an ↑ICP is accurate observe the patient for: headache, vomiting, irritability. LATE signs include: brady-cardia, hypertension, change in pupils, etc.

Must have order from neurosurgery to flush for patency. Only flush AWAY from the patient.

Mannitol can be used for ↑ICP

52

Lost Waveform √ All connections are tight √ No Kinks √ Transducer level is accurate √ Stopcocks positioned

53

Bedside Checklist EVDs √ Pressure Waveform √ CSF drainage amt, clear, color √ EVD for patency √ Clamps (clamped/unclamped?) √ Patient’s position √ All aspects of drain from head to bag are tight √ If cylinder is at the prescribed reference level √ Document the reference level

Glasgow Coma Scale Activity Score Infant/Children Adult

Eye Opening

4 3 2 1

Spontaneous To Speech To Pain No Response

Spontaneous To verbal stimuli To Pain No Response

Verbal 5 4 3 2 1

Coos Babbles Irritable Cries Cries to Pain Moans to Pain No Response

Oriented Confused Inappropriate Words Incomprehensible sounds No Response

Motor 6 5 4 3 2 1

Normal Movements Withdraws to Touch Withdraws from Pain Abnormal Flexion Abnormal Extension No Response

Obeys Commands Localizes Pain Withdraws from Pain Abnormal Flexion Abnormal Extension No Response

Any combination score of < 8 = Significant risk of mortality

54

Collecting CSF Fluid Sample

WITH A PHYSICIAN ORDER; THE RN WILL OBTAIN 2 ML OF CSF FROM THE VENTRICULAR CATHETER. DAILY CSF SAMPLES ARE OBTAINED BY THE NIGHT SHIFT (05:00) EQUIPMENT NEEDED: 3 BETADINE SWABS 3 ML SYRINGE MASK STERILE GLOVES, TOWEL, COLLECTION TUBE PROCEDURE: Verify Order and Patient – Explain procedure to family

ASSEMBLE EQUIPMENT Don Mask Place syringe & CSF Collecting tube on sterile towel Open Betadine Swabs Close the WHITE clamp proximal to the BLUE port Open the catheter to drain position on the stopcock Don Clean Gloves Clean the BLUE port w/ Betadine swabs Place the tubing on the sterile towel DON Sterile Gloves and affix the 3ml syringe to the blue port SLOWLY ASPIRATE 2ML of CSF fluid Remove the syringe and place the fluid in the collecting tube Open the WHITE CLAMP and turn the stopcock to original position LABEL TUBE AND SEND TO LAB WITH COPY OF ORDER AND LAB SLIP

BP ↓ ↑

Pulse ↑ ↓

Respiratory Rate ↑ ↓

Temperature ↓ ↑

Pulse Pressure ↓ ↑

LOC ↓ ↓

Shock VS ↑ ICP

55

Cerebrospinal Fluid (CSF) Analysis Bacterial Meningitis

Glucose Normal to marked decrease <40 mg/dL

Protein (Marked Increase) >250mg/dL

WBCs >500 (usually >1000) Early May be <100

Cell differential Predominance of Neutrophils (PMNs)

Culture Positive

Opening Pressure Elevated

Viral Meningitis Glucose Normal (>40 mg/dL)

Protein <100 mg/dl (moderate increase)

WBCs <100 cells/uL

Cell differential Early: Neutrophils. Late: Lymphocytes

Culture Negative

Opening Pressure Usually Normal

Fungal Meningitis Glucose < 40 mg/dL (Low)

Protein (Moderate to Marked increase) 25-500mg/dL

WBCs Variable (10-1000 cells/uL) < 500 cells/uL

Cell differential Predominance of Lymphocytes

Culture Positive (fungal)

Opening Pressure Variable

56

Meningitis Meningitis is an inflammation of the membranes that cover the brain and spinal cord. Bacterial meningitis is rare, but is usually serious and can be life-threatening if it's not treated right away. It is highly infectious and pa-tients should be placed on droplet isolation. Viral meningitis (also called aseptic meningitis) is relatively common and far less serious. It often remains undiagnosed because its symp-toms can be similar to those of the common flu. Can be divided into three categories based on symptoms: Acute-symptom onset less than 1 day Subacute– symptom onset 1-7 days Chronic– symptom onset greater than 7 days Acute meningitis is almost always a bacterial infection caused by one of several organisms. Neonates - Group B or D streptococci, nongroup B streptococci,

Escherichia coli, Listeria monocytogenes and Klebsiella 1-23 months-H influenzae , S pneumoniae, N meningitides and E.

Coli Greater than 23 months-S pneumoniae, H influenzae, N meningiti-

des Endotoxic shock with vascular collapse (meningococcemia) is charac-teristic of severe Nisseria meningitidis infection. Nisseria is treated with Ceftriaxone

Meningitis Complications:

Obstructive Hydrocephalus Cerebral abcesses Seizures-status epilepticus SIADH (Syndrome of Inappropriate AntiDiuretic Hormone) DI (Diabetes Insipidus)

57

Notes

____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

58

Renal

59

Renal Anatomy The kidneys take their blood supply directly from the aorta via the renal arteries Blood is returned to the inferior vena cava via the renal veins. The kidney has two regions: the cortex and the medulla. The cortex and the medulla are made up of nephrons; these are the functional units of the kidney, and each kidney contains about 1.3 mil-lion of them.

Functions of the Kidney Stimulation of bone marrow erythrocyte production Elimination of drugs toxins and metabolic wastes filters the blood of its small molecules and ions reclaims the needed amounts of useful materials Surplus or waste molecules and ions are left to flow out as urine Through reabsorption and secretion of several :substances the kidneys function to maintain: Electrolyte Balance Acid Base Balance Water and Sodium Balance

60

ESRD •Chronic kidney disease is the slow loss of kidney function over time •The loss of function usually takes months or years to occur. It may be so slow that symptoms do not appear until kidney function is less than one-tenth of normal. •The final stage of chronic kidney disease is called end-stage renal dis-ease (ESRD) •At this stage, the patient needs dialysis or a kidney transplant •Common causes of pediatric ESRD: Polycystic Kidneys and Nephrotic Syndrome Polycystic kidneys Polycystic kidney disease is a genetic kidney disorder in which many clusters of cysts form in the kidneys. These cysts are filled with fluid. And can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure Nephrotic syndrome Nephrotic syndrome is a group of symptoms that include protein in the urine, low blood protein levels, high cholesterol levels, high triglyceride levels, and swelling. Nephrotic syndrome is caused by different disor-ders that damage the kidneys including glomerulonephritis. In children, it is most common between ages 2 and 6

61

Func

tions

of

the

kidn

ey

Fun

ctio

n

Dys

func

tion

Sal

t, w

ater

and

aci

d ba

se b

alan

ce

Na

K

H

CO

3

Mg

Pho

s

Hyp

onat

rem

ia a

nd f

luid

ret

entio

n, C

HF,

HT

N

Hyp

erka

lem

ia

Met

abol

ic a

cido

sis

Hyp

erm

agne

smia

H

yper

phos

phat

emia

Exc

retio

n of

nitr

ogen

end

pro

duct

s U

rea

Cre

atin

ine

U

ric A

cid

A

min

es

Gua

nadi

ne d

eriv

ativ

es

Ano

rexi

a, n

ause

a, p

rurit

is,

peric

ardi

tis,

poly

neur

o-pa

thy,

enc

epha

lopa

thy,

thro

mbo

cyto

path

y

End

ocrin

e-M

etab

olic

C

onve

rsio

n of

vita

min

D to

ac-

tive

met

abol

ite

prod

uctio

n of

ery

thro

poie

tin

reni

n

Ost

eom

alac

ia,

oste

odys

trop

hy

Ane

mia

H

yper

tens

ion

62

Continuous Renal Replacement CRRT is a continuous 24 hour a day ongoing treatment where

blood is removed from the body through a catheter and is circulated through a filter with a semi-permeable membrane

Filter contains 8,000 hollow strands per filter; blood is pushed inside these hollow tubes while dialysate flows around them

Semi-permeable membrane allows certain sized molecules through and bigger molecules cannot go through

Using the patient’s own blood pressure or a pump, fluids and sol-utes such as electrolytes, BUN, and creatinine are filtered and re-moved.

The filtered blood is then returned to the patient through a catheter in a vein

This therapy can be used in patients with acute renal failure, pulmo-nary edema, cerebral edema, sepsis, post transplant. ATN, burns, CHF, rhabdomyolysis, ARDS, hyper-catabolic states.

Advantages of CCRT Effective management of fluid balance Adequate uremic toxin removal Correction/maintenance of electrolyte abnormalities Facilitations of nutrition management Gentle continuous treatment over 24 hours Disadvantages of CRRT Increased potential for bleeding due to the need for prolonged co-

agulation

AKA SCUF– Slow Continuous Ultrafiltration CVVH– Continuous Veno-Venous Hemofiltration CVVHD– Continuous Veno-Venous HemoDialysis CVVHDF– Continuous Veno-Venous HemoDiaFiltration

63

C

entr

al V

enou

s C

ath

e-te

rs

Art

erio

veno

us G

raft

s

A

rter

iove

nous

Fis

tula

e

Imm

edia

te u

sab

ility

Usa

ble

as

soon

as

two

to

thre

e w

eeks

Take

s m

inim

um f

our

to s

ix

wee

ks to

ma

ture

Hig

h m

alf

unct

ion

rate

s

Re

liab

le b

lood

flo

w

rate

s O

ptim

al b

lood

flo

w

rate

s

Hig

h m

orb

idity

due

to

infe

ctio

n ra

tes

Mod

era

te in

fect

ion

Low

est in

fect

ion

rate

Nee

dle

-les

s a

cces

s

Lo

w p

rim

ary

/ hi

gh

sec-

ond

ary

fa

ilure

H

ighe

st lo

ng-t

erm

p

ate

ncy

rate

No

hem

odyn

am

ic e

ffec

ts

H

igh

sten

osis

/ th

rom

bos

is

risk

Pote

ntia

l ad

vers

e he

mo-

dyna

mic

eff

ects

64

CRRT Transport Mechanisms Ultrafiltration– (squeezing a wet rag) movement of fluid through a semi-permeable membrane; goes with pres-sure gradient

Diffusion- (tea bag effect) movement of solutes from area of higher concentration to area of lower concentration; solutes in dialysate Convection- (waves pulling shells off beach) movement of solutes with water flow aka “slvent drag”; the more fluid moved through a semi-permeable membrane, the more solutes are removed.

65

Semi-Permeable Membrane

66

Notes

____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

68

DIC is a serious bleeding disorder. It is a complication of an un-derlying disorder or injury that causes the normal blood-clotting mechanism to malfunction.

Etiology: Not a disease, but rather an abnormal response to the normal clotting cascade stimulation by another disease process or disorder.

Definitions: Acute: Develops within hours to days after an initial assault to

the body system Subacute: May not be apparent initially, but may fulminate as

the clinical course progresses Chronic: May persist in a suppressed state until a coagulation

defect intensifies

Etiology of Acute DIC: Introduction of tissue factors into the circulation

Tissue necrosis, crush injury, fat embolism, amniotic fluid, etc Damage to vascular endothelium

Bacterial Sepsis, Aneurysm, Sickle cell, major surgery, etc Stagnant blood flow

Shock, acidosis, cardiac arrest, etc. Infectious agents

Bacterial diseases, viral diseases, parasitic infections

Etiology of Subacute DIC: Malignant disease

Acute leukemia, Metastatic Cancer Obstetric

Retained dead fetus

Etiology of Chronic DIC Liver Disease Systemic Lupus Erythematosus (SLE) Localized malignancy

Disseminated Intravascular Coagulation

69

Pathophysiology of DIC A massive activation of the clotting cascade triggered by

rapid accumulation of thrombin leads to… Production of large amounts of fibrin leads to.. Deposits of fibrin in the microcirculation leads to… Thrombi formation throughout the capillary system Thrombi activates the fibrinolytic pathway to dissolve the

fibrin clots Rapid accumulation of fibrin clots in the capillary system

quickly depletes the body’s supply of available platelets and coagulation factors

Results in generalized bleeding The hyperactive fibrinolytic mechanism works at maximum

speed to dissolve the clots by splitting them into “fibrin spilt products”

Normally cleared by the RES Contribute to the uncontrolled bleeding because of antico-

agulant properties deplete clotting factors Summary: Widespread occlusion in the microcirculation Tissue hypoxia, hypovolemia, uncontrolled bleeding Clinical Manifestations: Petechial rash, Bleeding with no previous history or obvious

cause Nonspecific manifestations: Weakness, malaise, fever

Subjective Data History of recent illness, surgeries, & past medical condition Changes in mentation, visual impairment, headache Localized pain in abdomen, back, joints, or muscle Nausea and vomiting Sudden Dyspnea, feeling of anxiety

Assessment with Diagnosis of DIC

70

Objective Data Neurologic System: Altered mentation, ptosis, asymmetric alignment, papillary response, Visual impairment, altered sensory/motor function Skin: Petechiae, diffused ecchymosis, necrosis over digits, nose, genitals Oozing from mucosal membranes, orifices puncture sites or incisions Cardiovascular System: ↓BP, CVP and MAP, Changes in car-diac rate/rhythm, Weak, thread pulses, peripheral edema Respiratory System: Dyspnea, tachypnea, crackles, hemoptysis, hypoxemia, absence of ventilated areas GI System: GI bleeding, absence of bowel sounds

Labs: elevated PT, PTT, FSP, WBC, glucose; possible ele-vated BUN, creatinine; Possible elevated liver enzymes

Assessment with Diagnosis of DIC

Management of DIC

Early Recognition Treat cause Chronic DIC may require no treatment

Supportive Care Blood products Anticoagulation therapy

Nursing Diagnosis

Altered tissue perfusion related to bleeding and dimin-ished blood flow

Risk for fluid volume deficit related to bleeding impaired gas exchange Pain related to bleeding into tissues & diagnostic tests Anxiety related to fear of the unknown Potential for injury related to bleeding

71

Platelets <100,000

Fibrinogen Reduced

Thrombin Time Prolonged: Defect in rate of fibrin formation

PT & PTT Prolonged: Lack of enzyme converting fibrinogen into fibrin

FSP”s Increased

D– Dimers Elevated: Confirm previous formation and breakdown of clots

Diagnosis of DIC

Nursing Therapeutic Care Assist physician with intubation and line placement Monitor respiratory & cardiovascular status. ABG’s, vital

signs, capillary refill time, administer fluids/blood prod-ucts as ordered

All patients need foley, NG, arterial line Monitor for bleeding: Bleeding precautions Maintain adequate cardiac output with fluid boluses,

PRBCs, FFP, Cryoprecpitate, vasopressors Skin care, nutrition

72

Definition: A state characterized by hyperglycemia (Glucose > 250 mg/dl) Acidosis (pH < 7.35) and low serum bicarbonate Pathophysiology: The inabilities of cells to take up and utilize glucose and an in-crease degree of lipolysis and proteolysis. Since the insulin de-rived cells can’t utilize glucose their response is the rapid me-tabolism of protein, which results in the loss of intracellular K+ and phosphorus and excessive liberation of amino acids. The liver converts these acids into urea and glucose, As a result of these processes, blood glucose levels are grossly elevated, The aftermath is increased serum osmolarity and glucosuria leading to osmotic diuresis.

The absolute insulin deficiency causes cells to convert fats into glycerol and fatty acids for energy. The fatty acids can’t be me-tabolized as quickly as they’re released, so they accumulate in the liver, where they’re converted to ketones. (ketoacids). These ketones accumulate in the blood and urine and cause acidosis.

The end result is volume depletion and metabolic acidosis

During DKA beta-hydroxybutyrate is converted to Acetoacetate

RISK FACTORS FOR DEVELOPING DKA Inadequate insulin use Inadequate fluid intake Excess of counter-regulatory hormones Steroid excess eg: Cushing syndrome or steroid therapy Stress secondary to concurrent illness or infection Drugs (sympathomimetics, pentamidine, thiazides, dilantin,

calcium channel blockers)

Diabetic Ketoacidosis

73

Examination Hypotension could be secondary to massive volume deple-

tion or sepsis or precipitating causes of DKA eg. Cardiogenic shock or massive pulmonary embolism

Hyperventilation (Kussmaul breathing) compensatory to blow off excess carbonic acid as water and CO2

The fruity odor of acetone on the breath may only be detect-able by 50% of people

Of acidosis Any altered mental status is variable in degree and does not correlate with the degree

Diagnostic Testing—Blood Work Routine including serum glucose. Electrolytes, CBC,

ketones and may include serum magnesium and phosphate Increased WBC (10,000-40,000 cells/ml) is common in DKA

and only suggests infection if significant left shift with bandemia is present

Blood cultures are indicated in the febrile DKA patient The serum betahydroxybutyrate (BHBT) is the best measure

of the degree of Ketoacidosis. Because it is the predominant serum ketone present, and changes in the serum BHBT can be used to monitor successful treatment of DKA anddeter-mine how long the sugar regulations was uncontrolled.

The urine ketone test may be more sensitive than serum ketone test in early DKA, because acetoacetate is concen-trated in the urine; however, the urine ketone test cannot be used to monitor the successful treatment of DKA

ABG An arterial or venous blood gas is required to determine the

degree of acidosis and the degree of compensatory hypocar-bia

Venous blood gases can be used to follow the course of aci-dosis during therapy of DKA, as it closely parallels the arterial blood gas reading

74

DKA Medical Decision Making and Treatment First focus your attention on stabilizing the patient ABCs Then focus your attention on fluid resuscitation if hemody-

namically unstable with 20ml/kg of isotonic crystalloids until normotensive and electrolyte replacement therapy

Insulin therapy should begin after pt is hemodynamically sta-ble. Fluid deficit replacement should be given over 24 hours added to maintenance to prevent cerebral edema.

Cardiac monitoring for early electrocardiographic evidence of hyperkalemia or hypokalemia

Correction of Potassium deficit: K+ replacement should be started as soon as it is determined

that the patient is urinating and not hyperkalemic A high serum K+(despite total body deficiency) could be due

to the insulin deficit as insulin is required to move K+ from the blood to the cells, Could also be due to the metabolic acido-sis secondary to increased ketoacids, decreased renal perfu-sion and any accompanying tissue catabolism

Expect a precipitous drop in the serum K+ when starting insu-lin therapy (mainly due to insulin mediated re-entry of K+ into cells)

Correction of Hyperglycemia Fluid therapy alone will result in a significant decrease in glu-

cose levels as they are at least partially falsely elevated from dehydration.

Regular insulin is given by constant IV infusion per MD or-ders, typically 0.05units/kg

IV insulin should be given by constant infusion until the acido-sis and ketosis is corrected

Remember , the body needs insulin to carry glucose into the cells for energy production. Without insulin, the body is starv-ing.

The serum glucose should not decrease more than 75-100 mg/dl/hour: to prevent complications such as cerebral edema

75

Correction of Acidosis There is no definite evidence that bicarbonate administration

is therapeutic (even in patient with a severe metabolic acidosis)

Therefore bicarbonate administration should only be given to patients with profound metabolic acidosis (pH <7.0) if the acidosis does not corrects within 1 hour of fluid and insulin therapy

REMEMBER THAT THE END-POINT OF THERAPY IS NOT

THE CORRECTION OF HYPERGLYCEMIA, BUT CORRECTION OF THE KETOACIDOTIC STATE

76

Acute Tumor Lysis Syndrome (ATLS)

Acute tumor lysis syndrome consists of several metabolic consequences of rapid tumor cell breakdown. Initial S&S will start to occur within 48 to 72 hours after chemotherapeutic agents have been initiated. ATLS is most likely to develop in chemo-therapy initiation of untreated newly diagnosed patients with rapid growing tumors such as Burkitts Lymphoma T Cell Leukemia Any bulky lymphomas or leukemia Patients with high initial WBC counts Rapid destruction and lysis of tumor cells causes the release of intracellular contents into circulation including excessive amount of metabolites. These of which are most destructive include: 1. Uric Acid - Hyperuricemia precipitates in the kidneys causing potential renal failure with its complications Clinical Presentation includes: Decreased urinary output Urine pH <7 Renal tubular obstruction Renal Failure Note: A previous history of renal impairment increases the

risk of development of renal failure in association with ATLS

2. Potassium - Hyperkalemia, can cause: Weakness, tingling, and loss of sensation ECG changes, Peaked T waves, increased PR interval, wid-

ening of the QRS complex, and arrhythmias

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3. Phosphate - May precipitate with calcium in the kidney, re-sulting in ionized hypocalcemia. Clinical Signs include:

Tingling, muscle cramping, and carpal pedal spasms or posi-tive Chvostek’s sign (contraction of facial muscles after tapping the facial nerve just anterior to the parotid gland)

Seizures ECG changes, which may include prolonged QT interval or

bradycardia 4. Tissue Thromboplastin - release may precipitate DIC Microscopic or gross bleeding Prolonged mucosal or skin oozing Laboratory abnormalities including thrombocytopenia, pro-

longed PY or PTT, decreased fibrinogen, elevated fibrin deg-radation products (fibrin split products), and anemia

The presence of fibrin monomer is an early indication. This indicates that fibrinogen is being broken down by thrombin and a clot is being formed

Management of ATLS Management of ATLS is prevention; accomplished through the identification of rapid cell breakdown. Some of these include: Initial antineoplastic doses to be adjusted to prevent ex-

tremely rapid cell breakdown Monitoring renal function and electrolytes Aggressive fluid administration (1.5 to 2 times maintenance

fluid requirements) to prevent uric acid crystal formation Closely monitoring urine output. Notify MD if UOP decreases

Allopurinol administration to reduce uric acid production Diuresis to treat decreased UOP Renal replacement therapy or hemodialysis may be required Severe hyperkalemia requires urgent treatment with calcium,

sodium bicarbonate, glucose, and insulin, and sodium poly-styrene sulfonate (kayexalate) enema

Hypocalcemia is treated with calcium administration. This problem will persist as long as hyperphosphatemia continues.

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Tips to care for Oncologic/ Neutropenic Patient

Neutropenia - A hematological disorder characterized by an ab-normally low number of neutrophils. Neutrophils are types of white cells that help to fight off infections. Neutrophils make up approx 50-70% of circulating whit cells. If a patient is neutro-penic they must be put on reverse isolation in order to help pro-tect them against potential infections. Calculate the patients ANC (absolute neutrophils count) in order to determine if the patient is neutropenic

Risk of Infection Mild Neutropenia (1000>= ANC<1500) - minimal risk Moderate Neutropenia (500>=ANC<1000) moderate risk Severe Neutropenia IANC <500) - Severe risk

ANC = (NEUT + BANDS) (WBC) remove decimal from WBC to calculate

Example: Neuts = 14 Bands = 7 WBC = 1.2

ANC = (14 + 7)(1.2)

ANC = (21)(12) = 252 ANC = 252

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Nursing Precautions No IM/SQ injections unless approved by Oncologist No rectal temps or rectal medications unless approved by

Oncologist Call Oncologist for fever DO NOT GIVE Ibuprofen products

for fever Check for mouth sores and assess skin folds and perianal

areas for signs of infection Most important of all, everyone who enters the patient's room

must WASH THEIR HANDS Neutropenic diet and good daily personal hygiene for patient Patient to wear a mask whenever out of the room Dispose of any product that may have come into contact with

body fluids into the yellow chemo waste container for 48 hours after completions of chemotherapy (diapers, gloves, gauze, etc.) Yellow chemo waste container to remain in patient’s room until full. Be familiar with the following Oncologic Emergencies:

Tumor Lysis Syndrome (TLS) DIC Mediastinal Masses Spinal cord compression Typhlitis Superior Vena Cava Syndrome Septic Shock SIADH Anaphylaxis

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Sickle Cell Disease

Normal RBC’s contain HbA. RBC’s in sickle cell have Hbss. When oxygen levels fall, RBC’s with Hbss become crescent shaped and get trapped in small vessels leading to erythrostasis.

Masses of sickled RBC’s occlude blood vessels leading to thrombosis, ischemia, and infarction.

Specific organs involved will have signs of hypoperfusion, vascular occlusion and tissue ischemia.

The body hemolyzes the abnormally structured RBC. Sickled cells may return to normal when blood is more oxygenated but after repeated episodes the cells become more sensitive and may not return to normal shape

Complications Infection is a major cause of morbidity and mortality. The

spleen becomes compromised and this leads to increased susceptibility to infection. S. Pneumoniae is a leading cause of death in the first 3 years of life. CXR will show infiltrates if infection involves pulmonary system. Obtain blood cultures immediately and start antibiotics when an infection is sus-pected.

Acute chest syndrome is caused by vasoocclusion resulting

in painful crisis; associated with infections, thromboembolism, and sickling of RBC’s in the pulmonary vasculature. Vascular occlusion of branches of the pulmonary artery leads to infarc-tion of the lung. The syndrome may be self limiting but can rapidly progress and become massive and fatal. Chronic pat-tern of this will lead to chronic scarring of the lung seen on CXR. Repeated episodes lead to restrictions of vital capacity, pulmonary hypertension, and cor pulmonale. Child will have fever, chest pain and Dyspnea.

81

Vasoocclusive crisis (pain crisis) is one of the most debilitat-

ing problems for pts. with SS disease. It is caused by obstruc-tion of small arterioles by sickled RBC’s, resulting in ischemia of tissues. Frequency, intensity, and severity are variable. Onset may be precipitated by infection, fever, dehydration, trauma, or exposure to cold. May last minutes to weeks. Child will show deep pain at any site, commonly musculoskeletal, extremities, back, chest or abdomen. Will have fever, resp. distress, lethargy and joint swelling. Must hydrate well, pro-vide oxygen and maintain good pain control.

Splenic sequestration crisis is the second most common

cause of morbidity and mortality in the first decade of life. The exact cause is unknown but often is associated with viral ill-nesses and prior sequestration crises. Blood pools in the spleen, further leading to acute splenic enlargement, in-creased anemia, and if severe, signs of hypovolemia leading to shock and death. May treat with oxygen, transfusion and frequent hemoglobin checks.

Cerebrovascular accident (CVA) in younger children is usu-

ally from cerebral thrombosis, and in older children is usually from intracranial bleeding. Child may show hemiparesis, headache, dizziness, lethargy or seizures. Goal is to prevent progression of the CVA. Partial exchange transfusion is used to decrease Hbss level to less than 40%.

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Electrolyte Imbalances Hypokalemia <3.5mEq/l Arrhythmia, drop in diastolic BP,

polyuria, muscle weakness, headache, dizziness, myocardial irritability, diminished reflexes

Hyperkalemia >5.5mEq/l Bradycardia, asystole, muscle weakness, confusion, peaked T waves, flat P waves, V-Fib, nausea

Hyponatremia <120mEq/l Hypotension, headache, tachy-cardia, lethargy, seizures, nausea, vomiting, dry mucous membranes, muscle weakness, weight gain, disorientation

Hypernatremia >150mEq/l Hypertension, rales, tachycardia, oliguria, lethargy, irritability, tremors, flushed skin, hypoten-sion

Hypocalcemia <9mmg/dl Bronchospasm, muscle cramps tremors, tetany, seizures, decreased cardiac output and long QT interval

Hypercalcemia > 10.5 mg/dl Hypertension, anorexia, nau-sea, vomiting, abdominal pain, headache confusion, polydipsia, polyuria, short QT interval

Hypomagnesemia <1.8 mg/dl Dysrhythmias, enhanced digitalis effect, confusion, lethargy, coma, seizures, facial twitching, T wave flattened, ST depressed, Long QT interval

Hypermagnesemia >3mg/dl Bradycardia, apnea, hypoten-sion, muscle weakness, lethargy, peaked T wave

Hypoglycemia <60 Labile, irritable, difficulty focusing, shaky, hunger, shallow respiration, hyperflexia, dilated pupils, con-vulsions, shock coma, sweating, headaches

Hyperglycemia >250 Lethargy, dulled sensorium confused thirst, weakness, nausea, vomiting, abdominal pain, flushed dry mucous membranes. Deep rapid respirations, fruity ace-tone breath, diminished reflexes, paresthia, acidosis and coma

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Notes

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84

NUTRITION IN PEDIATRICS

85

Early EN may promote high gastric residuals: Increasing the risk of aspiration pneumonia Increasing the risk of bacterial colonization of the

stomach Increased incidence of complications

The potential risks associated with EN can be offset with appropriate monitoring and management strategies to avoid complications. The risks of not using the GI tract for nutrition are outweighed by its benefits.

Choice of access dependent on several factors: Expected duration of therapy :

EN < 3 months = temporary means (NG, OG) EN >3 months = permanent means (GT, JT)

Anatomic and functional abnormalities: Known strictures Delayed gastric emptying or severe GER – bypassing the stomach may be necessary

Monitoring/ Maintenance and care: Please see Policy and Procedure: policy number 100.486-1

Enteral Nutrition Intervention

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Infants

Breast milk- expressed maternal or donor milk. Stored in appropriate freezer and labeled appropriately. Label should include Formula Standard (20 cal/oz): Enfamil Lipil, Similac Advance, Gerber Goodstart High calorie standard: Enfamil 24 cal/oz

Soy (20 cal/oz): Gerber Goodstart Soy, Similac Isomil, Enfamil Prosobee Lactose free: Similac Sensitive, Enfamil Gentle Ease

NICU discharge formulas

(22 cal/oz): Enfacare Lipil, Similac Neosure Advance Hydrolyzed protein: Alimentum Advance, Pregestimil (20 and 24 cal RTF):Nutramigen Elemental: Elecare, Neocate (both powder) Renal: Similac PM 60/40 (powder) Chylothorax/ long chain fatty acid deficiency: Enfaport (liquid concentrate) GER: Enfamil AR Specialty high kcals- unless otherwise specified above, cals/oz >20 must be mixed from powder and are not available as RTF

Additives: MCT oil Polycose powder Beneprotein powder

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Children: 1-10 years Standard: Pediasure Enteral Standard with fiber: Pediasure Enteral w/ fiber Hydrolyzed protein: Vital Junior Elemental: Elecare High calorie: Pediasure 1.5 Blenderized: Compleat Pediatric

Children: >10 years (adult formulas) Standard: Osmolite Standard high calorie: Osmolite 1.5 Standard with fiber: Jevity 1 cal Standard with fiber high calorie: Jevity 1.2 or Jevity 1.5 Renal: Nepro Hydrolyzed protein: Vital 1 cal or Vital 1.5 cal Elemental: Elecare, Vivonex RTF Diabetes: Glucerna 1 cal or Glucerna 1.5 cal Acute lung injury/ ARDS/ SIRS: Oxepa

Age in Years Kcal/kg/day

0.5 110

1 98

1-3 102

4-6 90

7-10 70

Male Female

11-14 55 47

15-18 45 40 (subcommittee, 1989: Merch, 2005)

Caloric Requirements for Healthy Children

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Notes

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90

*Pediatric Maintenance Fluid Requirements *(NIH, 2008)

Ex. 5kg infant: maintenance = 500ml/24hr = 21 ml/hr Ex. 15kg child maintenance = 1250m//24hr = 52ml/hr Ex. 25kg child maintenance = 1600ml/24hr = 66 ml/hr

Weight Range 24 hour Maintenance Fluid

Neonate (<72hrs)

60-100 ml/kg/day

0-10kg 100ml/kg/day

11-20kg 1000ml-1st 10kg PLUS 50ml/kg-11-20kg

21-30kg 1500ml-1st 20kg PLUS 20ml/kg for each additional kg over 20kg

Weight Range Hourly Maintenance Fluid Rate

<or = 10 kg 4 ml/kg/hr

11-20 kg 40ml/hr PLUS 2ml/hr for each kg over 10kg

>20kg 60 ml/hr PLUS 1 ml/hr for each kg over 20 kg

Ex. 5kg infant: 20 ml/hr Ex. 15kg child: 50ml/hr Ex. 25kg child: 65 ml/hr

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Hypertonic Solutions - a solution with higher Osmolality than blood serum Solution causes cells to shrink Used in severe symptomatic hyponatremia (very rare) Used as nutrient source (10% dextrose) Examples of solutions: 5% dextrose in 0.45% normal saline;

10% dextrose in water; 3% normal saline

Hypotonic Solutions - a solution with lower Osmolality than blood serum Hydrates cells, causes them to expand Used to correct dehydration Examples of solutions: 0.45% Normal Saline; 0.2% normal

saline; 2.5% dextrose

Isotonic Solutions - a solution with the same Osmolality as blood serum Cells remain unchanged Used for replacement or maintenance (expands extracellular

volume). Especially used to expand circulating (intravascular) volume

Examples of solutions: 5% dextrose in water; 0.9% normal saline (NS); Lactated Ringer’s

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*Sedation Therapy

LORAZEPAM: Benzodiazepine, Hypnotics, Sedative (Other CNS depressants may increase adverse effects)

Oral: Onset 15 -45 min, peak 1- 6 hrs IV: Onset rapid, peak 15 – 20 min

Adverse Effect: Apnea, hypotension, bradycardia, respiratory depression, drowsiness, confusion & dizziness

VERSED: Benzodiazepine, Hypnotic, Sedative Oral: Onset 10 –20 min, peak 30-60 min I.V.: Onset 1-5 min, peak 10 min I.N.: Onset 5 min, peak 10 min

Adverse Effect: CNS and Respiratory depression, hypotension, bradycardia, amnesia, paradoxical excitement, combativeness

FENTANYL: Analgesic, Sedative, Opoid Onset: Almost immediate Duration: 30-60 minutes

Adverse Effect: Skeletal muscle and chest wall rigidity if given to rapidly IV, hypotension, bradycardia, CNS & respiratory depression

MORPHINE: Analgesic, Sedative, Opoid Oral Onset:1 hour, duration 3-5 hrs IV Onset: 20 min, duration 3-5 hrs May be given PO, IV, IM, PR, SQ, Intrathecal

Adverse Effect: CNS depression, Hypotension, Respira-tory Depression, Bronchospasm

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PRECEDEX: Sedative/ alpha 2 agonist Onset: Duration: 2-3 hours

Special care: Not FDA approved for use in pediatrics. Adverse reactions associated with infusions greater than 24 hours in duration include ARDS, respiratory failure, and agitation

KETAMINE: Dissociative/ Anesthetic

Onset: Immediate Duration: 5-10 minutes

Beneficial Effect: causes bronchodilation, may be bene-ficial to asthmatics over other types of sedation Adverse Effect: Hypertension, tachycardia, Emergence Delirium. There is no reversal. Nurses may not push on non-intubated patient Precaution: Concentration is mg/mL, bolus dose in mg/kg, drip is mcg/kg/min

PROPOFOL: Anesthetic

Onset: Almost immediate Duration 5-10 minutes

Adverse Effect: Respiratory depression, hypotension. There is no reversal. Nurses may not push on non-intubated patients. Adverse reactions associated with in-fusions greater than 24 hours in duration include renal impairment and elevated lipids and triglycerides due to medication in lipid base. Precaution: Concentration is mg/mL, bolus dose in mg/kg, drip in mcg/kg/min

**REFER TO LEXICOMP FOR ALL MEDICATIONS**

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Intravenous Gamma Globulin (IVIG) Administration Protocol

General Information IVIG - is a purified preparation of human antibodies adminis-

tered intravenously to provide protection to people whose immune systems do not make enough antibodies or make antibodies that do not work properly.

There is a major shortage of IVIG because demand in-creased and supply decreased.

Clinical Indications for Use– IVIG is sometimes used in the fol-lowing diseases related to immunologic dysfunctions:

Advanced HIV infection Bone Marrow Transplant HIV-associated thrombocytopenia Idiopathic thrombocytopenia purpura (ITP) Kawasaki disease Prevention of sepsis in premature neonates Primary immunodeficiency

Before IVIG Administration General Information

DO NOT administer IVIG two hrs post blood transfusion DO NOT shake IV bag containing globulins *****HANDLE WITH CARE*****

Assessment Assess prior IVIG use and previous reaction to IVIG Assess if patient received live vaccination in the last 3

months (MMR and Varicella). Notify MD if any Assess if patient is IgA deficient. If so, patient should receive

products with low concentrations of IgA (Polygam and Gam-magard are both contraindicated

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Interventions Record baseline vital signs Have Oxygen, suction, and code cart readily available in an

event of anaphylactic reaction Administer pre-medication (per FHFC protocol) 30 minutes to

1 hour prior to IVIG infusion, if ordered IVIG ADMINISTRATION General Information

DO NOT MIX WITH ANY OTHER MEDICATION Infuse through a separate line. May flush primary line before

and after IVIG administration with D5W or NS (except Gamimmune, use D5W only)

Administration (Per FHFC Protocol)

Vital Signs During IVIG Infusion Assess for changes in vital signs, & symptoms of adverse reaction

Intervention Decrease IVIG administration rate by half, and call MD for thera-peutic interventions if patient experiences: Headache Nausea Chest tightness Sweating Fever Vomiting Palpitations Dizziness Flushing Chills Itching Rash Joint/muscle/Back Pain Irritation at needle site Notify MD STAT and stop IVIG infusion if patient experiences: Drop in BP equal to & over 20% of baseline and/or shortness of breath, Dyspnea, Wheezing, Sneezing, and Hives

First Hour Every 15 minutes

After every dose change Every 15-30 minutes

After Last dose change Every 1 hour until complete

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Drugs and Solutions – Filter Prior to Administration

Amphotericin B lipid Complex(abelcet)

5 micron filter needle

Amphotericin B liposome(Ambisome)

5 Micron filter needle

Amiodarone 0.2 micron in-line filter

Atgam and Cytogam 0.2 micron in-line filter

Hyperalimentation (TPN) 1.2 micron filter set

Mannitol 1.2 micron in-line filter

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Each time a new PCA cartridge is started, the medication must be documented in PRN section of the MAR with required nurse witness.

The PCA Med Administration Record form must be completed for monitoring pts on PCA. Pump setting details must be documented and verified by second nurse on PCA Med Admin Record (ad hoc or task form) before:

PCA is initiated Change in rate/dosing Change in shift Transfer of care

4 PCA tasks will generate when pharmacy enters medication. Form is also available directly from ad hoc folder (this may change and may only be available as an ordered task—PCA 24 hour Med Administration Records). Form has 2 tabs on far left and both need to be filled out (PCA Med Admin. Record and Pain Eval.)

PCA drug/concentrations are grouped into standard, opioid tolerant, and chronic to match available text order sets– select only on drug/concentration at a time (Adjust date and time to reflect when action was actually performed)

Select PCA activity, any of the five 1st options will cause fields for pt respiratory, rate, O2 sats, and pain to become required.

Under PCA activity box are fields that may have values pulled forward from previous charting in last 6 hrs. This includes:

PCA dose unit measure Continuous/basal infusion dose/hr PCA dose 4 hr limit Lockout interval

Once this form is charted, the verifying nurse must log into own computer with own OPID, go under forms tab, right click on PCA med Admin Record and select modify. The verifying nurse then types his/her own name in verifying nurse field and signs form. Do not change performed date and time.

Contributed by Melissa Carril BSN, RN

PCA Med Administration Record

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Saline Flush Protocol FHFC Policy 140.601-1

Heparin Flush Protocol FHFC Policy 140.601-1 Must have physician order for heparin flush

Patient Weight

Percutaneous (Subclavian,

Fem, Jug)

PICC

Tunneled (ex Broviac)

Implanted Port

< 10kg < 10kg < 10kg < 10kg < 10kg

Maintenance flush Pre/Post med flush Post Blood draw flush

3 ml 3 ml 5 ml

3 ml 3 ml 5 ml

3 ml 3 ml 5 ml

3 ml 3 ml 5 ml

10 - 39kg 10 - 39kg 10 - 39kg 10 - 39kg 10 - 39kg


5 ml 5 ml

10 ml

5 ml 5 ml

10 ml

5 ml 5 ml

10 ml

5 ml 5 ml

10 ml

40kg or > 40kg or > 40kg or > 40kg or > 40kg or >


5 ml 5 ml

20 ml

5 ml 5 ml

20 ml

5 ml 5 ml

20 ml

5 ml 5 ml

20 ml

Table 1: Weight-based Saline Flushing Volumes-Central Line specific Patients: Infant>28 days to Adolescent

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< 10kg < 10kg < 10kg < 10kg < 10kg < 10kg < 10kg

Line not in use

10

units/ml

Flush 1st w/ NS then

2ml (20units) Q 12 hrs

10

units/ml

2ml (20 units) Q 24 hrs

10

units/ml

5ml (50 units)

Q 4 weeks

Line in use once/day or

port accessed

10 units/ml

2ml (20 units) Q 24 hrs

10 units/ml

5ml (50 units)

Q day

Line used more than

once per day

10

units/ml

2ml

(20 units) per MD

10

units/ml

5ml (50 u) 1st flush of the

day then Saline for

subsequent flushes

> 10kg > 10kg > 10kg > 10kg > 10kg > 10kg > 10kg

Line not in use

10

units/ml

Flush 1st w/ NS then

2ml (20units) Q 12 hrs

100 units/ml

2ml (200units) Q24 hrs

100 units/ml

5ml (500units) Q 4 weeks

Line in use once/day or

port accessed

100 units/ml

2ml (200units) Q24 hrs

100 units/ml

5ml (500uits) once per

day

Line used more than

once per day

10 Units/ml

2ml (20 units) per MD order

100

units/ml

5ml (500 u) 1st flush of the

day then Saline for

subsequent flushes

Percutaneous CVL (Subclavian, Femoral, Jugular)

Tunneled CVL (Broviac, Cook, Hickman)

Implanted Portal Device (Port-a-Cath

Concentration

Amount/ Frequency

Concentration

Amount/ Frequency

Concentration

Amount/ Frequency

Table 2: Weight-based HEPARIN Flushing Protocol-Central Line specific Patients: Infants more than 28 days to Adolescent Tunneled CVL & Ports flush protocol unless otherwise ordered by physician Percutaneous CVL flush per Dr order which may include table recommendations

* Total daily dose of heparin flush should not exceed 50 units/kg/day

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CLABSI Prevention Measures Decreasing CLABSI (Central Line Associated Blood Stream In-fection) is everyone's job. We should care about this because it:

Increase morbidity and mortality to our patients Increases hospital length of stay Increases cost to the hospital. Medicaid and Medi-

care no longer pay for iatrogenic (something we caused) illness so the hospital has to pay for the cost of care related to this.

Each CLABSI carries excess health-care costs of $16,550 and mortality of up to 25%, (CDC Morbidity and Mortality Weekly Re-port March 4, 2011) What do we do about it:

Wash Your Hands Use Ultrasound guidance to place central lines Use sterility when placing lines Place biopatch (chlorhexidine gluconate impregnated

sponge) around insertion site Use sutureless securement device (StatLock) on all

lines Wash Your Hands Change central line dressings once per week, more

frequently only if dressing compromised Change IV tubing every 96 hours for clear continuous

infusions, change tubing every 24 hours for colloids (ie lipids, albumin, etc)

Wash Your Hands Use a needless system (blue claves) Place green caps on all available ports on all lines or

Scrub the hub Use chlorhexidine wash for daily skin cleansing on

critically ill patients Assess daily if central line is necessary and remove

promptly Wash Your Hands

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Notes

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Notes

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Notes

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Notes

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106

LMA Insertion 1. Verify that the size of the LMA is correct for the patien

2. Visually inspect the LMA cuff for tears or other abnor-malities

3. Inspect the tube to ensure that it is free of blockage or loose particles

4. Deflate the cuff to ensure that it will maintain a vacuum

5. Inflate the cuff to ensure that it does not leak

6. Slowly deflate the cuff to form a smooth flat wedge shape which will pass easily around the back of the tongue and behind the epiglottis.

7. Lubricate the back of the mask thoroughly

8. Open the airway

9. Grasp the LMA by the tube, holding it like a pen as near as possible to the mask end.

10. Place the tip of the LMA against the inner surface of the patient’s upper teeth.

11. Press the mask tip upwards against the hard palate to flatten it out.

12. Using the index finger, keep pressing upwards as you advance the mask into the pharynx to ensure the tip re-mains flattened and avoids the tongue. .

107

LMA Insertion 13. Press the mask into the posterior pharyngeal wall using the index finger.

14. Guide the mask downward into position

15. Do not touch the LMA tube while it is being inflated unless the position is obviously unstable.

16. Connect the LMA to a Bag-Valve Mask device or low pressure ventilator

108

IO Insertion 1. Choose proper site and needle size. Available sites for pedi-

atric patients includes Proximal Tibia, Distal Tibia, Distal Fe-mur, Iliac Crest

2. Insert Needle onto EZ-IO® driver

3. Palpate landmarks and prep insertion site with chlora-prep. Allow to dry.

4. Position and stabilize extremity to insert EZ-IO® needle.

5. For insertion into the proximal tibia, insert the needle perpen-dicular (90°) to the bony cortex.

6. Penetrate bone by squeezing driver trigger, apply gentle, steady, downward pressure.

7. Remove the trochar and confirm placement by aspirating bone marrow using an empty 5 ml. syringe. Failure to aspi-rate marrow does NOT necessarily mean that insertion was unsuccessful, it may mean that the needle is blocked by a piece of marrow

8. Gently flush the needle with 5-10 ml of saline.

9. Observe and palpate for swelling in the calf or fluid leakage around the needle. If you are unsure of proper placement, remove the needle and attempt in the other leg.

Gently advanced the needle through the skin and set into position. Without forcing. Stop when contact is felt with bone Verify at least one (1) black line still visible on needle.

109

IO Insertion 1. Secure in position IO stabilizer. Do not pad the needle. Do

not tape around the calf circumferentially, or obscure the in-sertion site.

2. Primed EZ connect set with normal saline, connect stop-cock and solution and begin infusion.

3. Placed pressure bag on solution to be infused. Electronic in-fusion device NOT USED.

110

Shunt Tap

CSF Collection

Universal Protocol Signed consent Sterile Gloves Shunt tap kit 23G butterfly needle 5 ml syringe 3 sterile culture tubes 2 red top tubes Betadine swabs

MD order: RN obtains 2ml of CSF from Ventricular Catheter port Daily CSF samples may be obtained usually by night shift (05:00)

Equipment: 3 Betadine Swabs ; 3 ml syringe; Mask; Sterile gloves/ towel; Clean glove; Collection tube (refer to lab)

PROCEDURE: (unless manufacture procedure differs) Organize Equipment: DON Mask Place syringe & CSF collection tube on sterile towel Open Betadine Swabs Close White Clamp Proximal to Blue port Open catheter to drain position (on the stopcock) DON Clean Gloves: Clean Blue Port with Betadine swab Place the EVD drain tubing on the sterile towel DON Sterile gloves; affix 3ml syringe to blue port Slowly aspirate 2ml of CSF fluid/Remove syringe Place CSF fluid in collection tube Open the white clamp/ Return STOPCOCK to original position Label per lab protocol

111

EVD Placement Equipment Signed consent/Universal Protocol Subarachnoid tray or cranial access kit Ventricular catheter set External ventricular drainage system (Atrium Dry) Sterile glove/gown/mask Cap Sterile 4X4’s Betadine 1% lidocaine with Epi Razor Ultradex (pcmx) scrub Sterile towels Preservative free normal saline vials 2-10 ml syringes & 2-5ml syringes 2-15g blunt needles 4.0 suture or physician preference 3 sterile culture bottles Transducer kit if monitoring ICP’s Codman ICP pressure module & cable for ICP’s

Consent form/Universal precautions Order for Emla Cream A-line box Arrow or Angiocath catheters Betadine Sterile 4X4’s Alcohol pads Heparin 1:1 in syringe Heparinized flush bag For pts < 10kg use syringe pump and 1:1 heparin Veni-guard/Tegaderm/Bard skin protectant

A-Line Placement Equipment

112

Signed consent Universal Protocol Sterile gloves Mask LP tray-appropriate size LP needle-appropriate size Betadine Sedation as ordered Sterile 4X4’s 1% Lidocaine & 25 G needle if MD requests Labels Biohazard bag Band-Aid Copy of order must go with specimens.

Universal Protocol Signed consent Line Cart

Sterile Gloves Mask for each person in the room Hat Gown Central line kit (catheter size determined by MD)

Saline flushes Heparin flushes (2-3 syringes, 10unit/ml) Blue claves (one for each lumen) Biopatch Curos caps Ordered sedation drawn up in syringes Ultrasound machine

Lumbar Puncture

Central Line Placement

113

NPASS The Neonatal Infant Pain Scale (NIPS) is a behavioral

assessment tool for measurement of pain in preterm and full-term neonates. This can be used to monitor a neonate before during and after a painful procedure such as venipuncture. It was developed at the Children's Hospital of Eastern Ontario.

Parameters: (1) facial expression (2) cry (3) breathing pat-terns (4) arms (5) legs (6) state of arousal neonatal infant pain scale = SUM (points for the 6 parame-ters) Interpretation:

• minimum score: 0 • maximum score: 7

Limitations: • A falsely low score seen in an infant who is too ill to respond or who is receiving a paralyzing agent.

The CRIES Pain Scale is often used in the neonatal

healthcare setting. CRIES is an observer-rated pain assessment tool which is performed by a healthcare practitioner such as a nurse or physician. CRIES assesses crying, oxygenation, vital signs, facial expression and sleeplessness. The CRIES Pain Scale is generally used for infants 6 months old and younger.

Pain Scales

114

The Wong Baker Faces Pain Scale combines pictures and numbers to allow pain to be rated by the user. It can be used in children over the age of 3, and in adults. The faces range from a smiling face to a sad, crying face. A numerical rating is assigned to each face, of which there are 6 total.

The Face, Legs, Activity, Cry, Consolability scale or FLACC scale is a measurement used to assess pain for children between the ages of 2–7 or individuals that are unable to communicate their pain. The scale is scored between a range of 0–10 with 0 representing no pain. The scale has 5 criteria which are each assigned a score of 0, 1 or 2.

The Universal Pain Scale is a pain assessment system in which patients are asked to rate their pain on a scale from 1 to 10, with 10 representing the worst pain they have experienced or could have imagined.

Pain Scales

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Pain Scales

NPA

SS

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Pain Scales

118

CRIES

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State Behavioral Scale (Study):

-3

Unresponsive

No spontaneous respiratory effort No cough or coughs only with suctioning No response to noxious stimuli Unable to pay attention to care provider Does not distress with any procedure (including noxious)

-2

Responsive to

noxious stimuli

Spontaneous yet supported breathing Coughs with suctioning/repositioning Responds to noxious stimuli Unable to pay attention to care provider Will distress with a noxious procedure

-1

Responsive to

gentle touch or

voice

Spontaneous but ineffective non-supported breaths Coughs with suctioning/repositioning Responds to touch/voice Able to pay attention but drifts off after stimu-lation Distresses with procedures Able to calm with comforting touch or voice when stimulus removed

Score Description Definition

Objective: To develop and test the reliability and validity of the State Behavioral Scale for use in describing sedation/agitation levels in young intubated patients supported on

mechanical ventilation (Curley, et al 2006)

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0

Awake and Able

to Calm

Spontaneous and effective breathing Coughs when repositioned/Occasional spontaneous cough Responds to voice/No external stimulus is required to elicit response Spontaneously pays attention to care provider Distresses with procedures Able to calm with comforting touch or voice when stimulus removed

+1

Restless and

difficult to

calm

Spontaneous effective breathing/Having difficulty breathing with ventilator Occasional spontaneous cough Responds to voice/ No external stimulus is required to elicit response Drifts off/ Spontaneously pays attention to care provider Intermittently unsafe Does not consistently calm despite 5 min attempt/unable to console

+2

Agitated

May have difficulty breathing with ventilator Coughing spontaneously No external stimulus required to elicit response Spontaneously pays attention to care provider Unsafe (biting ETT, pulling at lines, cannot be left alone) Unable to console

Score Description Definition

State Behavioral Scale score as patient’s response to voice, then gentle touch, then noxious stimuli (planned

endotracheal suctioning or _5 secs of nail-bed pressure)

122

Restore Project The Randomized Evaluation of Sedation Titration fOr Respiratory failurE is an NIH sponsored study at 31 pediatric intensive care units across the United States. The purpose of the study is to evaluate if sedatives used in children with acute respiratory

failure affects how long they need to be mechanically ventilated, how much it costs, and their quality of life and emotional health

after hospital discharge.

Pediatric Assessment: Withdrawal assessment, especially in preverbal or nonverbal children, can be challenging. The WAT-1 is used to identify iatro-genic withdrawal syndrome. The nurse should tailor their assess-ments to the child’s developmental level, medical status and tem-perament using the WAT-1.

Definition of Iatrogenic Withdrawal Syndrome: Iatrogenic withdrawal syndrome is the term used for a character-istic pattern of unpleasant signs and symptoms that typically fol-lows too rapid tapering or abrupt cessation of narcotics (opioids), benzodiazepines or other drugs with central nervous system de-pressant effects. Prominent manifestations include nervous sys-tem hyperirritability, autonomic system dysregulation, gastroin-testinal dysfunction and motor abnormalities.

Definition of the Start of Weaning: The date and time associated with a deliberate attempt to discon-tinue narcotics (opioids) and/or benzodiazepines.

Assessment Frequency and Documentation: Assess and document the patient’s WAT-1 in the designated col-umn of the Patient Care Flowsheet.

Start WAT-1 scoring from the first day of weaning in patients who have received narcotics (opioids) +/or benzodiazepines by infu-sion or regular dosing for prolonged periods (e.g., ≥ 5 days). Continue twice daily scoring until 72 hours after the last dose.

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The WAT-1 is completed and documented in the PICU with the SBS at least once per 12 hour shift at 08:00 and 20:00 ± 2 hours until 72 hours after the last PRN narcotic (opioid) and/or benzodi-azepine dose. If a patient is transferred to the floor prior to 72 hours after the last PRN narcotic (opioid) and/or benzodiazepine dose, WAT-1 scoring is completed and documented daily at 08:00 +/- 2 hours. More frequent assessment may be necessary in patients who show symptoms of withdrawal from narcotics (opioids) and/or benzodiazepines. The increased frequency of the WAT-1 as-sessments in these patients should follow the assessment – in-tervention – reassessment cycle for treating patients' withdrawal.

Description: The WAT-1 is an 11 item/12 point scale for monitoring narcotic (opioid) and/or benzodiazepine withdrawal symptoms in pediatric patients. Assessment Method: 1. Review the WAT-1, familiarizing yourself with the indicators

and how they are scored. 2. Review nursing documentation in the previous 12 hours. 3. Complete a 2 minute observation period with the patient at rest 4. Assess patient during a progressive arousal then assess

patient during an observation period following the stimulus. Use progressive stimuli to elicit the patient’s response; specifically, using a calm voice, call the patient’s name. If no response, call the patient’s name and gently touch the patient’s body. If no response, asses the patient’s re-sponse to a planned noxious procedure, e.g., endotracheal suctioning. If a noxious procedure is not planned then, us-ing a pencil/pen, provide < 5 seconds of direct pressure to the patient’s nail bed.

5.Complete a post-stimulus recovery observation period. Interpretation: A higher WAT-1 score indicates more withdrawal symptoms while a lower score indicates fewer withdrawal symptoms. WAT-1 scores should be interpreted based on their trend over time.

124

RESTORE Scoring Method Presence and intensity of withdrawal symptoms consist of:

Three indicators obtained from the nursing documentation in the previous 12 hours are scored with one point: 1. Loose/watery stools that are not consistent with the patient’s age,

medical condition or baseline stooling pattern. 2. Vomiting/retching/gagging that cannot be attributed to other causes or interventions. 3. Temperature elevation that remains >37.8 more frequently than not during the previous 12 hours and not believed to be associated with an infection.

Five indicators assessed during a 2 minute observation of the patient at rest are scored with one point:

1.State behavior based on observation (asleep/awake/calm = 0 or awake/distressed = 1) or based on the SBS score for sedation in mechanically ventilated patients (SBS ≤ 0 = 0 or SBS ≥ +1 = 1). See SBS guidelines for instructions on completing the SBS score.

2. Tremors that are moderate to severe and cannot be attributed to another clinical cause.

3. Sweating that is observed and not related to an appropriate tem-perature regulation response .

4. Uncoordinated/repetitive movements that are moderate to se-vere including head turning, leg or arm flailing or torso arching.

5. Yawning/sneezing that is observed more than once in the 2 minute observation period.

Two indicators assessed during a progressive arousal stimulus scored with one point: 1. Startle to touch that is severe 2. Muscle tone that is increased

One indicator assessed during an observation period following the stimulus scored with up to two points: 1. Time to return to calm state that is greater than 5 minutes will receive 2 points. If the time to return to calm state is 2-5 minutes, it will receive 1 point. The final WAT-1 score is the total sum of all indicators (0-12).

125

Withdrawal Assessment Tool Version 1

Any loose/watery stools No=0 Yes = 1

Any vomiting/wretchings/gagging No = 0 Yes =1

Temperature> 37.8°C No = 0 Yes =1

Information from patient record, previous 12 hours

2 minute pre-stimulus observation State SBS 0 or asleep/wake/calm = 0

Tremor SBS +1 or awake/distressed = 1

Any sweating No=0 Yes = 1

Uncoordinated/repetitive movement

None/mild = 0 Moderate/severe=1

Yawning or sneezing None or 1=0 2=1

1 minute stimulus observation Startle to touch None/mild = 0

Moderate/severe = 1

Muscle tone Normal = 0 Increased = 1

Post-stimulus recovery Time to gain calm state (SBS

< 2min = 0 2-5 min = 1 >5 min = 2

Total Score (0-12)

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Notes

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Notes

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Abad-Sinden, A., Sutphen, J. (2003). Nutritional management of pedicatirc short bowel syndrome. Practical Gastroenterolgy, 28-48 Abrams, S., (2001). Chronic pulmonary insufficiency in children and its effects on growth and development. [Electronic version]. Journal of Nutrition, 131, 938-941. All medication references in Handbook. In: Lexi-Drugs Online [database on the Internet]. Hudson (OH): Lexi-Comp, Inc.; 2011 [cited 20 May 2011]. Available from: http://online.lexi.com. subscription required to view on FH intranet American Academy of Pediatrics. (2009). Pediatric nutrition handbook. (6th edition). Elk Grove Village. American Dietetic Association (2010) Pediatric Nutrition Care Manual. Atrium University (2011). Managing dry suction chest drainage: nursing education program. Video/DVD. Bamhart, D. Czervinske, M., (1995). Perinatal and pediatric respiratory care. (1st Ed). St. Louis, MO. Saunders Company. Brizee, L., (2007). Short bowel syndrome. Retrieved October 31, 2009 from http://depts. Washington.edu/growing/Assess/ SBS.htm Center for Disease Control and Prevention (CDC, 2009). Morbidity and Mortality Weekly Rate, Guidelines for the preven tion of intravascular catheter-related infections, (2005). October 14, 2005.55(40);1013-1016. Retrieved May 10, 2011, from http://www.cdc.gov/mmwr/preview/mmwrhtml/ mm5540a2.htm. Curley, M., Sion, K,. Fraser, K., Johnson, R., Arnold, J., (2006). State Behavioral Scale: A sedation assessment instrument for infants and young children supported on mechanical ventilation Pediatric Critical Care Medicine Vol. 7, No. 2

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References Cystic Fibrosis Foundation. (n.d.). Staying healthy. Retrieved October 31, 2009 from http://cff.org/Living WithCF/ Stayinghealthy/. Florida Hospital Policy #140.601-1. (2009). Central venous, peripherally inserted central and arterial access catheters: care and maintenance—neonatal & pediatrics. Florida Hospital:(2010) Policy and Procedure. 2003-2004 The A.S.P.E.N.; Pediatric Nutrition Support Core Curriculum. Franck, L., Harris, S., Soetenga, D., Amling, J., Curley, M., (2008). The withdrawal assessment tool – 1 (WAT-1): an assessment instrument for monitoring opiod and benzodi azepine withdrawal symptoms in pediatric patients. Pediatr Crit Care Med 2008 Vol. 9, No. 6 Hockenberry, M., Wilson, D. (2006) Wong's Nursing Care of I nfants and Children, (8th Ed.) St. Louis, MO: Elsevier Mosby Lawrence J Alcock D et al. The development of a tool to assess neonatal pain. Neonatal Network. 1993; 12 (6 September): 59-66. Maguiness, K., Casey, S., Fulton, J., Luder, E., McKenna, A. & Hazle,L., (2006). Nutrition: Pancreatic enzyme replacement. Retrieved October 31, 2009 from http://www.cff.org/ uploadedfiles/Living With CF/Staying Healthy/Diet/ EnzymeReplacement/Nutrition%20-%20Pancreatic% 20enzyme%20Replacement%2002-06.pdf Merck Manuals:Online Medical Library. (2005). Nutrition. Retrieved October 31, 2009 from http://www.merck.com/mmpe/ sec19/ch266c.html. Slota, M., (ed.). (2006). Core curriculum for pediatric critical care nursing. Philadelphia, PA: W.B. Saunders Company Smith, S., Duell, D., & Martin, B., (2008). Clinical Nursing Skills:Basic to Advanced skills. (7th Ed.). Upper Saddle River, NJ: Pearson Prentice Hall

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References Solodiuk, J., Curley, M.,(2003). Severe cognitive impairments: the individualized numeric rating scale (INRS).Journal of Pediatric Nursing, Vol 18, No 4. Subcommittee of the Tenth Edition of the RDA, Food and Nutrition Board, Commission of Life Sciences, and National Research Council. (1989). Recommended dietary allowances. (10th ed.) Washington, D.C.: National Academy Press. Taketoma, C. K., Hodding, D. & Krause, D. (2008). Pediatric Dosage Handbook (15th Ed.) Hudson, OH: Lexicomp The A.S.P.E.N.; (2007).Nutrition Support Core Curriculum: A Case Based Approach- The Adult Patient. Trivits, V. & Lebet, R. (2008). Procedure Manual for Pediatric Acute and Critcal Care. St Louis: Saunders Company Sucommittee of the Tenth Edition of the RDA, Food and Nutritiona Board, Commission of Life Sciences, and National Research Council. (1989). Recommended dietary allowances. (10th ed.) Washingong, D.C. National Academy Press Whitaker, K. (1992). Comprehensive Perinatal and Pediatric Respiratory Care. Delmar Publishers. Clifton Park, NY: Delmar Thomson Learning Zerran, J. (2007). Bronchopulmonary dysplasia, Retrieved October 31, 2009 from http://dept,washington.edu/growing/ Assess/BPD.htm USDA. (2011).My Food Pyramid. Retrieved May 16, 2011from http://www.mypyramid.gov/ American Academy of Pediatrics. Use of Inhaled Nitric Oxide. Pediat-rics. 125 (4): e978 CDC 2011 CLABSI guidelines CDC Morbidity and Mortality Weekly Report March 4, 2011

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