PICU Handbook

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Guidelines for student/resident/fellow coverage in the Pediatric Intensive Care Unit

Purpose of Guideline: To clarify issues relating to patient care coverage and work for the various care
providers in the PICU
Caregivers in the PICU and level of responsability
1. Attending coverage
a. Day attending: Primary attending or consulting/co-attending on all pediatric patients and
selected adult patients admitted to the PICU
b. Backup attending: A backup attending is available during the day and is called at the
discretion of the day attending
c. Night attending: Night attending for admission, cross coverage, transport calls/consults,
code team response.
d. Sedation attending: Available some days
2. Resident Coverage
a. Pediatric residents: PL2 and PL3. Residents each take patients primarily. PL3 should
strive to mentor and guide the PL2 as needed with PICU or hospital procedures.
b. Emergency Medicine Intern. The EM intern will take patients primarily. Not all months
have an EM intern.
3. Fellow Coverage (varies by month)
a. PICU Fellow. The PICU fellow will act in a supervisory capacity, under the direction of
the PICU attending, for all patients admitted to the PICU.
b. Cardiology Fellow. The cardiology fellow will act in a supervisory capacity, under the
direction of the PICU attending, for all cardiology or cardiac surgery patients admitted to
the PICU. The cardiology fellow may go to the cath lab or OR for optimal educational
experiences.
c. Anesthesia Fellow. The anesthesia fellow will take patients primarily along with the
Pediatric residents and EM intern.
d. Surgical Fellow. The role/responsibilities of the surgical fellow will vary depending on
their educational goals.
4. Students
a. Subintern (MS4). The subintern will follow patients as the primary caregiver. One of the
pediatric residents should be assigned to back-up the subintern on each patient.
b. Student (MS3). The student will follow patients as the primary caregiver. One of the
pediatric residents (generally the PL3) should be assigned to follow the patient along with
the student. (see student info page for more specific guidelines re MS3 experience)
Responsibilities of Primary Resident/student
1. Write admission orders and admission note (medical patient) or review admission orders and
write admission note (surgical patient)
2. Pre-round on patients and be prepared to present on rounds. (note, residents should not pre-round
on subintern patients, and should very briefly pre-round on MS3 patients)
3. Write daily notes. Surgical patients do not need notes on the day of transfer (except cardiac
surgical patients, who transfer to the cardiology service on the ward/dncc).
4. When gone from unit (post call, clinic, etc), communicate/sign out with resident/s who remain in
the unit. Please also notify the attending that you are leaving and summarize any patient care
tasks that still need to be done.
5. Write transfer note for medical patients, communicate patient data to receiving resident.
6. For Shriners discharges or home discharges, dictate admission (students should not dictate).

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Division of Patients
1. Pediatric PL2, Pediatric PL2, EM PL1, sub-intern, and anesthesia fellow will take patients
primarily
2. The above caregivers will distribute patients relatively evenly, within the following guidelines
a. The EM intern and pediatric sub-intern should take more straightforward medical and
surgical patients until he/she is comfortable with taking more difficult patients. They
should follow up to 3-4 patients
b. The anesthesia fellows generally do not have substantial pediatric experience, and usually
are not familiar with how to get things done at OHSU. Because of this, initially they
should have fewer patients so that they can familiarize them selves with the various
hospital/unit procedures. They should follow up to 3-4 patients.
c. The Pediatric PL2 and PL3 should follow up to 5 high-acuity (nursing acuity 6 or 7) or a
maximum of 8 patients primarily. Some of these patients will also be followed by a
MS3.
d. The Sub-intern should follow 1-3 patients (backed-up by one of the pediatric residents)
e. The MS3 should follow 1-3 patients (co-followed with Pediatric resident)
3. Patients admitted by the cross cover residents should be divided up the following day, with
attention to evening up the distribution of patients according to the above guidelines.
Triage of work when the unit is busy or there are fewer caregivers
1. Round on sicker patients first. If not all patients can be pre-rounded on, surgical patients who are
expected to transfer to the floor after a one day stay should be rounded on last. If not all patients
are pre-rounded, their data will be reviewed by the entire team at the time of work rounds.
2. The night resident should include an assessment of whether or not the patient might transfer to the
floor in sign-out.
3. If urgent transfer to floor orders are needed prior to rounds beginning, the cross cover resident
should do them.
4. Daily notes are not needed on surgical patients transferring to the floor.
5. If unable to complete daily notes on all patients, prioritize medical patients over surgical patients.
6. Transfer notes for patients transferring after one day can be very brief.
7. If unclear about what tasks should take priority, ask the attending.

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Table of Contents
Introduction to the PICU ...........................................................................................

Common Conditions in the PICU .............................................................................

11

Procedures in the PICU .............................................................................................

37

Mechanical Ventilation ..............................................................................................

47

General Post-operative Care ......................................................................................

51

Cardiac Perioperative Care ........................................................................................

58

Cardiac Perioperative Care, Part II ............................................................................

72

Medications in the PICU............................................................................................

74

Useful Equations in the PICU ....................................................................................

85

Sedation in the PICU .................................................................................................

87

Transfusion in the PICU ............................................................................................

97

Death and Dying in the PICU .................................................................................... 101

Pediatric TPN Guidelines .......................................................................................... 106

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PEDIATRIC INTENSIVE CARE UNIT (PICU) INTRODUCTION

Purposes
1. The provision of specialized care for children with critical illness which may best be
provided by concentrating these patients in areas under the supervision of skilled and
specially trained team of physicians and nurses.
2. The continuing education of health-care team members.
Administrative Structure
The Medical Directors of the PICU are Dr. Dana Braner and Dr. Laura Ibsen. Attending
Pediatrics Intensivists are Dr. Dana Braner, Dr. Laura Ibsen, Dr. Miles Ellenby, Dr. Ken
Tegtmeyer, Dr. Aileen Kirby, and Dr. Bob Steelman. The Pediatric Intensivists are the primary
caretakers (medical patients), or consultants (surgical patients), for each patient admitted to the
PICU. There is an intensivist in house 24 hours/day.
The Clinical Manager of the PICU is Christine Pierce. She supervises the nursing and
administrative staff of the unit and is responsible for the day-to-day operations of the unit.
Nursing Staff
1. General organization. The PICU nursing staff consists of RNs and appropriate ancillary
personnel. Nursing assignments and acuity decisions are made by the nursing staff. If
parents make a request to you that relates to nursing staffing, please inform the charge nurse.
2. Continuing education of the nursing staff. An on-going program of education in pediatric
intensive care nursing has been the responsibility of the nursing service. In addition,
appropriate seminars discussing subjects of pertinence in pediatric intensive care have been
and will continue to be organized with physician participation. This will be an effort to
maintain and further the critical care skills of nursing personnel in the PICU.
Respiratory Care
The personnel of PICU will work jointly with the Director of Respiratory Therapy so that
optimum respiratory care may be provided. The respiratory therapy staff are responsible for
setting up and maintaining the ventilators, delivering respiratory treatments, and assisting with
patient care that involves respiratory care (i.e., suctioning).
Pediatric Respiratory Therapists rotate through the PICU, DNCC, and the floors.
Physicians and Students
A PL-3 and PL-2 are assigned to the PICU, and they with the Pediatric Critical Care staff and
other services will care for all pediatric patients. The Pediatric Intensive Care Unit is available
to all pediatric patients regardless of the service primarily responsible for the child.

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Other physicians who may rotate through the PICU include PICU fellows, cardiology fellows,
pediatric anesthesia fellows, surgical fellows, and emergency medicine interns. Cardiology
fellows should supervise the care of cardiac surgery and cardiology patients. PICU fellows will
supervise the care of all patients in the PICU. Emergency medicine interns and anesthesia
fellows should follow patients as the primary physician. Other visitors (surgical, dental, etc)
may tailor their experience to their needs.
Students who may rotate through the PICU include 4th year subinterns and 3rd year students who
are in their required Child Health 1 rotation. PICU subinterns will follow their patients as the
primary physician, under the supervision of the residents and attending physicians. Subinterns
are expected to function as the patients intern. Third year students will follow patients under
the supervision of one of the pediatric residents, and will have greater supervision than do the
subinterns. The 3rd year students are expected to attend all required student lectures for their
CH1 rotation.
Admission and Discharge
Any child requiring pediatric intensive care must be admitted to PICU. This is accomplished by
calling the PICU attending physician. If a bed is available the patient may be admitted. If the
PICU is full, and all beds are occupied, then the physician wishing to admit a patient to the PICU
must contact the PICU attending. The critical care attending will then make the disposition
regarding discharge of another patient from the PICU after appropriate consultation with the
patients primary service and the PICU nursing staff, or other appropriate disposition. There are
policies in place regarding triage of surgical and medical patients that are used when beds or
nurses are scarce.
These policies are necessary to insure optimum care for all children who require pediatric
intensive care.
Type of Patients admitted to the PICU
Medical patients from the ED. The ED will contact the PICU attending. The intensivist is
the attending of record
Medical patients from the floor. The floor attending or resident will contact the PICU
attending who will decide about transfer, then call the PICU charge RN and resident. The
intensivist is the attending of record
Medical patients transported in for outside institutions. The PICU attending will contact the
PICU charge RN and resident about the admission. The intensivist is the attending of record
Cardiac patients may be admitted from the OR, the floor, the ED, or DNCC. If they are
immediately post or pre-operative, the primary service is Pediatric Cardiac Surgery, with
medical consultation. Functionally, these patients are managed on an hour-to-hour basis by
the PICU attendings. Pediatric residents are the primary residents for the pediatric cardiac
surgery patients. If they are not pre or post-operative patients (i.e., they are medical cardiac
patients), the attending of record is the PICU attending and cardiology is a consulting service.
Surgical patients from the ED or the floor. The surgical attending or resident must contact
the PICU attending to admit a patient to the PICU. The surgical attending is the attending of
record. The PICU acts as a consultant for medical issues. Surgical residents write admission

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orders. The degree to which the surgical services manage the medical issues of their patients
will depend on the service and the patient.
Surgical patients from the OR. Surgical attending is the attending of record. The PICU acts
as a consultant for medical issues. Surgical residents write admission orders. The degree to
which the surgical services manage the medical issues of their patients will depend on the
service and the patient.
Orthopedic patients from Shriners are admitted to the service of the Pediatric Intensivist if
the orthopedic surgeon does not have privileges. The pediatric residents write admitting
orders for most of these patients.
BBBD/IAC patients. The BBBD service is the primary service and writes all orders on the
patients. They should be called for anything that is needed short of immediate resuscitation.

Routine Procedures
There are pre-printed orders for general PICU admits, CV surgery admits (track A and general),
and ECMO admits. If you use a pre-printed order and want to write more things, use regular
order paper. There are also pre printed orders for sedation drips, muscle relaxant drips, cardiac
patient ventilator weaning. Others are being added on an ongoing basis. Admitting orders to the
PICU should include the following categories:
Diagnosis
Attending physician
Condition
Vital sign frequency (routine is q2). If you want things documented more frequently, be
specific. (Hourly is reasonable for sick patients)
Allergies
Nursingspecific nursing requirements
Dressing changes
Chest tube orders
CVP/A-line orders
NG
Foley
Diet/NPO
IVF (type/rate)
Meds
Drips written in amount/kg/minute (vasoactive) or amount/kg/hour (sedation/narcotic);
consult with PICU MD or nursing staff about concentration to order.
Labslabs wanted on admission as well as lab schedule if needed.
Ventilator settings along with weaning parameters (i.e., wean oxygen for O2 sat>???)
Call HO orders. It is best to write these and also to speak with the RN caring for the
patient about specific issues you are worried about, to ensure accurate communication.
There are special order sheets for muscle relaxants, sedation, and PCA. If you are
unfamiliar with them, ask the intensivist or the nurse to assist in using them.
Post operative cardiac patients and ECMO patients have pre-printed orders. These will
be completed by the intensivist or the pediatric resident with attending supervision.

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Verbal Orders
Verbal orders may be taken only when necessary. These must be written and signed as soon as
possible after having been executed.
Emergency Procedures
In the absence of a physician, if a child's condition changes while waiting for the physician
caring for the child, the nurse may do the following where appropriate:
1. Draw blood gases, electrolytes and hematocrit, and send these to the lab for stat results.
2. Call for chest x-ray or other appropriate x-ray.
3. Administer oxygen.
4. Institute cardio-pulmonary resuscitation with Ambu bag and external cardiac massage.
5. The PICU attending should be called immediately for any sudden, unexplained change in a
patients condition. In the event of a cardio-respiratory or respiratory arrest where the PICU
attending is not immediately available, the Pediatric Code 99 team may be called.
6. If an anesthesiologist is needed emergently, the pediatric on call anesthesiology number
should be paged. At the present time, the pediatric anesthesiologists are in house 24
hours/day.
Discharge/Transfer Procedures
Decisions regarding transfer of patients from the PICU to the ward will be made in conjunction
with the primary service and RN staff. Confirmation of the availability of a ward bed as well as
an accepting physician must be made prior to transfer. The PICU attending will contact the
receiving attending for medical patients, the residents should contact the receiving resident to
give report.
For surgical patients, the surgery service will write transfer orders. For medical patients, the
PICU residents write transfer orders. On occasion, the PICU residents can help the flow of
patients by writing transfer orders on surgical patients (confirm with surgical service first).
On medical patients, the PICU resident should write a transfer summary prior to transfer to the
floor. Any patient discharged from the PICU (including Shriners patients going back to
Shriners) need a dictated summary.
The Medical Record
A record of patient admissions, diagnoses, date of discharge, and attending physician will be
kept in the PICU.
Visiting Regulations
1. Visitors other than parents may be present with parental permission.
2. Visitors may be limited to two persons at a time at the discretion of the bedside RN.
3. One immediate family member may stay with the patient 24 hours a day.
4. Visitors must check at the desk outside PICU for permission to visit the child.

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Pediatric Resuscitation Course

Pediatric resuscitation courses such as Pediatric Advanced Life Support (PALS) will be offered
several times per year. All residents are required to complete this course. You will need to
recertify for this course at the end of your second year.
Schedule and other rules
Call is generally q4. We dont make your schedule. Emergency medicine interns are on call
with the cross cover 2nd year pediatric resident. Subinterns take call with the PICU senior
resident.
Rounds start at 7:30 M-F. Prerounding, including gathering information about events of the
night, vitals with I/Os, labs, and examining the patient must be accomplished prior to rounds.
The time needed for this will depend on the acuity of the unit. Residents should not arrive
before 6:00 am. If you are unable to pre round on all patients, do so on the most ill or acute
patients so that decisions can be made on rounds. It is helpful if the post call person gives
accurate, summative sign-out so that pre-rounding is not bogged down by trying to figure out
what generally happened over night. The post call person should make a quick go-around the
unit prior to the day people coming in so any last minute changes can be relayed. Discovery
Rounds should be avoided.
Rounds on the weekend start at 9:00 am. The resident on call the previous night will preround on all the patients (subject to change by residentshow you do this is up to you).
Signout rounds M-F generally start at 4:30. The PICU residents are responsible for signing
out to the incoming resident.
The patient signout sheet is kept up to date by the residents. Help each other, do a good job
with it.
When one of the PICU residents has clinic, he/she should sign out to the other resident. If
both residents will be gone for a given time period, please notify the attending on service as
soon as possible (i.e., when you figure it out). The attendings have a backup system in place,
we need to know when 2 attendings will be needed.
The residents are responsible for assuring their compliance with work hours regulations, both
daily and weekly. We do not keep you schedule. If you are finding it difficult to comply
with the regulations, please let us know.
PICU attending lectures generally occur daily in the conference room, generally at 11:00am.
It is assumed you will be present and the attending on service will cover issues during the
lecture.
Procedures: Procedures will generally be done by the resident covering the patient, with
supervision by the attending. There will be times when the attending will do the procedures
and times when a more senior resident will do the procedure. Our first priority is patient
care. As a general rule, lines on infants or hemodynamically unstable patients will be done
by the attending. Intubation of patients who are not NPO, who are known to have difficult
airways, who are extremely hypoxemic, or patients who are hemodynamically unstable will
be done by the attending or an experienced resident.
Orders: Bedside charts MUST stay at the bedside. Orders should be written on rounds as
decisions are made. You MUST tell the nurse if you are writing an order if you would like it
to be carried out in a timely fashion.

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You will take on exam at the end of the rotation. It has been developed by a collaboration of
Peds intensivists around the country and is used to tailor our educational objectives. It stays
with us.
A PICU reference guide is being developed in collaboration between residents and the
attendings. It will exist at some point.

Helpful tips
PICU nurses are very experienced and invested in the care of these patients. Learn from
them. Take their advice and concerns seriously.
If you disagree with a nurse, please discuss the issue with the attending.
If a nurse asks you to call the attending, do it.
If in doubt, call the attending.
The only stupid question is the one you didnt ask.
Follow up on anything that was supposed to happen (including labs and x-rays and CT scans.
Even if you arent a neurologist, you will likely notice something really bad that we should
know about).
Keep the surgical residents apprised of any changes in their patients.
If in doubt about orders on surgical patients, ask the attending the best course of action.
Double Pages and Code 99
A "double page" is a page indicating the emergency need for the house officer named to respond
immediately. A "Code 99" page indicates the need for cardiopulmonary resuscitation. One of
the PICU residents must carry the code pager at all times. The PICU resident is a member of the
code team.

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Organ System Issues and Specific Diseases Commonly

Encountered in the PICU
A. Endocrine
Diabetic Ketoacidosis
Definition:
1. Metabolic acidosis
2. Ketonuria/ketonemia
3. Hyperglycemia (not mandatory)
4. Dehydration
5. Associated electrolyte disturbances: psuedohyponatremia, hypokalemia,
hypophosphatemia
PICU admission criteria: (depends on case/attending)
1. PH<7.25, HCO3 <15, mental status changes, cardiac arrhythmia
2. Insulin infusion that requires titration
Pathophysiology:
1. Occurs due to an absolute or relative insulin deficiency along with an excess of counter
regulatory hormones (e.g. glucagon, catecholamines, cortisol, and growth hormone) as
seen with infection or stress results in stimulation of lipolysis and increased levels of
circulatory free fatty acids
2. Fatty acids are oxidized in liver resulting in elevated levels of circulating ketone bodies
(beta-hydroxybutyrate and acetoacetate)
3. Counter regulatory hormones stimulate hepatic ketogenesis as well as gluconeogenesis
and glycogenolysis resulting in excess glucose production and hyperglycemia
4. DKA can occasionally present without hyperglycemia such as during pregnancy, in
patients who have been partially treated and those with prolonged vomiting with little to
no carbohydrate intake as blood glucose rises, the ability of the proximal tubule to resorb
glucose is exceeded and glycosuria occurs resulting in osmotic diuresis and dehydration
Evaluation:
1. Careful history: vomiting, abdominal pain, polyuria, polydipsia, nocturia, weakness,
heavy breathing or shortness of breath, symptoms of intercurrent illness, mental status
changes, sweet odor to breath, weight loss
2. Physical exam: dehydration (dry mucous membranes, poor skin turgor, poor perfusion),
tachycardia, hypotension, Kussmaul respirations, somnolence, hypothermia, impaired
consciousness
3. Laboratory studies:
- venous blood gas
- metabolic panel/blood glucose
- urine or serum ketones
- complete blood count
- anion gap
- consider: HgA1C, TSH, freeT4

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other signs of infection i.e. urinalysis/culture

Useful Equations:
1. Correction for psuedo/dilutional hyponatremia: Na+ (corrected) = Na+ (measured) +
[(serum glucose 100)/100] x 1.6
2. Anion gap: [(Na+ + K+) (HCO3- + Cl-)]
Treatment:
1. ABCs ensure adequate airway, ventilation and circulation
2. Correct fluid deficits
- calculate fluid deficit (may assume 5-10% dehydration)
- i.e., total fluid deficit = 10ml/kg for each 1% dehydrated
- consider administering a 10-20 ml/kg bolus NS over 1 hour
- replace evenly over 48 hours in addition to maintenance fluids
3. Correct electrolyte deficiencies
- consider normal saline or 1/2 normal saline
- potassium shifts extracellularly due to acidosis- therefore despite normal
- serum potassium levels a total body deficit usually exists
- if serum K < 5, replace with 40 mEq potassium in fluids initially. You may need to
add more.
- replace hypophosphatemia by using Kphos for 1/2of potassium replacement
- example fluids: NS + 20 mEq KCl/L + 20 mEq Kphos/L
4. Correct metabolic acidosis by interrupting ketone production
- begin with continuous insulin drip 0.05- 0.1 units/kg/hr IV
- start with lower dose and titrate to achieve glucose drop no more than 50-100
mg/dL/hour
- monitor blood glucose q1-2 hours when glucose reaches 250-300 mg/dL add D5 to
fluids, change to D10 (try to increase dextrose in IVFs to keep blood sugar 200-300
rather than decreasing rate of insulin drip until acidosis is corrected)
- monitor venous blood gas and electrolytes q2-4 hours until out of DKA
- monitor urine for ketones and glucose with each void
- when acidosis resolved (HCO3 >18), pt tolerating PO and mental status normal
consider switching to SQ insulin = 0.5-1.0 unit/kg/day
2/3 total dose in am (1/3 Regular, 2/3 NPH)
1/3 total dose in pm (1/2 Regular at dinner, 1/2 NPH at bedtime)
5. Assess for and treat any underlying causes for DKA (e.g. infection)
6. Closely monitor for and treat any complications of DKA
Complications:
1. Cerebral edema- the leading cause of mortality; occurs in 1-2% of children with DKA;
risk factors include rapid shifts in osmolality, excessive fluid administration, use of
hypotonic fluid; symptoms include declining/fluctuating mental status, symptoms of
increased intracranial pressure such as dilated or unequal pupils, Cushings triad.
Treatment: Mannitol, consider intubation, mechanical ventilation
2. Cardiac arrhythmia- due to electrolyte disturbance (hypo/hyperkalemia)

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3. Fluid overload
4. Hypoglycemia
Reference:

White, Heil. Diabetic Ketoacidosis in Children. Endocrinology and Metab

Clinics 29(4): December 2000.

Diabetes Insipidus:
Definition:
1. Absence of or inability to respond to argentine vasopressin (AVP)
2. Polydipsia, polyuria with dilute urine, hypernatremia and dehydration
3. Polyuria exceeding 5cc/kg/hr, specific gravity < 1.010
4. Serum sodium > 145mmol/L
5. Central DI vasopressin deficiency
6. Nephrogenic DI renotubular resistance to vasopressin
Pathophysiology:
1. The secretion of antidiuretic hormone, argentine vasopressin, occurs from the posterior
pituitary gland in response to changes in serum osmolality and is regulated by the
paraventricular & supraoptic nuclei AVP acts at the cortical collecting ducts in the kidney
and binds to the vasopressin2 receptor
2. Binding initiates a G protein/cAMP signaling cascade leading to the insertion of
aquaporin protein in the cortical tubular cells allowing water to enter the cell
3. A deficiency of vasopressin is caused by destruction of the posterior pituitary gland by
tumors or trauma
4. Nephrogenic diabetes arises from end-organ resistance to vasopressin, either from a
receptor defect or medications that interfere with aquaporin transport of water
Epidemiology:
1. Incidence of diabetes insipidus in the general population is 3 in 100,000 slightly higher
incidence in males (60%)
2. Central diabetes insipidus:
- approximately 29% cases are idiopathic (isolated or familial) 50% of childhood cases
are due to primary brain tumors of the hypophyseal fossa
- up to 16% of childhood cases result from Histiocytosis X
- 2% of childhood cases are due to postinfectious complications and another 2% result
from head trauma
- inherited forms of central DI may be autosomal dominant (usu. present >1year of life)
or autosomal recessive (present <1 year)
3. Nephrogenic DI:
- may be x-linked recessive, autosomal dominant or recessive and usually presents <1
week of life
- acquired forms of nephrogenic DI may be secondary to medications (lithium,
amphotericin, cisplatin, lasix, gentamicin, rifampin, vinblastine), electrolyte disorders
(hypokalemia, hypercalcemia or hypercalciuria) or due to systemic disorders (Fanconi

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Syndrome, diffuse renal injury, obstructive uropathy, RTA, sarcoidosis, Sjogren

syndrome, Sickle cell disease and trait)
Evaluation:
1. Clinical history: poor feeding, failure to thrive, irritability, soaking of diapers in infants;
polyuria, polydipsia, nocturia, large volume of water; growth retardation, seizures
2. Physical examination: irritability, signs of dehydration (decreased tearing, depressed
fontanelle, sunken eyes, mottled or poor skin turgor), signs of shock (hypotension, weak
pulses)
3. Laboratory tests:
- hypernatremia >145 mmol/L, (>180 in nephrogenic DI)
- hyperchloremia, azotemia, acidosis, high osmolarity
- low urinary sodium and chloride, osmols
- urine specific gravity < 1.010 (first morning void)
- 24 hour hure collection- usu. > 5cc/kg/hour
4. Diagnostic tests:
- water deprivation test (perform only w/close monitoring and involvement of
endocrine team)
- a rise in plasma osmolality >10mOsm/kg over baseline with specific gravity
remaining <1.0101 establishes diagnosis of DI to differentiate types, administer
DDAVP; if urine osmolality rises by more than 450 mOsm/kg, central DI is
established; if urine osmols remain <200 mOsm/kg, nephrogenic DI is the likely
diagnosis
5. Imaging: consider MRI scan to delineate cause of central diabetes insipidus
(suprasellar mass/ pituitary cyst/ hypoplasia/ ectopic gland, etc)
Differential Diagnosis:
1. Diabetes mellitus/DKA
2. Compulsive water ingestion
3. Medications i.e., mannitol
4. Small volume urine loss as in cystitis, urethritis, etc.
Treatment:
1. IV forms (aqueous vasopressin or desmopressin) are used for central DI in acute
hypophysectomy or in intensive care settings until able to transition to intranasal forms
2. Monitor urine specific gravity and urine output closely, titrate drip or IV doses
appropriately; monitor serum sodium q2-4 hours initially
3. When stable, transition to intranasal DDAVP 5-20 mcg daily (absorption may be poor
with rhinitis or sinusitis); oral preparations also available
4. Treat dehydration with oral repletion or if necessary, parental rehydration if severely
dehydrated.
5. For nephrogenic DI, a low-osmolar, low-sodium diet should be initiated, and thiazide
diuretics administered which increases sodium loss by inhibiting its reabsorption in the
cortical tubules

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Complications:
1. Mental retardation
2. Seizures
3. Nonobstructive functional hydronephrosis and hydroureters
4. Chronic renal insufficiency
5. Life threatening dehydration and its complications
Reference: Saborio et al. Diabetes Insipidus. Pediatrics in Review: 21(4) April 2000.

B.

Neurology

Status Epilepticus
Definition:
1. A life-threatening medical emergency defined as frequent or prolonged epileptic seizures
2. Many definitions including a continuous seizure lasting longer than 30 minutes or
repeating convulsions lasting 30 minutes or longer without recovery of consciousness
between them. Current thinking involves shorter periods of time.
3. Onset may be partial or generalized
Epidemiology:
1. A common neurologic medical emergency, affecting 65,000 to 150,000 persons in the
United States yearly
2. Estimated that 1.3-16% of all patients with epilepsy will develop SE at some point in
their lives (in some may be the presenting seizure)
3. More common in childhood than in adults, no sexual predominance
4. Mortality rate is as high as 10%, rising to 50% in elderly patients
5. Many possible etiologies as listed below:

Causes of Status Epilepticus

Background of Epilepsy
Poor compliance with medication
Recent change in treatment
Barbiturate or benzodiazepine withdrawal
Alcohol or drug abuse
Pseudostatus epilepticus
Underlying infection/fever

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Presenting de novo
Recent stroke
Meningo-encephalitis, meningitis, encephalitis
Acute head injury
Cerebral neoplasm
Demyelinating disorder
Metabolic disorders (e.g. renal failure, hypoglycemia, hypercalcemia)
Drug overdose (e.g. TCAs, phenothiazines, theophylline, isoniazid, cocaine)
Inflammatory states (e.g. systemic lupus erythematosus)
New onset seizure disorder
Evaluation and Treatment:
1. Evaluate and support ABCs
2. Obtain IV access if possible
- check glucose
- if access, draw: lytes including Ca/Mg, Bun/Cr, LFTs
- consider CBC/blood cx if infection possible
- draw anticonvulsant levels, tox screen if indicated
3. Administer a rapidly acting benzodiazepine
- if IV: lorazepam (ativan) 0.5mg-1mg/kg (max 10mg)
- may repeat ativan
- administer long acting AED
+ fosphenytoin 15-20 mg/kg IV or
+ phenobarbitol 15-20 mg/kg IV
4. If seizures persist, consider additional ativan or additional bolus of phenytoin or
phenobarb 5mg/kg IV
5. ABCs: continue to eval; may need intubation if not able to manage airway
6. Last resort may need to induce pentobarb or general anesthesia (propofol) coma after
airway secured
7. Watch for potential complications including hypothermia, acidosis, hypotension,
rhabdomyolysis, renal failure, infection and cerebral edema
8. Continue to search for and treat any underlying cause
Complications:
1. Hypoxia
2. Metabolic and respiratory acidosis
3. Increased or decreased cerebral blood flow
4. Hypo or hyperglycemia
5. Rhabdomyolysis
6. Hyperkalemia
7. Hyperpyrexia
8. Cardiac dysfunction, arrythmias, hypotension
9. Permanent neurologic sequelae (e.g., motor deficits, MR, epilepsy)
10. Death

- 16 -

Reference:

Hanhan, U. et al. Status Epilepticus. Pediatric Clinics of N. America: 48(3): June

2001.

Traumatic Brain Injury and Increased Intracranial Pressure

Definition:
1. Increased intracranial pressure results when the volume of one of the cranial contents
(brain parenchyma, cerebrospinal fluid, or blood) increases and adaptive measures are
unable to compensate
2. Increased ICP is dangerous when it compromises cerebral perfusion, leading to further
cell damage, cerebral edema and eventual displacement and herniation of the brain
3. Classification of brain edema:
vasogenic- characterized by increased permeability of brain capillary endothelial cells, as
in tumor, abscess, hemorrhage, infarction contusion, lead intoxication, and
meningitis; the neurons and glia are relatively normal
cytotoxic- characterized by failure of the normal homeostatic mechanisms that maintain
cell size: neurons, glia and endothelial cells swell; prominent in hypoxic-ischemic
injury, osmolar injury, some toxins, and secondary injury following head trauma
interstitial- characterized by an increase in the water content of the periventricular white
matter due to obstruction of CSF flow
Pathophysiology:
1. The brain is composed of three components: brain (cells and intercellular fluid), blood
and CSF; increases in the size of any of the three compartments can lead to increased ICP
2. pO2, pCO2, pH and blood pressure all effect cerebral blood flow, but may act differently
in an injured brain compared to a normal brain
3. Increased pCO2 will cause an increase in cerebral blood flow, and hence an increase in
ICP. Low pO2 will also cause an increase in cerebral blood flow and ICP
4. Brain injury occurs in 2 phases: (1) the primary injury that occurs at the moment of
impact and results from a transfer of kinetic energy to the brain and (2) the secondary
injury that is a biochemical and cellular response to the initial trauma
5. The primary injury causes direct cellular damage; we cannot do anything to reverse the
primary injury as neurons do not regenerate
6. The secondary injury is delayed, usu. peaking at 48-72 hours and occurs in response to
the hypoxia, hypoperfusion and cell damage that result from the initial trauma; our goal
in management is to prevent, as much as possible, secondary injury
Epidemiology:
1. In pediatric trauma patients, head injuries occur in more than 70-80% of those children
who require hospitalization and death occurs in 20-40% of those patients
2. Each year, between 29,000 and 50,000 children younger than 19 years suffer permanent
disability as a result of TBI
3. The etiology of brain injury and increased ICP is important to understand and is essential
in formulating a treatment plan

- 17 -

Causes of Brain Injury and Increased ICP

Generalized Brain Injury
Hypoxic-ischemic injury
Diffuse head injury i.e. shaken baby syndrome
Osmolar injury (hypo-osmolality, hyerosmolality, DKA)
Encephalopathies (Reyes syndrome, hepatic encephalopathy)
Infection (meningitis, encephalitis)
Toxins
Focal Intracranial Lesion
Vascular: subdural, epidural, intraparenchymal hemorrhage, AVM
Focal traumatic lesion, focal edema w/o bleeding
Tumor
Abscess
CSF Obstruction
Evaluation:
1. Clinical history: -h/o trauma, symptoms including headache, vomiting, depressed level of
consciousness i.e. confusion, restlessness, progressive unresponsiveness
2. Physical exam: abnormal posturing, abnormal breathing pattern, abnormal cranial nerve
findings, papilledema, hypertension with bradycardia or tachycardia, bulging fontanelle
3. Cushings triad: increased ICP, hypertension, bradycardia or tachycardia bradycardia
and Cushings triad is a late sign of increased ICP
4. Radiology: CT (non contrast) to evaluate for blood, edema, mass effect
Equations:
Cerebral perfusion pressure (CPP) = MAP-ICP or MAP-CVP
Management:
1. Airway -remember avoid manipulation of neck in trauma; a child w/ a GCS <8 should be
intubated as a general rule to protect the airway; use meds during intubation that will
reduce the ICP response to intubation.
2. Breathing- ensure adequate oxygenation and avoid hypercapnia (mild hyperventilation is
appropriate)
3. Circulation- provision of adequate cardiac output and blood pressure is essential; avoid
lowering the osmolarity of blood (NO hypotonic fluids, normal saline or LR are good
options as is albumin). Initial Neurologic Assessment (GCS, neuro exam, seizures)
4. IV access and Lab evaluation: consider blood gas, electrolytes including Ca/Mg/Phos,
Osmolality, blood glucose, LFTs ammonia, CBC/coags, toxicology screen,
blood/urine/spinal tap
5. CT scan without contrast- evaluate for signs of trauma, bleed, edema
6. Evaluate and treat possible complications: hyperthermia, glucose abnormalities, seizures
7. Provide analgesia and sedation if indicated
8. Positioning- HOB elevated with head midline to avoid impeding venous return

- 18 -

9. Surgical management if indicated (drainage of blood, removal of tumor, drainage of CSF

or shunt revision)
10. Intracranial pressure monitoring (intraventricular drain, intraparenchymal catheter
(Camino), subarachnoid bolt). The goal is to maintain cerebral perfusion pressure 50-70
mmHg/ ICP <20, and detect events: rebleed, herniation, etc.
11. Mechanical ventilation: sats >95%, avoid hypercapnia, consider short- term
hyperventilation
12. Mannitol- decreases blood viscosity by lowering hematocrit, may reduce brain water
content in the uninjured portion) give rapidly, chronic dose is 0.25-0.5 mg/kg, in
impending herniation give a large 1 gram/kg dose quickly; watch blood pressure and
renal function
13. Lasix- synergistic in combo with mannnitol for reducing ICP
14. Other: barbiturates-controversial, steroids- will help reduce vasogenic edema (around
tumors), no effect on cytotoxic brain edema or in the management of head trauma
15. Fluid Management- avoid hypotension and hypo-osmolality; look for SIADH; reasonable
regimens include D51/2 NS or D5NS at slightly less than maintenance (so as to avoid Na
overload) follow electrolytes and volume status closely. Do not restrict volume early in
resuscitation.
Reference:

C.

Enrione, M. Current Concepts in the Acute Management of Severe Pediatric

Head Trauma. Clin. Ped Emergency Medicine: 2(1): March 2001.

Pulmonary

Status Asthmaticus
Definition:
1. The condition of severe, life threatening asthma
2. Unresponsive to the initial doses of bronchodilating agents
3. Progressive respiratory failure
Pathophysiology:
1. Reversible, diffuse lower-airway obstruction caused by airway inflammation and edema,
bronchial smooth muscle spasm and mucous plugging
2. Airway obstruction hyperinflation/VQ mismatch hypoxemia
Evaluation:
1. Exam: level of consciousness, breath sounds (distant or absent is ominous),central
cyanosis, accessory muscle use
2. Chest radiograph- if concerned for foreign body, pneumonia, pneumothorax
3. Arterial blood gas:
- Early phase hypoxemia, hypocarbia
- Impending respiratory failure hypercabia
Treatment:
1. Beta agonists: intermittent versus continuous inhaled treatments vs. IV terbutaline, reevaluate frequently
- 19 -

2. Steroids: give early

3. Cardio-respiratory monitoring
4. High flow supplemental oxygen (Non-rebreather if necessary, use blender if possible to
avoid 100 % FiO2)
5. Fluid replacement, avoid vigorous hydration. If severely ill, make sure patient has 2
large bore, well functioning IVs.
6. Antibiotics if clinically indicated
7. Other: anticholinergics, magnesium
8. Intubation can usually be avoided and requires considerable skill. Mechanical
ventilation is also difficult and should be managed by an experienced pediatric
intensivist. aggravates bronchospasm, worsens hyperinflation, risks barotrauma
If necessary, use low tidal volumes and long expiratory time. Support modes of
ventilation (pressure support and volume support) are used frequently.
Asthma Drugs and Doses
Drug
Albuterol

Nebulized

Prednisone
Methylprednisolone

Oral
IV

Ipratropium
Terbutaline

Nebulized
IV

Magnesium Sulfate

IV

Aminophylline

IV

Route

Complications:
1. Respiratory failure
2. Death
3. Barotrauma with mechanical ventilation

- 20 -

Dose
0.15 mg/kg max 5mg
continuous: 0.3mg/kg/hr
Typically ordered as 5, 10,
15, or 30 mg/hour.
2mg/kg/d max 60mg
2mg/kg loading dose
max 80 mg, 1mg/kg q 6
hours.
250-500 micrograms
Bolus: 10g/kg max 500g
Drip: 0.4g/kg/min, titrate
up as needed. Usually max
2-4g/kg/min.
25-75 mg/kg/dose max 2g
infuse over 20 minutes.
Watch for hypotension. If
effective, may continue as
infusion or bolus q3-4
hours.
6 mg/kg load followed by
infusion 1mg/kg/hr
(0.1-0.8 mg/kg/hr for
neonates and infants).
Uncommonly used.

4. Beta agonists- tachycardia, arrhythmia, hypertension or hypotension,

agitation/tremulousness, hyperactivity
5. Anticholinergics- anxiety, dizziness, headache, GI upset; aerosol chamber,
contraindicated in soy or peanut allergy
6. Magnesium- hypotension, respiratory depression, heart block, flushing, nausea,
somnolence
7. Methylxanthines- nausea, vomiting, tachycardia, hypotension, arrhythmia
8. Steroids- hypertension, pseudotumor cerebri, GI bleeding, hypergylcemia
Reference:

Werner, H. Status Asthmaticus in Children. Chest: 119 (6) June 2001.

Acute Respiratory Distress Syndrome

Definition:
Acute respiratory distress characterized by acute lung injury, noncardiogenic pulmonary edema
and severe hypoxia.
The respiratory distress syndrome in 12 patients was manifested by acute onset of
tachypnea, hypoxemia, and loss of compliance after a variety of stimuli, the syndrome did
not respond to usual and ordinary methods of respiratory therapy. The clinical and
pathological features closely resembled those seen in infants with respiratory distress and
to conditions in congestive atelectasis and postperfusion lung.
Reference:

Ashbaugh, Lancet, 1967

Diagnostic Criteria: 1. Identifiable associated condition

2. Acute onset
3. Pulmonary artery wedge pressure < or = to 18mm or absence of evidence of left atrial
hypertension
4. Bilateral infiltrates on chest radiography
5. Pao2/Fio2 ratio < or = to 200
*[Pao2/Fio2 ratio < or = to 300 is defined as Acute Lung Injury]
-American-European Consensus Conference Statement, 1994
Risk Factors:
Pulmonary
Bacterial pneumonia
Viral pneumonia
Aspiration
Inhalation injury
Fat emboli
Near Drowning

Extra-pulmonary
Sepsis
Trauma
Multiple transfusion
Cardiopulmonary bypass
Pancreatitis
Peritonitis
Anything really bad

- 21 -

Pathophysiology:
1. Direct lung injury or systemic insult occurs
2. Release of pro-inflammatory agents i.e. TNF, interleukins
3. Migration of neutrophils producing oxygen radicals and proteases
4. Endothelial and epithelial cell damage leads to increased permeability and the influx of
fluid into the alveolar space. (pulmonary ARDSepithelial damage, extra-pulmonary
ARDSendothelial damage initially)
5. Surfactant is abnormal
6. Impaired fibrinolysis leads to capillary thrombosis/microinfarction

Pathology of ARDS
Exudative Phase
(Day 1-7)
Interstitial and intraalveolar edema

Proliferative Phase
(Day 7-21)
Interstitial myofibroblast
reaction

Fibrotic Phase
(> Day 21)
Collagenous fibrosis
Microcystic honeycombing

Hemorrhage
Leukoagglutination

Lumenal organizing fibrosis

Chronic inflammation

Necrosis-Type I
Pneumocytes

Parenchymal necrosis

Hyaline membranes

Type II pneumocyte
hyperplasia

Platelet-fibrin thrombi

Obliterative endarteritis

Reference:

Traction bronchiectasis
Arterial tortuosity
Mural fibrosis
Medial hypertrophy

Macrothrombi
Tomashefski, J. Acute Respiratory Distress Syndrome. Clinics in Chest
Medicine: 21(3) Sept. 2000.

Evaluation:
1. Physical exam: tachypnea, tachycardia, altered mental status
2. Blood gas monitoring: initial respiratory alkalosis may precede infiltrates, later:
alveolar edema VQ mismatch/shunt severe hypoxia
3. Imaging: CXR progression from diffuse interstitial infiltrates to diffuse, fluffy alveolar
spaces; later reticular pattern suggests interstitial fibrosis. CT demonstrates dependent
(posterior if supine) infiltrates and atelectasis, with anterior hyperinflation.
*Most patients with ARDS develop diffuse alveolar infiltrates and progress to
respiratory failure within 48 hours of the onset of symptoms

- 22 -

Treatment:
1. Treatment of underlying cause or associated condition
2. Ventilatory support- ensures adequate oxygenation/ventilation while minimizing
ventilator induced lung injury.
- Appropriate recruitment of alveoli through appropriate levels of PEEP. Avoid under
(atelectrauma) or over (volu/barotraumas) inflation.
-Limit pressures and tidal volumes (<30-35)
-Tolerate hypercapnia permissive hypercapnia well accepted
-Tolerate hypoxemia? permissive hypoxemia ?
- Consider high-frequency oscillatory ventilator
- Consider prone position
3. Pharmacologic treatment- no proven role as yet. Drugs sometimes used include steroids
(late phase), NitricOxide (no proven survival benefit),
4. Monitor and/or Prophylaxis for complications- GI bleed.
- Thromboembolism
- Nosocomial infection
5. Supportive care- nutrition, sedation/pain control
6. ECMO: not proven to improve survival
Ventilator Strategy:
1. Usual mode is PRVC (pressure regulated volume control).
2. Avoid over or under-inflation: Usually this requires PEEP of 6-12, depending on
severity. Remember things tend to get worse before they get better-it is not unusual for
patients to require increasing PEEP as their disease worsens.
3. Use low tidal volumes, 5-7 cc/kg. Monitor peak pressure (PIP or plateau pressure). It
should be less than 30-35.
4. Use longer aspiratory times than usual for age.
5. Tolerate hypercapnia, monitor pH, try to keep >7.2
6. Tolerate hypoxemia if necessary to keep FiO2 <60%. If on <60%, Sat goal should be
~92, if not able to maintain 92 on <60%, tolerate 85%. Monitor trends closelyabsolute
numbers are not usually important, trends in numbers are often extremely important.
7. Remember that cardio-pulmonary interactions occur, and ventilator maneuvers may
affect hemodynamics.
Complications:
1. Barotrauma- pneumothorax, pneumomediastium, subcutaneous emphysema
2. Cardiac- hypotension
3. GI- stress-related gastrointestinal hemorrhage
4. Death estimated to occur in 20 (low risk)-90% (highest risk, BMT) of cases. Previously
well children and those with extrapulmonary ARDS have a better prognosis. The
mortality from ARDS has fallen significantly since it was first described in 1967.
Reference:

Mortelliti, M. Acute Respiratory Distress Syndrome. American Family

Physician: 65(9) May, 2002.

- 23 -

D.

Infectious Diseases

Meningitis
Definition:
1. Inflammation of the membranes surrounding the brain and spinal cord including the dura,
arachnoid and pia mater
2. May present in combination with inflammation of the cerebral cortex, then called
meningoencephalitis
3. Associated with evidence of an inflammatory response in the CSF
4. Most commonly caused by viral or bacterial infection, but must consider infection with
fungus, mycobacterium and cryptococcus and anaerobes.
Epidemiology:
1. Prognosis depends on age, etiology, time of onset to therapy, and complications
2. Case fatality rate range from 3-5 % for meningococcal meningitis to 10% for
pneumococcal meningitis and 15-20% in neonatal cases
3. The common etiologic agents of meningitis can be divided by age group as follows:
<1 Month

1-3 Months

Immunocompromised

Group B Strep

3 Months through
School Age
N. meningitides

Group B Strep
E. coli

S. pneumoniae

S. pneumoniae

Toxoplasma

Listeria

N. meningitides

H. influenza

Tuberculosis

Enterococcus

H. influenza

Enterovirus

Aspergillus

Enterovirus

Enterococcus

Arbovirus

And all others

HSV

Enterovirus

HHV6

CMV

HSV

EBV

Ureaplasma

HHV6

Mycoplasma

Candida

Cryptococcus

Mycobacterium

Pathophysiology:
1. Inflammation of the meninges is initiated when cell wall and membrane products of an
organism disrupt the capillary endothelium of the CNS (e.g. blood brain barrier)
2. The organism/offending agent may enter the CNS by hematogenous spread or by direct
invasion
3. Disruption of the endothelium causes transmargination of PMN and subsequent release of
cytokines and chemokines

- 24 -

4. Inflammation of the vessels produces capillary leak, leading to edema and potentially to
increased ICP
5. Further inflammatory response occurs following antibiotic administration due to rapid
bacterial lysis and release of cell wall/fragments
Evaluation:
1. History- fever, headache, neck pain or stiffness, nausea, vomiting, photophobia and
irritability; young infants may only exhibit irritability, somnolence and fever; seizures
also possible
2. Physical exam- alterations in level of consciousness, stiff neck (Kernig and Brudzinski
signs not sensitive in young children), bulging fontanelle, rash, fever, focal neurologic
abnormalities in complicated cases, hemodynamic instability
3. Studies- lumbar puncture-CSF studies are key to diagnosis. Include cell count, diff,
protein, glucose, culture, gram stain, specific stains/cultures as indicated, PCR for
enterovirus/HSV, etc.
4. Lab studies- CBC w/diff, blood culture, electrolytes (eval for SIADH), consider LFTsmay be elevated with enteroviral infections or disseminated HSV
5. Imaging -consider CT scan or MRI if concerned for increased ICP or abscess, or for
evaluation in a complicated clinical course (hydrocephalus, subdural effusion,
hemorrhage or infarction may be seen). MRI is also helpful in diagnosis and
management of herpes meningitis and tuberculosis meningitis
6. Other -all patients should have urinalysis, urine culture. When viral meningitis is
suspected, swabs of rectum, nasopharynx and eyes indicated in addition to CSF studies
CSF Findings in Infants and Children
Component
Normal
Normal
Bacterial
Viral
Children
Newborn
Meningitis
Meningitis
Leukocytes/mcL 0-6
0-30
>1,000
100-500
Neutrophils (%)
0
2-3
>50
<40
Glucose (mg/dL) 40-80
32-121
<30
>30
Protein (mg/dL)
20-30
19-149
>100
50-100
Erythrocytes/mcL 0-2
0-2
0-10
0-2
*Adapted from Wubbel, et. Al, Pediatrics in Review. 1998: 19(3) page 80.
*CSF in tuberculous meningitis is notable for low glucose

Herpes
Meningitis
10-1,000
<50
>30
>75
10-500

Treatment:
1. Management of ABCs
2. If bacterial meningitis suspected and if possible after all cultures obtained, begin
appropriate empiric antibiotic treatment on basis of age and epidemiologic factors
(remember meningitic doses!)
- in neonates/infants, consider ampicillin and gent or cefotaxime
- in children consider cefotaxime or ceftriaxone, and addition of vancomycin in cases
of possible resistant S. pneumonia
- if herpes meningitis is suspected, intravenous acyclovir is appropriate
3. In cases of aseptic meningitis, supportive care
4. Evaluation for and treatment of complications i.e. SIADH, seizures
5. Isolation precautions and chemoprophylaxis for exposed individuals if indicated

- 25 -

6. Consider neurosurgical evaluation if indicated (drainage of subdural, placement of ICP

monitor)
7. Increased intracranial pressure may rarely occur. In there is clinical evidence of
increased ICP, consider ICP monitoring and treatment. The most common cause of death
in meningitis is brain death.
8. Supportive care, pain control, GI prophylaxis, nutrition.
Complications:
acute:
seizures
increased ICP
effusion/empyema/abscess/subdural
SIADH
herniation
death
chronic:
hearing loss
seizure disorder
hydrocephalus
developmental delay
Reference:

Wubbel et al. Management of Bacterial Meningitis: 1998. Pediatrics in Review.

1998: 19(3), pages 78-84.

Encephalitis
1.
Definition:
- involves inflammation of the cerebral cortex
- often present with some inflammation of the meninges, i.e., meningoencephalitis
- an unusual complication of common viral infections, can be subdivided based on
etiology and pathogenesis: 1) acute encephalitis, 2) postinfectious encephalomyelitis,
3) slow viral infections of the CNS
2.

Pathophsiology:
- a virus gains access to the CNS by either hematogenous or neuronal routes
- in anthropoid-borne viral disease there is local replication of the virus at the skin
followed by transient viremia which causes seeding of the reticuloendothelial system
and later the CNS
- in contrast, viruses such as HSV and rabies gain access to the nervous system intraneuronally
- in acute encephalitis, capillary and endothelial inflammation occurs primarily in the
gray matter or gray-white junction; subsequent lymphocytic infiltration results.
- as the disease progresses astrocytosis and gliosis become evident on histopathology

3.

Epidemiology:
- approximately 20,000 cases of encephalitis occur in the US each year
- the two endemic causes of encephalitis include rabies and HSV

- 26 -

- HSV accounts for approximately 10% of all US cases of encephalitis

- MMR and polio vaccinations have significantly decreased the incidence of
postinfectious encephalitis
- postinfectious encephalomyelitis is still seen with upper respiratory tract, although
uncommon, and is most often seen with influenza infection
- anthropoid-borne viruses causing encephalitis that are seen in the US include St.
Louis encephalitis, Eastern equine encephalitis, Venezuelan equine encephalitis, and
La Crosse virus
- other viruses that have the potential to cause encephalitis include enteroviruses,
coxsackieviruses, and echoviruses, CMV, EBV, varicella, HHV-6
- rarely bacteria are the cause of diffuse encephalitis and may include listeria and
mycoplasma pneumoniae
- Japanese encephalitis is a major cause of encephalitis in China, SE Asia, and India
and must be considered in persons who recently traveled or moved from these areas
4. Evaluation:
- clinical history
- fever, headache, disorientation, altered consciousness, behavioral changes; in more
severe cases hemiparesis or seizures; photophobia and nausea also seen
- history of travel, season, bite from animal or insect, URI
- n cases of meningoencphalitis, may also see nuchal rigidity
- physical exam- eval for focal neurologic signs, lethargy or somnolence, fever, rash,
nucal rigidity
- HSV infection has predilection for the temporal lobes and thus can lead to findings of
aphasia, anosmia, temporal lobe seizure and focal neurologic findings
- studies: labs- CBC, blood and viral cxs including mucous membranes, electrolytes
to eval for SIADH CSF evaluation
- may be normal but can see elevated protein levels and mononuclear cell pleocytosis;
rarely helpful for isolating the virus
- include viral cultures as well as PCR for HSV, CMV, HHV-6 and enteroviruses if
indicated CT
- eval for tumor or abscess that may mimic encephalitis
MRI- may see areas of inflammation, edema
EEG- to eval for seizure activity
5. Treatment:
- ABCs
- management of increased intracranial pressure
- acyclovir to treat possibility of herpes infection until ruled out
- antibacterial therapy for suspicion of bacterial involvement
- rabies vaccine and immune serum for those potentially exposed to rabies
- supportive care
6. Complications:
- seizures
- neurologic deficits

- 27 -

death

Reference:

E.

Whitley et. al., Viral Encephalitis. Pediatrics in Review. June 1999: 20(6).

Gastroenterology

Gastrointestinal Bleed
1.

Definition:
- upper GI bleed- originating above the ligament of Treitz
- usually presents with hematemasis or melena; may present as hematochezia if large
amount of blood/rapid transit
- lower GI bleed- originating below the ligament of Treitz
- presents as hematochezia
- must be confirmed by gastroccult, guaiac, hemoccult or hematest for the presence
of blood (to rule out food coloring/medications)

2. Risk Factors: liver failure- coagulopathy, esophageal varices

- surgery/burns/steroids/brain tumors- gastrointestinal ulceration
- NSAIDs/steroids- ulceration
- GERD/neuromuscular disease- esophagits
- cirrhosis/portal hypertension- gastroesophageal varices
- constipation- anal fissure/ hemorrhoids
- family history- inflammatory bowel disease
- recurrent vomiting- Mallory-Weiss syndrome
3.

Diagnosis: -careful history and physical exam, evaluation of vital signs as indicator of
volume of blood loss
- immediately establish IV access (as large an IV as possible x 2)
- place nasogastric tube to assess extent of active bleeding/confirm presence of fresh
blood
- confirm presence of blood by appropriate testing (i.e. hemmocult)
- baseline blood count; may be misleading in recent bleed, use as comparison
- other labs: liver function, platelet counts, coagulation times, Apt test
- imaging: plain films- not very helpful but can see free air/foreign body
ultrasonography
- eval for portal hypertension, vascular anomalies
+ Endoscopy- method of choice; offers both diagnosis and tx (banding, sclerosissee below)
+ Meckels scan- consider in painless, massive bleeding Angiography- when
bleeding is massive
+ MRI/CT- to evaluate mass lesions, vascular malformations

4.

Treatment: endoscopic therapy-electrocoagulation, laser tx, sclerosing, elastic band

ligation, mechanical clips
- arteriographic embolization by interventional radiology
- transjugular intrahepatic portosystemic shunt placement (TIPS)
- 28 -

surgical repair/excision- Meckel diverticulum, polyp, ulceration

antibiotics- in few cases of infectious enterocolitis
H-2 blockers- esophagitis, ulcers, GERD
Proton pump inhibitors- as above
Octreotide- a somatostatin anolog
Corticosteroids- for inflammatory bowel disease exacerbations

Causes of GI Bleeding In Children

Infancy

Infant to 6 months

Swallowed maternal
blood
Hemorrhagic
disease- newborn

Anal fissure

6 months to
5 years
Epistaxis

Esophagitis/gastritis

Esophagitis/gastritis

Infective
enterocolitis

Esophageal varices

Mallory-Weiss
syndrome

Polyps

Gastritis

Infective colitis

Peptic ulcer

Lymphonodular
hyperplasia

Chronic ulcerative
colitis

Intussusception

Crohns disease

Meckel
diverticulum

Hemorrhoids

Anal fissure
Protein-sensitive
enterocolitis

Infective
enterocolitis

Intussusception
Protein sensitive
enterocolitis

Lymphonodular
hyperplasia

Necrotizing
enterocolitis

Volvulus

Hirschsprungs

Hirschsprungs

Midgut volvulus

Vascular
malformations

Vascular
malformations

Duplication cysts

Gastric ulceration

5-18 years
See 6mos-5years,
and:

Coagulopathy
Vascular
malformations
Henoch-Schonlein
purpura
Hemolytic uremic
syndrome

Duplicaton cysts
4.

Pearls:
- Currant-jelly stools- indicates mixture of blood, mucous and stool, consider Meckel
diverticulum or intussusception massive, painless bleeding
- Meckels

Reference:

Vox, Victor. Gastrointestinal Bleeding in Infancy and Childhood.

Gastroenterology Clinics: 29(1) March, 2000.

- 29 -

F.

Renal

Hemolytic Uremic Syndrome

1. Definition:
- combination of microangiopathic hemolytic anemia and variable degrees of
thrombocytopenia and renal failure
- usually occurs ages 6 months-5 years, previously healthy children
- most commonly preceded by watery diarrhea that can evolve into hemorrhagic colitis
proceeds to hemolysis, thrombocytopenia, then oliguria/anuria several days later
2. Pathogenesis:
- typically occurs with infection and associated toxin production/release
- oxin binds and destroys colonic mucosal epithelial cells resulting in blood diarrhea
- also enters systemic circulation and binds to endothelial cells (especially in the
kidneys) causing release of vWF, PAF and plasminogen activator inhibitor resulting
in platelet/fibrin thrombi
- may involve endothelium in the CNS, pancreas, liver, etc.
- red blood cells become deformed in the occluded vessels and platelets consumed,
resulting in hemolytic anemia and thrombocytopenia
3. Etiology/Epidemiology:
- two types of HUS which differ by presence or an enteritis prodrome
- the most common type is accompanied by enteritis and is strongly linked to a shigalike toxin associated with E.coli 0157:H& and others such as enterohemorrhagic
E.coli and shigella
- usually acquired by consumption of raw/undercooked meat, unpasteurized milk and
contaminated water/apple juice; person to person spread also possible
- atypical HUS lacks the preceding diarrheal illness and is less common; has been
associated with strep pneumo, drugs and collage vascular disorders; has been
associated with higher complication rates
5.

Evaluation:
- exam: vitals
- hypertension, tachycardia CNS
- drowsiness, personality changes, hallucinations, hemiparesis
Abdomen- surgical abdomen, tenderness, Hepatosplenomegaly
Skin- pallor, petechiae, jaundice, edema
Labs:
CBC- normochromic, normocytic anemia; thrombocytopenia, WBC
Smear- schistocytes
Coags- normal
Urine- hematuria, proteinuria, anuria, red cell casts
CMP- elevated creatinine/BUN, electrolyte disturbances
Stool- +E.coli/shigella, +fecal leukocytes
- 30 -

6.

Differential Dx: TTP, DIC, IBD

7.

Complications: 5-10% mortality rate

ESRD 10%
CNS involvement 20-30% (seizures most common)
Pleural/pericardial effusions
Pancreatic insufficiency 4-15% (diabetes most common)
Intussuception, gangrenous bowel
*poor prognostic factors include: WBC >20,000
anuria > 1 week
CNS involvement

8.

Management: supportive care

Blood pressure control (calcium channel blockers, nitroprusside)
PRBC infusions
Fluid management
Correction of electrolyte imbalance
Dialysis, indications for: BUN > 100
Fluid overload
Electrolyte imbalance
*avoid platelet transfusions- may contribute to microthrombosis
*plasmapheresis may be helpful, more likely in atypical cases

Reference:

Corrigan et al. Hemolytic-Uremic Syndrome. Pediatrics in Review: 22(11)

November 2001.

G. Hematology/Oncology
Tumor Lysis Syndrome
1. Definition:
- acute tumor lysis syndrome is the consequence of the rapid release of intra-cellular
metabolites (potassium, phosphorus and uric acid) in quantities that exceed the
excretory capacity of the kidneys
- potential complications include acute renal failure and hypocalcaemia-onset of tumor
lysis is most commonly seen at the onset of therapy for malignancies that are
especially sensitive to chemotherapy (i.e., Burkett lymphoma, T cell lymphoma, and
other lymphoid malignancies especially with hyperleukocytosis) -usually seen
between day 1 and 5 of treatment but may present before onset of therapy secondary
to spontaneous tumor degradation
2. Pathopysiology:
- lymphoblasts contain 4 times the content of phosphate of normal
- lymphocytes; when the calcium phosphate product exceeds 60, calcium
- phosphate precipitates in the renal tubules and microvasculature causing renal failure
- 31 -

hyperkalemia can result from tumor lysis or renal failure

an elevation in uric acid results from the breakdown of nucleic acids; urates
precipitate in the acid environment of the kidney, causing renal failure
hypocalcaemia occurs secondary to compensatory mechanisms to maintain the
calcium phosphate product at 60

3. Evaluation:
- repeated physical examination
- monitor urine output, blood pressure; check weight at least twice daily
- monitor serum creatinine, uric acid, calcium, sodium, phosphate and potassium at
least every 8 hours until the high risk period is over
- if oliguria occurs, consider imaging with ultrasound or CT scan to look for
obstructive uropathy
- EKG with hyperkalemia
4. Prevention:
- aggressive hydration to maintain urine output at >5ml/kg/h before chemotherapy
and at >3ml/kg/h once chemotherapy begins
- allopurinol 300mg/m2/day divided TID- a xanthine oxidase inhibitor, inhibits the
breakdown of amino acids into uric acid
- alkalinization of the urine pH from >6.5 to <7.5 with NaHCO3 to increase the
solubility of urates and avoid precipitation of crystals in the kidneys
- consider diuresis with lasix or mannitol to achieve desired urine volume
- avoid potassium in fluids
5. Management:
Hyperuricemia
- continue allopurinol/alkalinization
Hyperphosphatemia
- maintain urine output, low-phosphate diet, aluminum hydroxide 150mg/kg/day
divided q4-6 hours hyperkalemia
- administer calcium to stabilize cardiac cell membranes sodium bicarbonate at 1-2
mEz/kg IV to drive K into cells
- administer insulin at 0.1U/kg/h simultaneously with glucose (1/2 gram/kg) to move
excess potassium into cells, monitor serum glucose carefully sodium polystyrene
sulfonate (Kayexalate) to remove K, not useful in emergencies
Hypocalcaemia
- treat with CaCl or Ca gluconate if symptomatic
Dialysis
- indications include: fluid overload with CHF, anuria, electrolyte disturbances
intractable to other treatment or with symptoms/EKG findings
Venoocclusive Disease
1. Definition:
- a serious complication of bone marrow transplantation that occurs early in the posttransplant course, with clinical onset usually between day +7 and day +20

- 32 -

clinical syndrome consisting of sudden weight gain, ascites, and hyperbilirubinemia

2. Pathophysiology:
- caused by occlusion of the hepatic venules by cellular debris and endothelial swelling
related to the toxic effects of the conditioning regimen
- results in sclerosis of the terminal hepatic veins which leads to increased resistance
and the development of portal hypertension
3. Evaluation:
- monitor urine output and fluid balance closely
- twice daily weight measurements
- blood pressure monitoring
- daily labs including bilirubin, LFTs
4. Prevention:
- aggressive hydration during pre-conditioning phase to preserve filling pressure and
prevent further collapse of the hepatic venules
5. Treatment:
- aggressive hydration
- renal dose dopamine 3-5 mcg/kg/min to maintain urine output
- diuretics i.e., metolazone, furosemide, bumetanide
- maintain serum albumin >3g/dL to help maintain intravascular volume
Dilutional coagulopathy (coming)
Disseminated intravascular coagulation (coming)
Heparin Induced Thrombocytopenia
1. Cause and Clinical Significance of Heparin-Induced Thrombocytopenia (HIT):
HIT is the most common drug-induced thrombocytopenia in adults, complicating 1-4% of fulldose exposures to standard heparin. Unlike other thrombocytopenias, HIT carries a high
thrombotic morbidity (30-50%) and mortality (10-15%) because it is a syndrome of platelet
activation. Heparin forms a complex with platelet factor 4 (PF4) which is released from
platelets by platelet activation. Antibody directed against the heparin-PF4 complex binds via its
Fab region. The antibody-heparin-PF4 immune complex binds to the Fc receptor on the surface
of the platelet leading to activation of the platelet. [Fig. 1]

- 33 -

2. Clinical Characteristics of HIT:

In HIT, the platelet fall is usually 40-50% and the thrombocytopenia is moderate (30-100). The
onset is 5-10 days after first exposure to heparin and hours to 2-3 days with re-exposure. In reoperative cardiac surgery in adults either the platelets do not rise post-op, or rise, then fall with
no other cause evident. Venous thrombosis (DVT, PE) is more common than arterial (limb
ischemia, stroke, MI). Thrombosis may localize to sites of pre-existing pathology (CVLs,
shunts, surgical repairs) and be present in unusual locations. Less common presentations include
delayed thrombocytopenia (2-3 weeks), heparin-induced skin necrosis (SQ sites), adrenal
infarction/hemorrhage, heparin resistance and anaphylactoid reactions
3. Laboratory testing:
Antibody (PF4) ELISAs are sensitive but not specific. More specific for clinical HIT are
functional assays based on in vitro heparin-dependent platelet activation (14C serotonin release,
heparin-dependent platelet aggregation, lumi-aggregometry). Unfortunately functional assays
are less sensitive and often negative or indeterminate in the first 24-48 hours of HIT. Both
assays usually become negative in about 3 weeks, making it difficult to diagnose previous HIT.
4. Treatment:
ALL heparin (lines, flushes, heparin-coated catheters, low molecular weight heparins) must be
stopped. Platelet transfusion should be AVOIDED (transfusion may precipitate thrombosis) as
should warfarin in the acute phase of HIT (its use may precipitate venous gangrene and
thrombosis). Use of alternative anticoagulation is imperative in pre-existing or new thrombosis
and should be strongly considered for prophylaxis (up to 50% of asymptomatic patients
thrombose). Argatroban, a hepatically excreted, synthetic anti-thrombin with a t 1/2 of ~ 40-50
minutes, is presently our choice. It is only available IV. Usual dose is 2mg/kg/min by
continuous infusion. All patients with HIT should have a hemostasis/thrombosis consult.

- 34 -

I. Shock, SIRS, MOSF

Shock
1. Definition:
- inadequate tissue perfusion to supply oxygen and nutrients to meet the metabolic
demands of the body
- three major types include hypovolemic, distributive and cardiogenic
- hypovolemic shock is the most common form, and is due to an absolute loss of
volume from the vasculature (blood loss (hemorrhage), body water loss (dehydration)
or loss of plasma)
- distributive shock results when total circulating volume has been redistributed and a
functional hypovolemic state results (seen in sepsis, Neutrogena shock and
anaphylaxis)
- cardiogenic shock occurs when the heart is unable to maintain cardiac output (may
be intrinsic i.e., heart failure or extrinsic i.e. tamponade)
- compensated shock is the state of tissue hypoperfusion in which adaptive
physiologic responses are still able to maintain blood pressure
- decompensated shock is the state in which the adaptive physiologic responses can no
longer compensated and central organ perfusion is no longer maintained as heralded
by hypotension
2. Evaluation:
rapid evaluation of airway, breathing and circulation
Clinical history
- underlying disease, recent infection or illness, trauma, surgery, etc.
- physical exam- ABCs first, heart rate, blood pressure, respiratory rate, pulses, skin
perfusion, altered mental status, decreased level of consciousness, urine output, other
signs of trauma or focus for indication of infection
Studies- labs including CBC, CMP, blood gas, coagulation panel, blood culture; consider
amylase in trauma, lactate
- imaging including chest xray, others in trauma (pelvis/abdomen)
- consider CT of head/abdomen if stable
- consider echocardiogram if possibility of cardiogenic shock
- urine and CSF studies in suspected septic shock
3. Treatment:
- establish a patent airway, ensure adequate oxygenation and ventilation (support
cervical spine if trauma suspected)
- establish intravascular access
- fluid resuscitation (crystalloids i.e. normal saline/lactated ringers, colloids i.e., 5% or
25% albumin, or blood products)
- use of inotropes if fluid resuscitation not adequate (dopamine, dobutamine,
norepinephrine among others)
- maintain electrolytes
- evaluate for and treat underlying cause

- 35 -

Clinical Signs

Hypovolemic
Shock

Distributive Shock

Cardiogenic Shock

Thready

Respiratory Rate
Respiratory Effort
Heart Rate
Pulse Quality

Normal

Thready

Pulse Pressure
Skin Perfusion

Narrow
Pink, cool distally,
nl or prolonged CR

or
Normal to
to
Early-bounding
Late-thready
Widened
Pink, often warm
early, nl to long CR

Level of
Consciousness
Urine Output
Stroke Volume
Preload
Afterload
Acidosis

Usually normal
unless severe
Decreased
Low
Low
High
Mild to moderate

Lethargic or
confused
Decreased
Normal to increased
Low
Low
Mild to marked

*Adapted from PALS Provider Manual, AAP, 2002

- 36 -

Narrow
Mottled gray or
blue, cool to cold,
prolonged CR
Lethargic to coma
Markedly decreased
Markedly decreased
Often high
High
Moderate to marked

Intubation
This is a general review of issues relevant to intubation. While the hand skills necessary for
performing intubation do take a certain amount of practice, the decision of when to intubate and
the choice of technique is of at least equal importance, and is often ignored. While you may not
acquire significant hands on training in intubating non-neonates during your pediatric
residency, you will have the opportunity to learn how to decide when someone should be
intubated, as well as the potential complications and problems that may be encountered. THIS
KNOWLEDGE MAY BE LIFE-SAVING.
I.

Indications for intubation--Thinking about the indications will help you decide on a
technique.
A. Airway patency
B. Requirement for positive pressure ventilation due to pulmonary disease (ie, hypoxia
or hypercarbia)
C. Significant cardiovascular compromise, shock
D. Neurologic-seizures, weakness, head injury

II.

Techniques
A. Awake, without drugs
B. Sedated but not paralyzed
C. Anesthetized-+/- rapid sequence induction

III.

Considerations in determining technique used for intubation

A. Airway anatomy-if primary airway problem, i.e., croup, epiglottitis, foreign body,
abnormal anatomy, etc., DO NOT BURN BRIDGES. These patients should not be
paralyzed. Paralysis relaxes the pharyngeal muscles, which may obscure landmarks
in the difficult airway, and may make bag-mask ventilation difficult. Sedation, along
with local anesthetics (i.e., lidocaine spray) may be used to facilitate intubation.
B. Cardiovascular stability-hemodynamically unstable patients (i.e., sepsis, toxic shock,
certain ingestions) may become even more unstable when sedated, due to loss of
sympathetic tone. Any drugs used should be used in smaller doses and titrated to
effect. Patients with primary cardiac disease, however, generally do not tolerate
unsedated intubations, and carefully titrated anesthesia is warranted.
C. Cardiopulmonary arrest-there is no reason to use any pharmacologic intervention.
Bag-mask ventilation with cricoid pressure and intubation can generally be
accomplished without difficulty.
D. Full stomach--risk of pulmonary aspiration. These patients should be intubated
awake to preserve airway protective reflexes, or by rapid sequence induction with
cricoid pressure.
1.
Recent oral intake
2.
Delayed gastric emptying from ascites, peritonitis, bowel obstruction
3.
Swallowed blood from trauma
4.
Increased intra-abdominal pressure from masses or ascites
5.
Abnormal lower esophageal tone-pregnancy
6.
Gastro-esophageal reflux
7.
Altered level of consciousness

- 37 -

E. Head injury-laryngoscopy and intubation may lead to increased intracranial pressure

in the unanesthetized patient with an evolving head injury. Trauma victims are
frequently hypovolemic. Drugs and doses used need to be carefully considered.
IV.

The awake intubation

A. Indications (all relative)
1. Cardiopulmonary arrest
2. Airway anomalies, acute severe upper airway disease
3. Cervical spine injury
4. Facial Trauma
5. Significant hemodynamic instability
6. Any suspicion of difficulty intubating, for any reason.

B. Technique
1. Local anesthetic sprays can be used to topicalize the tongue and pharynx.
Nebulized lidocaine (2cc 1% lidocaine in nebulizer) will decrease the
laryngospasm and bronchospasm with intubation.
2. Laryngoscopy and intubation should proceed firmly but gently, with attention
to the teeth and tongue if the child is struggling
V. The sedated intubation
A.
Indications
1. Potentially difficult airway
2. Lung disease with moderate to high O2 requirement (may desaturate during
period of apnea necessary for rapid sequence intubation)
B.
Technique
1. Carefully titrated drugs, watching for hemodynamic as well as sedative
effects. If hemodynamics are stable, more drug can be given if necessary.
a. Versed, 0.05-0.1 mg/kg. Use lower doses in the setting of
hypovolemia, sepsis, or poor cardiac function.
b. Ketamine, 0.5-2.0 mg/kg. Indirect sympathomimetic preserves cardiac
output and systemic BP in acutely hypovolemic patients. Direct
bronchodilatory properties. Potent sialogogue (premedicate with
atropine or glycopyrrolate). Co-administration of a small dose of
benzodiazepine will reduce emergence phenomena.
2. Monitor degree of sedation carefully. Watch for signs of impending vomiting
or respiratory depression. Gentle ventilatory assistance through cricoid
pressure is sometimes necessary in extremely hypoxic or unstable patients.
VI. The anesthetized intubation--rapid sequence induction
A. Indications
1.
Full stomach conditions
2.
Head injury
3.
Asthma
4.
Common theme-Desire to blunt undesirable physiologic response to
intubation-hypertension, tachycardia, bronchospasm, increased
intracranial pressure.

- 38 -

B. Contraindication-anticipated difficulty with securing airway, i.e., anatomic

abnormality or airway pathology. NEVER sacrifice airway safety for the sake of
pharmacologic intervention.
C. Technique-rapid sequence refers to rapid infusion of medications, followed by a brief
period where airway protective reflexes are lost, followed by ideal intubating
conditions. During the period after medications are given, cricoid pressure is
applied and positive pressure ventilation is avoided.
1. Preoxygenate with 100% O2
2. NG (if present) to suction. Have suction (LARGE Yankauer) available!!!
3. Medication sequence--cricoid pressure should be applied from the moment
drugs are given until the ETT is confirmed to be in the proper position. No
positive pressure ventilation.
a. Atropine
b. Sedation
c. Paralysis
4. When fully relaxed, intubate the trachea, remove the stylet, and attach bag.
5. If difficulty with intubation arises, or the patient had more lung disease than
you anticipated and desaturates significantly without positive pressure
ventilation, GENTLY BAG MASK VENTILATE the patient, get the
saturations up, and try again.
6. Confirm ETT placement by breath sounds, mist in tube, ETCO2 device.
Confirm correct placement with CXR.
D. Drugs to facilitate intubation
1. Atropine 0.02 mg/kg, minimum 0.1 mg
2. Sedation-Benzodiazepine +/- narcotic, or ketamine, or thiopental.
a. Versed 0.05-0.1 mg/kg
b. Morphine 0.2 mg/kg or fentanyl 1-2 mcg/kg
c. Ketamine 0.5-2 mg/kg
d. Thiopental 2-6 mg/kg
3. Paralysis
a. Rocuronium 1.2 mg/kg achieves intubating conditions in 60 seconds.
Duration of paralysis 30-60 minutes. Should not be used if there is any
anticipated difficulty achieving intubation.
b. Succinylcholine 1-2 mg/kg, achieves intubating conditions in 45
seconds. Duration of paralysis 5-8 minutes. This is a long time if you
cant get the airway or bag mask ventilate the patient. BE CAREFUL.
E. Untoward effects of succinylcholine
1. Cardiovascular-succinylcholine stimulates the vagus nerve and sympathetic
ganglia leading to bradycardia, hypertension, or hypotension. Atropine prior
to administration may prevent bradycardia.
2. Hyperkalemia-With depolarization there is opening of acetylcholine receptor
channels, allowing efflux of potassium from the cell through receptors in the
muscle end plate and extra-junctional receptors. In normal patients, there is a
rise in serum potassium of 0.5 meq with a dose of succinylcholine. In certain
disease processes, there is an upregulation of acetylcholine receptors, and
hence, a massive increase in serum potassium with the administration of

- 39 -

3.

4.
5.
6.
7.
8.

succinylcholine. These include: burns (3 days to 6 months after injury), spinal

cord injury (3 days to 1 year after injury), tetanus, severe intra-abdominal
infections, Guillain-Barre syndrome, Duchennes Muscular Dystrophy,
Myotonic Dystrophy, multiple sclerosis, many progressive neuromuscular
diseases.
Malignant hyperthermia-Succinylcholine is one of the agents that trigger
MH, a hypermetabolic response to a triggering agent characterized by fever,
tachycardia, tachypnea, acidosis, hyperkalemia, ventricular dysrhythmias, and
rhabdomyolysis. The mortality is high. Risk factors include positive family
history, Duchenes Muscular Dystrophy, and certain myopathies.
Increased intraocular pressure
Rhabdomyolysis and myoglobinuria
Muscle pain-reduced if a defasciculating dose of pancuronium is used
Increased intragastric pressure
Increased intracranial pressure-blunted by pretreatment with adequate
sedation and a defasciculating dose of pancuronium.

Equipment
For any and all intubations, have available:
Large suction catheter Yankauer and reliable suction.. 2 suction setups if
bleeding. DO NOT use small suction catheters.
Bag and appropriate sized mask
Oxygen source
Endotracheal tubes--one up, one down from anticipated size needed
Laryngoscopes-at least 2, preferable 1 straight blade, one curved blade. CHECK
LIGHTS
Stylet, with lubrication
Oropharyngeal airways

Tape
CO2 monitoring device
Ventilation system

Extubation

Confirm that there is an airleak around the ETT. The airleak should occur at <20cm H20.
If there is no leak, there may be increased risk of stridor and airway obstruction due to
tracheal edema. Consider decadron (0.5-1.0 mg/kg/dose, 4 hours before extubation,
generally continued for 3-4 doses q6.
The patient should have been off feeds for 4-6 hours prior to extubation. EVERY
EXTUBATION IS A PLANNED RE-INTUBATION.
Confirm that patient is sufficiently awake and spontaneously breathing, oxygenation is
adequate on PEEP </=5, and </=40% O2, and ventilation is adequate.
Obtain all supplies at bedside for intubation. EVERY EXTUBATION IS A PLANNED
RE-INTUBATION. If there is significant concern, have meds drawn up.
Have epinephrine aerosol available if there is concern that the patient will have stridor
Suction mouth well, suction trachea via ETT
- 40 -

Untape ETT and remove

Observe for ventilation and oxygenation, air movement, stridor or weakness.

Central Line Placement

A. Indications: Need for central venous pressure monitoring, need for reliable venous
access.
B. Procedure:
1. Decide on site: subclavian vein, internal jugular vein (contraindicated in
patients with increased intracranial pressure), femoral vein (contraindicated in
patients with severe abdominal trauma).
2. Prep and drape area in sterile manner
3. Approach:
a. Internal jugular: place patient in 15-20 angle Trendelenburg position,
hyperextend the neck and turn head away from site of line placement,
palate sternal and clavicular heads of the muscle and enter at the apex
of the triangle formed, insert needle at 30 angle to skin and aim
toward ipsilateral nipple
b. Subclavian vein: place patient in Trendelenburg position, hyperextend
back with towel roll under thoracic spine, aim needle from distal third
of clavicle toward sternal notch
c. Femoral vein: flex and abduct hip, locate femoral pulse just distal to
inguinal crease, place finger on femoral artery to locate, insert needle
at 30 angle to skin medial to pulse which should be 2-3cm distal to
inguinal ligament, aim for umbilicus
4. When blood return occurs, remove syringe and insert guidewire through needle
1/2 to 3/4 the length of the wire. If wire does not thread easily and smoothly, do
not force it. Wires are designed to be the appropriate length for the catheter being
inserted. If you need an additional wire, it must be at least twice the length of the
catheter including the hub.
5. Remove needle-holding guidewire firmly. NEVER let go of the wire.
6. Enlarge the entry site with a small dilator. You may need to make a skin nick with
blade.
7. Slip catheter (preflushed with sterile saline) over wire into vein with a twisting
motion until hub is at the skin. NEVER let go of the wire.
8. Remove the guidewire
9. Secure catheter with sutures
10. Attach IV tubing
11. Apply sterile dressing
12. For IJ or subclavian line, obtain CXR to rule out a pneumothorax. For a femoral
vein on the left, obtain abdominal XR to confirm that the line is in the vena cava.

- 41 -

Intraosseous needle placement

A. Indications: Need for emergency venous access, for infusion of fluids or medications.
B. Procedure
1. Prep area in sterile manner
2. If the patient is conscious (i.e., not a code situation) using 1% lidocaine,
anesthetize puncture site down to the periosteum
3. Insert the IO needle perpendicular to skin and down to the periosteumuse a
boring motion, a decrease in resistance indicates penetration to marrow and
needle should stand firmly without support
4. Secure needle with dressing and tape. Leave the back of the leg free so you can
assess for extravasation
4. Remove stylet and aspirate marrow (can be sent for glucose, chemistries, type and
cross but not CBC)
5. Infuse 10-20 ml NS and watch for extravasation
6. Attach standard IV tubing. Any crystalloid, blood product, or drug that can be
infused in PIV can be infused in IO with high pressure system. Dress the IO so
that it is not dislocated.

Lumbar puncture
A. Indications: Obtain CSF to evaluate for infection, other disease, evaluate opening
pressure.
B. Procedure:
1. Apply EMLA to lumbar area, if there is sufficient time (about 20 min prior to LP).
Patients who are intubated may be sedated and/or relaxed for the procedure. If
they are on a spontaneous mode of ventilation, change to a controlled mode for
the procedure and sedation. Consider increasing FiO2 for the procedure.
2. Position child in lateral decubitus or sitting with hips, knees and neck flexed.
3. Locate L3-4 or L4-5 intervertebral space
4. Prep and drape in sterile manner
5. Infiltrate skin and interspinous tissue with 1% lidocaine
6. Use a 20- or 22-gauge spinal needle with stylet and 1.5 inches for infants and
small children, 2.5 inches for older slender children, and 3.5 inches for older
obese children
7. Insert the needle at the L3-4 or L4-5 intervertebral space advancing until there is a
decrease in resistance or the feeling of a pop as the dura is penetrated
8. Remove the stylet and check for CSF flow
9. If measuring opening pressure, attach manometer once CSF is flowing. Read
opening pressure when CSF stops flowing up the manometer tubing. There will
be some respiratory and/or cardiovascular variation (i.e., bounce).
10. Collect about 1cc per tube and send tubes for 1) culture and gram stain 2) glucose
and protein 3) cell count and differential 4) hold. Consider whether or not you
want CSF for viral cultures or HSV PCR.

- 42 -

Chest Tube Placement (traditional chest tube):

A. Indications: Pneumothorax, pleural effusion, emphysema, chylothorax
B. Procedure:
1. Consider need for sedation.
2. Position child supine or with affected side up
3. Locate the 3rd to 5th intercostals space in the mid to anterior axillary line avoiding
breast tissue
4. Prep and drape in sterile manner
5. Anesthetize skin, subcutaneous tissue, periosteum of rib, chest-wall muscles and
pleura with 1% lidocaine
6. Make sterile incision one intercostal space below target and bluntly dissect with
hemostat until superior portion of rib is reached (Remember nerve-artery-vein run
along the inferior side of the rib!)
7. Push hemostat over tope of rib, through pleura and into pleural spacedont go
deeper than 1 cm into pleural space
8. Spread open hemostat and place chest tube in clamp, then guide to desired
distance
9. Placement: pneumothoraxinsert tube anteriorly toward apex, pleural effusion
insert tube inferiorly and posteriorly
10. Secure tube with purse-string sutures: suture first tied to skin, then wrapped
around tube once and tied at the tube
11. Attach tube to drainage system with -15 to 20 cm H2O pressure
12. Apply an occlusive dressing
13. Obtain CXR to confirm position

Chest Tube Placement (pigtail chest tube):

A. Indications: Pneumothorax, pleural effusion, chylothorax. These tubes work well for
most things except blood and thick empyemas.
B. Procedure: (basically Seldinger technique)
1. Consider need for sedation.
2. Position child supine or with affected side up
3. Locate the 3rd to 5th intercostals space in the mid to anterior axillary line avoiding
breast tissue
4. Prep and drape in sterile manner
5. Anesthetize skin, subcutaneous tissue, periosteum of rib, chest-wall muscles and
pleura with 1% lidocaine
6. Insert needle with 10cc syringe attached, aim to midpoint of rib, then walk
OVER the rib into the pleural space. (Remember nerve-artery-vein run along the
inferior side of the rib!)
7. Withdraw air or fluid to confirm placement
8. Insert guidewire
9. Withdraw needle over guidewire. NEVER LET GO OF THE WIRE.
10. Insert dilator over wire to dilate the tract. Remove dilator

- 43 -

11. Insert pigtail catheter over the wire. Aim up and anteriorly for pneumothorax,
down and posteriorly for fluid.
12. Remove wire.
13. Secure tube: suture first tied to skin, then wrapped around tube once and tied at
the tube
14. Attach tube to drainage system with -15 to 20 cm H2O pressure
15. Apply an occlusive dressing
16. Obtain CXR to confirm position
17. Send fluid for studies if needed.

Arterial Line Placement:

A. Indications: Need for minute to minute blood pressure monitoring, need for arterial
blood gas monitoring, need for frequent labs in the absence of a functioning central
venous line.
B. Procedure: (There are multiple techniques for placing an arterial line. This is one
method.)
1. Test with Allen test first: clench hand while simultaneously compressing ulnar and
radial arteries, watch for hand to blanch, then release ulnar artery and entire hand
flush. If entire hand flushes, procedure is safe to perform.
2. Locate radial pulse
3. Secure hand to arm board, leaving fingers exposed
4. Prep and drape in sterile manner
5. Infiltrate area of maximal impulse with 1% lidocaineaspirate first to ensure that
youre not in the artery
6. Use a needle to make a small skin puncture over point of maximal impulse and
discard needle
7. Insert an IV catheter with needle through the puncture site at 30 angle to
horizontal
8. Pass needle and catheter through artery to transfix it and then remove needle
9. Very slowly withdraw the catheter until free flow of blood is noted
10. Insert wire. Wire should pass easily
11. Advance catheter and remove wire. Secure in place with sutures or tape
12. Apply an antibiotic ointment dressing
13. Infuse heparinized isotonic fluid (1 unit heparin/ml)
14. Attach pressure transducer
NOTE:
Do not infuse any mediation, blood products, or hypotonic or
hypertonic solution through an A-line
RADIOLOGY:
CT Head/Body:
Ordering guidelines: always give an indication
Specific considerations: Head--order with contrast to r/o infection or abscess, order with IV
and PO contrast when evaluating the abdomen. PO contrast takes time to administer and
is not needed to evaluate the liver or spleen. Consider the need for sedation.
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MRI head/body:
Ordering guidelines: always give an indication. Consider if you need DWI, FLAIR, etc. If
in doubt, ask neuroradiologist or neurologist.
Specific considerations: consider sedation for infants or children. If the patient is intubated,
the PICU staff can provide continued sedation. If the patient is not intubated, consider
the need for sedation service.
Angio Head/Body:
Ordering guidelines: always give an indication
Specific considerationsyou will need to speak with the radiologist to determine the best
study and any special considerations. Many of these will need to have sedation or
anesthesia.
Vascular lab:
Ordering guidelines: always give an indication. Specify exactly what vessels you want
Specific considerations. If evaluating for SVC syndrome, you need to get an
echocardiogram.
Ultrasound:
Ordering guidelines: always give an indication
Specific considerations: call radiology resident if done at night or on weekends

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Mechanical Ventilation in the PICU

This fundamental tool in the PICU serves to support the patient in respiratory failure by ensuring
adequate ventilation and oxygenation.
Mechanical Ventilation Basics:
Volume Control

Pressure Control
Controls

Rate
PEEP
FiO2
Tidal Volume (TV)
Inspiratory Time (IT)
Known TV

Rate
PEEP
FiO2
PIP
IT
Relative Advantages/Disadvantages
No guarantee of TV

Ventilators used in the PICU

Ventilators Types of Ventilation
Modes
PC/VC/SIMV/SIMVcPS/PS,
Servo 300
volume and pressure
PRVC/VS/CPAP
Infant Star
pressure
SIMV and Assist Control
LP-10
volume and pressure
SIMV and Assist Control
Sensormedics
High frequency
High frequency
300 A, B

Volume Control Ventilation

Theses ventilators work by delivering whatever pressure is necessary to achieve a set volume.
You can set the respiratory rate and the tidal volume (TV). To control the pO2 you can adjust the
FiO2, the PEEP, and the inspiratory time. PCO2 is controlled by adjusting the tidal volume and
the rate.
Pressure Control Ventilation
In these ventilators, the operator sets the PIP and the machine generates the volume necessary to
achieve the set pressure. PCO2 is controlled by adjusting the respiratory rate and TV. TV is
directly proportional to P (PIP-PEEP). As in Volume Control, you can adjust the FiO2, PEEP,
and inspiratory time to affect the pO2.

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Modes of Mechanical Ventilation: Control Modes (Assist Control Modes) vs. Support
Modes
Control modes (VC, PC and PRVC) deliver a set breath which is set by the physician. If the
patient breathes over the set rate, he or she will receive a fully supported breath, regardless of
how much effort is generated. Support Modes (VS, PS, CPAP, BiPAP, and SIMV with PS)
serve to augment breaths being generated by the patient spontaneously and reliably.

Characteristics of Ventilation Modes

IMV (Intermittent Mandatory Ventilation

SIMV (Synchronous IMV)

Set breath delivered at a fixed interval. No patient

interaction, pressure or volume modes.

Set breath delivered within an interval based on the

set rate (master rate). Ventilator waits for a
spontaneous breath by the patient as a trigger to
deliver a full breath. If this is not sensed it
automatically gives a breath at the end of the
interval period. Any other breaths during the cycle
are not supplemented

Uses: Commonly for neonates.

Contraindications: uncomfortable
Advantages: Regular breaths guaranteed.
Disadvantages: Patient is not allowed to breathe
with the ventilator, i.e. doesnt work with the
patient.
Ventilator: Sechrist and most others.

Uses: Common in many settings. Can be used as a

weaning mode (See SIMV w/ PS).
Contraindications: None.
Advantages: Works with the patient. Friendlier
mode.
Disadvantages: Any other breaths during cycle are
not supplemented.
Ventilators: All but the Sechrist.

PS (Pressure Support)

SIMV w/ PS

Supports each spontaneous breath with

supplemental flow to achieve a preset pressure.
Gives a little push to get air in.

Combination of SIMV and PS. Extra breaths in the

cycle are supplemented with pressure support.

Uses: Helps to overcome airway resistance of the

ET tube in the spontaneously breathing patient.
Useful as a weaning mode.
Contraindications: Patient who is not
spontaneously breathing.
Advantages: Helps overcome resistance of the ET
tube, making spontaneous breathing easier.
Disadvantages: Can be uncomfortable for small
patients, need to have appropriate sensing.
Ventilators: All but the Sechrist.

Uses: Most circumstances. Weaning mode.

Contraindications: None.
Advantages: Allows both synchrony with the
patient and helps in overcoming the ET tube
resistance, allowing easier spontaneous breathing.
Disadvantages: Occasional difficulty with the
pressure support for some patients. Not useful for
the patient who is not spontaneously breathing.
Ventilators: All but the Sechrist

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PC (Pressure Control)

AC (Assist Control) or
VC (Volume Control)

Essentially IMV. Breath is controlled by the

Preset rate and tidal volume (sometimes PIP),
either on the patients initiative or at the set interval Pmax, not the set tidal volume.
a full mechanical breath is delivered.
Uses: In neonates or patients with high airway
pressures (ARDS) to avoid barotrauma.
Uses: For patients who have a very weak
Contraindications: Not a friendly mode in the
respiratory effort. Allows synchrony with the
awake patient.
patient with maximal support. Patient is on
Advantages: Pressure limited, decreases
complete mechanical support in this mode.
barotrauma risk.
Contraindications: None.
Advantages: Provides a great deal of support; fairly Disadvantages: No guaranteed TV.
Ventilators: All.
comfortable.
Disadvantages: Can lead to hyperventilation if not
closely monitored. Not a weaning mode.
Ventilators: LP-10, Servo 900, Infant Star
CPAP (Continuous Positive Airway Pressure)
PRVC (Pressure Regulated Volume Control)
A volume control assist control mode. Adjusts
flow rate of the delivered air to achieve set TV at
or below the set maximum pressure. Decelerating
flow pattern.
Uses: All patients. Especially in patients with high
airway pressures. Perhaps more friendly to awake
patients than SIMV.
Contraindications: None.
Advantages: Delivers a guaranteed tidal volume
while minimizing barotrauma.
Disadvantages: None.
Ventilators: Only available on the Servo 300.

Same as PEEP.
Uses: For patients with upper airway soft tissue
obstruction or tendency for airway collapse. As a
final mode prior to extubation in some patients.
Contraindications: Any patient w/o spontaneous
respiratory effort. Not a good idea in a patient with
obstructive pulmonary disease (asthma, COPD)
Advantages: Simple, easy to use.
Disadvantages: Provides no supportive ventilation.

Where to Start: Initial Ventilator Settings

Obviously, the individual patient and clinical setting will determine the mechanical ventilation needs, but the
following is a good place to start, realizing that the settings will most likely require adjusting to achieve the
desired effect.

Rate

Preemie

Infant/Toddler

Child

40

30

20

- 48 -

Adolescent/Ad
ult
12

Inspiration
Time (IT)
sec
PIP
(P-Peak)
cm H20
Tidal Volume
(TV) ml/kg

0.4

0.6

0.7

.9

16

20

20

20

5-10

5-10

5-10

5-10

PEEP

4-5

4-5

4-5

4-5

FiO2

1.0

Titrate

Down

As Tolerated

Things to Watch Out For:

1. Peak Pressures: Keep below 30-35 to reduce risk of barotrauma.
2. Oxygenation: Want to wean down as quickly as is safe to about 0.6. Inability to wean implies V/Q
mismatch. May need to increase PEEP, I-time.
3. Ventilation: Utilize blood gases to guide your ventilation rate. Obtain first gas 15-20 minutes after
initially starting ventilation or after major changes. Non-invasive monitoringETCO2 and Oxygen
saturation may allow you to do many fewer blood gases.
4. Follow the trend. The trend is your friend, know what it is. The trend is more important than any
specific blood gas, oxygen saturation, or chest film.

Resources:
1.

Hammer GB, Frankel LR. Mechanical ventilation for pediatric patients. Int Anesthiesiol Clin. 1997; 35(1): 139-67.
2. Lectures and printed material provided by Ken Tegtmeyer MD (http://homepage.mac.com/tegthmeyer/residents/vents.html);
Mohan Mysore MD; Mark Wilson MD.

High Frequency Oscillatory Ventilation (HIFOV)

Candidates for HFOV:
1. Hyaline Membrane Disease (HMD), aspiration etc. as evidenced by bilateral diffuse,
homogenous lung disease on CXR.
2. Patients requiring hyperventilation including ECMO candidates and patients with
pulmonary hypertension.
3. Pediatric patients with acute lung injury/ARDS, general guidelines include PEEP >10,
FiO2 >60%.
What to set
1. MAPMean airway pressure. Affects degree of recruitment of alveoli and expansion of
the lung.

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2. HzHertz, cycles per second. Affects ventilation. The LOWER the Hz, the more the
piston moves, and the BETTER the ventilation.
3. PowerHow MUCH the piston moves, works like tidal volume. The amount of gas
displaced is less than dead space.
How to start
1. Patient <30K, use 300A, patient >30 kg, use 300B.
2. MAP4-8 higher than the MAP on conventional ventilation. The worse the
complacence, the more the increase will need to be.
3. Hzsmaller patient, higher Hz. Infant-10-14, toddler-6-10, child-5-8, adolescent 4-6.
4. Powerlook for CWF (chest wiggle factor). The chest should wiggle, and you should
see the wiggle down to the groin.
5. Check x-ray soon and repeat in 6-12 hours.
6. Suction as INFREQUENTLY as possible
7. Treat bronchospasm aggressively.

- 50 -

Evaluation and Management of the Post-Surgical Patient

in the PICU-An Overview
Why should the Pediatrician know anything about surgery and surgical patients?
There are a number of reasons for our involvement with the surgical patients. Surgical patients
are excellent examples of organisms under stress, and a great deal of acute physiology can be
learned by caring for them--airway and pulmonary issues, fluid/electrolyte issues,
neuroendocrine response to stress, pain and sedation, etc. The patient in ICU must be cared for
in a collaborative fashion with the primary surgical service. In general, pediatricians know about
infants and children, and medical issues, and surgical attendings/residents know about
surgical/technical issues. If a collaborative relationship is formed, the patients will receive the
best of both sets of knowledge. Finally, because of the potential for miscommunication to lead
to mis-understandings and problems with care, these patients present excellent opportunities to
practice the art of communication and finesse.
Post-operative care must be approached in an organized, timely manner, with attention to the
acute nature of the patients changing physiology. Before the patient arrives, you should
familiarize yourself with the patients past medical/surgical history and the planned surgical
procedure. If you dont know what the disease and/or the operation is--ASK or READ! There is
usually information available somewhere. Only when you know what they planned to do, and
what they did it on, will you be prepared to evaluate your patient when he/she arrives, and
anticipate potential problems that you must watch for.

When the patient arrives--the initial evaluation

The patient has just undergone general anesthesia, been intubated +/- extubated, and had some
fairly invasive procedure performed.
Thus:
ABCs
Look at the breathing pattern
Listen to the chest--breath sounds, stridor?
Listen to the heart--gallop, murmur?
Feel the pulses--strong, weak, thready?

The Anesthetic Record--what it contains, what you need?

The anesthetic record can be viewed as the history of present illness for the surgical patients--it
contains information related to maintaining physiologic stability during the course of the
operation. You will need to learn to read it and interpret the information it contains. Each
hospitals record is somewhat different, but all will contain the following information:
1. Induction of anesthesia--IV or mask, smooth or difficult?
2. Intubation--rapid sequence?, blade and tube size used, number of attempts, any notations
about anatomy?

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3. Maintenance of anesthesia--potent inhalational agents

(halothane/isoflurane/sevoflurane), nitrous oxide, narcotics, propofol. Regional
techniques--epidural, caudal, local infiltration or Nerve block.
4. Ventilator parameters-rate, tidal volume, FiO2
5. Vital signs-BP, HR, SaO2, temp
6. Fluids--ins and outs-type or fluid, crystalloid/colloid/blood
7. Blood loss
8. Any events should be recorded
9. Extubation-problems, especially bronchospasm or stridor
10. ANY drugs given (including antibiotics)
11. Lines and tubes

Fluids in the Operative and Post-operative patient

Pediatrician: Why do they always get so much fluid?
Anesthesiologist: Because they need it
The anesthesiologist must provide maintenance (=preoperative hydration status+length of
NPO+normal 4,2,1 maintenance needs) + replacement of third space losses (open belly, hot
lights, extensive dissection of tissues) + replacement of blood loss (see later discussion). Major
abdominal procedures can lead to losses of 15 cc/kg/hr in third space losses which must be
replaced.
Effect of Anesthesia on Fluid Balance:
General anesthesia produces vasodilatation and some degree of myocardial contractility (usually
overcome by sympathetic drive induced by the surgical stimulus), and thus a volume bolus may
be needed. Mechanical ventilation can increase evaporative loss if gases are not adequately
humidified, which is often the case during long OR procedures. These factors will increase the
need for volume/fluid. Other factors, including increased intrathoracic pressure brought about by
mechanical ventilation, a stress response to surgical stimulus, or the prone position, may lead to
increased ADH production and decreased urine output. Hence, usual fluids are isosmotic (L. or
NS, with or without Dextrose), and urine output may not reflect intravascular volume status.
Assessment of Fluid Balance:
Vital signs (HR/BP) combined with a knowledge of the amount of anesthesia being delivered,
urine output (with above caveat in mind), acid-base status, and occasional invasive monitoring
(CVP, PA catheter) are used to estimate how balance the patients fluid/volume status is. As you
might imagine, this can sometimes be difficult.
Types of Fluids
For resuscitation purposes (including the OR), fluids are categorized as crystalloid (salt
solutions) or colloids. There is much discussion about which is better, what the cost/benefit ratio
is, etc. You should at least be aware of which is which, and of the implications of choosing one
over the other.

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Is There an Optimal Hematocrit?

ICF

ECF

Interstitial Space

H2O
H2O

Na

Water flows
along osmotic
gradient, thus
water follows
distribution
of osmoles

Viscosity

Relative O2
Transport Capacity

Distribution of Administered
Fluids

Albumin

Vascular Space
Hematocrit
Sodium will leave the vascular space and go into the interstitial
space, but be excluded from the intracellular space by the Na-K
exchanger. Albumin is retained more in vascular space, if the
capillaries are intact. Water flows along its concentration
gradient, hence, water will leave the vascular space with the
sodium, and less so with albumin. Thus, after about an hour for
fluid shifts, 1 liter gets you about 200ccs of intravascular
space if NS, about 500cc if albumin.
Others:
L.--125cc
NS--180cc
5% albumin--490cc
Hetastarch--710cc
Whole blood--900cc
7.5%
BLOOD loss and replacement
Blood loss in the operating room is estimated, but this may be inaccurate, especially during long
cases. One needs to consider replacing volume, cells, and coagulation factors. Coagulation
factors will only become a clinically relevant issues with massive transfusion or DIC. There is
controversy (in the literature and with respect to individual patients) regarding when one needs to
transfuse the patient. Remember that the function of red cells is to carry hemoglobin, carried by
cardiac output. O2 transport capacity will thus be a factor of Hg level and the ability of the Hg
to get to cells--which will be adversely affected by hyper viscosity. Thus the optimal
hematocrit is probably somewhere around 30-35. This does not, however address the issue of
tolerable hematocrit--healthy patients will tolerate much lower hematocrits, and there is a risk
involved in any transfusion. Hence, debate.

- 53 -

When to transfuse?
MABL=(EBV X (patient hct - minimum tolerated hct))/Patients pre-op hct
MABL--maximum allowable blood loss, EBV--estimated blood volume
Example--10 kg healthy child, without significant lung disease
MABL=70cc/kg x 10 kg x (42-25)/42=285cc
Thus, up to 285cc, blood loss can be replaced with crystalloid (at a ratio of 4:1), and any further
blood loss should be replaced with packed cells.
Component Therapy
During a massive transfusion, coagulation factors and platelets will be reduced due to dilution, as
they are not present in packed cells. What constitutes a massive transfusion varies, but 0.753.0 blood volumes is a reasonable range. If not replaced, bleeding will be greater, necessitating
greater packed cell transfusion, etc. Whole blood does contain coagulation factors, but is very
rarely available. One must remember, however, that those injuries which necessitate massive
transfusion (IE, large blood loss with resultant acidosis and shock, severe trauma, sepsis) may
also lead to DIC (disseminated intravascular coagulation), in which factors/platelets are
consumed as well as diluted.
Large Volume Transfusion--other Complications
Hyperkalemia (increased K+ in supernatant of packed cells)
Hypocalcaemia (citrate binding of Ca++)
Hypothermia is blood warmer inadequate or not used

- 54 -

Altered Oxygen-Hg dissociation curve--shift to left with most blood products (decreased 2,3
DPG), thus, Hg holds onto O2.

Extubation
Criteria for extubation in the operating room are the same as those elsewhere--the patient must
have an adequate airway, maintain oxygenation and ventilation (adequate strength as well as
lung function), and have a neurologic status able to protect the airway and maintain adequate
drive. Patients can be extubated awake or deep (i.e., asthmatics), but one should avoid
extubation in a light plane of anesthesia, which can lead to laryngospasm.
Airway--Is there a tube leak? Is the pre-existing airway pathology that might now be worse?
Did the operation affect the airway (trachea, cords, pharynx)
Breathing--Are the lungs normal or abnormal. Has there been enough fluid administered that
there is concern about pulmonary edema? Did the operation involve the chest or abdomen in a
way that will adversely affect the patients ability to breathe deeply?
Neuro--Has anesthesia worn off to a degree that the patient can protect his airway and have
adequate drive. (Awake, following commands, spontaneous eye opening, protective airway
reflexes) How much/what type of narcotic has been used? Has paralysis worn off/been
reversed? (typically, paralytics will be reversed with glycopyrollate/neostigmine at the end of a
case). Small/young infants are at increased risk of apnea following general anesthesia.
Any problems related to extubation should be noted on the anesthesia record, and communicated
in report form the OR or PACU.

Post-Operative Issues and Problems

Respiratory
Airway--check ETT size and position if patient returns
intubated (CXR).
Stridor--causes include trauma to trachea or cords, laryngeal edema, recurrent nerve
damage, arytenoid dislocation. Treatment is as for viral croup--racemic epi, decadron,
and re-intubation if necessary.
If patients airway is compromised due to decreased mental status, a jaw thrust and nasal
airway may temporize the problem.
Pulmonary--Assess quality of breath sounds, respiratory drive. Check CXR if intubated.
Generally patients will require some oxygen due to atelectasis, narcotics, and splinting.
Cardiovascular
Most pediatric patients will not have invasive monitoring in place (IE, CVP, PA line).
Some will have arterial catheters. CV status must be assessed clinically, therefore, in the
majority of patients. Remember that the In/Outs will not necessarily reflect the patients
intravascular volume status (due to blood loss replacement, third space losses,
evaporative losses). Of note, hypercarbia will lead to sympathetic nervous system
activation, with impressive hypertension and tachycardia.

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Pain
Most post-operative patients will have pain, which must be addressed in some
fashion. Pain relief is best managed presumptively (i.e., dont wait till the
patient is in tremendous pain before treating it, and drugs must be TITRATED
to effect. Modalities include narcotics (scheduled, prn, PCA), non-steroidals
(ketorolac, ibuprofen), Tylenol, and regional techniques (epidural, caudal
catheters, nerve blocks). Titration of drugs in the infant or
ventilated/sedated/paralyzed patient requires assessment of vital signs.

Common Procedures and Common Problems

Spinal Fusion--Respiratory, Pain, Fluid Balance
The post-operative course will be affected by the patients general medical history, degree of
curvature, extent of the repair, and intraoperative course (fluid balance, blood loss, narcotics
given). The most dreaded complication is paralysis, and patients who are cognitively able to
follow commands will be submitted to a wake-up test intra-operatively, before closure of the
wound. Potential post op problems include respiratory depression (excess analgesia), respiratory
difficulty due to splinting (inadequate analgesia), pain control (difficult), and fluid balance.
Spinal fusion patients can develop SIADH with some frequency, likely due to manipulation of
the spine and spinal cord. They also might not urinate due to inadequate volume restoration.
Thus, if a post-op fusion does not have adequate urine output, you must decide if he is dry or
developing SIADH. This can be difficult to assess on purely clinical grounds, as the overall fluid
balance is always quite positive, and the HR may be high due to pain. Look at the anesthesia
record for clues as to volume status (IE, is fluid replacement adequate given blood loss and
duration of the case). Check a serum sodium--if high, the problem is likely inadequate volume,
if low, the problem is likely SIADH. If its still not clear, you can check a urine sodium--it
should be high (>40) if the patient is volume replete (SIADH), low if volume depleted. Treat
accordingly.

LeFort Osteotomy--AIRWAY, AIRWAY, AIRWAY

Various bones of the face are broken and the face re-aligned in this operation. There is typically
a fair bit of blood loss and there can be significant swelling of the involved tissues. The most
important things to monitor are the status of the airway and continued bleeding. If the jaws are
wired shut, there should be wire-cutters at the bedside. Pain and nausea must be treated as well.

Tracheostomy--Airway, sedation, ventilation

The most critical issues for the fresh trach is not losing it. Until the tract heals, the swelling can
make replacing the trach tube difficult. Hence, patients who are wild should be adequately
sedated, especially if they were trached because they were impossible to intubate. In other
situations, remember that an ETT is still an option if the tube comes out and cant be replaced
(but try to avoid that situation!!!). Mechanical ventilation will depend on the underlying lung
status--typically the patients return from the OR on a ventilator, and are weaned according to
- 56 -

their pulmonary status. There are stay sutures which are at the base of the incision and can be
held up to help provide a tract should the trach tube come out.

Craniosynostosis--Blood Loss
During craniectomy for craniosynostosis one or more of the sutures of the cranium are cut. As
one might expect, there is typically a large blood loss. You should be aware of whether the
patient is syndromic or not (those with a syndrome typically have more sutures in need of
repair, and might well have other problems), and the extent of the repair. Because of the large
blood loss, they typically receive quite a bit of fluid intra-operatively as well as post-operatively.
Monitor fluid balance, respiratory status, and blood loss (dressing).

- 57 -

Perioperative Management Of Patients

With Congenital Heart Disease:
A Multidisciplinary Approach

Basic Principles
The perioperative care of the infant, child, and adult with congenital heart disease
requires a coordinated, multidisciplinary approach to patient care that emphasizes teamwork and
the unique contributions of all those involved in the continuum of patient carepediatric
cardiologist, pediatric cardiac surgeon, pediatric cardiovascular anesthesiologist, perfusionist,
pediatric intensivist, nurses, advanced practice nurses, physicians assistants, respiratory
therapists, child life therapists, and family members. Each member of the team brings unique
knowledge and perspective to the care of the patient and recognizing and integrating all members
of the team in the ongoing care of the patient is essential in providing optimal care for these
patients. The presence of trainees from medicine, nursing, respiratory therapy, or other
disciplines adds to the size and complexity of the team caring for the patient, and the roles and
responsibilities of these individuals must be explicitly acknowledged.
Perioperative care encompasses both pre and post operative care of the patient with
congenital heart disease. Although many infants and children with congenital heart defects are
managed as outpatients until their repairs, some infants or older children with severely abnormal
physiology require stabilization and critical care prior to surgery. Many of the basic principles of
cardiac intensive care apply to both pre and post operative care and will be considered in this
chapter. In addition to supportive care and stabilization, pre operative management includes
thorough evaluation of the anatomy and physiology of the heart and the physiologic status of the
patient as a whole so that appropriately planned and timed surgery can take place.
Basic principles of pediatric critical medical and nursing care remain relevant in the pediatric
congenital cardiac patient. Pediatric cardiac patients are cared for in specialized cardiac
intensive care units and in multidisciplinary intensive care units. There is some data that
institutions that perform more surgeries have improved outcomes (info herebased on
surgeon, unit, hospital?? Is it surgeon numbers that really matter?). Regardless of the focus
of the unit, a commitment to ongoing education and training, as well as a collaborative and
supportive environment is essential. We feel strongly that a unit dedicated to the care of
infants and children is best able to care for these patients (down on the adult units caring for
kids).
General Principles of Oxygen Delivery and Utilization
Oxygen delivery (DO2) is described by the following equation: DO2=Qs (CaO2), where
Qs is the systemic cardiac output and CaO2 is arterial O2 content. In turn, CaO2 (ml/dl) = Hgb
(g/dl) * SaO2 * 1.34 (ml/g) + PaO2 (mmHg) * 0.003 (ml/dl/mmHg) where, Hgb is the
hemoglobin concentration, SaO2 is the arterial O2 saturation, and PaO2 is the arterial O2
tension. Oxygen utilization (VO2) is Qs (CaO2-CvO2), where CvO2 is the mixed venous
oxygen content. Oxygen delivery is therefore primarily dependent on systemic cardiac output,

- 58 -

hemoglobin concentration, and oxygen saturation. Dissolved oxygen (PaO2) makes a small
contribution to oxygen delivery.
Ventricular output (Q) is directly related to heart rate and stroke volume. Stroke volume
is in turn dependent on preload, afterload, and myocardial contractility. Both pulmonary blood
flow (Qp) and systemic blood flow (Qs) are determined by these fundamental forces. In the
patient with two ventricles, ventricular interdependence, or the affect of one ventricle on the
other, may play a role in pulmonary or systemic blood flow. In some situations, including the
post operative state, the pericardium and restriction due to the pericardial space may also play a
role in ventricular output.
When evaluating the loading conditions of the heart and myocardial contractility, it is
important to consider the two ventricles independently as well as their affect on one another. In
previously healthy pediatric patients without heart disease, right atrial filling pressures are
commonly assumed to reflect the loading conditions of the left as well as the right ventricle. In
the patient with congenital heart disease, this is frequently not true. Pre-existing lesions and the
affects of surgery may affect the two ventricles differently. For example, the presence of a right
ventricular outflow tract obstruction will lead to hypertrophy of the right ventricle. That right
ventricle will be non-compliant, and the right atrial pressure may therefore not accurately reflect
the adequacy of left ventricular filling.
Oxygen content (CaO2) is primarily a function of hemoglobin concentration and arterial
oxygen saturation. Thus, patients who are cyanotic can achieve adequate oxygen delivery by
maintaining a high hemoglobin concentration. Arterial oxygen saturation is commonly affected
by inspired oxygen content, by mixed venous oxygen content of blood, by pulmonary
abnormalities, and by the presence of a R to L intracardiac shunt. Arterial oxygen content in the
patient with a single ventricle and parallel pulmonary and systemic circulations will depend on
the relative balance between the circulations as well. In the patient with intracardiac shunt or the
single ventricle patient, arterial oxygen content is also affected by the relative resistances of the
pulmonary and systemic circuits, as this determines how much blood flows through the lungs
relative to the systemic output. Low mixed venous oxygen content contributes to desaturation
and suggests increased oxygen extraction due to inadequate oxygen delivery, which in turn is
either due to inadequate systemic cardiac output or inadequate hemoglobin concentration.
A thorough understanding of these fundamental principles of cardiac output and oxygen
delivery is essential for the perioperative care of the patient with congenital heart disease.
General Principles of Anatomy and Pathophysiology Affecting Pre-operative and Postoperative Management
An understanding of the anatomy and pathophysiology of the congenital cardiac lesion
under consideration allows one to determine the pre-operative care or resuscitation needed and to
predict the expected post-operative recovery.
Acyanotic Heart Disease
Children with acyanotic heart disease may have one (or more) of three basic defects: 1)
left-to-right shunts (e.g., atrial septal defect, ventricular septal defect); 2) ventricular
inflow/outflow obstructions (e.g., aortic stenosis, coarctation of the aorta); and 3) primary

- 59 -

myocardial dysfunction (e.g., cardiomyopathy) (Table 22-1). These lesions may lead to
decreased systemic oxygen delivery by causing maldistribution of flow with excessive
pulmonary blood flow (Qp) and diminished systemic blood flow (Qs) (Qp/Qs >1), by impairing
oxygenation of blood in the lungs caused by increased intra and extravascular lung water, and
decreasing ejection of blood from the systemic ventricle.
Maldistribution of Flow: Qp/Qs >1
In infants with left-to-right shunts, pulmonary blood flow (Qp) increases as pulmonary
vascular resistance (Rp) decreases from the high levels present perinatally. (37,132) If Qp is
sufficiently increased, pulmonary artery pressure may also increase, particularly with left to right
shunts distal to the tricuspid valve, such as large VSD or truncus arteriosus. As pulmonary flow
increases, left ventricular volume overload may occur with cardiac failure, decreased systemic
output, pulmonary congestion and edema. Over time, increased Qp leads to a series of
pulmonary microvascular changes which first produce reversible pulmonary vasoconstriction
and later fixed pulmonary vascular disease (see Chapter 4 on 'Regulation of Pulmonary Vascular
Tone'). As Rp increases over time, Qp decreases (Table 22-3). The primary determinant of
pulmonary blood flow is pulmonary vascular resistance. In patients with increased and reactive
Rp, LV function may be normal but oxygen delivery may be limited by decreased RV output or
by the development of intracardiac right-to-left shunting. If pulmonary pressures exceed
systemic pressures, right to left shunting predominates and the patient becomes cyanotic.
Depending on the type and size of the lesion, pulmonary over circulation that remains
uncorrected may lead to pulmonary vascular obstructive disease as early as 6 months of age.
Pulmonary over circulation can lead to congestive heart failure through several
mechanisms. Increased Qp leads to left (systemic) ventricular volume overload and raises left
ventricular end diastolic, left atrial, and pulmonary venous pressures. The increases in
pulmonary artery and pulmonary venous pressures raise the pulmonary hydrostatic pressure
gradient and these promote transudation of fluid into the interstitial space and ultimately lead to
alveolar edema. Right ventricular end diastolic pressure, and hence, right atrial and systemic
venous pressures, are also elevated. Venous return may be decreased. High systemic venous
pressure contributes to interstitial edema and may lead to decreased organ perfusion. The
maldistribution of flow with reduced Qs is accompanied by a reduction in renal blood flow and
resultant stimulation of the renin-angiotensin system (see Chapter 5 on Renal Function in Heart
Disease). Fluid accumulation is aggravated by sodium and water retention by the kidney.
Pulmonary edema reduces CaO2 through increased intrapulmonary shunting in the lungs.
In addition to pulmonary over circulation, other causes of pulmonary edema in patients with
acyanotic heart disease include left ventricular inflow- or outflow obstruction and diastolic
dysfunction of the left ventricle. These children demonstrate an increased respiratory rate,
diffuse rales and increased work of breathing. The chest x-ray demonstrates diffuse interstitial
and alveolar infiltrates.
Myocardial Dysfunction
Diastolic and to a lesser extent systolic dysfunction decrease oxygen delivery in patients
with cardiomyopathy.50, 77 Diastolic dysfunction raises LVEDP and pulmonary venous
pressures ultimately leading to pulmonary edema. Systolic dysfunction decreases ejection
fraction and systemic output. Cardiomyopathy represents the primary defect in a variety of
heritable and inflammatory heart diseases (See Chapter 47 on Heritable Heart Disease and 44 on

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Inflammatory Heart Disease). Patients with structural congenital heart defects may also develop
myopathic changes in the heart. Graham et al. (32,51,58,73) have shown that cardiomyopathy
may be produced by volume or pressure overload depending on the type of defect (Table 22-4).
The myopathic changes will be important both pre and post-operatively.

Cyanotic Heart Disease

Children with cyanotic heart disease have a right-to-left shunt and therefore always
demonstrate systemic arterial desaturation. 95 As with acyanotic heart disease, there may be
some combination of shunt, obstruction, and myopathic changes, all of which must be
considered. Infants with cyanotic heart disease may be divided into two physiologically distinct
groups, those with decreased pulmonary blood flow and those with increased pulmonary blood
flow.
Ductal Dependent Pulmonary Blood Flow (Decreased Pulmonary Blood Flow)
These patients have decreased systemic venous blood entering the pulmonary circulation.
Patients in this group may have obstruction to flow from the pulmonary ventricle either at the
outlet (e.g., Tetralogy of Fallot, Pulmonary Atresia) or inlet (e.g., Tricuspid Atresia). Patients
whose pulmonary blood flow is dependent on a patent ductus arteriosus may present with severe
hypoxemia and acidosis as the ductus closes. With decreased Qp and the obligatory presence of
an atrial or ventricular septal defect, the blood in the systemic ventricle consists of desaturated
systemic venous blood (via the septal defect) and a smaller volume of saturated pulmonary blood
(Qp/Qs < 1). The decreased Qp results in decreased oxygen uptake from the lungs, and thus
decreased systemic oxygen delivery. In the initial stages, Qs may be normal. If systemic oxygen
delivery remains inadequate, anaerobic metabolism and myocardial dysfunction develop,
resulting in a further reduction in oxygen delivery. The end result can be severe hypoxemia and
acidosis. Patients with decreased Qp require a stable conduit for pulmonary blood flow and a
high hemoglobin concentration (> 14 mg/dl) to maximize oxygen content CaO2) and oxygen
delivery (D02).
Ductal Dependent Systemic Blood Flow (Increased Pulmonary Blood Flow)
Patients with ductal dependent systemic blood flow have increased pulmonary blood flow
but decreased systemic blood flow due to obstruction of systemic output which can occur at a
variety of locations. (61,114,116) These infants may have acceptable arterial saturation but
develop decreased oxygen delivery as a result of decreased systemic output (i.e., hypoplastic left
heart syndrome, interrupted aortic arch, co-arctation.) Patients may present with profound shock
due to dramatic reduction in systemic perfusion and oxygen delivery if the ductal flow is
inadequate. Systemic blood flow in patients with severe left ventricular outflow obstruction is
dependent on flow through a patent ductus arteriosus into the aorta distal to the obstruction.
Pre-op Stabilization, Surgical Planning
The degree to which infants and children will require pre-operative stabilization will
depend on the nature and severity of the lesion, the degree to which the lesion has affected the
myocardial function, and the presence of other organ system involvement. Many of the concepts
involved in pre-operative stabilization will be applicable to post operative care.

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Preoperative stabilization of the ill infant or child focuses on establishing adequate

oxygen delivery through manipulation of total cardiac output, Qp, Qs, hemoglobin concentration,
and oxygen saturation. Additionally, any abnormalities of other organ systems, such as
pneumonia, renal insufficiency, or seizures, must be evaluated and corrected if possible.
Manipulation of Qp and Qs and the balance between the pulmonary and systemic
circulations is achieved by manipulation of the preload, afterload, and inotropic state of the right
and left ventricle. Pulmonary vascular resistance is affected by pH, alveolar pO2, lung volume
(atelectasis or overdistension), noxious stimuli, hematocrit, and many medications. The patient
with excessive pulmonary blood flow and consequent low systemic oxygen delivery can be
managed with maneuvers to increase pulmonary vascular resistance (Rp), which will lead to
decreased Qp and increased Qs. In the patient with ductal dependent pulmonary or systemic
blood flow, the balance of pulmonary and systemic flow can be manipulated by manipulation of
pulmonary vascular resistance or the systemic vascular resistance if needed.
Afterload reduction may improve myocardial function by decreasing ventricular wall
tension, thus improving stroke volume and decreasing myocardial oxygen consumption. .
Systemic vascular resistance can be lowered by agents that vasodilate (milrinone, dobutamine)
and by avoiding agents that raise SVR (high dose dopamine, epinephrine, norepinephrine) or
situations that raise SVR (pain, agitation). Patients with left to right shunts and LV volume
overload show improved LV function after cautious reduction of elevated systemic afterload. 11
CHF in infants with VSD is associated with stimulation of the renin-angiotensin system.
Angiotensin converting enzyme inhibition with captopril and enalapril reduces systemic vascular
resistance (Rs), decreases Qp/Qs and increases LV output in a dose dependent manner.19 Potent
intravenous vasodilators such as nitroprusside have unpredictable effects on Rp/Rs and therefore
on Qp/Qs, and should be avoided in infants with left-to-right shunts and volume overload.10
Children with LV outflow obstruction and pressure overload such as severe aortic
stenosis may have massively increased, fixed afterload. Vasodilator administration will not
increase Qs, but rather may cause shock, myocardial ischemia, or life threatening arrhythmias.
In this situation afterload reduction is accomplished by relief of the fixed obstruction by surgical
or catheterization techniques.
The myopathic ventricle requires a greater than normal preload to maintain output. If the
infant presents with CHF, pulmonary edema, and a stable systemic blood pressure, diuretics may
be useful to reduce LVEDP and relieve pulmonary edema without compromising ventricular
output. On the other hand if the infant with a myopathic ventricle presents with hypoperfusion,
hypotension and acidosis, carefully titrated fluid administration may be necessary to optimize
preload and increase cardiac output.
Inotropic drugs increase contractility at least in the short term. Unfortunately, inotropic
drugs which increase cytosolic Ca++ concentration may also impair relaxation of the heart and
decrease ventricular compliance (see Chapter 2 on Normal and Abnormal Myocardial
Contraction) and limit preload.78 In addition, increased inotropy is associated with increased
myocardial energy requirements.. Therefore, in patients with a pressure overloaded ventricle and
risk of myocardial ischemia, inotropic agents with minimal chronotropic activity should be
selected. Finally, CHF may be associated with desensitization of beta-adrenergic receptors and a
blunted response to beta adrenergic agonists.21 There is an important role for use of inotropes
which do not rely on beta adrenergic stimulation such as milrinone, a phosphodiesterase
inhibitor.4,5,28

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Treatment of pulmonary edema without pulmonary overcirculation are directed at

increasing both oxygen content and delivery. These children will benefit from oxygen
administration to treat the hypoxia and diuretic therapy to reduce the intravascular volume and
left atrial pressure. Positive pressure ventilation with positive end expiratory pressures (PEEP)
can improve end expiratory lung volume, decrease intrapulmonary shunting by opening
collapsed alveoli, improve compliance, increase tidal volume and decrease the work of
breathing. (59) In addition, increased intrathoracic pressure with positive pressure ventilation and
PEEP reduces LV afterload, thus improving systemic ventricular function and lowering end
diastolic pressure (LVEDP). Because positive pressure ventilation will affect systemic venous
return, LV afterload, and pulmonary vascular resistance, the net effect on oxygen delivery will
depend on intravascular volume status, myocardial function, and lung mechanics. Assisted
mechanical ventilation of the child with pulmonary edema may directly increase both CaO2 and
systemic output.
Post Operative Care
Postoperative care requires a thorough understanding of the anatomic defect, the
pathophysiology of the pre-operative heart as well as any other organ system involvement, the
anesthetic regimen used, cardiopulmonary bypass issues, and the details of the operative
procedure. Invasive and non-invasive monitoring and laboratory or radiographic monitoring is
tailored to the needs of the individual patient and will depend on the lesion, the repair, and
expected post-operative issues.
Mechanical Ventilation and Pulmonary Support
Patients who require mechanical ventilation post-operatively do so for a variety of
reasons: airway control, abnormal lung function, reduction of oxygen delivery needs, assurance
of stability during the immediate post operative period, because of the affect of positive pressure
ventilation on cardiac loading conditions, or due to neurologic concerns or residual anesthesia.
Mechanical ventilation, either in the operating room or the intensive care unit, is continued until
there is adequate hemostasis, the heart rate and rhythm are stable and close to normal for age,
cardiac output is adequate with minimal inotropic support, oxygen saturation is adequate and
lung function is close to normal, and the patient is awake enough to have adequate respiratory
drive and airway protective reflexes. Depending on a number of factors, these conditions may be
met in the operating room or the intensive care unit much later in the post-operative course.
Cardiopulmonary interactions can exert important influences on the hemodynamics of the
postoperative patient but must be evaluated critically and optimized for the specific patient
situation. For example, while early extubation and spontaneous ventilation after Fontan
operation is often thought to improve hemodynamics, if atelectasis or hypoventilation occurs,
pulmonary vascular resistance will increase, and hemodynamics will be adversely affected.
Monitoring of mechanical ventilation and pulmonary adequacy is accomplished via
physical examination, non-invasive monitoring of oxygen saturation and end tidal carbon
dioxide, attention to lung mechanics, blood gases, and chest radiographs. The need for tracheal
suctioning and the quality and quantity of secretions should be followed as well.
Once patients are weaned from mechanical ventilation, care must be taken to avoid
atelectasis. Infants and young children typically will move and cry spontaneously, but older
children and adolescents frequently will need assistance with sitting and standing, and will need

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encouragement to deep breathe and move. Incentive spirometry and a guided program of
progressive ambulation is essential and should be initiated as soon as physiologically safe.
Cardiac Evaluation and Support
The routine evaluation of the cardiovascular system after surgery depends on a
combination of physical exam, non-invasive monitoring, and invasive monitoring.
Repeated physical examination is an essential part of the evaluation following cardiac
surgery. Although a vital part of patient assessment, physical examination remains the least
quantifiable and most subjective. Distal extremity temperature, capillary refill and peripheral
pulses suggest the adequacy of tissue perfusion. A prolongation of capillary refill greater than 3
- 4 seconds indicates poor systemic perfusion. Changes in the character of murmur or attenuation
of a shunt murmur may reflect significant changes in the childs condition. The child should
(frequently) be examined for changes in cardio respiratory status.
Noninvasive monitoring includes examination, pulse oximetry, central and peripheral
temperatures, and surface ECG monitoring. The surface ECG provides information on heart rate
and rhythm. Cool extremities with normal or rising rectal temperature suggests decreasing and
inadequate systemic cardiac output.
Before invasive monitoring is planned, the risk-benefit ratio of catheter placement should
be considered. Vascular catheters are commonly placed in the operating room, and include
central venous catheters, right atrial catheters, left atrial catheters, pulmonary artery catheters,
and arterial catheters. Central venous or right atrial catheters provide right-sided filling
pressures, as well as information about tricuspid valve function. They enable indirect assessment
of cardiac output by providing systemic venous oxygen saturation119, and they provide a site for
infusion of pharmacologic agents. Because of their relative safety and extraordinary utility, most
cardiac surgery patients will have a central venous/right atrial line. Central venous
catheterization can be obtained by percutaneous cannulation of the internal jugular vein or by
placing the catheter directly into the right atrial appendage at the time of surgery.
Left atrial catheterization provides measurement of pressures in the left side of the heart,
information about mitral valve function, and measurement of left atrial desaturation due to rightto-left shunting in the lung. The indications for left atrial catheter placement are abnormal mitral
valve function, abnormalities of left ventricular diastolic and/or systolic function, and abnormal
lung parenchyma. Left atrial catheter placement carries the serious risk of introduction of air
into the systemic arterial circulation. This can be kept to a minimum by careful management of
these lines, the use of air filters, and appropriate education of the care team. The recent
introduction of intraoperative echocardiography has resulted in a more selective use of left atrial
lines.145
Pulmonary artery catheters provide access for measurement of pulmonary pressures,
pulmonary arterial saturation, and cardiac output.46,71 Indications include the risk of
pulmonary hypertension, residual left-to-right shunts, and decreased cardiac output. Pulmonary
artery catheters should be used in children whose postoperative pulmonary artery pressure is
greater than 1/2 systemic arterial pressure and in children who are at a high risk for pulmonary
artery hypertension (Table 22-6). Pulmonary artery catheters are placed during surgery through
the right ventricular outflow tract and advanced into the main pulmonary artery.
Contraindications for pulmonary artery catheter placement are a large right ventricular outflow
tract patch or any anatomic condition which will not allow placement of the catheter through a
muscle bundle.

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Arterial catheterization is required in all children who undergo surgery for congenital
heart disease and allows for continuous blood pressure monitoring as well as repeated
measurements of a variety of laboratory studies,
Support of the cardiovascular system is directed at optimizing cardiac output and oxygen
delivery. This is accomplished by optimization of heart rate, preload, afterload, and entropy, and
is guided by invasive, non-invasive, and laboratory monitoring. When cardiac output
measurement is not available, mixed venous oxygen saturation trends can provide information
regarding the adequacy of oxygen delivery. Studies have demonstrated that mixed venous
saturations are a reliable and early indicator of cardiovascular dysfunction and failure to measure
this may worsen outcomes in some situations.8 A decreasing mixed venous oxygen saturation,
despite escalating support, indicates abnormal convalescence and the need for aggressive
intervention. Another indicator of failing oxygen delivery is the development of lactic acidosis...
The sequential evaluation of serum lactate levels provides important assessment of the adequacy
of oxygen delivery. Lactate levels are usually high immediately after surgery but should
decrease to < 2.0 mmol/L if oxygen delivery is adequate.30 Persistent elevation of lactate
requires evaluation. Metabolic acidosis that is not accompanied by elevated lactate is usually a
hyperchloremic metabolic acidosis (non anion gap metabolic acidosis) and generally resolves
without treatment.
Hematology, thrombosis and hemostasis
Postoperative bleeding is the result of inadequate surgical hemostasis or of coagulopathy,
either due to residual heparin, to dilutional effects, or to disseminated intravascular coagulation.
If bleeding is not corrected after correction of coagulopathy or if the blood loss is greater than 10
cc/kg/hour, surgical bleeding should be considered and exploration strongly considered. Chest
tubes and mediastinal drainage tubes must be kept clear and patent if there is ongoing bleeding in
order to prevent the occurrence of cardiac tamponade.
Heparin induced thrombocytopenia (HIT) is increasingly recognized in the pediatric
population. HIT is the most common drug-induced thrombocytopenia in adults, complicating 14% of full-dose exposures to standard heparin. We have reported as similar rate of occurrence of
HIT in a pediatric cardiac surgical population. In HIT, the platelet fall is usually 40-50% and the
thrombocytopenia is moderate (30-100). The onset is 5-10 days after first exposure to heparin
and hours to 2-3 days with re-exposure. Thrombosis may localize to sites of pre-existing
pathology (CVLs, shunts, surgical repairs) and be present in unusual locations. Less common
presentations include delayed thrombocytopenia (2-3 weeks), heparin-induced skin necrosis (SQ
sites), adrenal infarction/hemorrhage, heparin resistance and anaphylactoid reactions.
Antibody (PF4) ELISAs are sensitive but not specific. Positive ELISAs are found in 4060% of asymptomatic adult re-operative cardiac surgery patients. A recent abstract found them
in 31/64 children (median age 29 months) undergoing re-operative cardiac surgery, only 1 of
whom had clinical HIT. Unfortunately a negative ELISA does not exclude HIT. More specific
for clinical HIT are functional assays based on in vitro heparin-dependent platelet activation (14C
serotonin release, heparin-dependent platelet aggregation, lumi-aggregometry). Unfortunately
functional assays are less sensitive and often negative or indeterminate in the first 24-48 hours of
HIT. Both assays usually become negative in about 3 weeks, making it difficult to diagnose
previous HIT.
If HIT is diagnosed, all heparin (lines, flushes, heparin-coated catheters, low molecular
weight heparins) must be stopped. Platelet transfusion should be AVOIDED (transfusion may

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precipitate thrombosis) as should warfarin in the acute phase of HIT. Use of alternative
anticoagulation is imperative in pre-existing or new thrombosis and should be strongly
considered for prophylaxis. Argatroban, a hepatically excreted, synthetic anti-thrombin with a t
1/2 of ~ 40-50 minutes, is presently our choice. Usual dose is 2mg/kg/min by continuous
infusion. Anticoagulation is monitored by either PTT (target 1.5 3.0 x normal) or by ACT
(target on ECMO 180-200).
Normal versus Abnormal Convalescence
Convalescence after cardiac surgery may be characterized as normal or abnormal.
Normal convalescence is recovery that is expected given the pre-operative state of the patient,
the procedure performed, and the expected effects of cardiopulmonary bypass or other
interventions. Abnormal convalescence is recovery that is prolonged or unexpected given what
is known about the patient and the interventions that have been performed. It may be due to
unknown or under appreciated abnormal pre-operative anatomy or physiology, to unexpected
complications of bypass, to residual anatomic defects, or to abnormalities in other organ systems
such as pneumonia or sepsis. It is crucial to identify abnormal convalescence and to characterize
it thoroughly so that appropriate intervention can take place in a timely fashion.
The effects of cardiopulmonary bypass (CPB) have been described as a "whole body
inflammatory response" because of the generalized activation of complement, neutrophils,
cytokines, and other mediators.25 These effects of cardiopulmonary bypass (CPB) and related
techniques are discussed in detail in Chapter 21. It is important to appreciate those effects which
are anticipated sequelae of CPB and those that suggest abnormal convalescence.
Most congenital heart defects are repaired on cardiopulmonary bypass and require a
period of time during which the circulation to the heart is interrupted by aortic cross clamping
and infusion of cardioplegia. This provides the surgeon with a still, flaccid heart on which to
operate, however, the heart may be "ischemic" during this time. Ischemic injury to myocardium,
produced (or unable to be prevented) by the protection used for operative repair, can present
serious problems in the postoperative period. Depressed ventricular function in the immediate
period following CPB, or inability to wean a patient from CPB, may be due to ischemic
injury.150,27 This condition can usually be treated with inotropic support, recognizing that
inotropic support following CPB further increases myocardial oxygen demand. For patients with
severe ventricular dysfunction, consideration of ventricular extracorporeal support with ECMO
(patients less than 5 kg), or with RVAD or LVAD (for selected patients over 5 kg) is reasonable
if it is felt that the ventricular dysfunction may be reversible. For the intensive care physician,
knowledge of the aortic cross clamp time (ischemic time) and the period of total circulatory
arrest is important. These times can be predictive of the degree of postoperative ventricular
dysfunction and the amount of support that can be predicted. ?? numbers here??
Patients who require extracardiac repair only and patients with simple shunting lesions
who require closure (patch or ligature) without valvar involvement should require minimal
inotropic support. When performed in the neonatal period, these children may require inotropic
support with a single agent. Requirement of multiple agents and increasing inotropic
requirements indicate abnormal convalescence. Patients with more complicated perioperative
pathophysiology and those who require circulatory arrest will require more intensive myocardial
and respiratory support. In the first 24 - 48 hours inotropic support may be generous and
escalation of inotropic support should be anticipated in the first 24 hours due to myocardial
edema/injury. Failure to respond to moderate increases in inotropic therapy and the need for
high levels of inotropic therapy (Dopamine/Dobutamine > 15 g/kg/min, Milrinone > 1.0

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g/kg/min, Epinephrine > 0.1 g/kg/min) indicate abnormal convalescence and the need for a
thorough investigation.
Pulmonary dysfunction is a common occurrence after cardiopulmonary bypass.35,150
Lung injury is mediated by a variety of mechanisms including an inflammatory response
initiated by activation of complement which occurs during cardiopulmonary bypass.69 This also
occurs after hypothermic cardiopulmonary bypass which causes complement activation,
leukocyte degranulation, an increase in capillary permeability, and widespread endothelial injury
(See Chapter 21 on Cardiopulmonary Bypass).23 Microvascular dysfunction with platelet
aggregation and mediator release increases pulmonary vascular resistance, extravascular lung
water, and airway resistance and decreased lung compliance. All of these increase
intrapulmonary fluid and can decrease oxygen delivery.
Management of pulmonary insufficiency in the postoperative period requires an
understanding of the physiologic consequences of cardiopulmonary bypass. Pulmonary function
tests after cardiopulmonary bypass demonstrate reduced static and dynamic compliance, end
expiratory lung volumes less than physiologic FRC, an increase in alveolar-arterial oxygen
gradient, and atelectasis.75,156 These abnormalities are related to endothelial injury and
interstitial edema and result in alveolar collapse and microatelectasis. Therapy for children with
pulmonary insufficiency is directed at reducing atelectasis and improving the
ventilation/perfusion mismatch with positive end-expiratory pressure (PEEP) and an inspiratory
time adequate to aerate all lung units. Very low PEEP (<4) and very short inspiratory times do
not provide adequate lung expansion or aeration of all lung units. Diuresis consistent with the
hemodynamic status of the child may encourage the resolution of pulmonary edema and
atelectasis.
The effects of cardiopulmonary bypass on renal function are not completely understood.
Cardiopulmonary bypass with hypothermia, non-pulsatile perfusion, and reduced mean arterial
pressure causes the release of angiotensin, renin, catecholamines and antidiuretic
hormones.44,48,49,66,67,82 These circulating hormones result in reduced renal blood flow.
There are no confirmatory studies linking low-flow, low pressure, and non-pulsatile perfusion
during CPB with postoperative renal dysfunction,49,67 but reduction in cardiac output in the
postoperative period is associated with the development of renal dysfunction. After total
circulatory arrest, it is common to observe a period of oliguria or anuria which usually resolves
after 24 hours.44,49 This oliguria is seen less frequently in infants whose CPB perfusion flow
rates are maintained at 150-200 cc/kg/min during the recovery following circulatory arrest.
Treatment of renal dysfunction in the postoperative period includes increasing renal
perfusion pressure using inotropic agents. Diuretics are the primary agents for promoting urinary
output after cardiopulmonary bypass. Furosemide (1-2 mg/kg) every 6-8 hours induces a
vigorous diuresis and reduces renal cortical ischemia associated with cardiopulmonary bypass.66
Continuous infusion of diuretics is useful in patients sensitive to fluid shifts. During the
immediate postoperative period diuretics should be used cautiously because of the ongoing
capillary leak that is the result of CPB. After resolution of the capillary injury, usually 24-48
hours postoperatively, a vigorous diuresis can be initiated.
Nutrition is an essential component in the care of the postoperative patients. Early
aggressive feeding is now advocated for the majority of patients. Early feeding reduces gut
translocation of bacteria and decreases the need for total parenteral nutrition and its attendant
risks. Feedings are usually begun when bowel sounds are present.. Feedings are withheld in
high-risk patients, such as those with severe pre-operative acidosis or those with marginal post-

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operative hemodynamics.104 In those children, a delay in feeding is usually indicated until the
patient has demonstrated resolution of acidosis and organ dysfunction. Necrotizing enterocolitis
in the post-operative period can lead to significant morbidity and mortality.81,104 The diagnosis
of necrotizing enterocolitis should be considered in any infant with abdominal distention, bloody
stools, and pneumatosis intestinalis. Children who cannot tolerate enteral feeds require
parenteral nutrition to support caloric needs (see Chapter 17 on Nutrition and Metabolism).
Cardiac surgical patients are frequently hyperglycemic in the initial postoperative period.
Many infants have received steroids pre and intraoperatively, and all patients have undergone a
physiologically stressful event. There is evidence in the adult literature that control of
hyperglycemia significantly improves outcome in patients in the intensive care unit (NEJM
article). At the present time, there is no data on any beneficial or detrimental effect of control of
hyperglycemia in critically ill pediatric patients. If blood glucose is controlled with insulin, care
must be taken to avoid hypoglycemia.

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Terminology and Definitions

Atriotomy - an incision into the wall of the atrium. Allows visualization of the interior of the
atrium, the AV valve, and allows access to the ventricle through the AV valve. Puts the patient at
some risk for dysrhythmias because it can alter electrical conduction in the atrium. Used
commonly in many procedures.
Complete Repair - is a repair in which post-operatively the patient has separation of pulmonary
and systemic blood flow and an otherwise functionally normal heart, if not anatomically normal.
Conduit - an artificial pathway forming a track for blood to follow. Can be from a ventricle to
the aorta or pulmonary artery, can be across a stretch of a blood vessel or between vessels.
Commonly made of Gore-Tex, but can be cadaveric or porcine in origin, can also be valved or
unvalved.
Cross Clamp - consists of placing a clamp across the entire diameter of the vessel described
(usually refers to the aorta). Cross clamping the aorta interrupts blood flow beyond the point of
the clamp. This prevents blood flow from entering the surgical field in an area of the aorta being
manipulated and can also be used to prevent air embolization during surgery on the left side of
the heart. The risks involved with cross clamping involve interruption of blood flow to the spinal
arteries with some risk of paralysis. Also requires retrograde perfusion of the coronary arteries to
allow oxygen supply to the myocardium.
CVP - central venous pressure. This is the pressure usually measured in the right atrium through
a central venous catheter. This reflects the filling pressure of the right side of the heart.
Cyanosis - literally means blueness. To appear cyanotic a patient must have 4-5 gms of
deoxygenated hemoglobin floating in bloodstream. Can be difficult to detect in severely anemic
patient. Generally, anyone who has oxygen saturations less than 85% on room air, in the
absence of pulmonary disease should be suspected of having cyanotic heart disease. A patient
without a right to left shunt should be expected to show a significant rise in pO2 on an ABG after
30 minutes on 100% FiO2.
Filling Pressure - this refers to the pressure required by each side of the heart to generate
optimum force of contraction. We can speak of right or left sided filling pressures. Filling
pressure is measured by right atrial, left atrial, or CVP lines.
Palliative repair - usually a palliative procedure is one which overcomes a lethal problem in a
defect without totally correcting it. Post-operatively these patients are usually still cyanotic, with
mixing lesions, still functionally and anatomically abnormal hearts
Pulmonary Hypertension - as the name implies increased vascular resistance to blood flow in
the pulmonary vascular bed. This is the normal state in the fetus where systemic vascular
resistance (SVR) is lower than PVR. It can be seen as part of the disease entity of Persistent
Pulmonary Hypertension of the Newborn (PPHN). It can also be reactive to prolonged increased

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pulmonary blood flow related to a left to right shunt, or to any number of obstructive lesions
distal to the pulmonary outflow tract.
Pump Run - when a patient is placed on cardiopulmonary bypass. This is done in any patient
with an open-heart procedure to allow emptying the heart of blood to ease visualization of the
abnormalities which the surgeon is trying to repair. During the pump run the coronary arteries
must receive perfusion, and the heart must be kept cold to decrease its metabolic demand. This is
done by inserting a canula into the coronary sinus and infusing a fibrillation solution with highly
oxygenated blood and high potassium. Clotting factors and platelets can get consumed and/or
activated while on the pump, so the longer the pump run the more like coagulopathy will be
present.
Side Biting Clamp - a clamp used to allow manipulation of a large vessel without necessarily
stopping the flow through the vessel (i.e. the aorta). Clamps onto the side of the vessel giving
substrate to operate on while diminishing the risk of bleeding. Used often in shunt placement,
sometimes in coarctation repair.
Total Circulatory Arrest - stoppage of all blood flow, including the pump. Can be done for
brief periods in infants kept at low temperatures (~15-20C). Allows a clear operating field, free
of blood return.
Ventriculotomy - an incision into the ventricular wall during surgery exposing the interior of the
ventricle. Can be done when the atrial approach does not adequately expose VSD's or when the
surgical repair otherwise mandates it. Puts patient at risk for right bundle branch block from
interrupting the conduction system. Also leads to more myocardial insult and thus a somewhat
stiffer ventricle. Can be difficult in the face of aberrant coronary arteries.
Pacing
Temporary
Atrial and ventricular wires are commonly placed in the epicardium at the time of surgery
to allow for potential treatment if dysrhythmias develop post-operatively, particularly
heart block. These are intended to be temporary and can be removed without difficulty
after the patient recovers by gentle tension.
Atrial pacing
For a patient with pure sinus node dysfunction and intact conduction through the AV
node. This mode is used if a higher heart rate is desired
Ventricular pacing
Usually only done as a short-term treatment in patients who only have ventricular wires
in place.
AV sequential pacing
Commonly done in post-operative patients requiring pacemaker support due to faulty or
delayed conduction, generates both atrial contraction and ventricular contraction allowing
for some AV pause
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Theshold: the setting at which there is capture of the atrium or ventricle (i.e., pacing works to
create a conducted beat). The pacemaker should be set at twice the threshold. There is an atrial
setting and a ventricular setting. Thesholds should be checked every 12 hours (by RN or
attending) in patient who is pacemaker dependent.
Sensitivity: The setting at which the pacemaker senses an intrinsic beat. If it is too sensitive,
it picks up noise and thinks there is a beat, and inhibits the paced beat. If it is not sensitive
enough, it will not sense an intrinsic beat and will produced a paced beat regardless of what the
heart is doing.
Permanent Pacemakers
Internationally Standardized Nomenclature
1
2
Chamber sensed
Chamber paced
V
V
A
A
D
D
O

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3
Mode of Response
Triggered
Inhibited
Dual
None

4
Rate Modulation
Programmable
Multiprogrammable
Communicating
Rate modulation
nOne

Extracorporeal Membrane Oxygenation/Ventricular Assist Device

ECMO/VAD
Note: There are pre-printed orders for ECMO patients. Please use the appropriate preprinted orders.
What is it?
ECMO - Basically, prolonged cardiopulmonary bypass outside of the OR.
VAD Mechanical assist of cardiac output outside of the OR
What is the difference between ECMO and VAD?
Essentially they are mechanically the same except the VAD does not have a membrane
oxygenator in the circuit, hence oxygenation and ventilation in the VAD patient are
entirely dependent on the patients own lung function and mechanical ventilation
Indications:
ECMO: Reserved for patients who would otherwise not survive because of either severe
pulmonary disease making conventional or high frequency ventilation not practical, or
reversible myocardial depression that prevents adequate cardiac output to be compatible
with life.
VAD: used as a device for ventricular rest following major cardiac surgery, particularly
those procedures that lead to a single ventricle supporting output to both the pulmonary
and systemic circulations. At OHSU, all patients undergoing Stage I repair of HLHS and
some other single ventricle repairs are supported with VAD immediately after surgery.
Contraindications:
<35 weeks gestational age (risk of IVH bleeds too high)
<2000g (limited by size of canulas and effectiveness of pump)
Intracranial hemorrhage prior to going on ECMO (>Grade I IVH).
Uncontrollable bleeding at any site
Irreversible condition
Mechanics: for VenoArterial ECMO/VAD
Patient=>Venous Canula=>Pump=>Membrane Oxygenator=>Heat Exchanger=>
Arterial Canula=>Patient
Venous Canula: usually placed in the right atrium, if placed intra-operatively the canula
usually directly enters the right atrium, if post (or non)-operatively placed access is
achieved through the right IJ.
Pump: Roller pump.
Membrane Oxygenator: both oxygenates and removes carbon dioxide, manipulated by
sweep gas composition.
Heat exchanger: rewarms the blood before return to the body
Arterial canula: tip usually placed at the arch of the aorta. If placed non-operatively
access is achieved through the right common carotid.
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Anticoagulation:
Conventional Circuit: advantage is that the circuit lasts longer than the bonded circuit.
The disadvantage is that risk of bleeding is higher. Significant consideration must be
made before any invasive procedure (chest tube, line placement, etc.) is performed on a
patient on ECMO with systemic anticoagulation as the bleeding risk is high.
Monitor anticoagulation with ACT (activated clotting time).

Monitoring
In addition to coagulation there are three main labs that are watched
Pre-lung Blood Gas
This represents the patient's mixed venous saturation.
Post-Lung Blood Gas
This measures the function of the membrane itself. PO2's should be very high in a
well functioning membrane.
Arterial Blood gas
This is measured from a peripheral (or umbilical) artery. It gives you an idea of
how much blood flow is going through the patients lungs and how well they are
functioning. A higher PO2 most likely correlates with minimal blood flow
through the lungs

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Medications
GENERAL ORDERING INFORMATION:
mg/kg dosing: Doernbecher has instituted a policy regarding ordering medications to reduce
errors. The policy states:
Medication orders written in the Pediatric Intensive Care Unit (PICU) will comply with
all existing PICU / OHSU / Doernbecher policies with the following additions:
All medication orders must be written in dose per kilogram of body weight (e.g. mg / kg /
per day or per dose, mcg / kg / per day or per dose) until the adult dosage is reached.
Medications that are traditionally written on a per m2 basis may continue to be written in
this fashion (i.e., chemotherapy).
The RN signing off the order is responsible for validating calculation accuracy.
Orders will not be faxed to pharmacy without the dosage / kilogram information.
Pharmacists will not accept orders that are not written utilizing the dosage / kilogram
method.
This policy applies mainly for patients weighing less than 50 kg, but it is a good
habit to get into for all patients, regardless of weight. The following
components are required for all medication orders:
Date and time of order
Drug name
Dose and dose per kg of body weight or mg/m2 calculation
mg/kg/day or mg/kg/dose
mcg/kg/day or mcg/kg/dose
units/kg/day or units/kg/dose
Route of administration
Dosing interval
Patient weight on order sheet containing medications, usually at top right hand
corner
Legible signature and legible pager number
For example, a 10 kg patient needing vancomycin would be written:
Joe Patient
10 kg
7/1/03 1400 Vancomycin 100 mg IV q6h (10 mg/kg/dose)
Signed: Sally Resident, 14793
OTHER MISCELLANEOUS MEDICATION HELPFUL HINTS:
GI Prophylaxis: Most all PICU patients are made NPO, and are placed on GI prophylaxis
meaning an acid blocker to prevent stress gastritis. Ranitidine is commonly used, doses include:
2-4 mg/kg/day IV divided q6-8 hours or
2-10 mg/kg/dose PO/NG/NJ q6-8 hours.

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Once the patient is eating (or getting feeds via NG or NJ) and is transferred to the ward, the
ranitidine can often be discontinued.
Therapeutic Levels:
When ordering medications for a patient, make sure you know which ones need therapeutic
levels monitored. You can order the level at the time of initial drug ordering. Most medications
are at steady state within 3 doses. In most instances, in patients with normal renal and hepatic
function, obtaining only a trough prior to giving the 3rd dose will allow you to adjust the dosing
frequency up or down to get a therapeutic level. In patients with hepatic or renal insufficiency or
failure, ordering both a peak and trough around the 3rd dose will allow you to adjust the
frequency (if the trough is high or low) and/or the dose (if the peak is high or low).
Common medications requiring therapeutic level monitoring:
Antibiotics:
Aminoglycosides Gentamicin, Tobramycin, Amikacin,
Vancomycin
Cardiac:
Digoxin
Procainamide
Anti-epileptic:
Carbamazepine (Tegretol), Phenytoin (Dilantin), Phenobarbitol, Valproic Acid
Asthma:
Theophylline
DRIPS:
In the PICU, drips are often used for their vasoactive properties (post-operative heart patients or
patients in shock) or sedative/anxiolytic or pain-reducing properties. Some helpful general
information about drips and how to calculate them follows.
1. All medications must be ordered as mg or mcg mixed in some solution, i.e., NS or D5W.
This gives the concentration of the medication (mg/ml or mcg/ml.)
2. The orders for drips must include the drip dose (mcg/kg/hr or mg/kg/min) AND the drip
rate (ml/hr). TRA means to run at.
3. Some medications are ordered as milligrams in some volume of fluid and then run at
mcg/kg/min so you must make sure that the units have been properly converted.
4. The drips are run through an infusion pump and have a minimum rate of 0.2 ml/hr.
5. Many medications that are infused as drips come in standard concentrations and are written
on pre-printed order sheets. Sedative/narcotic/paralytic drips have their own order sheet.
Vasoactive medication drips are listed on the cardiac admission order sheets. If you dont know
the appropriate standard drip concentration, ask the attending or RN.
Example:

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3 kg post-operative heart baby, returning to the PICU on ECMO needs a dopamine drip written.
(Post-CPB Order Sheet has a section for IV fluids and medications with dopamine for <10 kg as
an option.) You decide the dose will be 10 mcg/kg/min. For 3 kg patient, the dose calculation is
therefore (3 kg) (10 mcg/kg/min) = 30 mcg/min.
On the order form the concentration is written for you, 80 mg in 50 ml D5W.
Then rearrange the fractions to have the units cancel to end up with ml/hr.
( 50 ml ) ( 1 mg ) (30 mcg) (60 min) = 1.125 ml/hr
( 80 mg ) (1000 mcg) ( min ) ( 1 hr )
Your final order will look like this:
Please mix 80 mg of dopamine in 50 ml D5W TRA 1.1 ml/hr = 10 mcg/kg/min.
This order:
Tells the pharmacist how much medication to put in the bag of IV solution.
Tells the RN how fast to run the drip on the infusion pump.
Tells you and everyone else what the dose is (10 mcg/kg/min) because this is what you
adjust based on the patients clinical picture. Once the drip is made up and brought to the
bedside, subsequent orders can be written simply as, increase dopamine gtt to 15 mcg/kg/min
and the RN will calculate what infusion rate is needed for that dose.

Analgesics
Morphine sulfate (MSO4) (0.05 - 0.2 mg/kg initial dose)
Class: Opiate Analgesic
Half-life: 2-4 hours (4.5-13.3 hours in neonates)
Duration of action: 3-4 hours
Metabolism: by liver, excreted in urine and bile
Dosing Frequency: Q1-4 hours or as a continuous drip
Precautions: respiratory suppression with increasing doses, histamine release, has caused
seizures in neonates
Uses: post-operative pain control, sedation, tet spells, can also increase cardiac output
Fentanyl (1-2mcg/kg per dose initially)
Class: opioid analgesic
Half-life: 2-4 hours
Duration of action: 1-2 hours
Metabolism: by liver, excreted by kidney (<10%)
Dosing Frequency: Q30min-1hour, continuous drip
Precautions: may cause chest wall rigidity in neonates at high doses.
Uses: Post-operative pain management, rapid tolerance develops, may need to increase
drip rate daily to maintain equianalgesic dose.

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Nalbuphine (Nubain) (0.05-0.1mg/kg initial dose)

Class: Partial opioid agonist (mixed agonist/antagonist)
Half-life: 5 hours
Duration of action: 3-6 hours
Metabolism: by liver, excreted in urine
Dosing Frequency: Q1-4 hours (as with MSO4) can be in drip
Precautions: equal respiratory depression in standard doses as MSO4, at higher doses the
effect plateaus.
Uses: in post-operative pain management or to relieve itching related to narcotics.
Frequently used with epidural opiods
Sedatives
Midazolam (Versed) (0.05-0.1mg/kg initial dose)
Class: benzodiazepine
Half-life: 1-4 hours
Metabolism: extensively by liver (microsomally), excreted in urine, some in feces
Dosing Frequency: Q1-2 hours, to continuous drip
Precautions: respiratory depression, when used alone in some patients can produce
paradoxical effect. Cimetidine can prolong half life when used concomitantly
Uses: as anxiolytic/sedative in association with analgesic agents for patients with severe
pain, or in whom sedation is desired for various reasons.
Lorazepam (Ativan) (0.03-0.09mg/kg/dose)
Class: benzodiazepine
Half-life: 10-12 hours (40 hours in neonates)
Metabolism: liver, excreted in urine
Dosing Frequency: Q4-8 hours
Precautions: as with Versed, longer acting so prolonged effect of respiratory suppression
Uses: Sedative for patients who will need prolonged sedation. Can also be used to help
wean patients from Versed drips
Chloral Hydrate (25-75mg/kg max dose 2gm/day)
Class: sedative hypnotic
Half-life: around 8 hours
Metabolism: by liver to trichloroethanol (active metabolite) then excreted in urine
Dosing Frequency: Q6hours to Qday
Precautions: Trichloroethanol is carcinogenic in mice, prolonged usage may put patient
at risk. Arrhythmias with high levels, withdrawal similar to EtOH withdrawal after
prolonged, regular usage.
Uses: additional sedation of a different class, sedation for procedure
Propofol (Diprivan) (25-50 mcg/kg/min drip, 0.5-1mg/kg bolus)
Class: sedative hypnotic
Half-life: minutes, increases with increasing duration of therapy
- 77 -

Metabolism: by liver excreted in urine

Dosing Frequency: Only used as continuous drip or short acting bolus
Precautions: severe myocardial depressant proportionate to dose. No preservatives in
solution so at high risk for infection unless aseptic technique is adhered to, particularly
for prolonged drips.
Uses: Insoluble in water so supplied in solution of 10% Intralipid. Used for short term
sedation when extra sedation is needed. Also used overnight prior to extubation on
patients who have had prolonged sedation to allow decreasing other sedatives, rapid
wean prior to extubation. FDA does not approve use in pediatric patients for sedation in
the PICU

Paralytic Agents
Vecuronium (Norcuron) (0.1mg/kg, 0.2mg/kg for rapid sequence intubation)
Class: non-depolarizing neuromuscular blocker
Duration of action: 30-40 minutes
Metabolism: excreted primarily in bile, partially in urine
Dosing Frequency: Q1-2 hours prn to continuous drip
Precautions: must be prepared to manage airway or intubated prior to use. Do not use
without adequate sedation/pain control. Prolonged administration can produce prolonged
muscle weakness after stoppage
Uses: as a paralytic in patients who need prolonged mechanical ventilation with
significant lung disease, those with significant pulmonary hypertension,
Pancuronium (Pavulon) (0.04-0.1mg/kg initially then 0.01mg/kg per dose as needed)
Class: non-depolarizing neuromuscular blocker
Duration of action: 35-45 minutes
Metabolism: excreted mostly unchanged in urine, some metabolism by liver and
elimination in bile
Dosing Frequency: Q25-60minutes
Precautions: must be prepared to manage airway or intubated prior to use. Do not use
without adequate sedation/pain control.
Uses: as a paralytic in patients
Cisatracurium (Nimbex) (0.1mg/kg)
Class: non-depolarizing neuromuscular blocker
Duration of Action: 20-35 minutes, up to 45 minutes
Metabolism: rapid non-enzymatic degradation (Hofman elimination) in bloodstream
Dosing Frequency: usually a continuous drip or prn
Precautions: Cis form minimizes Histamine release caused by Atracurium
Uses: ideal as neuromuscular blocker in patient with compromised renal and/or hepatic
function
Diuretics

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Furosemide (Lasix) (0.5-1mg/kg, Max Dose 10mg/kg/day)

Class: loop diuretic
Half-life: 30min-2 hours, duration of action 2 hours
Metabolism: minimally by liver, 50-80% excreted in urine
Dosing Frequency: Q2 hours to Qday
Precautions: Ototoxicity, hypokalemia, hypocalcemia
Uses: diuresis, treatment of hyperkalemia
Bumetadine (Bumex) (0.02-0.1mg/kg, Max Dose 0.35mg/kg/d)
Class: loop diuretic
Half-life: 1-1.5 hours duration of effect 2-4 hours
Metabolism: by liver, excreted in urine (80%) and feces (10-20%)
Dosing Frequency: can be continuous drip to prn
Precautions: same as for Furosemide
Uses: Diuresis when not responding to Furosemide; has less ototoxicity at equitherapeutic doses, should change usage when Furosemide dose gets high
Metolazone (Zaroxylyn) (0.2-0.4mg/kg/day)
Class: Thiazide-like diuretic
Half-life: approximately 14 hours, slowly absorbed from GI tract
Metabolism: 70-95% excreted unchanged in urine, also in bile, may undergo
enterohepatic recycling
Dosing: oral/enteral only
Precautions: dumps both Na and K, can cause bone marrow suppression
Uses: compliments activity of loop diuretics by functioning with a different mechanism.
Has been shown to improve urine output even with very low GFR not found in other
thiazides. Can improve urine output in patients whose renal function is not responding to
high dose loop diuretics. Does not decrease GFR as other thiazides can.
Antiarrhythmic Agents
Adenosine (Adenocard) (50mcg/kg initial dose, then increase by 50 for each subsequent dose)
Class: endogenous nucleoside
Half-Life: <10 seconds
Metabolism: rapidly taken up by erythrocytes and vascular endothelial cells, becomes
part of body pool of nucleosides
Dosing Frequency: repeat doses can be given as early as 2 minutes after initial dose
Administration: should be given in most central venous access site as rapidly as possible.
Central venous access is preferred but not essential
Precautions: may produce a short-lasting first, second or third degree av block.
Use: Adenosine works by decreasing conduction through the av node. It is used
exclusively in supraventricular tachycardia to convert to sinus rhythm. If unsuccessful
after 3 doses, or patient becomes unstable, synchronized cardioversion should be
performed (This would include fresh post-op heart patients as they may not be able to
withstand the significant transient decrease in BP that can occur with this agent).
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Lidocaine (1mg.kg iv slowly, 20-50mcg/kg/min as a drip)

Class: a Class 1b anti-arrhythmic agent (membrane stabilizing), also an amide local
anesthetic
Half-Life: Initial 7-30minutes, terminal 1.5-2 hours
Metabolism: by liver to active metabolites GX and MEGX, which are later metabolized
by the liver
Dosing Frequency: douses can be given Q3-5 minutes, otherwise can be used as a drip
Precautions: CNS depressant, may cause seizures at high doses (although does have anticonvulsant properties), can cause respiratory arrest. Also suppresses cough and gag
reflexes.
Uses: treatment of choice for premature ventricular contractions, used for ventricular
dysrhythmias
Procainamide (15mg/kg over 15 minutes, 20-80mcg/kg/min as continuous drip)
Class: a Class 1a anti-arrhythmic agent
Half-life: 3-4 hours
Metabolism: acetylated to active form N-acetyl procainamide (NAPA), actively secreted
in urine as well as filtered. All forms are excreted in urine.
Dosing Frequency: may be administered as frequently as Q5 minutes or as continuous
infusion.
Precautions: contraindicated in complete heart block, Lupus, and Torsades des Pointes.
Can cause transient hypotension
Uses: for lidocaine resistant ventricular tachycardia, reentrant tachycardias, atrial
fibrillation and flutter associated with WPW
Amiodarone (5mg/kg IV over 30 minutes)
Antihypertensives
Nifedipine
Class: Calcium Channel blocker, (a dihydropyridine)
Half-life: 2-5 hours
Metabolism: primarily hepatic
Dosing: must be drawn from capsule with TB syringe then dose is calculated from total
extracted.
Precautions:
Uses: in patients who can take oral, or sublingual meds, can be used for acute
hypertensive episodes
Labetolol
Class:
blocker
Half-life:
Metabolism:
Dosing:

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Precautions:
Uses:
Esmolol (as a drip 25-250mcg/kg/min)
Class: blocker
Half-life:
Metabolism:
Dosing:
Precautions:
Uses: Hypertension, frequently after coarctation repair
Nitroprusside (as a drip, usual range 0.1-10 mcg/kg/min)
Class: arteriolar vasodilator, NO donor
Half-life:
Metabolism:
Dosing:
Precautions: Monitor cyanide levels, especially in the setting of renal failure
Uses: Hypertension, afterload reduction
Hydralazine
Half-life: about 4 hours, although serum levels don't correlate well with activity
Metabolism: extensively by the liver
Dosing:
Precautions: can cause a Lupus like syndrome in as many as 10-20% of patients who
receive a prolonged course.
Uses: can be used for acute hypertensive episodes, but it is not the drug of choice
Cardioactive Drips
Adrenergic Receptors
Alpha - peripheral vasculature
stimulation causes vasoconstriction
Beta - (remember 1 heart, two lungs)
Receptor stimulation acts through adenylate cyclase forming cAMP
Beta 1 - cardiac receptors
stimulation increases contractile strength
and increases heart rate

Beta 2 - pulmonary receptors, and peripheral vasculature

stimulation causes smooth muscle relaxation of bronchial walls
smooth muscle relaxation in peripheral vasculature
Drugs to Improve Cardiac output
Dobutamine (3-20mcg/kg/min)
MOA: almost exclusively a Beta-1 agonist with no alpha effect, and minimal beta-2
effect

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Effect: inotropic and chronotropic effects on the heart, some decrease in peripheral
vascular resistance and some improvement of AV node conduction
Use: to improve cardiac output and blood pressure, can be administered peripherally
Risk: increases myocardial oxygen demand, may increase heart rate excessively

Dopamine (2-20mcg/kg/min)
MOA: precursor of norepinephrine, stimulates dopaminergic, alpha and beta adrenergic
receptors (little or no beta-2 effect)
Effect: at low doses (2-5mcg/kg/min) minimal alpha effects, causes more splanchnic
dilatation, improving renal blood flow (a dopaminergic response). At medium doses (510mcg/kg/min) beta effects start to predominate. At high doses (10-20mcg/kg/min) alpha
effects more prevalent
Use: good first line to improve cardiac output when used in mid-range
Risk: high doses may cause vasoconstiction. Adverse effects on immune function.
Epinephrine (0.01 to 1 mcg/kg/min, or higher in very critical situations, usual dose range in
cardiac patients is 0.03-0.3, in septic patients doses may be higher)
MOA: potent non-selective beta agonist also an alpha agonist (Beta>alpha)
Effect: increases inotropic and chronotropic cardiac activity also causes peripheral
vasoconstriction, decreasing peripheral perfusion
Use: to increase cardiac output and blood pressure, at lowest doses (<0.1mcg/kg/min
has primarily beta-1 effects)
Risk: can cause profound peripheral vasoconstriction, compromising tissue perfusion.
Long term use downregulates catecholamine receptors, decreasing effect, also increases
myocardial oxygen demand
Drugs to Improve Cardiac Output and cause Vasodilation
Milrinone (0.30-1.0mcg/kg/min)
MOA: phosphodiesterase inhibitor, prolonging the effect of cAMP, allowing increasing
ionized calcium entry into cardiac cells, increasing myocardial contractility, and cAMP
dependent vascular relaxation
Effect: peripheral vasodilator and positive inotropic effect on heart, improved diastolic
relaxation. May cause reflex tachycardia due to vasodilation
Use: afterload reduction, additional inotropic support when catecholamines already in
use.
Risk: as with other inotropes, can also potentially cause too much vasodilation leading
to hypotension, use caution in severely hypovolemic patients
Drugs to cause vasodilation
Nitroprusside (Nipride) (0.5-10mcg/kg/min)
MOA: it has direct activity on vascular smooth muscle (donates an NO group to be
specific)
Effect: peripheral vasodilator by relaxation of smooth muscles in vessels
Use: used as an afterload reducer, primarily an arterioloar vasodilator, can increase
tissue perfusion in patients receiving vasoconstrictors, can be given peripherally.

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Risk: Cyanide and Thiocyanate toxicity from prolonged usage of high doses (using Na
thiosulfate decreases risk 10mg/mg nitroprusside). Risk of severe hypotension in patient
who is intravascularly dry. Overcomes hypoxic vasoconstriction in the lungs, so initiation
can cause increased VQ mismatch and therefore more difficulty in oxygenation.

Nitroglycerin (0.5-5mcg/kg/min)
MOA: relaxes peripheral vascular smooth muscle by donating an NO group
Effect: causes peripheral vasodilatation, decreasing pre-load and decreasing blood
pressure, helps prevent vasospasm
Use: most commonly used in post-operative arterial switches to help prevent coronary
vasospasm, sometime used as a preload reducer, can be given peripherally.
Risk: can cause severe hypotension in patient who is intravascularly dry, risk of
methemoglobinemia, otherwise similar to nitroprusside.
Drugs to cause pulmonary vasodilation
Nitric Oxide (0-80ppm inhalation)
MOA: Activates cGMP pathway causing direct smooth muscle relaxation in local
vascular bed
Effect: since given as inhalational agent, causes relaxation of pulmonary vascular bed
only, with no systemic effect
Use: used to decrease pulmonary vascular resistance in patients in whom pulmonary
hypertension is a problem, either from a cardiac output standpoint or from a oxygenation
standpoint
Risk: can combine with Hgb to form methemoglobin, needs closed ventilatory circuit
and constant monitoring. NO is now FDA approved for PPHN, but the cost is $3000/day
for up to 4 days.
Drugs to increase systemic vascular resistance (increase afterload)
Norepinephrine (Levophed) (initial dose 0.05-0.1mcg/kg/min, titrate to effect)
MOA: Potent alpha adreneric agonist and beta agonist (alpha>beta)
Effect: vasoconstriction and inotropic and chronotropic effects, increasing blood
pressure, both by increasing SVR and by increasing CO
Use: in patients already on vasopressors requiring more support to maintain blood
pressures
Risk: decreases blood flow to all organs and tissues, can cause worsening metabolic
acidosis due to ischemia
Phenylephrine (Neo-Synephrine) (0.1-0.5mcg/kg/min as drip, 5-20mcg/kg as bolus)
MOA: alpha adrenergic agonist
Effect: constricts both arterial and venous blood vessels, increasing systemic vascular
resistance without changing cardiac dynamics
Use: In patients who need blood pressure support, where muscular outflow obstruction
may be worsened by the use of Beta agonists, such as unrepaired TOF or hypertrophic
cardiomyopathy.

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Risk: decreases flow of blood to all organs, reducing oxygen supply and potentiating
ischemia at very high doses can have some beta effect.

Also Epinephrine and Dopamine to some extent

Adjunct:
Steroids - can upregulate catecholamine receptors, improving function and decreasing dose
requirements of vasopressors

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Cardio Pulmonary Equations

Pulmonary to Systemic Blood Flow Ratio (Qp:Qs Equation):

Qp:Qs =

Sat (aorta)
- Sat(SVC)
Sat (pulm venous) - Sat (PA)

This equation can be used to determine the relative blood flow between the body and the lungs. The goal in
any patient is for this ratio to approach 1, so there is equal blood flow to the lungs and body. In patients
who have all of their pulmonary blood flow supplied by a shunt from the aorta (i.e., Norwood after stage 1
repair), you can use this equation to help determine the ideal oxygen saturation for a patient. For these
patients:
Sat (aorta) = arterial oxygen saturation (as measured from ABG)
Sat (SVC) = mixed venous sat, which in this case should be measured before the right atrium as mixing
occurs from pulmonary venous return, artificially elevating the MVS.
Sat (pulm venous) = as we usually cannot measure this we assume that, with healthy lungs the blood will
be fully oxygenated, i.e. =100%
Sat (PA) = pulmonary artery saturation, which in a patient whose entire pulmonary blood flow comes from
a shunt from the aorta, should equal the Sat (aorta).
Example:
A patient POD#3 s/p Norwood, relatively stable has oxygen saturations around 80% (by pulse ox, correlating with
gases). MVS from a jugular line is 60%. What is this patient's Qp:Qs?
Qp
Qs

80%-60%
100-%-80%

20 = 1
20

Oxygen Content (CxO2) (for any sample of blood)

CxO2 = 1.34x [Hgb] x (O2 Sat) + 0.003PxO2
Where:
[Hgb] is the concentration of hemoglobin in gm/dl
O2Sat is the oxygen saturation of the specimen of blood
PxO2 is the partial pressure of oxygen (in mmHg) of the sample of blood

Fick Principle
VO2 = (CaO2 - CvO2) * Q
Where:
VO2 is the oxygen consumption
CaO2 is arterial oxygen content
CvO2 is venous oxygen content
Q is cardiac output

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The following equations can be used in solving the Fick Principle, but give you values based on patients body size

Oxygen availability (DO2) (620+/-50 ml/min/m2)

DO2= CaO2*CI*10
CI = cardiac index = CO/Body surface area
Oxygen Consumption (VO2) (120-200ml/min/m2)
VO2 = CI*avDO2*10
avDO2 = DO2 (arterial blood) - DO2 (venous blood)
Oxygen Extraction (26 +/- 2 %)
O2 ext = (avDO2/CaO2)*100

Oxygenation Index
OI = MAPx (FiO2x100)/PaO2
Where:
MAP is the mean airway pressure
FiO2 is the set fraction of inspired oxygen the patient is receiving
PaO2 is the partial pressure of oxygen (in mmHg) from an arterial blood gas

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Sedation, Analgesia, Paralysis

making life in the PICU safer, more comfortable, and easier for all.
Laura Ibsen, M.D.

Goals of ICU Sedation

Analgesia for painful diseases and procedures
Compliance with controlled ventilation and routine intensive care
Amnesia for the perios of sedation
Reduce the pysiologic responses to stress

Avoid complications
How???
Know what you are trying to do
Know your drugs
Know your patient
If you dont know the indications and contraindications to the drug you are considering, and if
you are not prepared to deal with complications, DONT DO IT.
It is essential to get comfortable with the idea of titrating drugs to effect--there is no dose.
There are guidelines, but each situation, and each patient will be different. A dose of morphine
that wouldnt touch a narcotic-tolerant oncology patient could cause life-threatening respiratory
depression in an adolescent with a broken arm. Watch the nurses give the drugs, and watch their
effect. Keep in mind what the target response is. It is the ONLY way you will ever be
competent to provide adequate analgesia and sedation. WATCH, and PAY ATTENTION. You
will learn something and you will be able to provide better care.

Classes of drugs commonly used in the PICU

Narcotics
Benzodiazepines
Non-steroidal anti-inflammatory agents (Ketorolac)
Ketamine
Propofol
Neuroleptics
Barbiturates
Paralytics-depolarizing and non-depolarizing

Situations in which some combination of the above drugs are commonly

needed
Mechanical ventilation, post-operative
Mechanical ventilation, ARDS
Mechanical ventilation, Asthma
Mechanical ventilation, Epiglottitis or croup
Head injury
- 87 -

Post-operative
Chest syndrome
Intubation--various scenarios
Painful procedures--chest tubes, lumbar puncture, bone marrow aspirate, dressing changes,
endotrachal tube suctioning
As you think about the drugs you would choose for each situation, think concretely about what
you are trying to achieve--NO movement whatsoever in the patient with a tenuous airway,
analgesia while attempting to allow wake-up for extubation post-operatively, etc. Different
drugs do different things--often you should use a balanced approach.

Basic (very basic) pharmacologic principles

1. Onset of action--t1/2 reflects initial distribution from blood to highly perfused tissues.
Clinical onset of action is the time necessary to see effect of the drug.
2. Half life--the time it takes for the concentration of drug to decrease by 1/2. Elimination
constant, Kel=0.693xT1/2. (T1/2 =redistribution and metabolic clearance)
3. Volume of distribution--relates the amount of drug in the body to the concentration of drug in
the blood or plasma--the fluid volume that would be needed to account for all the drug in the
body. Small Vd implies that the drug is retained within the vascular compartment, large Vd
implies distribution through the body of sequestration in certain tissues. Vd (ml/kg)=Dose
(mg/kg) /concentration at time 0 (mg/ml).
4. Clearance--The ability of the body to eliminate a drug, expressed as a volume of blood
cleared of drug per unit time. Cl=Vd x Kel
4. Metabolism--mostly renal and/or hepatic for most drugs.
5. Bioavailability--the percent of the dose reaching the systemic circulation as unchanges drug
following administration by any route.

Opioids (a.k.a. narcotics)

Opioids provide both pain relief and sedation. They are the most commonly used class of drugs
for analgesia in the PICU. In addition to their analgesic properties, narcotics decrease
responsiveness to external stimulation and reduce the level of consciousness. Nevertheless, the
sedative properties of narcotics are inferior to those of the benzodiazepines, and amnesia
following narcotic administration is incomplete.

morphine
meperidine
fentanyl
methadone

Relative Dose

Elimination t1/2

Clearance
(ml/kg/min)

0.1 mg
1.0 mg
1-5 mcg
0.1 mg

114 min
222 min
202 min
15 hours

14.7
15.1
11.6

Morphine
Minimal direct effect on myocardial performance
Histamine release--may induce hypotension if large doses are given rapidly
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Dose related analgesia, sedation, euphoria

Dose related respiratory depression
Meperidine
Respiratory depression similar to other opioids
Normeperidine (metabolite) is epileptogenic
Mild vagolytic
Histamine release and myocardial depression in high doses
Less biliary tract spasm
Fentanyl
Synthetic opioids, highly lipid soluble, short distribution T1/2 but long elimination T1/2
Metabolized almost exclusively in the liver, thus may accumulate with altered hepatic blood flow
Provides hemodynamic stability, even in very high doses, and blunts pulmonary vascular
responses.
May produce Muscle rigidity (hest wall rigidity) if given as large fast bolus
Commonly causes lowering of HR (unrelated to pain relief or sedation)
Methadone
Potent analgesic effects, minimal hemodynamic effects
Long half-life
Absorption after oral administration reliably 50-7-% that of IV
Sedative and euphoric properties may be less pronounced than those of morphine
Useful for pain control as well as for treating abstinence phenomena.

Untoward Effects of Opioids (a.k.a. side effects)

Respiratory depression--All opioids cause dose related respiratory depression by shifting the CO2
response curve to the right, and abolishing the ventilatory response to hypoxemia. Depending on
the drug you can see decreased ventilatory rate or tidal volume (thus, the rate may be ok, but the
tidal volume may be inadequate). Respiratory depression may occur at any age.
Reversal--Naloxone (narcan)
Full reversal--0.1 mg/kg; >20 kg, 2.0 mg.
Partial reversal--titrate to effect--start with 2-10 mcg/kg.n The easiest way to do this
is to take 0.4 mg (i.e., 1 cc of 0.4mg/cc vial) and dilute in 10 cc NS=40mcg/cc. Thus,
1cc per
4 kg body weight equals 10 mcg/kg. Most useful for patients who are
expected to have significant residual pain (i.e., surgical, chest syndrome, Sickle Cell pain
crisis, oncology)
The half-life of naloxone is significantly shorter than morphine, demerol, or fentanyl. If
there has been a significant overdose, more than one dose will be necessary. A
continuous infusion may be needed.
Pruritis--Several of the opioids cause itching, and there is significant inter-patient variability in
susceptibility. It may be alleviated by beardy.

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Tolerance and Dependence--Tolerance generally develops after 2-3 days of frequent or

continuous usage. Dependence (i.e., the potential for withdrawal symptoms) generally develops
after 5-7 days of frequent of continuous use. Tolerance is treated by increasing the dose as
needed for pain relief. Dependence is treated with gradual withdrawal of the drug, either using
the initial drug, or converting to methadone for convenient dosing. Treatment of withdrawal can
be difficult if the patient has been receiving narcotics for prolonged periods. In general, the
longer the period of treatment, the longer the period of withdrawal needed. Alternatively, one
can treat symptoms with alternative drugs (a method usually reserved for those who have a
psychological as well as physical dependence on the drug).

Benzodiazepines
Benzodiazepines provide hypnosis, anxiolysis, aterograde amnesia, and anticonvulsant activity.
They DO NOT provide analgesia. Once more, they DO NOT provide analgesia. They are
useful for providing sedation and treating seizures, but one must remember to treat pain with an
analgesic
Midazolam has a short onset of action, short duration of action, and relatively short elimination
Relative
Dose
Diazepam

0.3-0.5

Lorazepam

0.05

Midazolam

0.15-0.30

t1/2

t1/2

(redistribution)

(elimination)

(min)

(hours)

30-60

6-15

Vd
(Liter/kg)

Clearance
(ml/kg/min)

21-37

1.0-1.5

0.2-0.5

10-20

0.8-1.3

0.7-1.0

1-4

1.0-1.5

6-8

half-life. For these reasons, it is useful for short procedures, but inconvenient for prolonged
sedation. It may be used as a constant infusion. Continuous administration may result in
prolonged sedation even after the infusion is discontinued if the rate of administration is to high.
There have also been reports of dystonia and choreoathetosis after midazolam infusion and may
represent benzodiazepine withdrawal, persistent effects of the drug, or the combined effect of
multiple drugs.
Diazepam has a short onset of action, like midazolam, and slightly longer duration of action, but
a long elimination half-life. Thus, with repeated doses, it may accumulate.
Lorazepam is less lipid-soluble, and has a longer duration of action with a shorter elimination
half-life, thus is more appropriate than diazepam for prolonged sedation. (Longer duration of
action but less risk of accumulation with repeated dosing.)

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Untoward Effects of Benzodiazepines

Tolerance--As with the narcotics, dose may need to be increased after 2-3 days
Dependence--Dependence and withdrawal phenomena can be severe. Withdrawal needs
to be done carefully, looking for signs of withdrawal (tremor, high HR, BP). Too rapid
withdrawal in severely dependent patient can cause seizures.
Choreoathetoid movement disorder--Usually improves with time
Personality changes--Usually improves with time, though after long term, high dose use,
personality changes may remain apparent to family members for weeks-months.
Respiratory depression--Dose related.
Reversal--Flumazenil--Benzodiazepine receptor antagonist
0.2 mg over 30 sec. may increase dose up to 0.5 mg/minutes. Up to 5 mg total.
Contraindicated--where benzodiazepines have been used to treat seizures, chronic
benzodiazepine use, TCAs present, mixed drug overdose.

Ketamine
Ketamine is chemically related to phencyclidine and cyclohexamine. Ketamine hydrochloride is
water soluble at commercial concentrations, but is quite lipid soluble as well and quickly crosses
the blood-brain barrier.
Pharmacokinetics are very similar in children and adults. With intravenous administration, the
distribution half-life is less than 30 seconds, the redistribution half-life 4.7 minutes, and the
elimination half life 2.2 hours. Clinically, one sees peak concentrations within one minute of IV
administration, with rapid absorption by the brain and early immediate induction of clinical
effects. With redistribution to peripheral tissues, the decrease in CNS levels correlates with
resolution of the clinical effect, generally within 15-20 minutes.
The anesthetic state produced by ketamine has been classically described as a functional and
electrophysiological dissociation between the thalamoneocortical and limbic systems. Ketamine
is a potent analgesic at sub-anesthetic concentrations, and the effects may be mediated by
different mechanisms. Ketamine blocks NMDA receptors, and there is some data that it interacts
with opiate receptors as well as CNS muscarinic receptors.

Clinical Effects of Ketamine

CNS
Ketamine produces a dissociative state. Its effect on intracranial pressure remains
controversial in practice, but controlled studies in which ventilation was controlled
showed no effect on intracranial pressure. It probably does, however, increase CMRO2,
and hence, use in patients with intracranial injury should probably be avoided if possible.
Emergence phenomena are frequently reported after the use of ketamine in older
adolescents. Concordant treatment with a benzodiazepine has been shown to prevent the
development of unpleasant emergence phenomena.

Cardiovascular System
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Ketamine inhibits reuptake of catecholamines in both the peripheral circulation and the
CNS in a dose-dependent fashion. It has a direct negative inotropic effect on the
myocardium, and a direct vasodilatory action on vascular smooth muscle. This is
generally overwhelmed by central sympathetic stimulation that occurs, however, leading
to increases in heart rate, systemic arterial pressure, and possibly systemic vascular
resistance. The cardiovascular effects of ketamine are attenuated by alpha and beta
blocking agents, verapamil, benzodiazepines, and high epidural blockade.
Respiratory effects
Ketamine is a mild respiratory depressant, and there is a dose related increase in
respiratory depression with incremental doses of ketamine. In children, respiratory rate,
tidal volume, and minute ventilation are unaffected, but the CO2 response curve is shifted
to the right. Ketamine generally preserves airway patency, and protective airway reflexes
are not repressed. Transient stridor or laryngospasm are rarely reported, and are
associated with coincident respiratory infection. Ketamine increases oral secretions, and
this may be more clinically important in those children with upper respiratory infections.
Laryngospasm and the potential for emesis/aspiration are more pronounced in infants and
patients with a full stomach, hence these patients should be considered at risk for airway
compromise.
Ketamine is a potent bronchodilator. The mechanisms of this response is considered to
be a combination of drug induced increase in circulating catecholamine, direct smooth
muscle dilatation, and inhibition of vagal tone.
Neuromuscular Effects
Ketamine increases skeletal muscle tone, and there are frequently random movements of
the head or extremities. Ketamine also appears to potentiate the effects of neuromuscular
blocking agents, both depolarizing and non-depolarizing.
Intraocular Pressure
The effects of ketamine on IOP are controversial, and the literature contains various
contradictory reports regarding the potential for increased IOP during ketamine
anesthesia.
Dosage Recommendations
In the intensive care unit all anesthetic/analgesic/sedative agents should be titrated to
effect, with the unique physiology of each patient kept in mind. This makes dosage
recommendations difficult. These children may be compromised from a pulmonary,
hemodynamic, or neurologic perspective, and judicial use of any agent is warranted.
Ketamine, for example, while supporting hemodynamics in the majority of patients, can
cause hypotension if the patients myocardial reserve is limited. Thus, these
recommendations are NOT to be interpreted as policy, but as simple guidelines.
Analgesia-.25-.75 mg/kg IV: Dissociation/anesthesia-1.0-2.0 mg/kg IV in a wellhydrated patient with good hemodynamics, 0.25-1.0 mg/kg in a severely dehydrated
patient of a patient with compromised myocardial function.
- 92 -

Continuous infusion-1 mg/kg IV followed by 0.5-1.0 mg/kg/hour

Tolerance develops with repeated doses, and the optimal dose will need to be increased.
Co-administration of benzodiazepines reduces the incidence of emergence phenomena in
older children, but will prolong the duration of sedation. This is not generally
problematic in the intensive care setting, but should be considered.

Propofol
Propofol (2,6 diisopropyl phenol, Diprivan) has low aqueous solubility, and the commercial
preparation is a 1% (i.e., 10 mg/ml) solution in intralipid (i.e., 1.2% egg phosphatide, 2.25%
glycerol.). It has a rapid onset and short duration of action, and produces respiratory and cardiac
depression that is dose related. It is most useful for short procedures or short continuous
infusions (see below).
Propofols unique pharmacokinetics are its most attractive feature-rapid onset of hypnosis and
rapid resolution of effects after discontinuation of the drug. The distribution of propofol is
describes by an open three-compartment model: rapid initial distribution from blood to highly
perfused tissues (brain, heart, lung, liver)-t/12 1.8-4.1 min, redistribution and metabolic
clearance-t1/2 21 to 69 min, and slow return from poorly perfused tissues to blood-t1/2 184834 min. Propofol has a large central volume of distribution, is highly protein bound, and has an
apparent high volume of distribution at equilibrium.
Propofol is extensively metabolized in the liver and possibly other sites to inactive glucuronide
and sulfate conjugates which are excreted in the urine. In adults with renal or hepatic disease,
propofol pharmacokinetic parameters are not significantly altered.
Clinical effects are realized within 40 seconds of administration, and emergence occurs within 10
to 30 minutes, depending partially on the length of administration.

Clinical Effects of Propofol

CNS
IV administration of propofol produces hypnosis with minimal excitation, usually within 40
seconds. Propofol is not an analgesic. It appears to decrease ICP, presumably by reducing CBF
and increasing cerebrovascular resistance, and also decreases CMRO2. CPP may be reduced to
unacceptable levels. Propofol may be an effective anti-convulsant for status epilepticus
unresponsive to other drugs.
Cardiovascular
Propofol may produce hypotension by a direct vasodilatory effect on both arterial and venous
beds and by reducing sympathetic tone. High concentrations of propofol have a direct negative
inotropic effect. Propofol is thus more likely to induce hypotension in patients with
hypovolemia, compromised myocardial function, or vasomotor instability.
Respiratory
- 93 -

Propofol acts as a moderate respiratory depressant, and blunts both hypoxic and hypercapnic
ventilatory drive. Minute ventilation, tidal volume, and FRC are all decreased during its use. As
well, as high levels, airway protective reflexes are blunted.
Propofol is a mild bronchodilator and pulmonary dilator, but does not affect hypoxic
vasoconstriction.
Metabolic
Propofol significantly decreased Vo2 and Vco2 in excess of its sedative effects, possibly due to a
decrease in cellular metabolism. Serum and urine cortisol levels are decreased, but the adrenal
response to ACTH is preserved. Hypothalamic function, thyroid function, or glucose
metabolism have not been shown to be affected.
There have been a number of reports of profound metabolic acidosis in children who have
received propofol for long-term (>24 hours) sedation. The etiology of the metabolic acidosis
remains unclear, but probably precludes routine use of propofol for long-term sedation in the
PICU.
Immunologic
Anaphylaxis has been reported with propofol use. Because of its carrier, it is contraindicated in
patients with known hypersensitivity to egg.
Untoward Effects
Pain on injection is relatively common, and can be ameliorated by concomitant injection
of 1% lidocaine, generally in a ratio of 1cc lidocaine to 10-20cc propofol.
Hyperlipidemia may occur with long-term use.
Green urine (no clinical significance)
Ability to support bacterial growth due to carrier media (thus, should be treated as a
sterile injection).
In vitro evidence of inhibition of neutrophil chemotaxis.
Excitatory phenomena when there are low serum levels of drug.
Dosage Recommendations
As with all anesthetics, keep hydration status, vascular tone, and inotropic state in mind. If
patient is not intubated, have available equipment to secure an airway.
Induction (i.e., intubation): 0.5-1.0 mg/kg (i.e., 0.5-1.0cc/10 kg)
Bolus method for short procedures: 0.1-0.5 mg/kg/bolus, every 3-10 minutes.
Maintenance (sedation-OR): 15-100 mcg/kg/min, (i.e., 0.075ml/kg/hour to 0.6 ml/kg/hour) start
low, increase as necessary. Occasionally need to use up to 300 mcg/kg/min.
ICU sedation: initial 5-10 mcg/kg/min, increase as necessary in 10 mcg /kg/min increments, up
to 100 mcg/kg/min.

Muscle Relaxants

- 94 -

Muscle relaxants are used when you need to have the patient NOT MOVE, and to have NO
MUSCLE ACTIVITY. They provide ZERO sedation or analgesia. Once more, ZERO sedation
or analgesia. DO NOT FORGET.
Indications for Muscle Relaxants (always relative)
Intubation
Mechanical ventilation where risk of estuation is great, or risk of bara/volutrauma is high
Procedures such as central line placement of biopsy in the intubated patient
Intractable intracranial hypertension (IF ICP being monitored)
Reduction of CO2 production/O2 consumption (??not clear if this is true)
Depolarizing Neuromuscular Blocker--Succinlycholine
Non-depolarizing neuromuscular blockers
Pancuronium, vecuronium
Atracurium, cis-atracurium
Doxacurium
Rocuronium
Succinlycholine
Sux is loved and hated both. You must understand why before you use it safely. It is a
depolarizing neuromuscular blocker--it depolarizes the neuromuscular junction by binding the
Ach receptor and further transmission of nerve impulses cannot be propagated. It has a rapid
onset of action--average 45 seconds to achieve intubating conditions, and short duration of
action--generally 5-8 minutes. It is vagotonic and bradycardia is common and may be
hemodynamically significant, necessitating premedication with atropine in most cases.
Fasciculations occur in children and adults, are rare in infants. There is a rise in serum K+ of
0.5 meq in normal patients (those w/o muscle disease), and hence is to be avoided in states of
hyperkalemia. The rise in serum K is massive in certain pathologic states--burn injury, crush
injury, spinal cord injury, certain neuromuscular disease. It is also a triggering agent for
malignant hyperthermia (which may be fatal), and patients who are known to have MH, who
have a family history of MH, or who have a condition that puts them at risk for MH should
NEVER receive sux.
Risk of Hyperkalemia--burn injury, tetanus, spinal cord injury, encephalitis, crush injuries,
certain neuromuscular diseases, intra-abdominal sepsis.
Risk of Malignant Hyperthermia--Positive family history, Muscular dystrophies (esp.
Duchenne), central core myopathy, remember to include unknown myopathies.
Other Untoward Effects of Sux:
Jaw stiffness, usually masseter muscle spasm. There is controversy about the relationship of
MMM to Malignant hyperthermia.
Arrythmias--usually vagal in origin. Premedicate with atropine.
Myoglobinemia--Relatively frequent (40 % if given Sux and halothane), occasionally significant
enough to produce myoglobinuria.
Increased Intraocular pressure-avoid in the presence of eye injury.
- 95 -

Inability to intubate--even 5 minutes can be a LONG TIME. Short duration of action is not a
license to use sux in a situation when the patient should not be paralyzed.
Non-depolarizing Neuromuscular Blockers
These drugs have a longer onset of action and longer duration of action than succinlcholine.
They act as competitive antagonists of Ach at the neuromuscular junction. They do not affect
potassium and are not MH triggering agents. They differ in their chemical structure, route of
metabolism and elimination, onset and duration of action.
onset

Duration

Side Effects

Metabolism

Pancuronium

Dose
(mg/kg)
0.1

2 min

4-6 min

tachycardia
with bolus use

Vecuronium

0.1-0.3

1.5-2
min

Atracurium

0.3-0.6

histamine
release (mild)

Hoffman degradation

Rocuronium

0.6-1.2

2-3
min
60sec

20-30
(children)
60-80
(infants)
15 min

Renal (60-80%) and

biliary excretion
hepatic metabolism,
biliary (80%) and renal
(20%) excretion

60 min

Problems Associated with Neuromuscular Blocker Use

Loss of a valuable patient monitor--without muscle activity you must depend on vital sign
changes to assess pain and anxiety, as well as abdominal assessment.
Fluid retention without muscle activity to stimulate venous and lymphatic drainage.
Long-term weakness has been associated with continuous infusions of neuromuscular blocking
agents, most commonly the steroid based NMBs (vecuronium) used in conjunction with steroids.
There are now reports of significant myopathy associated with Atracurium, however, so the
implication of the steroid base as etiologic may not be valid. Excessive blockade should be
avoided. This may be accomplished by Train of Four testing, giving drugs as intermittent
boluses, or by stopping paralysis on a regular basis and observing the time needed for return of
function.
Many antibiotics, especially the aminoglycosides, have neuromuscular blocking properties
(complex and varied mechanisms). Aminoglycosides should be avoided if possible if continuous
infusions of NMBs are used. If not avoidable, depth of paralysis should be monitored.

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Blood Products in the PICU

CONSENT:
Before giving any patient a blood product at OHSU, the parent should be given a copy of the
handout What You Should Know About Blood Transfusion to read. This sheet describes the
benefits and potential risks of transfusions, as well as describing blood safety measures,
alternatives to Red Cross donor blood and describes the Bloodless Medicine and Surgery
program at OSHU.
A Transfusion Blood Consent form should be signed before ordering blood products for a
patient for the first transfusion of that hospitalization. If the patient needs more blood products
after the first transfusion, a new consent form does not need to be signed each time during the
same hospitalization. However, if a patient receives a transfusion during one hospitalization, is
discharged, and then is readmitted, a new consent form needs to be signed.
There is also a Transfusion Blood Refusal form for any patient (or parent) who does not want
blood products given.
There is a blood product-ordering sheet that should be used to order all blood products.
DONOR SCREENING/BLOOD PROCESSING:
All blood that is given to patients at OHSU comes from the Red Cross. The blood that is
donated for transfusion is screened for antibodies including hepatitis B, hepatitis C, HIV-1, HIV2, human T-cell lymphotropic virus (HTLV) I and HTLV II. Additionally, a RPR/VDRL test for
syphilis, hepatitis B surface antigen and HIV p24 antigen are also done. If any donor unit is
positive for these tests, the test is repeated and if confirmed, the unit is destroyed. Because most
of the screening tests look for antibodies within the donors serum, it is possible for a donor to
have been infected with an agent but not produced antibody before donating blood. Therefore,
with these screening and confirmatory tests, the risk of infection from a unit of blood is small,
but not zero. The following is a list of approximate risk of transfusion, and may help you discuss
this issue in an educated manner with a concerned parent.
Syphilis
<1:100,000
Hepatitis A 1:1,000,000
Hepatitis B 1:250,000 1:30,000
Hepatitis C 1:100,000
HIV-1 &-2
1:2,000,000 1:500,000
HTLV I & II 1:600,000
Both donor blood and the recipient blood are also tested for type (ABO) and Rh status (positive
or negative), which reflects the D antigen on the red cells. In addition, an antibody screen is
done which detects autoantibodies or alloantibodies. Direct Coombs testing will detect IgG or
complement on the surface of the red cells. Indirect Coombs testing will detect the presence of
free-floating antibodies that will coat or activate complement on the surfaces of normal red cells.
If you need to transfuse any blood product, first you must order a type and screen for that
patient. The patients blood will be drawn and sent to the laboratory where ABO and Rh type
- 97 -

will be done, as well as the antibody screen. If you then order a blood product for the patient, a
cross-match will be performed so that washed donor red cells are incubated with the patients
serum. Agglutination is detected and graded. Direct Coombs testing is then done. If both the
antibody screen and the Direct Coombs test are negative, and the cross-match does not produce a
reaction, then the blood is compatible and can be given to the patient. If the antibody screen or
cross-match is positive, then an Indirect Coombs test is done to evaluate compatibility for the
patient.

- 98 -

CHOICE OF BLOOD PRODUCT AND AMOUNT TO GIVE:

PRODUCT
Whole Blood

COMPOSITION
RBCs, leukocytes
and platelets as
well as clotting
factors, especially
Factors VIII and
V.

PRBC

RBCs, no plasma.

FFP

Procoagulant and
anticoagulant
plasma proteins.

Cryoppt

Factors VIII, XIII,

fibrinogen and
fibronectin.

Apheresis
Platelets

Platelets from
single donors.

INDICATIONS
Oxygen carrying
capacity or
volume
replacement for
severe blood loss
(>20%).

ADMINISTRATION
10 ml/kg over 2-4
hours. This amount
will raise Hct by 5%.

COMMENTS
Not used
commonly
since it
contains
leukocytes
and has
higher risk of
transfusion
reactions.
Very
difficult to
obtain.
Oxygen carrying
10 ml/kg over 1-2
One unit =
capacity, trauma,
hours in patients with 250-350 ml.
bleeding, chronic
nl cardiac function.
Order in
anemia.
Slower if CHF, faster increments
if bleeding. Discuss
of 1/2 unit
or __ units
with attending the
or may give
amount to give for
cardiac patients.
60 ml or less
This will raise Hct by to neonate.
~5%.
Replacement of
10-15 ml/kg as
Give for
plasma
rapidly as tolerated
prolonged
procoagulant and
(15-30 minutes). This INR, aPTT
anticoagulant
will increase level of
plasma proteins.
all factors by 10-20%.
Deficiencies of
One button of cryo
May give
VIII, vWF or
= 7 ml = 1 unit. 1 unit with FFP or
fibrinogen.
per 5 kg will raise
alone.
fibrinogen ~50
Specify in
FFP or saline
Thrombocytopenia 10 ml/kg as rapidly as No crossor platelet function tolerated (usually 30- match
defects.
60 minutes). This
needed, but
will increase platelet
are ABO
count by 50,000.
typespecific.
One unit =
200-250 ml.

OTHER INFORMATION ON HOW TO ORDER BLOOD PRODUCTS:

- 99 -

Leukoreduced - Now, all blood products at OHSU are leukoreduced at the red cross, and
therefore considered CMV-safe. You do not need to write this in the order. This may change
in the future, so stay informed.
Irradiation - Order irradiated PRBC or platelets for patients who are immunosuppressed and
who may be at risk for transfusion associated graft-versus-host disease. In our PICU, this is
mostly for the Hematology/Oncology patients, infants <1 who had heart surgery. It takes only
five minutes for the blood bank to do this. It is not necessary to irradiate FFP or cryopreciptate.
Sickle-cell free Order this type of red cell for all post-operative cardiac patients.
Neonatal Order this type of PRBC for all patients under one month of age. Repeated
transfusions will be taken from the same unit.
RCL- Red cell leukoreduced. This is the basic type of blood.
RC5Red cells that are less than or equal to 5 days old. Potassium levels are low. Only
indicated for massive transfusion and hyperkalemia. Limited quantity.
Washed cellsindicated for massive transfusion and hyperkalemia, and certain antibody
problems. Usually necessitates discussion with transfusion medicine.
Calcium
Blood products contain citrate, which binds ionized calcium. Albumin binds ionized calcium.
Ionized calcium is active (NOT total calcium). The usual dose of Calcium chloride is 10 mg/kg
for Ca2+ <1.2. If large quantities of blood products or albumin are given (and sometimes small
amounts), the ionized calcium may fall.

- 100 -

Guidelines of the Task Force for the Determination of Brain

Death in Children
Brain death is defined as the irreversible loss of function of the brain, including the
brainstem. OHSU policy: http://ozone.ohsu.edu/HealthSystems/medstaff/x-e.htm
History Determination of cause of death is necessary to ensure the absence of treatable or
reversible conditions (i.e., toxic or metabolic disorders, hypothermia, hypotension, or surgically
remediable conditions).
Physical examination (documented by 2 examiners)
1. Coma or unresponsiveness, no motor response to pain.
2. Loss of consciousness and volitional activity
3. Absent brainstem function
1.
2.
3.
4.

Fixed and dilated or midposition pupils

Absent spontaneous and oculocaloric/oculovestibular eye movements
Absent movement of facial and oropharyngeal muscles
Absent corneal, gag, cough, sucking, and rooting reflexes

4. Apneano respiratory effort with pCO2 up to 60 or rise of 20 mmHg. Must document

pre and post test blood gas as well as lack of respiratory effort during period of exam.
Spinal cord reflex withdrawal not included
Consistent examination throughout the observation period
Table 1. Age-Dependent Observation Period
Age

Hours Between 2 Examinations

Recommended Number of EEGs

7 d-2 mo

48

2 mo-1yr

24

2 (not needed if angiography or flow study negative)

>1 year

12

Not needed

If hypoxic encephalopathy present, observation for 24 hours is recommended. This may be

reduced if an EEG shows ECS or a radionuclide study is negative for CBF. One report suggests
that a second EEG is not necessary at all; however, the number of patients in this study, aged 2
months to 1 year, was small.

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- 102 -

When a child may die

Talk with the family!! Understand their values and fears. Tell them as soon as the team knows
the child is going to die.
Determine the best place for the child to die (PICU, ward, Heme Onc, home, hospice facility)
Make sure the child is comfortable. Remember non-pain discomforts: nausea, constipation,
depression
Consider involving child life, pain team, ethics, PCP, chaplains as appropriate.

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** We need to discuss how much palliative care info we want here- just resources? What would
be helpful? Resources and how to get them.

When a child is dying: Dying, withdrawal, DNR, etcprobably need an explanation of

how people die and how different modes are treated differently?
1. Offer a chaplain to the family (available 24 hrs), or offer to contact their spiritual
supports. This offer is one many families, regardless of their personal beliefs, will take
advantage of.
2. Contact child life if they have been helpful to the family, or if there are siblings involved.
3. Discontinue labs and any meds not needed to maintain patient comfort.
4. Adjust the monitor (nurse will likely do). All the alarms need to be turned off. The
contrast on the monitor needs to be turned completely down (so the family cant see the
decreasing heartbeat). Some families really want the monitors left on. I try to ask them,
or at least tell them what Im doing. Sometimes we leave them on and look at the central
monitor, sometimes we take everything off. I tend to leave on so I can anticipate whats
happening.
5. Help get things cleaned up. Nurses and families will appreciate your involvement.
6. Give the family the opportunity to hold their child BEFORE we turn the vent off,
extubate, turn the inotropes off, etc. This way the family can hold their child before
death. Not all families want to hold their child, and depending on the mechanism of
injury and age of the child, may not be appropriate. They should always be given the
opportunity to participate as much as they want.
7. Continue pain management until the child is dead (this is either by bolusing by hand or
keeping the drip going; dose may be increased.
After a child dies:

Call the director of shift operations (4-8105), who will:

Provide the death certificate (to be signed by resident OR attending)
Discuss organ donation and autopsy with the family
Help the family start planning funeral/cremation
Provide a list of support groups

Remove machines, etc. from the room so the family can have time alone with their child
in as de-medicalized room as possible. The family is given all the time they need. Be
around to answer questions that the nurses cant answer. Even after the child dies, some
family members need reassurance that they did the right thing by taking their child off the
meds and vent, and some want the DOCTORS reassurance.

The nurses will give the family all the time they need, helping the family to bathe their
child, hold their child, do hand and foot prints, and hair clips. You may participate in any
and all of these activities

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Sign the death certificate if the attending is not available, and give to the director of shift
operations.

Special Situations:
B. Suspected NAT - the family cannot be left alone with the child after death. In some
cases, a total body bone scan will need to be done after the child dies and the child
can never be left alone.
C. Medical examiner cases - usually we take all tubes out of the child so the family can
hold them, but in these cases, we must leave all tubes in place.

How people die

i. Cardiovascular death
1. Failed resuscitation
2. Resuscitation not attempted (DNR)
3. Support withdrawn (inotropes, ventilator, etc)
ii. Brain death
1. Declared brain dead. In this case, support is not withdrawn,
machines are removed.

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OHSU SUGGESTED GUIDELINES FOR NUTRITION CARE

PEDIATRIC NUTRITIONAL SUPPORT
I. Preliminary Factors:
A.

Nutritional assessment:
1. Goals for calories, protein, fluid, fat, non-protein calorie to nitrogen ratio
2. Plot growth history on NCHS growth curve.

B.

Identification of primary objective for parenteral nutrition:

1. Supplemental.
2. Maintenance of present body stores.
3. Repletion of a mal-nourished patient.
4. Promotion of "catch up growth."

C.

Estimation of duration of parenteral alimentation.

1. Peripheral access for short-term use.
2. Central access for long-term use.
< 6 weeks - PICC line
> 6 weeks - Hickman, Bronac

II. CALORIES
A.

Primary Objective: Normal or Catch up growth/anabolism.

Central line is usually indicated.
Daily Energy Requirements (Non-protein kcal/kg) (13)
Non-protein kcal/kg/day
120-140
90-120
80-100
75-90
60-75
30-60

Age
Preterm
< 6 months
6-12 months
1-7 yr
7-12
>12-18

Circumstances that increase caloric requirements:

Fever
Cardiac Failure
Major Surgery
Burns
Long term growth failure
Protein calorie malnutrition
- 106 -

12% for each degree above 37oC

5-25%
20-30%
up to 100%
50-100%
50-100%

III. FLUIDS
A.

Calculate daily fluid allowance based on maintenance requirements. If additional

losses need to be replaced, use non-TPN fluid and Y into the line.

Maintenance requirements for fluid based on weight

Body weight
Fluid requirements per day
1-10 kg.
100ml/kg
11-20 kg.
1000 mls plus 50 ml/kg for
each kg > 10 kg.
> 20 kg.
1500 mls plus 20 ml/kg for
each kg > 20 kg.
D. Note that maintenance water requirements normally average 100ml/100 cal/day
(1ml/1cal used). Hence any physiological process that increases the caloric
requirements of a child will increase the fluid requirements as well.
E. Start with 100-120% of maintenance fluid for central TPN and 120-150 %
maintenance fluid for peripheral TPN.
IV. CARBOHYDRATE
A. Carbohydrate is required as a principal calorie source and should provide 50-60% total nonprotein calories.
B.
Hydrated glucose (dextrose) provides 3.4 cal/gm.
C.
Carbohydrates are initiated in a slow stepwise fashion to allow an appropriate
response to endogenous insulin and thus prevent glucosuria and subsequent
osmotic diuresis.
Glucose in excess of 16 mg/kg/min or 24 g/kg/day should be evaluated.
General Guidelines:
Maximum dextrose concentration (final concentration).
Peripheral: 10%-13%
>13% IV associated with an increased incidence of
phlebitis.
Central:
30% dextrose
2.

Central TPN
A.
Usually begin with 15% dextrose concentration, unless patient is
at risk for refeeding syndrome.
- 107 -

B.
C.

Monitor daily for tolerance particularly while advancing. Check

glucose after 1 hour on new solution.
Increase dextrose concentration by 2-5 gm/100ml per day as
tolerated until goals are met. Increase slowly if at risk for
refeeding syndrome.

Glucose intolerance is unusual in children with gradually advanced glucose

concentrations. Insulin is rarely necessary.
4.

Any infant or child who suddenly demonstrates glucosuria at a

concentration of dextrose that had previously been tolerated is suspect for
sepsis.

V. PROTEIN
A.

Daily protein requirements (g/kg)

Neonates
Infants
Children
Adolescents
Critically Ill

2.0-2.5 gm/kg
1.5-2.0 gm/kg
.8-2.0 gm/kg
1.5-2.0 gm/kg

B.

General guidelines:
1.
Begin with 2g/dl amino acids, except for patients with renal insufficiency.
2.
In general the amino acid concentration in peripheral veins should not
exceed 2% (because of increased osmolality). Amino acid solutions
through central line usually need not exceed 3% but may go up to 5% to
meet protein goals.

C.

The non-protein: nitrogen ratio.

The desired ration of 150-100:1 is generally recommended.

D.

Complications of Excess Protein Administration

Long Term Complications
Abnormal Plasma Aminograms
Cholestolic Jaundice

Short Term Complications

Azotemia
Hyperammonemia
VI.

2.5-3 gm/kg

INTRAVENOUS FAT
A.
B.

A concentrated source of calories, particularly beneficial during periods of fluid

restriction.
The low osmolality and high caloric density of lipid emulsions makes them useful
for peripheral parenteral alimentation.
- 108 -

C.

Administration prevents occurrence of fatty acid deficiency. Prevention of

E.F.A.D. can be accomplished with 2-3% of total calories as essential fatty acids
or linoleic acid per day, or 0.5 gm IL/kg body weight.
20% Intra-lipid provides 2 Cal/ml.
20-30 % of total calories (not to exceed 50%) as fat are recommended for normal
caloric balances.

D.
E.

General guidelines
1.
2.

Start infusing fat emulsion over 20-24 hours to improve clearance; may
gradually taper time to
10-12 hours.
Monitor tolerance closely. Draw triglyceride level initially and after each
dose increase.
If TG level is elevated to > 400 IL must be adjusted.

GUIDELINES FOR ADMINISTERING 20% LIPID EMULSION (2)(6)

Premature
SGA Infants
Initial
Dose

1gm/kg/day
(2.5ml/kg/day)
(5ml/kg/day)
(5ml/kg/day)

Increase Daily
Dose by
Maximum
Dose

VII.

Full-Term
Older
AGA Infants
Children
0.5 gm/kg/day
1gm/kg/day

0.25 gm/kg/day
(1.25ml/kg/day)

0.5 gm/kg/day
(2.5ml/kg/day)

1 gm/kg/day
(5ml/kg/day)

3 gm/kg/day

4 gm/kg/day

2 gm/kg/day
(15 ml/kg/day)
(20 ml/kg/day)
(10 ml/kg/day)

Recommended Maintenance Daily intake of Electrolytes and Minerals for Pediatric

Parenteral Nutrition Solutions
Element

Daily Amount

Sodium
Potassium

2-5 meq/kg
2-5 meq/kg
- 109 -

Chloride
2-5 meq/kg
Magnesium
0.25-0.5 mEq/kg
Calcium gluconate*
0.5-2.5 mEq/kg
Phosphorous
1-2 mmol/kg
* 110 mg is used in standard pediatric TPN at OHSU; gluconate is the recommended
Calcium salt in Parenteral Nutrition solutions since this salt dissociates less than chloride
salt.
Iron - is not a standard part of TPN solutions, but may be added to solutions as Iron
Dextran when oral iron therapy is precluded by GI problems. Monitor serum ferritin
levels. A test dose of iron dextran must be given.
VIII. Multi-Vitamins Pediatric (Used at OHSU)
Infants and children up to 11 years of age receive pediatric multi-vitamins. Above 11 years of
age, children receive adult dosage of vitamins for intravenous use.
Vitamin A - 2300 USP units
Vitamin D - 400 USP units
Vitamin K - 200 mcg
Vitamin C - 80 mg
Folic Acid - 140 mcg

Riboflavin - 1.4 mg
Thiamine - 1.2 mg
Vitamin B6 - 1.0 mg
Vitamin B12 - 1 mcg
Dexpanthenol - 5.0
mg
Biotin - 20 mcg

Niacin - 17 mg
Vitamin E - 7 mg equals
7 USP units

MVI Pediatric infused at OHSU --- Follow Protocol on Ped

Parenteral Nutrition Order sheet
< 3 kg 3.25 mls daily
> 3 kg < 11 years 5 mls daily
> 11 years = Adult multivitamin
IX. Pediatric Trace Elements mixture at OHSU --- Follow Protocol on Pediatric
Parenteral Nutrition Order Sheet (13)
Intravenous trace elements in pediatric patients (not neonates)
Unless specifically crossed out, the Pediatric Parenteral Nutrition form will always
provide trace elements according to out protocol.
Elements

Recommended
mcg/kg/day
- 110 -

Dose per out pediatric

TPN protocol
mcg/kg/day

Max mcg/day

Zinc

100

100

5000

Copper

20

20

300

Manganese

1 to 10

50

Chromium

0.14 to 0.20

0.17

Selenium

none

30

Dosing - Trace Elements:

Intravenous Dosing

Oral
Dosing

Infant
Pediatric
Infant
Pediatric
T.E.
Mcg/kg/day
(maxmcg/day)
(dose/day)
Zn

250 < 3 mo
100 > 3 mo

100 (5000)

3-5 mg

10-15 mg

Cu

20

20 (300)

0.5-1.0 mg

1-3 mg

Cr

0.2

0.14 to 0.20 (5)

10-40 mcg

20-200 mg

Mn

1 to 10 (50)

0.5-1.0 mg

1-5 mg

Se

2(30)

10-60 mcg

20-200 mcg

Manganese and copper may be decreased/not used in children with obstructive jaundice.
Molybdenum and selenium are usually present as contaminants in parenteral solutions.
X. Weaning Parenteral Nutrition
A.
B.
C.
D.

Goal is maintenance of optimal nutrition while progressing from parenteral to

enteral nutritional support.
Wean parenteral fluid gradually as enteral fluids are being advanced and
tolerated; document enteral and parenteral intake via calorie count.
Decrease parenteral calories the same amount enteral calories are increased.
Enteral feeding should be initiated and TPN weaned as soon as possible to
decrease the risk of cholestatic liver disease.

- 111 -

E.

Enteral feeds should be initiated in a slow continuous drip with age appropriate
elemental formula.

XI. Cyclic TPN

Cyclic TPN is needed for long-term use to increase mobility. Can be used to increase
oral intake. Tapering TPN off reduces risk of hyperglycemia and hypoglycemia.
Recommended:
1)
Taper volume: cut volume in half for 15 minutes then cut reduced volume
in half again for 15 minutes to start and stop TPN Taper for neonates and
infants over 1 hour
2)
Target for cyclic TPN:
a)
neonate - 16-18 hour cycle
b)
infants - 12 hour cycle
c)
children - 8-10 hour cycle
XII. Monitoring
A. When TPN is initiated:
1. Check blood glucose 1 hour after initiation and 1 hour after each increase in
dextrose concentration.
OR
Check urine glucose every shift after starting new TPN solution; if positive
check blood glucose.
2. Check Labs: liver panel, renal panel, lytes, glucose, magnesium.
3. Check serum triglycerides after each change in lipid prescription.
4. Monitor liver function tests daily while advancing TPN.
B. After target dextrose, amino acid, and lipid concentrations have been reached, check
all of the above weekly and after any change in prescription.
C. Refeeding syndrome - Severely malnourished patients who are given adequate
calories may develop critical hypophosphatemia and/or hypokalemia in the first few days.
Check levels prior to TPN initiation, replete if indicated, and monitor levels closely!!
D. Monitoring for long term TPN (> one month). (12)
1. Every 3 months check: serum ferritin, free carnitine
(in children with short gut or chronic diarrhea).
2. Every 6 months check: carnitine, zinc.
3. Annually check: copper, selenium, chromium, manganese.

References
- 112 -

1.

Oregon Health & Science University Pharmacy, Portland, Oregon.

2.

Mauer E.C., et al. Lipid Emulsion - Use in Neonates and Infants. Hosp. Pharm
1987. 22:185-187.

3.

Hohnbrink K and Oddlifson N. Pediatric Nutrition Support. Aspen 1991.

4.

Macfarlan, K, et al. Usage of total parenteral nutrition in pediatric patients. JPEN

15:85-88,1991.

5.

ASPEN Board of Directors. Guidelines for pediatric nutrition support. JPEN

17:(4)305A-495A,1993.

6.

Ekuall, S. Pediatric nutrition in chronic diseases and developmental

disorders.1993. 36-37.

7.

Colomb, V. Liver disease associated with long term Parental Nutrition in

Children. Transplantation Proceedings. 1994; 26(3);1467.

8.

Sapsford, A. Energy, Carbohydrate, Protein, and Fat Nutritional Care for High
Risk Newborns. Precept Press Chicago Illinois. 1994;71-87.

9.

Fitzgerald, K. et al. Hypermanganesemia in patients receiving total parenteral

nutrition. JPEN. 1999;23(6):333-6.

10.

ASPEN Safe Practices. JPEN. 1998; 22: 49-66.

11.

Samour, P. Handbook of Pediatric Nutrition. ASPEN Publishers. 1999. 551-588.

12.

Mc Donald, et al. Carnitine and cholestasis: Nutritional dilemmas for the

parenterally nourished newborn. Supportline. April 2003 Vol 25 No 2.

13.

Guidelines for the use of parenteral and enteral nutrition. JPEN 2002; 26 (1
suppl): 15a-1385A,

6/03

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