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Pediatric Emergency Manual

Pediatric Emergency Manual

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Published by: api-3840428 on Nov 27, 2009
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03/18/2014

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TABLE OF CONTENTS
Topic
Page
PALS Algorithms
Inside FRONT cover
Common Drips, Weight estimates, RSI, ETT sizes
Inside REAR cover
Selection of Proper Resuscitation Equip
REAR cover
Acid Base Disorders
2
Anaphylaxis
5
Bites and Stings
8
Cardiology Problems
17
Chemotherapeutic Agents
27
Child Abuse
33
Coagulopathies
40
Croup
48
Diabetic Ketoacidosis
52
Epiglottitis
61
Febrile Seizures
65
Fluid and Electrolyte Abnormalities
68
Gastrointestinal Bleeds
88
Hypertensive Crisis
94
Increased Intracranial Pressure
109
Neurologic Assessment, Altered MS, Glasgow Coma Scale
117
Newborn Resuscitation
126
Oncologic Emergencies
Acute Tumor Lysis Syndrome
141
Leukemia
144
Neutropenia and Fever
146
Spinal Cord Compression
149
Superior Vena Cava / Mediastinal Syndrome
150
Pediatric Rescusitation
151
Poisonings
General Management
165
Acetaminophen
174
Aspirin
177
Caustic Ingestions
181
Cyclic Antidepressants
187
Digoxin
193
Hydrocarbons
195
Iron
199
Lead
205
Rapid Cardiopulmonary Assessment
212
Rapid Sequence Induction
217
Renal Replacement Therapy
220
Sickle Cell Anemia
225
Status Asthmaticus
239
Status Epilepticus
249
Transfusion Rxns / Blood Component Tx
254
Trauma
259
2
APPROACH TO ACID BASE PROBLEMS

Acid base status in a patient is regulated by and affected by pathology in
two systems- 1) the metabolic system [HCO3] & 2) the respiratory system
[PCO2]. Abnormal \u201cprocesses\u201d in these systems cause acid base disorders. To
diagnose & understand a patient\u2019s acid base disorders the clinician must
interpret a complete database, which includes data from the history &
physical examination as well as laboratory data, mainly a blood gas, blood
chemistries and often urine chemistries. The clinician should suspect acid
bases disorders in certain clinical situations & seek to document them,
determine their severity & determine the need for treatment. Laboratory data
must always be related to the patient\u2019s clinical situation and cannot be
interpreted in a vacuum.

Laboratory evaluation of Acid base disorders.
A] First determine if the patient is ACIDEMIC or ALKALEMIC
These terms only refer to the netp H of blood, and do not describe the

process that led to the alteration of the pH. An ABG or free flowing venous

blood gas is required for this determination.
Acidemic: patient\u2019s pH < 7.35
Alkalemic: patient\u2019s pH >7.45

If the patient is acidemic or alkalemic there is at least one major abnormal
acid base process present which must be explained by further analysis of data
from the history, physical & lab. Acid base processes like metabolic
acidosis or respiratory acidosis refers to specific pathophysiologic states
which, if they are unopposed, would make the patient acidemic or alkalemic
respectively. Remember that patients with a normal pH could have severe,
counterbalancing, acid base processes. For example an ESRD patient with
vomiting could have a metabolic acidosis & metabolic alkalosis with a normal
pH.

B] Next try to explain the abnormal pH by a simple acid base disorder i.e.
one abnormal acid base process in one system with appropriate compensation in
the other system. Examine the directional change of PCO2 and HCO3 from
normal. If they are abnormal in the same direction there is a mixed
disorder. If they are abnormal in opposite directions only one can explain
the change in pH. Assume that that is the primary process & that the other
system is trying to compensate. For example if the pH is low & the PCO2 and
the HCO3 are low, only the low HCO3 can explain the low pH. Therefore an
initial guess as to what is wrong with the patient would be that the patient
has a simple metabolic acidosis with respiratory compensation.

C] Next determine if the compensation is appropriate- see table below for
appropriate compensation expected in various primary simple acid base
disorders. If the changes in the other system fall outside the expected
changes in this table then the acid base disorder is complex ie there are
disorders in both the respiratory & metabolic acid base systems.
Compensation never returns the pH to normal or over corrects. One easy rule
on compensation is Winter's rule which states that the last 2 digits of pH
greater than 7 predicts the CO2 in a patient with a primary metabolic

3

acidosis & appropriate respiratory compensation. So if a patient has a
metabolic acidosis with a pH 7.25 one should expect a CO2 of 25. If the CO2
is higher, than the patient is not having an appropriate compensation,
suggesting respiratory dysfunction, if it is lower then there is a coexisting
respiratory alkalosis.

Primary Disorder
Expected Compensatory
Response
Limits of Compensation
Metabolic Acidosis
\u0394PCO2 = 1-1.3 x \u0394\u0397C\u039f3
PCO2 not < 10 mmHg
Metabolic Alkalosis
\u0394PCO2 = 0.5-0.6 x \u0394\u0397C\u039f3
PCO2 not > 55 mmHg
Respiratory Acidosis
Acute Respiratory Acidosis
\u0394\u0397C\u039f3 = 0.1x \u0394PCO2
HCO3 not > 30 mEq/L
Chronic Respiratory Acidosis (3-5
days)
\u0394\u0397C\u039f3 = 0.4x \u0394PCO2
HCO3 not > 45 mEq/L
Respiratory Alkalosis
Acute Respiratory Alkalosis
\u0394\u0397C\u039f3 = 0.2x \u0394PCO2
HCO3 not < 17-18

mEq/L
Chronic Respiratory Alkalosis (2-4
days)

\u0394\u0397C\u039f3 = 0.5x \u0394PCO2
HCO3 not < 12-15
mEq/L

D] Next determine the serum anion gap [Na- (Cl+HCO3), normal 12 +/- 2]
especially if a potential metabolic acidosis exists (low HCO3-). Metabolic
Acidosis is commonly divided into anion gap and non-anion gap acidosis.

If the anion gap is greater than 17, it suggests the patient has an anionic
gap acidosis. Anion Gap acidosis differential is remembered by stating this
acronym: CAT MUDPILES.C for cyanide or carbon monoxide,A for alcohol,T for
toluene,M for methanol,U for uremia,D for DKA,P for paradehyde,I for
iron and isoniazid,L for lactic acidosis,E for ethylene glycol, andS for
salicylates and strycnine. In simple AG acidosis, the decrease in serum
bicarbonate should equal the increase in the AG (.ie 1 mmol of bicarbonate
titrates 1 mmol of acid which forms Na Acid. The Acid anion is an unmeasured
anion that increases the anion gap by 1.Calculate the excess anion gap. The
excess anion gap = total anion gap minus the normal anion gap (12 mmol per
liter). Add the excess anion gap to the measured bicarbonate concentration.
If the sum is greater than a normal serum bicarbonate (> 24-28 mmol per
liter) there is an underlying metabolic alkalosis (e.g. vomiting in a renal
failure patient). If the sum is less than normal bicarbonate (< 23) there is
an underlying non-anion gap metabolic acidosis process (e.g. shock &
diarrhea). If the value is not less than 23 or greater than 28 then no
additional metabolic process is going on.

If there is no anion gap but the bicarbonate is low, the patient has a non
anion gap acidosis. This usually means loss of HCO3 from the gut (diarrhea,
fistula) or the renal system (RTA, carbonic anhydrase inhibitors). Other
causes include dilution of HCO3 by large infusions of normal saline or
addition of a Cl acid or a GI/urinary diversion or augmentation. Aurinary

anion gap can help differentiate renal vs. GI loss of bicarbonate. Urine AG

=(Na + K)- Cl and correlates with urinary ammonium excretion. As ammonium
excretion increases the urinary gap narrows. With GI losses of HCO3 ammonium
excretion is unimpaired and increases with acidosis & the urinary AG becomes

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