Pediatric Fluid Management Lab Interpretation Case Studies

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Pediatric Fluid ManagementLab InterpretationCase
Studies
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Fluid Management

• Children's kidneys have less concentrating
  ability and maximum GFR than adults
• Recent weight, can be helpful in determining
  fluid losses
• Diagnosing and determining degree of volume
  depletion
• Decreased level of consciousness
• Decreased skin turgor
• Elevated respiratory rate
• Prolonged capillary refill
• Decreased BP (only decreased in extreme volume
  depletion)
• Decreased urine output (sensitive but
  nonspecific)
• Laboratory data serum HCO3 15-17mEq/L is
  associated with absence of severe dehydration in
  children with gastroenteritis (JAMA 2912746,
  2004--AFP)
• Not reliable for diagnosis per a systematic
  review (JAMA 2912746, 2004--AFP) Cool
  extremities, absence of tears, weak pulse,
  "sunken" eyes, dry mucous membranes, sunken
  appearance to fontanel(s) (if open), elevated
  heart rate

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What Kind of Dehydration?

• Isotonic volume depletion (Na 130-150)-60 of
  cases causes include diarrhea, vomiting,
  fasting
• Hypertonic volume depletion (Na gt150)-25 of
  cases don't look as sick b/c circulating volume
  preserved by diffusion or water from
  intracellular compartment caused by isotonic
  loss with hypertonic replacement.
• Hypotonic volume depletion (Na lt 130)-15 of
  cases causes by isotonic loss with hypotonic
  replacement also cystic fibrosis

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Degree of Dehydration

• Mild Dehydration
• Deficit
• Child 3 deficit (30 ml/kg)
• Infant 5 deficit (50 ml/kg)
• Signs and Symptoms
• Dry lips
• Thick Saliva
• Decreased Tears
• Anterior Fontanelle flat
• Decreased Urine output

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Degree of Dehydration

• Moderate Dehydration
• Deficit Child 6 deficit (60 ml/kg)
• Infant 9 deficit (90 ml/kg)
• Signs and symptoms
• Eyes sunken
• Tears absent
• Dry mucus membranes
• Sunken Fontanelle
• Pulse weak and rapid
• Skin turgur decreased
• Delayed capillary refill (gt2 seconds)
• Skin slowly retracts (tenting)
• Listless and Irritable
• Urine characteristics
• 1. Dark color
• 2. Oliguria (Urine output lt1-2
  cc/kg/hour)

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Degree of Dehydration

• Severe Dehydration
• Deficit
• Child 10 deficit (100 ml/kg)
• Infant 15 deficit (150 ml/kg)
• Limp and cold
• Lethargy or coma
• Acrocyanosis
• Thready pulse
• Grunting
• Deep and rapid Respiratory Rate
• Decreased Blood Pressure
• Skin retracts gt2 sec
• Oliguria or Anuria
• Capillary refill gt4 seconds
• Blood Urea Nitrogen (BUN) markedly increased
• Arterial pH lt7.10

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How Much Fluid?

• 20 cc/kg NS bolus to acutely replace circulating
  volume.
• Deciding on fluid replacement
• Calculate 24 hour maintenance requirements
• 1. Formula
• 1. First 10 kg 4 cc/kg/hour (100
  cc/kg/24 hours)
• 2. Second 10 kg 2 cc/kg/hour (50
  cc/kg/24 hours)
• 3. Remainder 1 cc/kg/hour (20 cc/kg/24
  hours)
• 2. Example 35 Kilogram Child
• 1. Hourly 40 cc/h 20 cc/h 15 cc/h
  75 cc/hour
• 2. Daily 1000 cc 500 cc 300 cc
  1800 cc/day
• Replacement of static deficits
• 10-20ml/kg over 1h of ISOTONIC
• Rest of replacement based on established degree
  ot H2O/electrolyte losses 50 of deficit in 1st
  24h 25 in next 8 25 in next 16
• Consideration of ongoing losses diarrhea is
  hypotonic sweat in CF is hypertonic

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Special Situations

• Hyponatremic Seizure
• Background
• 1. Serum Sodium raised 5 meq/L with 6
  ml/kg of 3 NaCl
• Protocol
• 1. Give 3 NaCl (0.5 meq NaCl/ml) IV
  over 1 hour
• 2. Give 3 NaCl at 6 ml/kg/hour until
  Seizure stops
• Burn Patient
• Parkland formula
• Total volume of the first 24 hours of
  resuscitation (with Ringer lactate RL solution)
  at approximately 4 mL/kg body weight per
  percentage burn TBSA. Half the volume is given
  in the first 8 hours postburn, with the remaining
  volume delivered over 16 hours.
• Congenital Heart Disease
• Diabetic KetoAcidosis
• Initial fluid repletion in pediatric patients
  should be 10-20 mL/kg over the first 1-2 hours
  with a maximum of 50 mL/kg over the first 4
  hours.

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Sodium

• Increase
• water loss in excess of salt loss
• profuse sweating, severe diarrhea or vomiting,
  polyuria (as in diabetes mellitus or insipidus),
  hypergluco- or mineralocorticoidism, and
  inadequate water intake.
• Drugs steroids with mineralocorticoid activity,
  carbenoxolone, diazoxide, guanethidine, licorice,
  methyldopa, oxyphenbutazone, sodium bicarbonate,
  methoxyflurane, and reserpine.
• Decrease
• intake of free water or hypotonic solutions
• sweating, diarrhea, vomiting, and diuretic abuse.
  
• Dilutional hyponatremia may occur in cardiac
  failure, liver failure, nephrotic syndrome,
  malnutrition, and SIADH.
• There are many other causes of hyponatremia,
  mostly related to corticosteroid metabolic
  defects or renal tubular abnormalities.
• Drugs other than diuretics may cause
  hyponatremia, including ammonium chloride,
  chlorpropamide, heparin, aminoglutethimide,
  vasopressin, cyclophosphamide, and vincristine.

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Potassium

• Increase
• excess destruction of cells, with redistribution
  of K from the intra- to the extracellular
  compartment
• massive hemolysis, crush injuries, hyperkinetic
  activity, and malignant hyperpyrexia.
• Decreased renal K excretion is seen in acute
  renal failure, some cases of chronic renal
  failure, Addison's disease, and other
  sodium-depleted states.
• Hyperkalemia due to pure excess of K intake is
  usually iatrogenic.
• Drugs hyperkalemia include amiloride,
  aminocaproic acid, antineoplastic agents,
  epinephrine, heparin, histamine, indomethacin,
  isoniazid, lithium, mannitol, methicillin,
  potassium salts of penicillin, phenformin,
  propranolol, salt substitutes, spironolactone,
  succinylcholine, tetracycline, triamterene, and
  tromethamine.
• Spurious hyperkalemia can be seen with the
  tourniquet in place prior to venipuncture.
• Hemolysis and marked thrombocytosis may cause
  false elevations of serum K as well. Failure to
  promptly separate serum from cells in a clot tube
  is a notorious source of falsely elevated
  potassium.
• Decrease
• Excess K loss, such as in vomiting, diarrhea,
  certain renal tubular defects, hypercorticoidism.
• Redistribution hypokalemia is seen in
  glucose/insulin therapy, alkalosis (where serum
  K is lost into cells and into urine), and
  familial periodic paralysis.
• Drugs causing hypokalemia include amphotericin,
  carbenicillin, carbenoxolone, corticosteroids,
  diuretics, licorice, salicylates, and
  ticarcillin.

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Chloride

• Increase
• Dehydration, renal tubular acidosis, acute
  renal failure, diabetes insipidus, prolonged
  diarrhea, salicylate toxicity, respiratory
  alkalosis, hypothalamic lesions, and
  adrenocortical hyperfunction.
• Drugs acetazolamide, androgens,
  corticosteroids, cholestyramine, diazoxide,
  estrogens, guanethidine, methyldopa,
  oxyphenbutazone, phenylbutazone, thiazides, and
  triamterene.
• Bromides in serum will not be distinguished from
  chloride in routine testing, so intoxication may
  show spuriously increased chloride.
• Decrease
• Excessive sweating, prolonged vomiting,
  salt-losing nephropathy, adrenocortical
  defficiency, various acid base disturbances,
  conditions characterized by expansion of
  extracellular fluid volume, acute intermittent
  porphyria, SIADH.
• Drugs bicarbonate, carbenoxolone,
  corticosteroids, diuretics, laxatives, and
  theophylline.

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Co2

• Increase
• Reflects increase in serum bicarbonate (HCO3-)
  concentration rather than dissolved CO2 gas, or
  PCO 2 (which accounts for only a small fraction
  of the total).
• Compensated respiratory acidosis and in
  metabolic alkalosis.
• Diuretics (thiazides, ethacrynic acid,
  furosemide, mercurials), corticosteroids (in long
  term use), and laxatives
• Decrease
• Metabolic acidosis and compensated respiratory
  alkalosis.
• Drugs ammonium chloride, acetazolamide,
  ethylene glycol, methanol, paraldehyde, and
  phenformin.
• Salicylate poisoning is characterized by early
  respiratory alkalosis followed by metabolic
  acidosis with attendant decreased bicarbonate.

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Glucose

• Hyperglycemia
• relation to time elapsed after meals
• Drugs caffeine, corticosteroids, estrogens,
  indomethacin, oral contraceptives, lithium,
  phenytoin, furosemide, thiazides, thyroxine.
• Decreased
• severe liver disease, poisonings (arsenic,
  alcohol, salicylates, and antihistamines),
  adrenocortical insufficiency, hypothroidism.
• Failure to promptly separate serum from cells in
  a blood collection tube causes falsely depressed
  glucose levels.

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Urea nitrogen (BUN)

• Increased
• acute and chronic intrinsic renal disease
• decreased effective circulating blood volume with
  decreased renal perfusion
• postrenal obstruction of urine flow
• high protein intake states.
• Decreased serum urea nitrogen (BUN)
• high carbohydrate/low protein diets
• increased anabolic demand
• malabsorption states
• severe liver damage.

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Creatinine

• Increase in serum creatinine is seen any renal
  functional impairment.
• Creatinine clearance is significantly reduced
  before any rise in serum creatinine occurs. The
  renal impairment may be due to intrinsic renal
  lesions, decreased perfusion of the kidney, or
  obstruction of the lower urinary tract.
• Deranged metabolic processes may cause increases
  in serum creatinine
• acromegaly and hyperthyroidism
• dietary protein intake does not influence the
  serum level
• Decrease in serum creatinine is seen in pregnancy
  and in conditions characterized by muscle wasting

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Liver Function

• ALT (SGPT)
• Increase of serum alanine aminotransferase
  (SGPT)
• any condition involving necrosis of hepatocytes,
  myocardial cells, erythrocytes, or skeletal
  muscle cells.
• AST (SGOT)
• Increase of aspartate aminotransferase (SGOT)
• any condition involving necrosis of hepatocytes,
  myocardial cells, or skeletal muscle cells.
  Decreased serum AST is of no known clinical
  significance.
• GGTP (GAMMA-GT)
• Markedly increased in lesions which cause
  intrahepatic or extrahepatic obstruction of bile
  ducts. Lesser elevations of gamma-GT are seen in
  other liver diseases, and in infectious
  mononucleosis, hyperthyroidism, myotonic
  dystrophy, and after renal allograft.
• Drugs causing hepatocellular damage and
  cholestasis may also cause gamma-GT elevation
• Gamma-GT is a very sensitive test for liver
  damage, and unexpected, unexplained mild
  elevations are common. Alcohol consumption is a
  common culprit.

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Bilirubin

• Increased
• hepatocellular damage (infectious hepatitis,
  alcoholic and other toxic hepatopathy,
  neoplasms), intra- and extrahepatic biliary tract
  obstruction, intravascular and extravascular
  hemolysis, physiologic neonatal jaundice,
  Crigler-Najjar syndrome, Gilbert's disease,
  Dubin-Johnson syndrome, and fructose intolerance.
  
• Disproportionate elevation of direct (conjugated)
  bilirubin is seen in cholestasis and late in the
  course of chronic liver disease. Indirect
  (unconjugated) bilirubin tends to predominate in
  hemolysis and Gilbert's disease.
• Decreased serum total bilirubin is probably not
  of clinical significance but has been observed in
  iron deficiency anemia.

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Albumin

• Increased
• Not seen as a natural condition. Relative
  increase may occur in hemoconcentration. Absolute
  increase may occur artificially by infusion of
  hyperoncotic albumin suspensions.
• Decreased
• Decreased synthesis (malnutrition,
  malabsorption, liver disease, and other chronic
  diseases)
• Increased loss (nephrotic syndrome, many GI
  conditions, thermal burns, etc)
• Increased catabolism (thyrotoxicosis, cancer
  chemotherapy, Cushing's disease, familial
  hypoproteinemia).

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Neutrophils

• Neutrophilia is seen in any acute insult to the
  body, whether infectious or not. Marked
  neutrophilia (gt25,000/µL) brings up the problem
  of hematologic malignancy (leukemia,
  myelofibrosis) versus reactive leukocytosis,
  including "leukemoid reactions."
• Neutropenia may be paradoxically seen in certain
  infections, including typhoid fever, brucellosis,
  viral illnesses, rickettsioses, and malaria.
  Other causes include aplastic anemia (see list of
  drugs above), aleukemic acute leukemias, thyroid
  disorders, hypopitituitarism, cirrhosis, and
  Chediak-Higashi syndrome.

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Eosinophils

• Eosinophilia
• allergic disorders and invasive parasitoses.
  Other causes include pemphigus, dermatitis
  herpetiformis, scarlet fever, acute rheumatic
  fever, various myeloproliferative neoplasms,
  irradiation, polyarteritis nodosa, rheumatoid
  arthritis, sarcoidosis, smoking, tuberculosis,
  coccidioidomycosis, idiopathicallly as an
  inherited trait, and in the resolution phase of
  many acute infections.
• Eosinopenia
• shock, major pyogenic infections, trauma,
  surgery
• Drugs corticosteroids, epinephrine,
  methysergide, niacin, niacinamide, and
  procainamide.

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Basophils

• Basophilia
• myeloproliferative disease as opposed to
  leukemoid reaction.
• allergic reactions, chickenpox, ulcerative
  colitis, myxedema, chronic hemolytic anemias,
  Hodgkin's disease, and status post-splenectomy.
• Estrogens, antithyroid drugs, and desipramine
  may also increase basophils.
• Basopenia is not generally a clinical problem.

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Lymphocytes

• Lymphocytosis
• Infectious mononucleosis, viral hepatitis,
  cytomegalovirus infection, other viral
  infections, pertussis, toxoplasmosis,
  brucellosis, TB, syphilis, lymphocytic leukemias,
  and lead, carbon disulfide, tetrachloroethane,
  and arsenical poisonings.
• Drugs aminosalicyclic acid, griseofulvin,
  haloperidol, levodopa, niacinamide, phenytoin,
  and mephenytoin.
• Lymphopenia
• AIDS, acute infections, Hodgkin's disease,
  systemic lupus, renal failure, carcinomatosis,
  Corticosteroids, lithium, mechlorethamine,
  methysergide, niacin, and ionizing irradiation.
  First to fall in radiation sickness.

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Monocytes

• Monocytosis
• Acure recovery phase of many infections.
• TB, syphilis, brucellosis, Crohn's disease, and
  sarcoidosis), ulcerative colitis, systemic lupus,
  JRA, polyarteritis nodosa.
• Poisoning by carbon disulfide, phosphorus, and
  tetrachloroethane
• griseofulvin, haloperidol, and methsuximide.
• Monocytopenia is generally not a clinical
  problem.

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Case Study 1

• You arrive at the referring hospital to find your
  patient is experiencing severe bronchospasms. 
  This is a 6 year old boy.  He is receiving 10mg
  albuterol/hour via continuous nebulizer. 
• His vitals are as follows 
• HR 166, RR 60, BP  70/48.  O2 SAT 88
• He is cold with poor perfusion. 
• The initial arterial blood gas is  7.22/62/59  
  HCO3 20   BE -2.2.  
• His LOC is decreased and he does respond well to
  verbal commands.

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Case Study 1

•  Is this patient stable? 
• What is your initial assessment?
• What priorities are urgent?
• Assess the airway  is it manageable, manageable
  with positioning, or unmanageable without
  intubation?
• What medications should you consider?
• Are steroids indicated in this situation?

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Case Study 1

• The patient's  is now unconscious and is having
  periods of apnea.  The heart rate is 68.
• What is your assessment of the situation?
• What are your interventions?

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Case Study 1

• What is the appropriate size tube?
• The age-based formula, ID (mm) age in years
  16/4
• Broselow Tape more accurate
• What would initial ventilator settings be for
  this 6 year old.
• What is the formula for determining tidal volume?
  
• How would inspiratory time effect this patient?
• After intubation, what do you assess?

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Case Study 1

• Upon making an assessment, you hear breath sounds
  louder on the right.  What must be done?
• Upon making an assessment, you hear breath sounds
  louder on the right.  What must be done?

29
Case Study 1

• What is your intervention?
• Is your patient stable?
• When is an appropriate time to call report?
• What thing do you need prior to departure to the
  base hopsital?

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Case 2

• You are going to stabilize and transport an eight
  year old female who has sustained severe head
  trauma secondary to motor vehicle accident.  She,
  also, has suspected internal injuries and is
  receiving a unit of PRBC when you arrive. 

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Case 2

• She is intubated with a 5.0 oral ETT and it is
  taped at the 10cm mark. 
• Her vitals are 
• HR- 166,
• RR- 0 ( spontaneous )
• BP - 165/110.  
• ABG - 7.35/45/86 HCO3 - 22   BE   - 1.1

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Case 2

• What are your priorities?
• What diagnostic tests are indicated?
• Are you satisfied with her ventilation? 
• Why, or why not? 
• What are your initial ventilator settings?
• Why did you choose these settings?
• What interventions should be made
  pharmacologically?
• What types of IV access do you need?

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Case 2

• Suddenly, the pressure and heart rate fall
  dramatically. 
• The O2 sats are 75 on 100 FIO2.  This occurred
  while hand bagging.
•  What could you expect to be happening?
• How do you confirm each  suspected problem?
• What are the interventions for each?

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Case 2

• Chest x-ray reveals a right tension pneumothorax.
• What is your intervention?
• Is this an emergency?
• How do you set-up for a chest tube on transport?
• What special equipment do you need for the
  transport?
• How could a flight effect a pneumothorax?

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Case Study 3

• The non-English speaking grandparents of a 15
  month old child brought him to an urban emergency
  department because of increasing respiratory
  distress. Obtaining a history was difficult. It
  was determined through an interpreter the child
  lives with the grandparents. They communicated he
  had been ill for one to two weeks with an upper
  respiratory infection which over the previous two
  to three days had worsened. His appetite had
  decreased as had his fluid intake. Because of
  increasing respiratory distress over the previous
  few hours, they presented him to the emergency
  department

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Case Study 3

• Physical examination by the emergency department
  staff demonstrated a child in obvious respiratory
  distress. He wanted to be in his grandmother's
  arms and appeared exhausted. Pulse rate 180,
  respiratory rate 65 with grunting and
  retractions. Weight 13 Kg. An inspiratory stridor
  and expiratory wheezes were noted on chest
  auscultation. Tidal volume was decreased.
• What other vital signs are important?

37
Case Study 3

• Initial treatment was directed toward alleviating
  his respiratory distress and included oxygen,
  subcutaneous epinephrine and IV
  methylprednisolone. Inhalation therapy was
  provided with albuterol and racemic epinephrine.
  Despite this therapy there was no evidence of
  clinical improvement. Arterial blood gases were
  evaluated pH 7.25, pCO2 56.6 mmHg, pO2 169 mmHg
  with a base deficit of -3.
• Additional vital signs obtained (answers the
  query above) demonstrated a blood pressure of
  90/60, oxygen saturation of 94, rectal
  temperature 37.5 C. Respiratory rate had
  increased to 60 and pulse rate to 200. Blood
  pressure was now 90/50, and capillary refill 5
  seconds. Peripheral (radial and dorsalis) pulses
  were weak and thready. His skin was cool, dry and
  pale.
• Laboratory determinations glucose 44 mg/dL
  electrolytes, BUN and creatinine were normal
  hemoglobin 10.8 Gm, hematocrit 33.6. White blood
  cell count 16,200

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Case Study 3

• How would you proceed?
• The trachea was intubated with a size 4.5 mm
  internal diameter endotracheal tube (ET) tube on
  the first pass. Vecuronium was then injected IV
  to maintain chemical paralysis. Ventilatory
  parameters chosen were rate 30, inspiratory time
  0.8 seconds, tidal volume 180 cc,
• PEEP 6 cm H2O, Synchronized Intermittent
  Mandatory Ventilation (SIMV) mode was selected.
  Resultant peak inspiratory pressure (PIP) was 28
  cm H20.
• 4 hours after the child was admitted to the
  emergency department, physical examination
  demonstrated blood pressure 88/44, heart rate
  143, respiratory rate 30, oxygen saturation 100,
  rectal temperature 37.5 C, skin slightly pale,
  slightly cool and dry, capillary refill 4
  seconds. Peripheral pulses remained 1,
  thready. Breath sounds were decreased but
  "better" on the right side.

39
Case Study 3

• As a consequence the tube was withdrawn cephalad
  (towards the head) one to two cm. Ten minutes
  later ETCO2 was 30 mmHg.
• Subsequent blood gases demonstrated pH 7.56, pCO2
  23.9, oxygen tension 215 and a base deficit of
  -5. Oxygen saturations were 100
• Is the child now stable for transport? Would you
  add any therapy? Would you change the ventilator
  settings?

40
Case Study 3

• Decrease the inspiratory time from 0.8 to 0.5
  seconds and eliminated the use of PEEP. Tidal
  volume was maintained at 180 ml. There was a
  slight increase in the PIP to 32 cm H20. An
  additional 260 cc normal saline fluid bolus (20
  cc/Kg) was administered IV. Glucose 6.5 Gm (0.5
  Gm/Kg) 25 solution was administered to treat the
  hypoglycemia.
• Just before helicopter lift-off the heart rate Is
  145, blood pressure 130/92, respiratory rate 30
  and oxygen saturation 100. ETCO2 72 mmHg. The
  patient remained chemically paralyzed.

41
Case Study 3

• A suction catheter was placed through the ET tube
  to be certain it was patent and to rule out a
  mucous plug. It was patent. Suction did not
  return any abnormal secretions. The entire
  circuit from the level of the endotracheal tube
  back to the ventilator was checked. There was no
  evidence of any restriction in the circuit.
  Ventilatory settingswere checked. Peak
  inspiratory pressures (PIPs) were unchanged.
  Chest rise appearedto be symmetrical bilaterally.
  Because of the noise of the helicopter it was not
  practicalto obtain conclusive information from
  chest auscultation . The 4.5 ET tube was noted to
  be taped at a depth of 15.0 cm as measured from
  its distal tip to the gums. ETCO2 remained
  markedly elevated, in the 70's. Oxygen
  saturations remained at 100. An airway breathing
  treatment with 1.25 mgm albuterol was
  administered in consideration of the possibility
  an increase in bronchospasm had occurred causing
  in the increase in ETC02 and PIPs

42
Case Study 3

• The staff slightly extended the childs head (do
  not do this when treating a trauma patient) and
  noted a rapid decrease in the end tidal ETCO2.
  The tube was then withdrawn two cm proximally and
  re-taped. Upon arrival to the regional pediatric
  center ETCO2 was 38 mmHg.
• After 24 hours in the intensive care unit of the
  regional pediatric center during which inhalation
  and IV therapy, including antibiotics, was
  continued, the child was extubated. He had
  developed x-ray evidence of pneumonia. His
  condition improved rapidly and he was discharged
  home six days later.

43
Case 4

• Pediatric transport responded to a request to
  transport an infant involved in a car versus semi
  truck accident. Another helicopter service was
  already at the scene tending to the mother and no
  report was available about the infant except a
  wide age range (6 weeks to 6 months) and mental
  status report, alert and active. The infant was
  being transferred to a local hospital.

44
Case 4

• The team came in contact with the child in the
  emergency room. The first assessment revealed an
  infant secured on a Pedi board, gray skin color
  with a GCS 10. A non rebreather with 15 liter
  oxygen flow was on the infants face with oxygen
  saturation of 99. Respiratory rate was 54 and
  auscultation revealed clear and equal breath
  sounds. Heart rate was 157 bpm with a capillary
  refill time of 3-4 second and pulses 1, blood
  pressure 99/79. An intraosseous needle was in
  the left tibia and a 24 gauge in the left arm.
• Peds Surgery is not available at this facility.

45
Case 4

• Is this patient stable? 
• What is your initial assessment?
• What priorities are urgent?
• Assess the airway  is it manageable, manageable
  with positioning, or unmanageable without
  intubation?
• What diagnosis should you consider?

46
Case 4

• What tests would you think about?
• What interventions are needed?
• What meds would you give?
• What meds would you consider before transport?

47
Case 1

• Call Received.
• Patient is a 9 yr. old s/p MVA
• En Route
• Last vitals Temp 37, Resp 18 HR 135 BP. 110/50,
  O2 sat 100 on room air
• Awake alert, PE significant for abrasion on
  chest, abdomen left flank, arm, leg

48
Case 1

• Pre Hospital History
• Patient brought in by paramedic
• Initial LOC then awake, alert appropriate in ER
• Open Tib/Fib fx bleeding controlled, dressed.

49
Case 1

• Where to start?

50
Case 1

• Airway Patent, child screaming.
• Breathing Still Screaming
• Circulation Blood Pressure 120/65
• What now?

51
Case 1

• Head Contusion on left temple, no depression
  bleeding briskly.
• Neck in C-Spine Trachea midline, no deformities
• Chest large bruise over left chest.
• Significance?

52
Case 1

• Abdomen flat, child screaming all the while.
  When touched or not.
• Ext Cap refill 5 secs. Tib/Fib open fracture

53
Case 1

• Studies
• CXR three rib fractures, moderate pneumothorax
• CT scan head- no bleed no shift
• CT Abd. No splenic/liver bleed.
• Labs
• Hct 37
• No blood in urine

54
Case 1

• What now?

55
Case 1

• Access Access Access
• TWO IVs
• Central Lines
• IJ/EJ, Scalp, Saphenous
• Cut Down capabilities?

56
Case 1

• Hospital Information
• No PICU
• Adult ICU
• Helipad
• Ground Transport 35 min
• Air Transport 10 minutes

57
Case 1

• Patient is screaming. Xrays are done
• IV is in.
• The Wanders set in.

58
Case 1

• Re-assessment is CRITICAL for pediatric patients.
• The patients O2 Saturation falls to 85 and the
  blood pressure to 90/35
• What is going on?
• What to do?

59
Case 1

• Causes of desaturation?
• Causes of patients hypotension?
• Treatment of hypotension- Aggressive!

60
Case 1

• How would you transfer this patient?
• Ground
• Air
• Paramedic in the referring Hospital offer to
  whisk him over

61
Ground vs. Air

• Severity of illness
• Distance
• Other transports in line
• Considerations
• Pressure changes, O2 tension

62
Airway

• The patient has a medium sized pneumothorax
  without mediastinal shift, no respiratory
  distress
• What do you do?
• Intubate
• Chest Tube
• Leave good enough alone watch patients clinical
  status

63
Case 1

• The patients gets the chest tube and is
  successfully transported out of your ER.

64
Case 2

• Parents call and tell you that they are bringing
  in their child who just swallowed a coin and is
  drooling and coughing.

65
Case 2

• What are your concerns?
• Who do you need ?

66
Case 2

• Child appears ill. Leaning forward, drooling.
• What now?
• IV?
• Who to call?

67
Case 2
68
Case 2

• Is this child stable for transport?
• What options are available?
• Who are your resources?

69
Case 2

• The rule is there is no rule.
• Flexibility is necessary but only from absolute
  necessity not convenience.
• The transport team has to ensure the safest
  transport possible.

70
Scenario

• 7 y.o. female brought to the ER by private car
  after suffering a skateboard accident. Patient
  is carried into ER in Dads arms. Patient is
  limp and unresponsive except to pain--moans and
  stiffens extremities.
• What is you first intervention for this patient?
• What do you do next?

71
Case 3

• Initial assessment
• T36.0C, HR65, RR25 w/ O2 sat100 on RA,
  BP145/90
• PERRL, left hemotympanum, clear nasal discharge.
  BSbilaterally, no chest deformity or contusion.
  RRR w/o murmur. Abdomen soft, NTND, pelvis
  stable, no blood at urethral meatus. Obvious
  left femur fracture with faint distal pulses.
• What tests do you order?

72
Case 3

• Is the patient stable for transport?
• Who makes the decision?
• Medico-legal ramifications.

73
Case 3

• CT scan. Large epidural hematoma, skull fracture.