pediatric respiratory illness
TRANSCRIPT
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Pediatric Respiratory Illness
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Case Presentation
! 24 y/o mother brings in her 9 month old child. She states that he seems to have a slight cough and he “just isn’t acting right”. He is more sleepy and fussy than usual.
! Sick contacts at daycare
! Missing 6 month immunizations, o/w UTD
! ? Fevers. No diarrhea. Maybe some vomiting, she attributes that to his reflux. Seems to be eating ok. Normal or increased amount of diapers.
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Your Patient
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Vital signs
! Wt 10 kilos, he is screaming at triage when vitals are taken. He readily calms and drinks from the bottle. He has a moderate sized snot bubble in the right nares.
! HR – 159
! RR – 56
! Cap refill ~ 2 sec, sat is 99%
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History
! What other questions do you have?
! FHX: ?
! Birth hx?
! Sick contacts?
! Immunizations?
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Physical Exam
! Pertinent positives:
! Slight nasal crusting – clear
! RR seems increased, slight retractions, no wheezing heard.
! Tachycardia at 149 on your exam, but he is crying
! Abdominal exam – normal except a small reducible umbilical hernia.
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You find this rash (what is it?):
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Differential Diagnosis:
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Lab Tests?
! RSV wash?
! CBC?
! Lytes?
! UA/urine culture?
! Blood cultures?
! CXR?
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Work Up:
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Patient Dispo
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Goals and Objectives
! Recognize DKA, especially new onset
! Select correct lab studies
! Fluid and insulin treatment
! Cerebral edema
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Pediatric DKA ! International Society for Pediatric and Adolescent
Diabetes (ISPAD) in 2007 defined:
! Hyperglycemia: glucose > 200 mg/dL AND
! Metabolic acidosis: venous pH < 7.3 and/or plasma bicarbonate < 15 mEq/L.
! Severity categorized according to the degree of acidosis: mild (pH 7.2-7.3), moderate (pH 7.1-7.2) and severe (pH < 7.1)
! DKA leading cause of morbiity/mortality in children with type 1 diabetes.
! Clinical manifestations related to degree of hyperosmolality, volume depletion, and acidosis.
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DKA v Hyperosmolar Hyperglycemic State
! Marked hyperglycemia: > 600
! Serum CO2 > 15 mmol/L
! Absent to mild ketonemia and ketonuria
! Effective serum osm >320
! Usually in adults but has been increasingly seen in adolescents. Still not common in the younger child.
! Associated with more severe hypotension and dehydration than DKA.
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Epidemiology ! DKA is frequently the initial presentation of children with
new onset type 1 DM.
! Factors associated with increased risk for DKA at presentation: ! Younger age ( < 5 y/o) – population study Germany –
higher incidence of DKA in <5 36% vs 26% of older children
! Ethnic minority status
! Diagnostic error
! Lack of health insurance
! Lower body mass index
! Delayed treatment
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DKA in type 1 DM
! Risk/predictive factors for recurrent DKA: ! Higher A1C values ! Higher reported insulin requirements ! Female adolescents >13 y/o ! Children over 13 y/o (regardless of
gender) who have no insurance and/or have psych issues
! Longer duration of DM
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DKA ! Almost 60% of DKA episodes occur in ~ 5% of
children.
! Patients with dm who had 4 or more episodes = 35% of all episodes of DKA in a UK surveillance study.
! Less common BUT ketosis and DKA can occur in type 2 DM.
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DKA – Precipitating Factors
! Poor metabolic control
! Frequently missed insulin
! Stress and infections
! Medications: corticosteroids, etc
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Signs and Symptoms
! Sxs/sxs related to the degree of hyperosmolality, volume depletion, and acidosis.
! Earliest sxs related to hyperglycemia
! Older children: polyuria, polydipsia, fatigue, wt loss, nocturia, vaginal or cutaneous moniliasis.
! Infants: More difficult – not toilet trained and can NOT express thirst. SXS: decreased energy and activity, irritability, weight loss, and physical signs of dehydration. Candidal diaper rash common.
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Signs/Symptoms Continued
! Polyphagia – early. As ketoacidosis worsens, appetite is suppressed. +/- abdominal pain, N, V
! Hyperventilation and deep respirations – respiratory compensation for acidosis.
! Children with DKA are volume depleted, but less likely to show classic signs of hypovolemia.
! Neurologic findings: drowsiness, lethargy, and coma – related to severity of hyperosmolality and/or the degree of acidosis.
! Cerebral edema: 0.5-1% of all DKA cases in children
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DKA – fluid deficits
! Most studies of fluid needs were done in the 40’s and 50’s on adults. Fluid losses in severe pediatric DKA: ! Water – 70 mL/kg
! Sodium – 5-13 mEq/kg
! Potassium – 6-7 mEq/kg
! Fluid losses more difficult to assess in pediatric DKA
! Generally present with a 5-10% fluid deficit.
! Initial fluid management is based on the assumption of a 5-7% deficit for moderate and 10% for severe.
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Volume
! Consensus: the maximal volume of isotonic solution used for initial treatment is 10 - 20 mL/kg unless the patient is objectively hypotensive.
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Lab Testing
! Initial labs: ! Serum glucose
! Electrolytes
! Creatinine and BUN
! Blood gases
! Hematocrit
! BHOB
! Urine testing – ok for initial test but may give false impression of continued ketoacidosis – use direct measurement of BHOB.
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Anion Gap
! Anion gap is useful for estimating the severity of ketosis.
! Normalization is a direct measure of the resolution of ketoacidemia.
! May underestimate the degree of acidosis.
! Calculated:
! Serum AG = Serum Na - (Serum Cl + bicarb)
! Normal pediatric value: 12 +/- 2
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Sodium
! Affected by hyperglycemia
! Hyperglycemia ! increase in plasma osmolality ! water movement out of cells ! lower serum Na (by dilution)
! Theoretical calculations: decrease in serum Na by 1.6 for every 100 mg/dL elevation in serum glucose. Am J of Med, Hiller, et al suggest better estimate is a reduction of 2.4 mEq/L for every 100
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Sodium
! Inability to independently access water in infants and young children may lead to hypernatremia despite the hyperglycemia.
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Potassium
! Osmotic diuresis and Increased ketoacid excretion promote urinary loss of K+.
! K+ loss in adults (on average) 3-5 mEq/kg
! K+ loss in pediatrics (less well studied): 6-7 mEq/kg.
! If hypokalemic at presentation, delay insulin therapy until K+ repletion begins.
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Serum Bicarb
! Study at the University of Oregon – looking at serum bicarb as a predictor of pH. 300 + patients enrolled. ! Serum bicarb of 18.5 or less – predicts pH < 7.3,
sensitivity – 93%, specificity – 91%
! Serum bicarb of 10.5 or less predicts pH of < 7.1, sensitivity – 97%, specificity – 88%
! Conclusion: venous pH may not be necessary in children.
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DX
! Glucose: serum glucose - >200
! Acid-base: bicarb < 15 mEq/L or venous pH < 7.3 The severity of metabolic acidosis is dependent on: ! Rate of ketoacid production
! Duration of increased ketoacid production
! Rate of acid excretion in the urine
! The adequacy of the compensatory respiratory alkalosis.
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Back to our patient:
! Labs: glucose 330
! Na+ - 130
! K+ - 3.7
! Cl- - 98
! HCO3 – 9
! BUN – 19
! Cr – 1.9
! Concerns? Plan for care?
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Our patient has:
! Hyperglycemia
! Acidosis
! Relative hypokalemia
! Dehydration
! Renal insufficiency
! Candidal diaper rash
! Anything else you really want to know right now?
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Neurologic Exam
! Neurologic compromise at presentation is a poor prognostic indicator.
! Retrospective study, 61 peds pts with DKA and cerebral edema: ! All who died or were persistently vegetative
presented with GCS < 7
! High morbidity and mortality – need to recognize and treat
! MORE TO COME later
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Back to our patient:
! He seems neurologically intact.
! What are your plans now? ! DKA
! Dehydration
! Renal insufficiency
! Relative hypokalemia
! Candidal diaper rash
! Fluids??? Insulin??? Treatment for cerebral edema
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Peds DKA Tx
! The approach and principles of management are essentially the same for all children in DKA.
! Treatment plans will be guided by severity.
! European Society for Pediatric Endocrinology and the Lawson Wilkins Pediatric Endocrine Society (ESPE/LWPES) have set forth guidelines.
! In the past MULTIPLE ways and guides to treatment for DKA
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Peds DKA Treatment
! The consensus from multiple societies is that the treatment protocol should be simple and relatively standardized to decrease errors in management
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Goals of Therapy
! Correct dehydration
! Correct the acidosis and reverse ketosis
! Restore blood glucose to near normal
! Avoid complications of therapy
! Identify and treat any precipitating event.
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Fluids
! First assess for dehydration.
! At best, the clinical assessment is imprecise.
! 3 most useful clinical signs: ! Prolonged capillary refill
! Abnormal skin turgor
! Hyperpnea
! > 10% ! weak peripheral pulses, hypotension, and oliguria
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Fluids
! Usually there is a deficit in extracellular fluid volume in the range of 5-10%.
! Shock with hemodynamic compromise is relatively rare in pediatric dka.
! Clinical estimates of deficit are subjective and inaccurate, therefore: ! Moderate DKA: 5-7%
! Severe DKA – 7-10%
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Goal of fluid & electrolyte replacement therapy:
! Restore circulating volume
! Replacement of sodium and ECF & intracellular fluid deficit of water.
! Improved glomerular filtration with enhanced clearance of glucose and ketones
! Reduce the risk of cerebral edema
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Fluids
! Fluid repletion should be done gradually and with isotonic fluids.
! Evidence of fluid resuscitation and cerebral edema is not conclusive either way.
! General consensus: initial volume expansion – is 10 ml/kg to be given over the first hour.
! May give a second bolus of 10 cc/kg IF hemodynamically compromised.
! DO NOT give more than 20 cc/kg, unless unstable.
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What fluid to use? ! NS for initial boluses
! K+??? ! If K+ is elevated, may wait until you get cr back
! If K+ is normal, add when the child urinates or with the initiation of insulin therapy
! If K+ is low, add immediately
! Do not begin insulin therapy with severe hypokalemia
! It is added to the maintenance fluids.
! Rate of fluids should then be 1.5-2 times maintenance.
! Do not need to replace urinary fluid losses.
! Continue NS or LR for first 4-6 hours (???)
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SUMMING UP FLUIDS
! 10 – 20 cc/kg bolus
! NS +/- K at 1.5 – 2 times maintenance
! Change to ! normal about 4 hours into it, ?earlier, ? Younger child
! Don’t exceed these rates unless patient is in extremis.
! Easy, right?
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Insulin
! After the first bolus is complete, initiate insulin.
! 0.1 unit/kg/hour
! For younger children (usually <3) the rate should be 0.5 units/kg/hour.
! NO BOLUS!!!!!!
! Study in Germany – less complications with low dose insulin 0.025 u/hr. Resolution took longer.
! Mix insulin with NS, 1 unit/ml and give on syringe pump to decrease extra fluids.
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Insulin continued
! If serum glucose decreases to <300-250 and the ketoacidosis is not corrected, change the iv to D5NS or D5LR.
! It is recommended to have serum glucose levels around 150-200 for younger children and 100-150 for older kids.
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Sum it up again
! 10-20 cc/kg fluid bolus NS
! Maintenance – 11/2 to 2 times
! K+: if low, give K+ and delay insulin therapy, K+ normal -add K+ when tx begins, high – begin therapy follow K+, initiate K+ when K+ is lowered and when child has urinated.
! Insulin: 0.1 u/kg/hr or 0.05 units/kg/hour (<3)
! Monitor for cerebral edema
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Bicarb??
! There is substantial evidence that bicarbonate therapy should not be used in DKA
! Risks from bicarb therapy: ! Excess NaHCO3 tx can lead to a paradoxical fall in
cerebral pH
! Administration of alkali may slow the rate of recovery of ketosis
! Can lead to a post-tx metabolic acidosis
! ADA & ESPE/LWPES “selective pts may benefit from NaHCO3 – severe acidemia – pH < 6.90
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Monitoring ! Monitor glucose hourly during the initial 4-6 hours.
! Electrolytes and venous pH initially evaluated hourly for the first 3-4 hours, then q 2
! Monitor vs
! Monitor for signs of cerebral edema
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Subcutaneous Insulin?
! Younger children (sensitive to insulin) should be hospitalized.
! Venous pH > 7.30, no neurologic impairment, and volume deficit estimate of < 3%. – can do regular insulin q 3-6 hours.
! Inhaled insulin – on the horizon
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Neurologic Eval – cerebral edema
! Major Criteria ! Altered mentation/fluctuating LOC
! Sustained HR decel (>20 bpm)
! Age inappropriate incontinence
! Minor Criteria ! Vomiting, HA
! Lethargy or being not easily aroused from sleep
! Diastolic BP > 90 mmHg
! Age < 5 years.
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Cerebral Edema ! Diagnostic criteria
! Abnormal motor or verbal response to pain
! Decorticate or decerebrate posture
! Cranial nerve palsy (most notably – III, IV and VI)
! Abnormal neurogenic respiratory pattern: ! Grunting
! Tachypnea
! Cheyne-stokes respiration
! apneusis
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Cerebral Edema
! Diagnosed if ANY diagnostic criteria present
! With two major criteria
! With one major and two minor criteria
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Cerebral Edema
! The incidence is 0.5 – 0.9% of DKA episodes
! Mortality rate 21-24%
! Pathogenesis unclear. Increased risk factors: ! Younger age
! New onset diabetes
! Longer duration of symptoms
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Cerebral Edema
! Factors present at time of presentation that increase risk of cerebral edema: ! Greater hypocapnia
! Increased serum nitrogen (may represent a greater degree of dehydration)
! More severe acidosis
! Bicarbonate therapy
! Attenuated rise in measured serum sodium concentrations during therapy
! Administration of insulin in the first hour of fluid treatment.
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Cerebral Edema
! Glaser, et al published in 2006, Pediatric Diabetes Journal. 41 children in DKA had MRI’s done: ! Lateral ventricles were significantly smaller during
treatment than afterwards.
! 56% of children had ventricular narrowing during treatment – these children were more likely to have mental status changes than those without narrowed ventricles.
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Pathophysiology
! Cause of cerebral edema is not fully understood.
! Only way to definitively prevent it is to avoid DKA.
! May be present before the initiation of treatment, but more commonly presents 4-12 hours into treatment.
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Proposed Mechanisms
! Ischemic/cytotoxic edema: MR spectroscopy have shown a decrease of N-acetylaspartate (NAA) – a marker of neuronal function/viability.
! Vasogenic edema: primary damage to the cerebral vascular endothelium!increased blood-brain barrier permeability or a disturbance in autoregulation.
! Osmotic edema secondary to fluid tx: osmotic pressure promotes water movement into the intracellular compartment. During tx, insulin and fluid repletion lowers the serum glucose and plasma osmolality ! promoting osmotic water movement into the brain.
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Cerebral Edema
! By the time the diagnostic criteria develop, cerebral edema is already advanced: ! Abnormal motor or verbal response to pain
! Decorticate or decerebrate posture
! Cranial nerve palsy (III, IV, and VI)
! Abnormal neurogenic respiratory pattern
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Treatment
! Essential part of DKA tx is monitoring for changes.
! Decrease rate of fluids
! Mannitol: 0.25 – 1.0 g/kg IV over 20 minutes – based only on case reports. Retrospective study – no benefit.
! 3% saline – 5-10 ml/kg over 30 minutes
! Intubation/ventilation – No hyperventilation. Poor outcome with pCO2 <22
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Case Review
! 10 month old with URI symptoms – tachypnea is seemingly out of proportion to his illness.
! Lab shows elevated AG, glucose and a decreased bicarb., initial K+ is 3.7.
! What is your treatment plan ?
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Treatment Plan
! IV fluid bolus: ns 10 cc/kg – 100 cc bolus over one hour. Does he need a repeat?
! IV – after initial bolus, NS at a rate of 1.5-2 times maintenance (4-2-1 rule), add K+
! IV insulin – what rate for this child?
! Monitor neuro status and transfer to pediatric institution.
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Take home points!!!
! Bolus NS – do not exceed 20 cc/kg unless unstable – Do not volume overload.
! Continue NS for the first several hours
! Add insulin after one hour – 0.1 units/hour or 0.05 units/kg if less than 3 y/o
! Monitor glucose every hour. Monitor lytes, ag and bhob every hour for the first 3-4 hours. Should you have the patient longer, go to q 2.
! Monitor for cerebral edema.