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39th National Conference on Pediatric Health Care

©2018

March 19-22, 2018 CHICAGO

The MUD in the PILE:

Case Studies in Acute Care: Acid/Base and Fluid Derangements

Heather Herrera MSN, CPNP-AC/PC

Jennifer Joiner MSN, CPNP-AC/PC

©2018

Objectives

• Review normal acid-base balance and strategies to correct serious abnormalities.

• Identify via the use of pediatric case studies uncommon, serious fluid and electrolyte abnormalities and best practice treatment strategies.

• Discuss complications associated with uncorrected fluid and electrolyte derangements.

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A River Runs Through It

Body Water Composition

• Term Infant- 80ml/kg

• Child- 70ml/kg

• Adult-60ml/kg

-ECF-1/3 of Total body water

-ICF-2/3 of Total body water

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Just Right…

Homeostasis

Body wants it JUST right!!

Fluid

Electrolytes

pH

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Breathe in, Breathe out!

• What Happens Normally?

-Large amounts of acid secreted as CO2 in the lungs

-Reabsorption of HCO3-occurs in the proximal convoluted tubules.

-Active transport of acid occurs in the Distal Convoluted tubules -urea is secreted as: NH4, H2, PO4

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Respiratory Acidosis and Alkalosis

• Respiratory acidosis: pH 7.20/ PCO2 60/PO2 78/ HCO3 28

– CNS depression, muscular weakness, and diseases of lung and airways (asthma, COPD)

• Respiratory alkalosis: pH 7.52 /PCO2 25 /PO2 90 /HCO3 18

– Hypoxemia, anxiety, and acute lung injury (pneumonia, acute asthma, early pulmonary edema and pulmonary embolism)

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Metabolic Alkalosis/Acidosis

• Metabolic alkalosis– pH 7.52 PCO2 58 PO2 86 HCO3 36– Chloride responsive: contraction alkalosis, diuretics, vomiting, gastric

suctioning, and corticosteroid therapy– Chloride resistant: hyperaldosterone state, Severe K depletion

• Metabolic acidosis– pH 7.10, PCO2 12, PO2 96, HCO3 10– Compensation is by hyperventilation-exhibited by low CO2– Bicarbonate losses occur as buffer system is imbalanced and other cations

must accompany loss in the kidneys subsequently causing a loss in these electrolytes-usually potassium and sodium.

©2018

Electrolytes and the  Anion Gap

• An electrolyte abnormality is often the first sign of an acid base disorder. The anion gap is the sum of routinely measured cations minus the routinely measured anions.

• Because of electrochemical balance, the concentrations of serum cations and anions are the same.

• In routine measurement of electrolytes, however, more anions are unmeasured than are cations; this leads to an expectedanion gap.

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Expected Anion Gap

Cations – Anions

OR

(Na + K) - (Cl + HCO3)

Normal range = 12+ 4 mEq/L

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Gap or Non-Gap: That is the Question???

Example Non-Gap

Na 140, K 4, Cl 110, HCO3- 25

(140+4)-(110+25)= 9

Gap 9

Example Gap

Na 140, K 3, Cl 108, HCO3- 15

(140+3)-(108+15)= 20

Gap 20

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Non-Gap Acidosis

©2018

Gap Acidosis-CAT MUDPILES

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Case #1 – The Salty Baby

• 6-wk-old female presents to the ER with new-onset seizures– PMH significant for one month NICU stay for methadone wean secondary

to maternal drug use during pregnancy

– MOC reported in ER that child took 2-3 oz of Similac Advance q3h

– Meeting all developmental milestones

– Lived at home with MOC, 4yo sibling and GMOC

– No new caregivers; no daycare attendance

• MOC unavailable for history since admission to PICU from ER– Unable to verify PMH/feeding tolerance/schedule/formula

– Concern for unusual behavior

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Case-ER Labs

• ER labs: 7.43/78.3/26.1/50.5/22.1; Na 179.3, K 2.87, Cl 113, gluc 124, iCa 0.66

• Seized in ER – given ativan x3, tylenol, phenobarb load (15mg/kg) IV x1, ampicillin, gentamicin, and an NS bolus

• Respiratory failure ER – intubated – transferred to PICU

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PICU Labs

• PICU arrival labs:– VBG: pH 7.51/CO2 80.0/pO2 29.7/HCO3 62.7/BE 34.3; Na 177, K 3.2, Cl

108, gluc 147, iCa 0.53

– Chem – Na 188, K 2.6, Cl 108, CO2 53, BUN 52, Creat 0.9, Gluc 165, Ca 6.0, PO4 7.8, Mg 2.3, Tbili 0.5, AST 110, ALT 59, alk phos 325, Tpr 5.5, alb 3.5

– Urine: osmolality 595, creatinine 24.3, Na 204, K 61.7, Cl < 20

– CBC: WBC 15.3, Hgb 10.7, Hct 36.8, Plts 628

– http://www.mylonghairjourney.co.uk/wp-content/uploads/2012/10/say-what-logo1.jpg

©2018

Question

• What is this child’s anion gap?

– A. 12

– B. 20

– C. 30

– D. 10

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Gap acidosis

(188 + 2.6) - (108 + 53)

= 20 mEq/L

©2018

Differentials

• Differentials

– Bartter syndrome

– Diabetes Insipidus

– Hypernatremia

– Dehydration

– Chemical poisoning

– Acute Kidney Injury

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Diagnosis: Hypernatremia, unknown etiology

• Severe hypernatremia along with multiple other electrolyte abnormalities

• Gap acidosis

• Seizures

• Respiratory failure

• Dehydration

• Acute Kidney Injury

©2018

FENA-Fractional excretion of sodium

• Used to calculate kidney function in oliguric state as a %

• Accurately suggests pre-renal disease, creatinine is only snapshot in time.

• Not accurate with chronic kidney disease, diuretic use, obstruction or acute glomerular disease

Calculated:

Serum Creatinine x Urine Sodium/Serum Sodium x Urine Creatinine x 100

©2018

FEUrea

• Used In oliguric states while on diuretics to measure degree of AKI

• Urea is not affected by diuretics

Calculated By:

• Serum Creatinine x Urine Urea/Serum Urea x Urine Creatinine

©2018

FENA/FEUrea

Prerenal Intrinsic Post-renal

FENA <1% >1% >4%

FEUrea <35% >50% N/A

(Carvounis, C. P. et. al, 2002)

©2018

Why so high?

• Why is this child’s Na so high???

– Calculate FeNa

– 0.9 x 204/188 x 24.3 x100

– 183.6/456,840

– 0.0004%

– Pre-renal 

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Continuing...

• Arrival to PICU:

– Femoral CVL placed

– Arterial line attempted – unsuccessful

– EEG placed

– Attempts to obtain more history from MOC but unable to locate

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IV fluids...so important

• IVFs – D5NS + 20 meq KCl/L at maintenance

– Why NS?

• Goal correction for hypernatremia is ~0.5 meq/h – a rapid decline in serum Na concentration can cause cerebral edema

• Dehydration should be corrected over 48-72 hours

©2018

Repeat Labs

• Repeat labs:

– Chem: Na 182, K 1.8, Cl 114, CO2 49, BUN 46, Creat 0.8, gluc 125, Ca 5.7, PO4 5.9, Mg 2.5, Tbili 0.6, AST 113, ALT 63, alk phos 335, Tpr 5.3, alb 3.3

– VBG: 7.42/79.6/26.0/49.9/20.2; Na >170, K 2.01, Cl 121, gluc 129, iCa 0.92

©2018

Continuing...

• First night:

– LP done to r/o meningitis; blood and urine cultures obtained in ER – pending

– VBGs checked q2h – closely monitoring

– One episode of brady/desat that improved with bagging and suctioning

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Seizures

• Next morning – episode of desaturation to 50-60% with bradycardia to the 80s; increased tone noted – thought to be secondary to seizures

– Ativan and vecuronium administered with improvement in status

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Neurology consult

• Neurology consulted

– EEG showed multiple seizures originating mainly from the right hemisphere, and at times from the left hemisphere, clusters of 10-30 seconds long electrographic seizures, some of which were associated with stiffening and changes in vital signs

• Loaded with keppra 20mg/kg, followed by maintenance dosing (100mg IV) q12h

• Also started on vitamin B6, 50mg IV BID (supports the GABAergic inhibitory interneuron system)

©2018

New labs

• AM labs (HD #2)

– Chem – Na 181, K 3.2, Cl 132, CO2 37, BUN 44, Creat 0.8, gluc 139, Ca 8.6, PO4 6.7, Mg 2.1

– VBG: 7.31/87.9/33.9/43.1/12.3; lactate 1.30, Na > 170.1, K 3.2, Cl > 127, iCa 1.21 (vent settings: rate 30, 90%, iT 0.60, TV 20, PS 10, PEEP 5

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Status update

• Update in status:– Neuro: medically sedated; continuous EEG

• Precedex 0.4 mcg/kg/hr

• Morphine 0.05 mg/kg/hr

• Ativan PRN seizures; morphine PRN pain/agitation

– CV: Hypotensive; epi drip, titrating to maintain goal MAP 45-50; calcium gluconate drip for decreased iCal

– Resp: on vent; adjusting as needed

– FEN/GI: NPO. IVFs (initially D5NS, changed to D5 1/4NS ~12 hrs after admission). Monitoring chemistries q2h.

– Renal: Foley secondary to urinary retention. Nephrology consulted.

– Heme/ID: Febrile in ER. Cefotaxime; following up cultures (blood, urine, CSF).

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Where is Mom??

• MOC continued to be unavailable, despite being asked to bring in the infant’s formula

– Center for Miracles consulted

– CPS (Child Protective Services) contacted

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Repeat labs

• Labs HD #3

– Chem: Na 163, K 4.0, Cl 132, CO2 28, BUN 27, Creat 0.6, gluc 108, Ca 9.3

– VBG: 7.39/49.7/25.8/30.0/4.1; lactate 1.02; Na 158.2, K 3.94, Cl > 127, gluc 99, iCa 1.38

©2018

Starting feeds

• On HD #3, NG tube placed

– Similac Advance started, goal of 7 ml/hr (low Na formula)

– Transitioned to monitoring chemistries q4h, still slowly bringing down Na and correcting other electrolytes as needed

©2018

HD #4 labs - improving

• HD #4 labs:

– Chem: Na 151, K 4.0, Cl 121, CO2 26, BUN 16, Creat 0.6, gluc 124, Ca 8.6

– VBG: 7.38/44.0/39.4/25.7/0.4; lactate 0.89; Na 144.9, K 3.88, Cl 118, gluc 116, iCa 1.11

©2018

Continues to be ill...

• HD #4

– Echo – normal; small right pleural effusion

– MRI ordered

– Some difficulty with feeding tolerance (abdominal distention, decreased bowel sounds) – feeds held, tolerance to be readdressed after MRI

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Improving but...

• Developed multiple seizures – phenobarbital started per neurology recommendations

• Continues intubated on vent

• Following CMPs and VBGs q8h

• Continues on epi drip at 0.05 mcg/kg/min, titrating for goal MAP 45-50

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MRI findings:

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The mother’s story

• She finally arrives...

– Mother of child reported that a box of baking soda was by the baby’s formula but stated that she did not mix it with the baby’s formula

• Said that her 4yo daughter was playing with it

• CPS/CFM investigating

©2018

Status update

• Gained seizure control on scheduled keppra and phenobarbitol

• Extubated HD #7

• Started PO feeding HD #9; swallow study done after discharge showing aspiration of thin liquids; requires feeds with thickener and outpatient speech therapy

• Removed from mother’s care and placed in CPS custody in a foster home

• At last check, doing well

• Will require close developmental follow-up

©2018

Hypernatremia

• Imbalance in the body’s water management

– Increases plasma osmolality in relation to total body water

– Two causes:

• Water loss that is not replaced

• Excessive salt intake relative to water ingestion

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Hypernatremia

• So what...what’s the big deal with hypernatremia??

• Body wants Na levels “just right”

– Hypernatremia: Na > 150

– Hyponatremia: Na < 135

– https://www.curesources.coop/blog.html?action=topic&topicId=36ff655f-44d3-4650-a15c-eb33bdee5e71

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Salt, Salt, Salt

• What is baking soda made of??

– Sodium bicarbonate

• Massive sodium load

• Unable to regulate thirst mechanism due to age

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Salt Poisoning

• Hypernatremia

– In this case – salt poisoning

• Infants and children at risk secondary to their inability to communicate thirst and their reliance on other individuals for water

• A single teaspoon of salt contains 100 meq of Na; this can increase the serum Na concentration in a 10 kg child by 17 mEq/L

• Rapid onset of hypernatremia can cause cerebral hemorrhage and subsequent irreversible neurological damage

©2018

Neurologic signs

• Initial manifestations can include

– Irritability

– Restlessness

– Weakness

– Vomiting

– Fever

– High-pitched cry and tachypnea in infants

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Hypernatremia

• May also have signs/symptoms of dehydration

– Tachycardia

– Hypotension

– Dry mucous membranes

– Decreased peripheral perfusion

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Neurologic symptoms

• In severe hypernatremia (Na > 160 mEq/L)– Altered mental status

– Lethargy

– Coma

– Seizures

**in severe cases such as salt poisoning with a rapid rise in Na level, the rapid rise leads to acute brain shrinkage, which then results in vascular rupture with cerebral and subarachnoid hemorrhage, demyelination, and irreversible neurologic injury

©2018

At risk for central pontine myelinolysis

• Associated with dysnatremias, both hypo and hyper (as well as aggressive correction of hyponatremia)

• Caused by severe damage of the myelin sheath of neurons in the brainstem

• In a literature review of 76 patients with CPM (worldwide over 5 decades), the majority (58/76) had moderate to severe neurological symptoms at time of diagnosis– 36/72 died but 7/72 had moderate to severe neurologic deficits and 26/72 had

mild deficits or were neurologically asymptomatic

• Imaging studies and increased awareness have likely improved the diagnosis of this disorder while also improving management and prevention of severe sequelae

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Acute hypernatremia

• Manifested by neurological symptoms as water moves out of the brain cells which leads to cerebral contraction

– Presence and severity of symptoms corresponds with the degree of plasma Na elevation and its rate of rise

https://www2.estrellamountain.edu/faculty/farabee/biobk/BioBooktransp.html

©2018

Hypernatremia

• Goal rate of correction should not exceed 0.5 mEq/L per hour (10-12 mEq/L per day)

– Gradual rehydration using hypotonic solution (D5 0.45% NS over ~ 48 hrs

• Faster correction is associated with increased risk for development of cerebral edema

Critical Illness

Fluid administration is necessary for maintenance of water balance as intravascular volume depletion

and/or third spacing occurs.

Balance is disrupted!

Fluid and electrolyte shifts occur with a loss of homeostasis.

©2018

Balance

• Need balance

• Fluid rate is as important as tonicity of the solution

• LR-Isotonic but Na is less than ECF content

• NS-At risk for hyperchloremic metabolic acidosis

• Plasmalyte-Isotonic

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Fluid Balance and Outcomes

• Systematic Review by Olobaidi, R. et. al.

• 44 Studies, from JAMA, Jan 2018

• Found 6% increase in mortality for every 1% increase fluid overload

• Fluid overload found in 10-83% of patients

• Increase in in-hospital mortality

• Survivors had lower total % of fluid overload

©2018

Hyponatremia

• Sodium loss will lead to release of ADH

• Leads to a total body volume contraction and subsequent release of aldosterone which worsens sodium and potassium losses.

• Despite isotonic fluid administration, sodium will get excreted in urine, free water will be retained and hyponatremia will persist.

• Remember its confined to ECF-creates a gradient

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ADH - Hold the water please!

• Released in response to increased osmolality and from hemodynamic and non-hemodynamic triggers.

• Release causes increased water permeability and reabsorption.

• Levels peak 6-12 hours after surgery

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What Does Aldosterone have to do with it???

• Sodium reabsorption

• Potassium and Hydrogen Ion excretion

• Insulin Resistance

• Hypertension

• Activates NF-kB(nuclear factor kappa light chain enhancer of activated B cells) and nuclear transcription factor

• Causes release of AVP (arginine vasopressin)

©2018

Case: Failure to Thrive

• C. R. is a 5 month old male admitted from OSH ER near Mexican border after approximately 1 week history of cough and rhinorrhea without fever. Initially diagnosed with viral URI by an ER in Mexico, but when when symptoms persisted 3 days later with diarrhea and increased respiratory rate, mother went to PCP who sent her to the ER on US side.

©2018

Past Medical History

• Born at 38 weeks gestation via C-sxn at 2kg weight and had an uncomplicated NICU stay for intrauterine growth retardation and feeding issues.

• Followed by PCP for poor weight gain and had a 2 month visit but had missed 4 month visit due to travel to Mexico. Normal newborn screen x 2.

• Recently switched to Mexican formula Nidal as Similac Advance was not available. Current intake 1-2oz every 2-3hrs.

©2018

History

• PSH: No previous surgeries

• Social History: Lives with mother and 2 year-old brother with mother’s cousin and her husband in border town. Father lives in Mexico with paternal GM and 2 older siblings. Father smokes outside, no pets.

• Family History: Brother - Leukemia, Maternal GM - diabetes

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Review of Systems

• Neuro: + tires with feeds; no seizures, AMS or lethargy

• CV: no cyanosis or diaphoresis with feeds

• Resp: tachypnea with cough and increased work of breathing

• FEN/GI: no emesis, spitting up or constipation; denies abdominal distention

• Heme/ID: afebrile, no rashes

• HEENT: + rhinorrhea

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Physical Exam

• Vitals: Temp 97.9, HR 118, RR 45, B/P 94/42, 100% sats• General: Thin, non-toxic• Neuro: Alert, cries with exam, tracks and makes eye contact• CV: RRR, no murmur, pulses 2+ to bilateral upper and lower extremities• Resp: Clear bilateral breath sounds, no distress or accessory muscle use• FEN/GI: Soft, non-tender, non-distended, normal bowel sounds, no

hepatosplenomegaly, no palpable masses• Extremities: Full ROM, no edema or joint swelling• GU: Normal uncircumcised male• Integ: No rashes, warm and dry, pink, brisk refill• HEENT: Normocephalic, atraumatic, AFOSF, dry mucous membranes and tongue

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Pertinent Lab Data

• Chemistry-Na 131, K 1.6, Cl 114, CO2 6, BUN 47, Creatinine 0.7, Glucose 127, HCO3- 6

• ABG- pH 7.2, CO2 20, pO2 116, HCO3 7.6, BD-19

• CBC-WBC 17.2, HGB 9.2, HCT 24, PLT 469

• Coagulation: PT 15.1, PTT 31.4, INR 1.1, Fibr 120

• Microbiology: Blood Culture pending

• Urine: ph 7.5, urine anion gap present

©2018

Question??

• The infants lab values demonstrate which of the following?

A Metabolic Alkalosis

B Respiratory Acidosis

C Metabolic Acidosis

D Respiratory Alkalosis

©2018

Fluid Deficit

Fluid Deficit = Pre-illness weight – illness weight

%Dehydration = Pre-illness weight – illness weight/illness weight X 100%

Subtract fluid bolus received to determine hourly fluid rate over 24hrs.

©2018

Question?

• What action should the nurse practitioner take immediately?

A Administer sodium bicarbonate

B Place on Oxygen

C Administer potassium chloride

D Order FFP

©2018

Fill The Tank Follies!

• PIV infiltrated on transport, unable to replace

• IO placed for bolus - infiltrated in leg after bolus

• New IO placed with failed CVL placement x2

• NG placed with pedialyte infusing

• Femoral CVL placed via cut down by CT surgery

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Radiologic

• Babygram- Symmetric hyperinflation with a left retro-cardiac opacity consistent with atelectasis or infiltrate. Left femoral CVL present.

• RUS-Right kidney with mild fullness of pelvis. Left kidney with mild dilatation of renal pelvis. Diffuse patchy echogenicity consistent with medullary nephrocalcinosis.

©2018

What do we have here??

• Non-Gap Hyperchloremic, Hypokalemic, Metabolic Acidosis

• Severe diarrhea, hypovolemic shock and failure to thrive.

• Urine anion gap positive

• Nephrocalcinosis

• Small for gestational age at birth

©2018

Differential Diagnosis

• Viral Gastroenteritis

• Metabolic Disorder

• Child Maltreatment

• Renal Tubular Acidosis (RTA)

• Sepsis

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Diagnosis: RTA Type 1

• Non-gap, hyperchloremic metabolic acidosis that is associated with FTT, polyuria, growth failure, anorexia, constipation and/or diarrhea

• Easily confused with concomitant diarrheal illness

• Tips in Diagnosis: Urine anion gap +, slow resolution of problem and history of FTT

• Bone ion buffering causes hypercalciuria in untreated patients resulting in nephrocalcinosis

©2018

Question

The urine anion gap measures which ion?

A NH4+

B HCO3-

C Cl-

D Na+

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Urine Anion Gap

• Urine anion gap measures amount of ammonia that is being excreted.

• RTA: positive urine anion gap

• Diarrheal illness: negative urine anion gap

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Actions

• Fluid resuscitated

• Nephrology Consult - started on Citra-3 TID

-Replaces Bicarbonate 12mEq/day, Potassium 6mEq/day and Sodium 6mEq/day.

• Long term follow up for growth

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Fluids and Electrolyte Problems:Which Kids are at Risk?

• Shock - Endothelial leak stimulates body to release ADH as osmolality rises; fluid repletion is required for correction; stress response occurs and cortisol is released

• Surgery - Causes non-osmotic stimuli for ADH release leads to hyponatremia; higher risk during neurosurgical and renal cases

©2018

Too much Fluid…Why do we care?

• Impacts Oxygen cascade-partial pressure of oxygen decreases at the alveolar, capillary, arterial and tissue level.

• Reduces the efficacy of gas exchange-diffusion of gases are hindered as extraction from capillaries is restricted and CO2 clearance is impaired.

• FEAST study - Increase in mortality, LOS and length of ventilation with fluid overload

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The Mighty Endothelium-The Gatekeeper!!

• Disruption of the endothelial glycolax and loss of pre-capillary vasoconstriction causes a leak from the intravascular space which creates increase in interstitial volume, tissue edema and impairs organ function.

©2018

Fluid management

• First step: fluid administration CONTROL!

• Total Fluid Goal

• Plan for safe return to euvolemia

• Change fluid and rate with patient changes.

Daily Fluid Requirement

• 3–10 kg: 100 ml/kg/day

• 11–20 kg: 10kg:1000 ml +50 ml/kg each additional

• 21-70 kg 20 kg: 1500 ml +20 ml/kg for each additional kg

©2018

Case study of “Sweetie”

• 12 y. o. female

– No past medical history

– Presented to OSH ER with c/o sore throat and abdominal pain at the umbilicus

– 30kg weight loss in the last month

– MOC reports noting recent polyuria and increased liquid intake over last week

– Day of admission lethargic at home, unable to ambulate, brought to ER by family late afternoon

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DKA

• Diagnosed with Diabetic Ketoacidosis at OSH

– Exam

• Lethargic

• Kussmaul breathing

• Only responsive to deep painful stimuli

– Interventions

• NS 1L IV x1

• Insulin 8 units IV x1

©2018

Altered mental status

• GCS reported to be 8-10 by OSH

– Received 3% NS x1 at OSH

• Transport team sent to pick up patient

– Upon arrival, worried about neuro exam – 3% NS bolus given

– Second bolus given prior to air transport departure

©2018

Concern for cerebral edema

• Why not intubate the patient at this point?

– Concern for cerebral edema

• Worsening respiratory acidosis could worsen cerebral edema/impending herniation

• At time of transport, she had a + gag reflex, was protecting her airway, she would withdrawal to pain, and she would open her eyes to stimulus

• Respiratory rate was upper 20s with ETCO2 reading 15-20

• Uneventful transport...but then....

©2018

Code Blue!

• CODE BLUE!

– Upon arrival to the PICU, after transfer from stretcher to bed, she suddenly stopped breathing and became cyanotic

– CPR was initiated, epi x1 then ROSC

– After ROSC, she seemed to be moving purposefully (trying to remove mask from her face) and was breathing spontaneously

– Decision made to intubate

©2018

Intubation

• Intubated on first attempt using RSI (fentanyl, versed, and vecuronium) – 6.5 cuffed ETT, Mac 3 blade

• Ensured hyperventilation with hand-bagging pre and post intubation

• No major desats/bradycardia with intubation

©2018

Question?

• Which of the following medications can be given in an emergency situation to treat suspected cerebral edema?

a. 3% Normal saline

b. Sodium bicarbonate

c. Potassium chloride

d. Magnesium sulfate

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©2018

Critically ill

• Hypotensive after intubation (70s/30s)

– LR 500ml IV x1 rapid IV push

– Central line and arterial line placed

– Epinephrine drip started at 0.1 mcg/kg/min followed by norepinephrine at 0.1 mcg/kg/min

– Vasopressin started due to continued hypotension

– Stress dose steroids given to improve hemodynamics – goal MAP > 60, SBP 90-110

©2018

Physical exam

• Exam consistent with shock

– 1+ pulses to upper and lower extremities

– Cool to touch

– CRT > 3 sec

– HR 130s-140s

– BP 70-80s/40s

©2018

Interventions

• Pain and sedation/neuro-protective maneuvers

– Morphine drip

– Precedex drip

– HOB elevated 300

– Temperature control – goal 34-36C

– Prevent fever spikes

– Monitor for seizure activity

– Goal serum Na > 150

©2018

Hyperventilate on the vent

• Intubated on ventilator

– Hyperventilate for goal ETCO2 15-20 (same as pre-intubation ETCO2 readings)

– Follow frequent ABGs – adjust vent accordingly; initial pH post-arrest was 7.6 with significant hemodynamic instability; bicarb 50 meq IV x1

©2018

Slow correction

• Slow correction of glucose and acidosis

– Low dose insulin drip 0.05 units/kg/hr

– IVFs at 1.5x maintenance using DKA protocol (2-bag system)

– Monitor pancreatic enzymes

Social work consult – significant weight loss, lethargy for extended period of time before seeking help

©2018

Improving but develops pancreatitis

• Extubated and vasopressors weaned off HD on hospital day #2

• Significant evidence of pancreatitis identified

– Elevated lipase and amylase

– Necrotizing pancreatitis – pancreatic insufficiency as evidenced by low fecal elastase – prescribed creon 24000 2 tablets before each meal and one tablet with snacks

– No surgical intervention at this time

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Sequelae

• AKI and hypertension diagnosed during admission– Amlodopine and PRN hydralazine given– Home with amlodopine with follow-up scheduled with nephrology

• Developed line associated thrombus– Discharged home on Lovenox with plans for follow-up with

hematology• Diagnosed with necrotizing pancreatitis

– Creon prior to meals– Scheduled follow-up as outpatient with GI

©2018

Finale

• Discharged home with multiple outpatient follow-ups:

– Endocrinology

– GI

– Nephrology

– Hematology

©2018

The Case of Sweetie

• So what happened??

http://www.freepik.com/free-icon/question-mark_731610.htm

©2018

What is DKA?

• Venous pH < 7.3

• Serum bicarbonate concentration < 15 mmol/L

• Serum glucose concentration > 200 mg/dL

• Along with ketonemia, glucosuria, and ketonuria

©2018

Pathophysiologyhttps://www.ncbi.nlm.nih.gov/pmc/ahttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC313

©2018

Pathophysiology of Diabetes

• the result of critical deficit of insulin

– Results in starvation of insulin-dependent tissues

– stimulates release of counter-regulatory hormones

• stimulation of lipolysis and proteolysis

• hepatic and renal production of glucose

• hepatic oxidation of fatty acid to ketone bodies

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Severity

• Determined by the degree of acidosis

– Mild – pH 7.2 - 7.3, bicarb < 15 mmol/L

– Moderate – pH 7.1 – 7.2, bicarb < 10 mmol/L

– Severe – venous pH < 7.1, bicarb < 5 mmol/L

©2018

How to do we manage DKA?

• Goals of treatment:

– Return of adequate perfusion

– Stop ketogenesis

– Replace electrolyte losses

– Monitor for cerebral edema

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Treatment

• Insulin drip (usual dose 0.05-0.1 units/kg/hr)

• 2-bag treatment for DKA

– LR + KCl and Kphos

– D10LR + KCl and Kphos

– Choice of IVFs also depends on K+ level

• Glucose checks q1h

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Question

• What is the maximum decrease per hour of glucose that is acceptable when treating DKA?

a. 50

b. 100

c. 200

d. 150

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Fluid and electrolyte shifts in DKA

• Rehydration/maintenance fluids – should use 0.45% NS

• When plasma glucose < 300, 5% glucose should be added

– Can use 2-bag system to do this

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Fluid and electrolyte replacement

• K+ should be provided as half KCl and half KPO4

– Replenishes low phosphate levels and reduces risk of hyperchloremia

• Can also use K acetate and KPhos

– Acetate converts to bicarbonate which helps correct acidosis

***K should only added to IV fluids after serum K is < 6 (our institution cut-off is 5.5) and/or urine output has been established

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Fluid and electrolyte replacement

• Serum K+ increases by about 0.6 mEq/L for every 0.1 decrease in pH

– Serum K+ does not accurately reflect the deficit from vomiting and diuresis

• Both K+ and Phos shift significantly from intracellular to extracellular compartments with acidosis

– Both re-enter the cells quickly with insulin-induced glucose uptake and rehydration

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Fluid and electrolyte replacement - Bicarb is BAD!!

• Bicarbonate is not indicated

– No evidence that it supports metabolic recovery

– By restoring the circulatory volume, renal function and tissue perfusion will improve which will then reverse acidosis

– Rapid correction of acidosis can cause hypokalemia, the additional Na can increase hyperosmolality and alkali therapy can increase hepatic ketone production – all of which can slow recovery

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Insulin Therapy

• Should be started after initial fluid resuscitation

• Start at 0.1 units/kg/hr

• Bolus dosing is not indicated and may contribute to the development of cerebral edema

• Goal rate of glucose decline is 50-150 mg/dL per hour

• Insulin should not be stopped – needed to prevent ketosis

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Monitoring

• Frequent neurochecks – monitor for changes in neuro status as these can signal cerebral edema development

• Follow chemistries closely

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Transition

• Can be converted to home insulin of regimen (if an established diabetic) once acidosis has corrected

• **In our institution, conversion is somewhat driven by endocrinologist

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Complications

• Renal failure

• Peripheral venous thrombosis

• Pancreatitis

• Rhabdomyolysis

• Mucormycosis

• Cerebral edema

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Cerebral edema in DKA

• Cerebral edema

– Increase in cerebral tissue volume secondary to increase of cerebral tissue water

– Mechanism is complex

– Approximately 2/3 develop within 6-7 hours; remainder develop 10-24 hours after the start of treatment

• Vasogenic – due to breakdown of blood-brain barrier

• Cytotoxic – poisoning or metabolic derangement

• Osmotic – hyponatremia

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Who is at risk for cerebral edema?

• Risk Factors

– Age under 5 years

• Due to rapid deterioration and greater delay in diagnosis (nonspecificity of presenting symptoms)

– Low pCO2

• indicator of severity of ketoacidosis and degree of dehydration

– High BUN

• Also an indicator of severity of ketoacidosis and degree of dehydration

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Treatment of cerebral edema

• If it occurs:

– IV mannitol 1 gm/kg over 20 minutes with repeat as necessary in 1-2 hours

• Closely monitor I/Os – causes an osmotic diuresis

– 3% hypertonic saline – 5-10 ml/kg

• Also elevate HOB (any maneuvers to decrease presumed elevated ICP)

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Diabetes

• As the incidence of obesity and type 2 diabetes diagnoses increase in children, there is another diagnosis to be concerned with/aware of for hyperglycemia differentials

– Hyperglycemic Hyperosmolar State (HHS)

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HHS vs. DKA

• DKA – characterized by severe depletion of water and electrolytes from both intra and extracellular fluid as well as absolute or relative insulin deficiency

• HHS – characterized by extreme elevations in blood glucose concentrations and hyperosmolality without significant ketosis as well as absolute or relative insulin deficiency

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DKA HHS

Criteria Hyperglycemia (>200mg/dL)

Hyperglycemia (>600 mg/dL)

Venous pH < 7.3 or serum bicarbonate < 15 mmol/L

Venous pH > 7.25; arterial pH >7.3

Ketonemia and ketonuria

Serum bicarbonate > 15 mmol/L

Small ketonuria, absent to mild ketonemia

Serum osmolality > 320 mOsm/kg

Altered level of consciousness (obtundation, combativeness) or seizures

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Fluid Correction

• How to calculate fluid correction in DKA • For moderate to severe DKA

– Initial bolus of NS or LR 10 ml/kg (max 1L) over 1 hr, may repeat x1 if needed; no more than 20 ml/kg unless hemodynamic compromise is present

• Once HDS, goal to replace remaining fluid deficit over 24-72 hours• 2500 ml/m2 or ~1.5x maintenance• Rate of fluid administration should not exceed 3000 ml/m2 in 24

hrs – increases risk of cerebral edema • After first 48 hrs, fluids can be liberalized to as much as 3500 ml/m2

to achieve full rehydration

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References

• http://www.freepik.com/free-icon/question-mark_731610.htm• Carvounis, C. P, Nisar, S., Guro-Razunan, S. (2002). Significance of the Fractional Excretion of Urea in the

Differential Diagnosis of Acute Renal Failure. Kidney Int:62(6) p. 2223-2229.• Ranger, Adrianna M, Chaudhary, Navjot, Avery, Michael, and Fraser, Douglas (2012). Central Pontine and

Extrapontine Myelinolysis in Children: A Review of 76 Patients. Journal of Child Neurology: 27(8) p. 1027-1037. • Raman,S. & Peters, M. (2014). Fluid management in the critically ill child. Pediatr Nephrol (2014) 29:23–34 DOI

10.1007/s00467-013-2412-0• Dellinger RP, Levy MM, Rhodes A, et al: Surviving Sepsis Campaign: International guidelines for management of

severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637 • Weitz, J. Fluid management in paediatric shock. (2016). PAEDIATRICS AND CHILD HEALTH 27:1 • Moritz, Michael L. and Ayus, J. Carlos. (2005). Preventing neurological complications from dysnatremias in

children. Pediatric Nephrology 20: 1687-1700. • Somers, Michael J. and Traum, Avram Z. (2017). Hypernatremia in children. Downloaded from

www.uptodate.com on October 18, 2017. • Alobaidi, R., Morgan, C. & Basu, R. (2018). Association Between Fluid Balance and Outcomes in Critically Ill

Children: A Systematic Review and Meta-Analysis. JAMA pedatr. Published online Jan 22, 2018. doi:10.1001/jamapediatrics.2017.4540

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References

• RAAS.png courtesy of Wikipedia. Retrieved from world wide web on November 28, 2017• Stress Response courtesy of VIBE_stressresponse_091913.png• What the endothelium does courtesy of med_hr.png• Fernando Santos, F., Flor A. Ordóñez, D.,Claramunt-Taberner, D. & Gil-Peña, H. (2015). Clinical and laboratory approaches in the

diagnosis of renal tubular acidosis. Pediatr Nephrol 30:2099–2107 DOI 10.1007/s00467-015-3083-9 • Bagga, A. & Sinha, A. Evaluation of Renal Tubular Acidosis. (2007). Indian J Pediatr 2007; 74 (7) : 679-686] • Madkaikar, M., Shabrish, S. & Desai, M. Current Updates on Classification, Diagnosis and Treatment of Hemophagocytic

Lymphohistiocytosis (HLH) Indian J Pediatr (May 2016) 83(5):434–443 DOI 10.1007/s12098-016-2037-y • Oh, G. & Sutherland, S. (2016). Perioperative fluid management and postoperative hyponatremia in children. Pediatr Nephrol (2016)

31:53–60 DOI 10.1007/s00467-015-3081y• Rosenbloom, Arlan I. The management of Diabetic Ketoacidosis in Children. Diabetes Therapy (2010) 1(2):103-120. • Orlowski, James P., Cramer, Cheryl L., and Fiallos, Mariano R. Diabetic Ketoacidosis in the Pediatric ICU. Pediatric Clinics of North

America. (2008). (55) 577-587.• Wolfsdorf, J.I., Allgrove, J., Edge, J., Glaser, N., Lee, Jain V., Mungai, L.N.W., Rosenbloom, A.L., Sperling, M.A., and Hanas, R. (2014).

Diabetic ketoacidosis and hyperglycemic hyperosmolar state. ISPAD Clinical Practice Concensus Guidelines 2014 Compendium. • Agus, Michael S. D. and Wolfsdorf, Joseph I. (2005). Diabetic Ketoacidosis in Children. Pediatric Clinics of North America. (52) 1147-

1163. • Jeha, George S. and Haymond, Morey W. Treatment and complications of diabetic ketoacidosis in children and adolescents.

Dowloaded from www.uptodate.com on October 18, 2017. • Image: pathophysiology of DKA, obtained from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138479/.