1. Cases in Pediatric Acute Care
Kevin Y. Ching MD
Cornell University
New York, NY
Jeannette R. Koziel, APRN, MSN, NP-C
Yale New Haven Children’s Hospital
New Haven, CT

2. CASE 1B Pulmonary Module

3. We have a 5 year old boy with a history of moderate persistent asthma presenting from his pediatrician’s office in severe respiratory distress who is deteriorating despite aggressive bronchodilator therapy
He was already given 3 Combivent (Albuterol/Atrovent) nebs by his pediatrician, and an additional 2 Albuterol nebs back to back on his arrival here. We also gave him 40 mg of Prednisone ten minutes ago.

4. Initial Vitals HR 145 (sinus rhythm), BP 95/45
RR 45, SpO2 88% (up to 91% w/ O2)
Temp 37.5

5. BUN 21 Hct 35.7 Glu 76 pH 7.14 Cl 104 pCO2 70 Na 138 pO2 35 K 3.2
I-Stat
BUN 21
Glu 76
Cl 104
Na 138
K 3.2
Hct 35.7
pH 7.14
pCO2 70
pO2 35
BE -8
Pre Intubation

6. I-Stat
pH 7.21
pCO2 55
pO2 95
BE -5
Post intubation

7. Asthma

8. Asthma: Pathophysiology
Lower airway hypersensitivity to:
Allergies
Infection
Irritants
Emotional stress
Cold
Exercise

9. Asthma: Pathophysiology
Bronchospasm
Bronchial Edema
Increased Mucus
Production

10. Asthma: Pathophysiology

11. Asthma: Pathophysiology
Cast of airway produced by asthmatic mucus plugs

12. Asthma: Signs/Symptoms
Dyspnea
Signs of respiratory distress
Nasal flaring
Tracheal tugging
Accessory muscle use
Suprasternal, intercostal, epigastric retractions

13. Asthma: Signs/Symptoms
Coughing
Expiratory wheezing
Tachypnea
Cyanosis

14. Asthma: Prolonged Attacks
Increase in respiratory water loss
Decreased fluid intake
Dehydration

15. Asthma: History How long has patient been wheezing?
How much fluid has patient had?
Recent respiratory tract infection?
Medications? When? How much?
Allergies?
Previous hospitalizations?

16. Asthma: Physical Exam Patient position? Drowsy or stuporous?
Signs/symptoms of dehydration?
Chest movement?
Quality of breath sounds?

17. Asthma: Risk Assessment
Prior ICU admissions
Prior intubation
>3 emergency department visits in past year
>2 hospital admissions in past year
>1 bronchodilator canister used in past month
Use of bronchodilators > every 4 hours
Chronic use of steroids
Progressive symptoms in spite of aggressive Rx

18. Silent Chest equals Danger

19. ALL THAT WHEEZES IS NOT ASTHMA
Golden Rule
ALL THAT WHEEZES IS NOT ASTHMA
Pulmonary edema
Allergic reactions
Pneumonia
Foreign body aspiration

20. Asthma: Management Airway Breathing Sitting position
Humidified O2 by NRB mask
Dry O2 dries mucus, worsens plugs
Encourage coughing
Consider intubation, assisted ventilation

21. Asthma: Management Circulation IV TKO Assess for dehydration
Titrate fluid administration to severity of dehydration
Monitor ECG

22. Asthma: Management
Obtain medication history
Overdose
Arrhythmias

23. Asthma: Management Nebulized Beta-2 agents Albuterol Terbutaline
Metaproterenol
Isoetharine

24. POSSIBLE BENEFIT IN PATIENTS WITH VENTILATORY FAILURE
Asthma: Management
Subcutaneous beta agents
Epinephrine 1: to 0.3 mg SQ
Terbutaline mg SQ
POSSIBLE BENEFIT IN PATIENTS WITH VENTILATORY FAILURE

25. Asthma: Management
Use EXTREME caution in giving two sympathomimetics to same patient
Monitor ECG

26. Asthma: Management Avoid Sedatives Antihistamines Aspirin
Depress respiratory drive
Antihistamines
Decrease LOC, dry secretions
Aspirin
High incidence of allergy

27. Status Asthmaticus Humidified oxygen Rehydration
Continuous nebulized beta-2 agents
Corticosteroids
Magnesium sulfate (controversial)

28. Special Thanks to
Yale New Haven Children’s Hospital for this presentation

29. CASE 2B Trauma Module

30. 5 year old boy who fell off a jungle gym at the playground and hit his head, now there’s a big bump on the side of his head
He’s been crying because of a headache for 30 minutes
He started vomiting 15 minutes ago

31. Initial Vital Signs HR 165 (sinus rhythm), BP 105/65 RR 25, SpO2 98%
Temp 37.5

32. Pediatric Blunt Head Trauma
…and when to CT…

33. Why we care about CT…
Obtaining CT exams must balance the importance of identifying significant injuries or illnesses with the risks of CT
Multiple studies (and more every day…) show that the estimated lifetime risk of cancer mortality from head CT is substantially higher in children than adults because of a longer subsequent lifetime and the greater sensitivity of some developing organs to radiation

34. Intracranial Injuries, Background
The leading cause of traumatic death in childhood
United States yearly data:
>600,000 visits to EDs for blunt head trauma
~95,000 have intracranial injuries
~5,700 die from the injuries
Morbidity and mortality are increased when extracranial injuries are present

35. Skull Fractures - Epidemiology
Bone involvement in order of incidence:
Parietal Bone
Occipital Bone
Frontal Bone
Temporal Bone
Most common causes:
Falls – 35% (most common <2yo)
Recreational Activities – 29%
MVC – 24%

36. Skull Fractures - Classification
Linear
Comminuted
Depressed
Open

37. Linear Skull Fractures
Single fracture lines, do not cross sutures
Account for 75% of all pediatric skull fractures
15-30% are associated with intracranial injury
Most have associated exam findings (hematoma, soft tissue swelling)

38. Linear Skull Fractures

39. Linear Skull Fractures
Complications
Most heal without any
Subgaleal hematoma is most common
Absorb without intervention but can cause anemia
Epidural hematomas rare, but can occur
Temporal bone fracture involving the middle meningeal artery
Occipital bone fractures involving a venous sinus may cause posterior fossa epidural hematomas

40. Comminuted Skull Fractures
Consist of multiple associated linear fractures
Usually from large force of impact
When seen on occipital bone may be from repeated blows against an object
Increased suspicion for NAT

41. Comminuted Skull Fractures

42. Depressed Skull Fractures
Result from significant force
Approx 30% are associated with underlying cerebral injury
Risks increase with depth of depression
Bony defects or step-offs may be palpable

43. Depressed Skull Fractures

44. Depressed Skull Fractures
Complications
Compression of the underlying brain parenchyma
Intraparenchymal bone fragments
Cosmetic deformity
Increased likelihood of posttraumatic seizures and infection

45. Open Skull Fractures 2 main types:
Compound Fractures – Skull fx with overlying laceration
Skull fractures that disrupt paranasal sinuses or middle ear
May be associated with CSF rhinorrhea or otorrhea
Greatly increased risk for CNS infection due to communication with mucosa, upper respiratory tract, or scalp

46. Basilar Skull Fractures
80% contain at least one of 6 classic physical examination findings

47. Basilar Skull Fractures
80% contain at least one of 6 classic physical examination findings
Subcutaneous bleeding over mastoid process
Subcutaneous bleeding around the orbit
Hemotympanum
CSF rhinorrhea
CSF otorrhea
Cranial nerve deficits

48. Basilar Skull Fractures
80% contain at least one of 6 classic physical examination findings
Subcutaneous bleeding over mastoid process
Battle Sign
Subcutaneous bleeding around the orbit
Raccoon Eyes
Hemotympanum
CSF rhinorrhea
CSF otorrhea
Cranial nerve deficits
Facial paralysis, anosmia, nausea, vomiting, vertigo, nystagmus, tinnitus, hearing loss

49. Basilar Skull Fractures

50. Basilar Skull Fractures

51. Basilar Skull Fractures
Complications
Hearing Loss
Cranial Nerve Impairment
CSF Leakage

52. Basilar Skull Fractures
Complications
Hearing Loss
Occurs in up to 50% of children with basilar skull fx
May be conductive – TM perf, blood in middle ear, ossicular injury
May be sensorineural – injury to the cochlear origin or Corti
Cranial Nerve Impairment
CSF Leakage

53. Basilar Skull Fractures
Complications
Hearing Loss
Cranial Nerve Impairment
Seen in up to 23%
About 50% of those completely resolve, 50% with some permanent deficits
Most commonly CN VI, VII, VIII
CSF Leakage

54. Basilar Skull Fractures
Complications
Hearing Loss
Cranial Nerve Impairment
CSF Leakage
Results from underlying dural tears
Most resolve spontaneously within one week
Increased risk of CNS infection
Meningitis occurs in 0.7-5%
Meningitis can occur months to years after injury
Strep pneumo, Group A beta-hemolytic strep, H flu

55. Greenes & Schutzman, PEC 2001; 17:88
Scalp Hematomas
Predictive of skull fractures in infants <1yo
Clinical significance of scalp abnormalities in asymptomatic head- injured infants.
Greenes & Schutzman, PEC 2001; 17:88
Prospective study, 422 asymptomatic infants
Hematomas in parietal (OR 38) or temporal (OR 16) regions increased likelihood of underlying skull fracture
Hematomas in frontal region did not (OR 0.6)
Risk of skull fracture increases with size of hematoma

56. Neuroimaging Skull Radiographs
Essentially no use as a screening tool to determine if a child with head trauma should undergo CT
If for some reason it has been done and there is a skull fracture of any kind, CT should be done
Presence of fx is not sensitive (59%) or highly specific (88%) for intracranial injury, but relative risk is 6.1% (95% CI )

57. Skull Radiographs May be useful when: Evaluating foreign body
The history of trauma is uncertain
(skeletal survey)
Perhaps not as useful for us in the ED

58. Head CT Direct quote from UpToDate:
“Children with head trauma who are at risk for intracranial injury should be initially imaged with computed tomography.”

59. Head CT Direct quote from UpToDate:
“Children with head trauma who are at risk for intracranial injury should be initially imaged with computed tomography.”
Awesome. So who should get scanned?

60. Minor Head Trauma: Definitions
Separated by age < or > 2 years old
Separated because those <2yo :
Are more difficult to assess clinically
Are frequently asymptomatic
May get skull fractures as the result of minor trauma
Are more often victims of NAT

61. Minor Head Trauma: Definitions
<2y0:
A history or physical signs of blunt trauma to the scalp, skull, brain in an infant or child who is alert or awakens to light touch
>2yo:
GCS of 15 (some say 13, but studies show intracranial injury in up to 20% with this GCS)
Normal mental status at initial examination
No abnormal or focal findings on neuro exam
No physical evidence of skull fracture

62. Increased risk for intracranial injury
Historical Features:
High-risk mechanism
Seizure, confusion, or loss of consciousness >5 sec
Significant headache
Known predisposition for intracranial hemorrhage (i.e. AV malformation, bleeding disorder)

63. Increased risk for intracranial injury
Physical Exam Features:
Scalp abnormalities such as hematoma, tenderness, depression
Bulging anterior fontanel in infants
Abnormal mental status
Focal neurologic abnormality
Signs of basilar skull fracture

64. Generally Accepted Summary Recommendations
Perform CT if <2yo and:
Focal neuro findings
Known fracture
Altered mental status
Irritability
Bulging fontanel
Persistent vomiting
Seizure
Definite LOC (>5 sec)
Suspicion of NAT
Underlying predisposition

65. UpToDate Summary Recommendations
Also perform CT if <2yo and:
Large nonfrontal scalp hematomas, especially <12mos
<3mos with nontrivial trauma
Vomiting that is delayed by several hours after incident or occurs more than once
Presence of >1 observational criteria below

66. UpToDate Summary Recommendations
Observe 4-6 hours or CT if <2yo and:
Vomiting only once soon after injury
Uncertain or very brief LOC
History of lethargy or irritability, now resolved
Behavioral changes reported by caregiver
Skull fracture >24 hours old
Injury caused by high-risk mechanism
Unwitnessed trauma that may be significant

67. UpToDate Summary Recommendations
Do NOT perform CT if <2yo and:
Normal mental status
No nonfrontal scalp hematoma
No LOC
No evidence of skull fracture
Normal behavior per regular caregiver
No high risk mechanism
Normal neuro exam

68. UpToDate Summary Recommendations
Perform CT if >2yo and:
Focal neurologic findings
Skull fracture
Seizure
Prolonged LOC
Altered mental status (agitation, lethargy, repetitive questioning, slow response to verbal questioning)

69. UpToDate Summary Recommendations
Observe 4-6 hours or CT if >2yo and:
Vomiting
Headache
Questionable or brief LOC with no other signs/sx
Skull fracture >24 hours old
Injury caused by high-risk mechanism
(Lean towards CT if multiple)

70. UpToDate Summary Recommendations
Do NOT perform CT if >2yo and:
Normal mental status
No vomiting
No LOC
No signs of basilar skull fx
No severe headache
No high risk mechanism
Normal neuro exam

71. Admission Criteria Non-Negotiable: Strongly Considered:
Anyone with intracranial injury on CT
Strongly Considered:
No evidence of intracranial injury, but:
Persistence of neurologic deficits
Significant extracranial injuries
Persistent vomiting
Suspected NAT
Unreliable parents

72. Special Thanks to
Dr. Matthew Thornton, MD – Yale New Haven Children’s Hospital for this Presentation

73. CASE 3B Vomiting

74. We have a 5 year old boy, who’s been vomiting and complaining of diffuse abdominal pain for 2 days and a headache for 1 day
Initial finger-stick glucose was “critical” high and a urine dip was positive for glucose and large ketones.
He’s stable, but appears moderately dehydrated. We’ve already started a bolus of 20 cc/kg NS one hour ago that should be finishing up now. We’re about ready to hang a 2nd 20 cc/kg NS bolus.

75. Initial Vitals HR 155 (sinus rhythm), BP 125/65 RR 25, SpO2 97%
Temp 37.5

76. I-stat BUN 31 Glu 415 Cl 101 Na 130 K 6.1 Hct 42 pH 7.21 pCO2 16
BE -13
AG 20

77. DKA
Is the most common cause of hospitalization of children with diabetes
Is the most common cause of death in children with diabetes
Is fatal in <1% (from 1-2% of children in the 1970’s)
Most DKA deaths are attributable to cerebral edema (62- 87%), which occurs in 0.4-1% of kids with DKA
Ciordano B, Rosenbloom AL, Heller DR, et al: Regional services for children and youth with diabetes.
Pediatrics. 1977;60:
Rosenbloom AL. Intracerebral crises during treatment of diabetic ketoacidosis. Diabetes Care 1990;13:22-33.
Edge J, Ford-Adams M, Dunger D. Causes of death in children with insulin-dependent diabetes
Arch Dis Child. 1999;81:

78. Background
Though it varies depending on the population, 20-40% of newly diagnosed T1DM patients are in DKA.
Therefore, a major goal of outpatient diabetes management is to prevent DKA
with a high index of suspicion with early DKA symptoms in new or established T1DM patients
with close supervision of established patients
Pinkney J et al. Presentation and progress of childhood diabetes mellitus: a prospective population-based study.
Diabetologia. 1994;37:70-74.
G, Fishbein H, Ellis E. The epidemiology of diabetic acidosis: a population-based study.
Am J Epidemiol. 1983;117:551

79. Etiology of DKA--New Onset DM
Always due to insulin deficiency--absolute or relative
Many previously undiagnosed patients have been seen in pediatric offices or ERs where a detailed history and lab studies could make the diagnosis before DKA ensues
A simple urine dip could be life-saving!
High index of suspicion is especially important in infants and young children

80. Etiology of DKA--Established Patients
***Failure to take insulin, especially in adolescents-- most common cause of recurrent DKA
Acute stress--trauma, febrile illness, psychological turmoil with elevated counterregulatory hormones (glucagon, epi, GH, cortisol)

81. Etiology of DKA--Established Patients (continued)
Poor sick day management
not giving insulin because the child is not eating
failing to increase insulin for the illness, as dictated by fingerstick blood sugars
failure to monitor ketones

82. Definition Mild 16-22 Moderate 10-15 Severe <10
Definitions vary, but in general:
Hyperglycemia > 200 mg/dl
Ketonemia/ketonuria--large serum or urine ketones
Acidosis with venous pH <7.3
Serum bicarb <18
Mild 16-22
Moderate 10-15
Severe <10
*Sometimes DKA can occur with normoglycemia when there is continued insulin therapy, vomiting, and/or reduced intake of carbohydrates

83. Presentation
Hyperglycemia
insulin deficiency causes decrease glucose uptake with tissue starvation, glycogenolysis, and gluconeogenesis from protein and lipid breakdown.
Thirst/Dehydration 20 Osmotic Diuresis/Vomiting
dehydration is usually hyperosmolar, so may be underestimated by clinical exam
Acidosis
from breakdown of lipids to ketone bodies to ketoacids
Fruity Odor from Acetone (ketone body, not a ketoacid)
from tissue hypoperfusion/dehydration

84. Presentation (continued)
Kussmaul (rapid deep) respiration
compensatory response to the metabolic acidosis, contributing to dehydration
Coma- due to hyperosmolarity, not acidosis
Calculated osm >320 is associated with coma
Hyperosmolarity- largely due to glucose, calculated as:
2(Na) + Glucose/ BUN/2.8
Other: Na, K, BUN, Cr, WBC

85. Management--General
Resuscitation (ABC’s, O2) if in shock/poor perfusion with NS or albumin cc/kg over min, may repeat as needed, NGT if vomiting and impaired LOC.
The cause of cerebral edema remains unclear.
Too rapid reduction of intravascular osmolality thought to aggravate the process. Recommended to rehydrate children with DKA more slowly than in other causes of dehydration.
However, newer evidence seems to question this.
Start, maintain, and utilize your flowsheet!

86. Initial Labs Fingerstick blood sugar Grey top glucose
Urine and/or serum ketones
VBG
Chem 20
HgA1c
Insulin level, C-peptide
Antibodies: anti-insulin, anti-islet cell, and anti-GAD (glutamic acid decarboxylase)
TFT’s

87. Management--Fluids
Initial fluid bolus with NS will depend on assessment of severity of dehydration
most kids in DKA are  10% dehydrated, unless there is hypotension, poor peripheral perfusion, etc.
e.g If 10% dehydrated, should get 10 cc/kg NS over 1 hour

88. Fluids
IVF needed =
Maintenance + Deficit + Ongoing Losses
Caution: Fluids should not exceed L/m2/day, as this has been associated with cerebral edema and poor outcome (?)

89. Fluids Maintenance-as per usual, amount based on weight (4/2/1 rule)
Deficit replacement usually over 48 hours
5% dehydration = 0.05 L/kg
10% dehydration = 0.1 L/kg
Consider deficit replacement over 72 hours if marked hyperosmolality (Gluc >1000 or serum osm >320) or if corrected Na is >150 mEq/L
e.g. 30 kg kid with 10% dehydration has a fluid deficit of (30)(0.1)=3 Liters, 300 cc of which have already been replaced with the 10 cc/kg NS bolus, leaving a 2700 cc fluid deficit

90. Fluids Ongoing losses-usually do not need to replaced
If very polyuric or vomiting excessively, can replace urine/vomitus output 0.5 cc/cc
Reassessment of I/O’s at least every 4 hrs for first 24 hrs

91. Sodium Maintenance = 3-5 mEq/kg/day Deficit = 6 mEq/kg
Serum Na may be high, normal, or low depending on fluid status
Many find calculation cumbersome, so can usually use 1/2 NS as replacement fluid and NS as deficit fluid (running piggyback)

92. Sodium
Use NS if the corrected sodium is <140 and/or if serum osm >310
*To correct Na: Add 1.6 mEq/L to the measured Na for every 100 mg/dl of glucose over 100 mg/dl
Monitor electrolytes every 2 hours at first, and then every 4 hours when trend is normalizing

93. Potassium
DKA is associated with total body K depletion, while correction of acidosis causes hypokalemia due to an intracellular K shift, so add K sooner rather than later
Add K once the patient has documented urine output and no peaked T’s on ECG or K  6
Hypokalemia on presentation is an ominous sign; beware of arrhythmias

94. Potassium Usually add 20 mEq KCl and 20 mEq of KPhos per liter to IVFs
Some centers prefer Kacetate instead of Kphos for theoretical improvement of acidosis
If even mildly hypokalemic, add 40 mEq KCl and 20 mEq of Kphos per liter. Consider K run(s) if hypokalemic.
If serum K <3, hold insulin until K has been added to IVFs

95. Phosphate Body Phosphate is depleted in DKA
Need for replacement is controversial
Phosphate should be given if there has been prolonged illness or if a prolonged period without food is anticipate
Can give half of K requirement as KPhos
If Phos <3, give half of K requirement as Kphos
If hypocalcemia develops, stop Phos and adjust total K as KCl

96. Bicarbonate: Don’t Do It!
May be given if pH < considering that severe acidosis can be life-threatening, but…
Sudden correction of serum pH can paradoxically lower CSF pH, it should be given by slow IV infusion over several hours
Endogenous production of HCO3 occurs as ketones are metabolized
The usual calculations for correction of acidosis greatly overestimate bicarbonate needed in DKA
May increase the risk of hypokalemia
Bicarb use has been associated with increased risk of cerebral edema*
*Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344:

97. Insulin
Goal is to decrease blood sugar by mg/dl/hr, after initial drop from rehydration, avoiding rapid drops
Usual starting dose is 0.1 u/kg/hr (100 units in 500 cc NS, 0.1 u/kg/hr=0.5ml/kg/hr)
Consider starting at 0.05 u/kg/hr if new diabetic, age < 2 yrs, marked hyperglycemia (>1200), or recent large SQ insulin dose in known diabetic

98. Insulin (continued)
If poor response on 0.1 u/kg/hr (e.g. insulin resistance, ongoing infection), may need to increase drip to u/kg/hr, but first make sure IV is infusing properly.
Continue insulin infusion until ketonemia is cleared/clearing. Adjust rate of drip to maintain blood glucose Do not decrease drip below u/kg/hr. If pt is becoming hypoglycemic at this rate, increase dextrose concentration.

99. Glucose
Add D5W to IVF when glucose drops below mg/dl. If necessary, may further increase dextrose concentration to D7.5 - D10.
Consider “2 Bag System” *: One bag NS/0.45NS & 2nd bag D10 NS/0.45NS given simultaneously to vary dextrose concentration while maintaining constant fluid and electrolyte adminstration.
More cost-effective than single bag system
Monitor glucose hourly either by fingerstick (if within range of the meter) or by grey top glucose.
*Grimberg A, Cerri R, Satin-Smith M, et al. The "two bag system" for variable intravenous dextrose and fluid administration: benefits in diabetic ketoacidosis management. J Pediatr. 1999;134:376-3

100. Other
If patient is not improving, reevaluate IVF calculation, insulin delivery system and dose, change insulin bag, consider sepsis and antibiotics.

101. Risks Factors for Cerebral Edema
New Onset DKA (OR-2.9) and Younger
Higher blood urea nitrogen concentrations
Presenting with greater hypocapnia (↓PCO2)
A lesser rise in the measured serum sodium concentration during treatment (as the serum glucose concentration falls)
Bicarbonate administration
No association found for rate of infusion, volume, rate of change of glucose or sodium concentrations
Edge JA, Hawkins MM, Winter DL, Dunger DB. The risk and outcome of cerebral oedema developing during diabetic ketoacidosis. Arch Dis Child. 2001;85:16-22.
Glaser N et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344:
Mahoney C, Vlcek B, DelAguila M. Risk factors for developing brain herniation during diabetic ketoacidosis. Pediatr Neurol. 1999;21:

102. Signs & Symptoms of Cerebral Edema during DKA Treatment
Most commonly occurs in the first 24 hrs (5-15 hrs) after starting rehydration therapy when the child may seem to be improving
Does occur prior to treatment in 5% of cerebral edema
Headache-most often sudden, severe
Altered Mental Status--agitation, combativeness, disorientation, increased drowsiness, incontinence
Focal Neurologic Signs-cranial nerve palsies, opthalmoplegia, posturing
Papilledema, seizures, resp arrest are late signs with a very poor prognosis

103. Signs & Symptoms of Cerebral Edema during DKA Treatment
pupillary changes (asymmetry, sluggish to fixed)
change in VS: hypertension or hypotension, tachycardia, bradycardia, or arrhythmia, apnea, gasping, decr 02 sat
falling corrected Na
must exclude hypoglycemia as a cause of the symptoms before instituting therapy

105. Cerebral Edema Treatment
Mannitol should be immediately available during DKA treatment
Exclude hypoglycemia
Mannitol 1 g/kg IV over 20 minutes
Cut IVF rate in half until situation improves
NGT in vomiting child with impaired LOC
Elevate head
Consider intubation/hyperventilation
But, has been associated with poorer outcome*
Consider continuous mannitol infusion
Head imaging (CT/Eyeball US) after stabilized as hemorrhage, thrombus, or infarct may also occur
*Marcin J, Glaser N, Barnett P, et al. Clinical and therapeutic factors associated with adverse outcomes in children with DKA-related cerebral edema. J Pediatr. 2003;141:

106. Other Complications to Watch For:
Pulmonary Edema
CNS hemorrhage or thrombosis
Other large vessel thrombosis (femoral catheter)
Pancreatitis (salivary amylase elevated; check lipase)
Renal Failure
Intestinal necrosis
Rhinocerebral Mucormycosis

107. Special Thanks to
Jim Tsung, MD – New York University, School of Medicine , Bellevue Hospital for this presentation