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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.

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Presentation on theme: "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."— Presentation transcript:

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 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

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

7 Asthma

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

9 Asthma: Pathophysiology Bronchospasm Bronchial EdemaIncreased Mucus Production

10 Asthma: Pathophysiology

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

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

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

26 Asthma: Management Avoid Sedatives 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 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 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

51 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 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 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: 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: 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: 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 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 Moderate 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 2 0 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/18 + 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 4 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 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 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 0.03 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 & 2 nd 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 ( ↓ PCO 2 ) 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: 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 0 2 sat falling corrected Na must exclude hypoglycemia as a cause of the symptoms before instituting therapy

104

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


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