Case Management

Richard Lirio, M.D. PGY-3&

Rachel Gast, M.D PGY-326th January 2010

November Cases HV 15 yo with R distal femoral metastatic,

progressive, recurrent Osteosarcoma with cranial mets causing uncal herniation with RF died upon extubation after a DNR was initiated

GS 17 yo with cranipharyngioma with distal R index finger amputation transferred to Union Memorial Hand Trauma Center

SD 5 mo ex-27 week infant with RF ,vent dependant after viral illness with severe subglotttic stenosis, transferred to UM for tracheostomy after failure of steroids

History P.S. 16 y/o healthy Hispanic male Sustained head trauma from fall from

the back of a car while riding/jumping a skateboard w/o a helmet

Report of + LOC and seizure like activity Emesis x 2 Arrived at outside hospital as trauma

AF, HR 84, RR 24, BP 157/85 GCS 15 on arrival – C/O HA; noted to have

amnesia to event

Physical Examination Neuro: GCS 15; Awake & oriented to person

and time, but not to place. Normal sensation; Motor strength 5/5 throughout; CN intact

HEENT: Left TM perforated with blood; Oropharynx clear; EOMI;

PERRLA; Trachea midline; C-collar in place

Chest: CTAB; good Air Entry throughout; CV: S1S2, RRR, no murmur Abdo: Normal MS: No deformities or swelling of extremities Skin: No apparent abrasions or lacerations

Imaging Head CT:

Diffuse cerebral edema Multiple hemorrhagic contusions of frontal lobes Small subarachnoid hemorrhage in b/l cerebral hemispheres Small epidural hematoma over L occipital bone Pneumocephalus in occipital area Fracture L petrous temporal bone

C-spine CT: No fracture or dislocation or vessel injury CXR : No pneumothorax or parenchymal injury Pelvic XR : No fracture Chest, Abdo, Pelvic CT – No evidence of trauma

Outside Hospital Course

6hr Head CT:Showed evolutionary changes of b/l frontal & temporal lobes, hemorrhagic contusions & stable epidural hematoma

12hr Head CT:No significant change of subarachnoid & hemorrhagic contusions; stable L occipital lobe epidural hematoma; did show slight interval re-expansion of the lateral ventricles with persistent mass effect – 3rd & 4th ventricles were still effaced

~24hr Head CT:Stable traumatic brain injury; Unchanged epidural hematoma, hemorrhagic contusions w/minimal midline shift, stable pneumocephalus; ventricles unchanged in size & configuration

Outside Hospital Course Throughout stay

Afebrile Vital signs stable, on RA

HD #2 Noted to act more agitated – thought

to be appropriate for his injuries Tolerating mechanical soft diet Cleared to go to rehabilitation facility

On TransferBMP CBC

138

3.8

10325

7

.76

1529.6

13.6

14.1

41.8PE: Obese adolescent, sleeping, difficult to arouse.

Neuro: Withdraws from pain; does not follow commandsHEENT: Head normocephalic, atraumatic,PERRLA, Oropharynx clear, C-collar Chest: CTAB. RRR.Abdo: Soft, obese, +BSExt: Full ROM. 3-4/5 strength throughoutSkin: Minor L shoulder abrasions noted – otherwise normal

~4h s/p arrival – increasing irritability noted; Oxycodone given<12 hours s/p transfer Cardiac Arrest Sinai ED Died

Objectives

To discuss Traumatic Brain Injury To discuss Trauma Scores To discuss when to image in TBI To discuss CT surveillance in TBI

Traumatic Brain Injury Head injury is common in children

TBI = Most Common Cause of death & disability in childhood (Krug et al & Luerrson et al)

CDC estimates ~475,000 ER visits for TBI’s in 0-14 y/o (2006)

Schneier et al (2006) noted in 2000, ~50,000 children </= 17y/o hospitalized for TBI

Dunning et al (2004) noted 98% of children presenting to the ED with head injuries had a GCS of 15

However, 2 studies in the 1980s by Mayer et al note that ~75% of children with multiple trauma have TBI & almost 80% of all trauma deaths are associated with TBI

Langlois et al estimates overall mortality among children with TBI is ~4.5% (vs. 10.4% among adults)

Definitions Glasgow Coma Scale

Mild (GCS 13-15) Moderate (GCS 9-12) Severe (GCS <9)

Peds Trauma Score Combines parameters

of: Weight Airway SBP CNS Skin Skeletal system

Revised Trauma Score RR SBP GCS

Types of Brain Injury

Diffuse brain injury MC type of severe brain injury in children Usually produced by accel/decel forces Concussions – mildest form of DBI Diffuse axonal injury – more severe form

Result of tissue shearing of grey & white matter

Types of Brain Injury Focal injuries

Brain contusions (accel/decel; coup/contrecoup)

Intracranial haemorrhage (from either blunt or penetrating trauma)

Epidural, subdural, or subarachnoid haemorrhages usually occur from blunt trauma

Subdural & subarachnoid haemorrhages usually occur secondary to severe trauma;associated with other intracranial injuries

Chung et al noted CT findings of swelling/edema, subdural, & intracerebral haemorrhage worse outcomes; while subarachnoid & epidural haemorrhages better outcomes

Pathophysiology of TBI 2 phases

Initial – direct injury to brain parenchyma Secondary – resulting from biochemical,

cellular, & metabolic responses hypoxia, hypotension

Cerebral swelling peaks 24-72 hours after initial injury Resulting in decreased cerebral perfusion

more ischemia, swelling, herniation, death

Timing in days of cytokine production, cerebral edema, scar formation, and delayed cell death after TBI. Walker et al Walker et al.. Journal of Trauma, Injury, Infection, & Crit Care. 67,2:S120-127

Cyt

Evaluation Hx: prolonged LOC, persistent

vomiting, severe HA PE: VS (hypoxic? hypotensive?

abnormal breathing?), C-spine; open wounds; Neurological status

Labs: Hct, Type & screen, Lytes, US Imaging: CT-head (moderate to

severe TBI)

Imaging

National Institute of Health & Clinical Excellence (NICE): GCS <13 at any point since injury GCS 13 or 14 at 2h s/p injury >1 vomiting episode

Dunning et al. The implications of NICE guidelines on the management of children presenting with head injury. Arch Dis Child 2004; 89:763

Issues No widely recognized protocol currently exists to

address the recommended interval or duration of CT surveillance

Increasing public concern about radiation exposure in pediatric patients during CT imaging

In numerous studies, a common conclusion noted that despite CT-documented progression of a traumatic intracranial lesion, the decision to undertake delayed neurosurgical intervention is typically based on changes in the patient’s clinical status rather than neuroimaging findings

Durham et al (2006) Retrospective cohort study

268 patients at Level 1 Trauma Center <18 y/o who underwent repeated Head CT scanning within 24h of their initial Head CT

In 61 of the 214 pts with abnormal findings on initial CT progression was noted

Pts with epidural hematoma, subdural hematoma, cerebral edema & intraparenchymal hemorrhage found to be at a significantly increased risk for progression & to require delayed neurosurgical intervention

No significantly increased risk for pts w/ subarachnoid hemorrhage, intraventricular hemorrhage, diffuse axonal injury, or skull fracture (if no clinical deterioration)

Durham et al. Utility of serial computed tomography imaging in pediatric patients with head trauma. J Neurosurg (5 Suppl Pediatrics) 105:365-369. 2006

Recommendations In light of pt’s hx

LOC Emesis x2 Diffuse cerebral edema Epidural hematoma Hemorrhagic contusions Slight mass effect ? irritability (pain??)

Longer observation at trauma center probably would have been beneficial to the patient – to at least encompass the 72 hour period of maximal cerebral edema

BibliographyKrug et al. The global burden of injuries. Am J Public Health 2000;90:523Langlois et al. Traumatic brain injury in the US: ED visits, hospitalizations, & deaths.

Atlanta (GA): CDC&P, Nat’l Center for Prevention & Control;2006Schneier et al. Incidence of pediatric traumatic brain injury & associated hospital

resource utilization in the US. Pediatrics 2006;118:483Dunning et al. The implications of NICE guidelines on the management of children

presenting with head injury. Arch Dis Child 2004; 89:763Mayer et al. Causes of morbidity & mortality in severe pediatric trauma. JAMA 1981;

245:719Mayer et al. The modified injury severity scale in pediatric multiple trauma patients.

J Pediatr Surg 1980; 15:719Langlois et al. The incidence of traumatic brain injury among children in the

US:differences by race. J Head Trauma Rehabil 2005;20:229Walker et al. Modern approaches to Pediatric Brain Injury Therapy. Journal of

Trauma, Injury, Infection, & Crit Care. 67,2:S120-127Martin et al. Pediatric traumatic brain injury: an update of research to understand

and improve outcomes. Curr Opin Pediatr. 2008. 20:294-299Chung et al. Critical score of GCS for pediatric traumatic brain injury. Ped Neurol

2006. 34;379-387Durham et al. Utility of serial computed tomography imaging in pediatric patients

with head trauma. J Neurosurg (5 Suppl Pediatrics) 105:365-369. 2006

D.V. 8 month old female Transferred from G.B.M.C. to Sinai

Pediatric Ward on 12/17/09 Bacteremia Fever Refusing to bear weight on right leg

l

12/14 Fever for 4 days Seen by PMD and placed on Amoxicillin for O.M.

12/15 Increasingly febrile and irritable Emesis Taken to G.B.M.C.; partial septic work-up

WBC = 22 CXR = normal Blood culture done, Ceftriaxone

12/16 Continued fever Blood culture grew out gram negative coccobacillus; mom called

and child admitted to G.B.M.C. Ceftriaxone, Vancomycin x 3 Repeated blood culture Spinal tap with 1 WBC, latex antigen negative for H. influenza

Birth hx FT, SVD, Breastfed Meds No medications NKDA Imm No immunizations G & D Appropriate Family hx Older sister (3 y.o.) with

seizure activity after vaccination (fully Hib immunized); older brother (2 y.o.) cried for 6 hours after

vaccination Soc hx Lives with parents and siblings,

no smokers, no daycare

VS: T 38.5 (R), HR 159, RR 44, O2 Sat 100% on RA

H : 73 cm (95th%) Wt: 8.9 Kg (75-90th%) HC: 45 cm (75-90th%) General: Well-hydrated, irritable but

consolable Normal PE except…

Held right knee flexed; refused to bear weight; no erythema or swelling; “When completely distracted, allowed passive movement of leg.”

Transferred to Sinai for Orthopedic consult

19.5

8.8490

26.8

N = 55; Bands = 12; L = 27; M = 3MCV = 80

113

9.6 21 0.23.

8

139 105 5

Albumin = 3.5Protein = 6.3Alk Phos = 114AST = 32ALT = 17Total Bilirubin = 0.4ICa = 5.01

CRP = 13.8CSF = Negative Gram Stain, Glu = 72; Pro = 12; WBC = 1, RBC = 2 Bacterial Antigen test negativeBlood Culture (12/15) = H. InfluenzaeBlood culture (12/16) = No growth

Orthopedics Possible transient synovitis Imaging – normal Motrin/Toradol

I.D. Leg – muscular soreness 2/2 fighting LP 72 hours meningitic dose of Ceftriaxone 7-10 days parenteral antibiotics Prophylactic Rifampin for all household members Hib vaccine 1 month post discharge and 2nd dose

after 1 year of age Neurology

No evidence of radiculopathy related to spinal tap

To discuss the Epidemiology of H. influenzae

To discuss the different vaccine types

To discuss the efficacy of vaccines To discuss Herd immunity To discuss AAP guidelines for

vaccine refusal

•Gram negative coccobacilli•Non-motile•Facultative anaerobe•Requires 2 erythrocyte factors for growth that are released following RBC lysis:

• Hemin• NAD

•Carried in nasopharynx of humans (only natural host)•Colonization occurs by age 5

Encapsulated Strains

6 serotypes a – f based on polysaccharide capsule

Responsible for invasive disease Bacteremia Meningitis Pneumonia Epiglottitis Septic arthritis Cellulitis Pericarditis Endocarditis

Non-encapsulated or non-typeable

Mucosal disease Sinusitis Otitis media Bronchitis Pneumonia Conjunctivitis

Responsible for 95% of invasive disease – 3 million cases annually worldwide

400,000 deaths from pneumonia or meningitis Leading cause of meningitis in US and

worldwide 1 in 200 children developed invasive disease

prior to age 5 60% had meningitis 5% mortality rate Permanent sequelae in 20-30%, ranging from

mild hearing loss to mental retardation

1985 Hib capsular polysaccharide – polyribosyl-ribitol phosphate (PRP) Licensed for children 18-59 months Efficacy 41-88% Ineffective in infants 3-17 months

Did not activate T-cell response Limited, short antibody response

1987-1989

PRP – protein conjugate

PRP – T : Hib and tetanus conjugateHbOC : Hib and diphtheria CRM197

conjugatePRP – OMP : Hib and meningococcal

conjugateLicensed for infants as young as 2 months

Schedule = 2, 4, 6 and 12-15 months Carrier protein processed internally by Β cells;

peptides presented to T cells

1993Incidence of Hib invasive disease declined > 95%

1995>90% of infants in US were covered by vaccine

Occurs if transmitters – individuals or cohorts who have high rate of colonization and transmit the organism to susceptible individuals – are immunized so that they no longer acquire the organism themselves and cannot drive transmission in the population

Vaccines serve to reduce oropharyngeal carriage in immunized infants and young children as well as their unimmunized siblings

Moulton, Lawrence H., et al. Estimation of the indirect effect of haemophilus influenzae type b conjugate vaccine in an american indian population. International Journal of Epidemiology, 2000; 29: 753-756.

Prior to vaccine, carriage at 2-5% of healthy pre-school and school aged children Lower rates among infants and adults

Non-typeable H. influenzae considered part of normal respiratory flora in 60-90% of healthy children

30% Navajo children <2 years received one or more doses of Hib-OMPC → 50% reduction in Hib invasive disease

50% immunized → reduction > 70%

General US population – Hib disease declined in infants <12 months prior to conjugate vaccines; presuming immunization at 15-18 months resulted in herd immunity

Prior to vaccine: Alaskan natives with highest annual

incidence of invasive Hib; > 400/100,000 Hib carriers had higher anti-PRP IgG and

IgM concentrations than noncarrier controls

Cases continue to occur in children < 5 at 5.6/100,000 exceeding 2003 US rate of 0.2/100,000

Prevalance of carriage in the Amish communities was similar to pre-vaccination carriage surveys in the US

Incidence of Hib also similar to that of pre-vaccine era

Resistance to vaccineLack of knowledgeLow priorityReligious/philosophical objections

“Despite striking decline in Hib disease incidence in the United States, the disease persists at low levels several years after the initial decline.”

Coverage with the Hib vaccine decreased nearly 2 percent from the 2007 level but, at 90.9 percent, was still above the Healthy People 2010 goal

The CDC attributed the decrease to a shortage of the vaccine that began in December 2007 and that led to a temporary recommendation to defer the booster dose

Vaccines

1905 – U.S. Supreme Court – Jacobson v. Massachusetts

Endorsed the rights of states to pass and enforce compulsory vaccination laws

The Court decided that the freedom of the individual must sometimes be subordinated to the common welfare

When Parents Refuse Vaccines: AAP Guidelines

1. Parents are free to make choices regarding medical care unless those choices place their child at substantial risk of serious harm

2. Restrictions may be placed upon individual choices when there is a potential threat to the community as a whole

3. Continued refusal after adequate discussion should be respected unless the child is put at significant risk of serious harm

WBC – 19 → 16.8 → 12.2Platelets – 484 → 1,012 → 903

CRP - >100 → 86 → 4.15 SED - 80 → 55 All cultures performed at Sinai =

negative Ceftriaxone x 10 days; 3 days at

meningitic dose, 7 days at 75 mg/kg Parents and 2 older siblings received

prophylactic Rifampin, 20 mg/kg, x 4 days

Adams, William G., et al. Decline of childhood haemophilus influenzae type b disease in the hib vaccine era. JAMA, January 13, 1993 – Vol 269, No. 2.

CDC “Haemophilus b Conjugate Vaccines for Prevention of Haemophilus influenzae Type b Disease Among Infants and Children Two Months of Age and Older Recommendations of the ACIP” January 11th, 1991. http://www.cdc.gov/mmwr/preview/mmwrhtml/00041736.htm

Pollard, Andrew J., Maintaining protection against invasive bacteria with protein-polysaccharide conjugate vaccines. Nature Reviews/Immunology Volume 9 March 2009.

Moulton, Lawrence H., et al. Estimation of the indirect effect of haemophilus influenzae type b conjugate vaccine in an american indian population. International Journal of Epidemiology, 2000; 29: 753-756.

Zhou, Fangjun, et al. Impact of universal haemophilus influenzae type b vaccination starting at 2 months of age in the united states: an economic analysis. Pediatrics Vol. 110 No. 4 October 2002.

Danovaro-Holliday, M. Carolina, et al. Progress in vaccination against haemophilus inflenzae type b in the americas. PLoS Medicine April 2008, Volume 5, Issue 4.

Jafari, Hamid S., et al. Efficacy of haemophilus influenzae type b conjugate vaccines and persistence of disease in disadvantaged populations. American Journal of Public Health, March 1999, Vol. 89, No. 3.

Lipsitch, M. Bacterial vaccines and serotype replacement: lessons from haemophilus influenzae and prospects for streptococcus pneumoniae. Emerging Infectious Diseases, May 1999.

Baggett, Henry C., et al. Immunologic response to haemophilus influenzae type b hib conjugate vaccine and risk factors for carriage among hib carriers and noncarriers in southwestern alaska. Clinical and Vaccine Immunology, June 2006, p. 620-626.

Fry, Alicia M., et al. Haemophilus influenzae type b disease among amish children in pennsylvania: reasons for persistent disease.