Transcript Case Management - LifeBridge Health

Case Management
Richard Lirio, M.D. PGY-3
&
Rachel Gast, M.D PGY-3
26th January 2010
November Cases
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HV
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GS
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SD
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
17 yo with cranipharyngioma with distal R index
finger amputation transferred to Union Memorial
Hand Trauma Center
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
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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
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AF, HR 84, RR 24, BP 157/85
GCS 15 on arrival – C/O HA; noted to have
amnesia to event
Physical Examination
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Neuro:
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HEENT:
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Chest:
CV:
Abdo:
MS:
Skin:
GCS 15; Awake & oriented to person and
time, but not to place. Normal sensation;
Motor strength 5/5 throughout; CN intact
Left TM perforated with blood;
Oropharynx clear; EOMI; PERRLA;
Trachea midline; C-collar in place
CTAB; good Air Entry throughout;
S1S2, RRR, no murmur
Normal
No deformities or swelling of extremities
No apparent abrasions or lacerations
Imaging
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Head CT:
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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:
12hr Head CT:
~24hr Head CT:
Showed evolutionary
changes of b/l frontal
& temporal lobes,
hemorrhagic
contusions & stable
epidural hematoma
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
Stable traumatic
brain injury;
Unchanged epidural
hematoma,
hemorrhagic
contusions
w/minimal midline
shift, stable
pneumocephalus;
ventricles unchanged
in size &
configuration
Outside Hospital Course
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Throughout stay
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Afebrile
Vital signs stable, on RA
HD #2
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Noted to act more agitated – thought to be
appropriate for his injuries
Tolerating mechanical soft diet
Cleared to go to rehabilitation facility
On Transfer
BMP
CBC
138
103
7
152
3.8
25
.76
9.6
PE:
Neuro:
HEENT:
Chest:
Abdo:
Ext:
Skin:
14.1
13.6
41.8
Obese adolescent, sleeping, difficult to arouse.
Withdraws from pain; does not follow commands
Head normocephalic, atraumatic,PERRLA, Oropharynx clear, C-collar
CTAB. RRR.
Soft, obese, +BS
Full ROM. 3-4/5 strength throughout
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
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To
To
To
To
discuss
discuss
discuss
discuss
Traumatic Brain Injury
Trauma Scores
when to image in TBI
CT surveillance in TBI
Traumatic Brain Injury
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Head injury is common in children
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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
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Glasgow Coma Scale
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Mild (GCS 13-15)
Moderate (GCS 9-12)
Severe (GCS <9)
Peds Trauma Score
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Combines parameters of:
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Weight
Airway
SBP
CNS
Skin
Skeletal system
Revised Trauma Score
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RR
SBP
GCS
Types of Brain Injury
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Diffuse brain injury
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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
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Result of tissue shearing of grey & white matter
Types of Brain Injury
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Focal injuries
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Brain contusions (accel/decel; coup/contrecoup)
Intracranial haemorrhage (from either blunt or
penetrating trauma)
Epidural, subdural, or subarachnoid haemorrhages
usually occur from blunt trauma
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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
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2 phases
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Initial – direct injury to brain parenchyma
Secondary – resulting from biochemical, cellular, &
metabolic responses  hypoxia, hypotension
Cerebral swelling peaks 24-72 hours after
initial injury
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Resulting in decreased cerebral perfusion more
ischemia, swelling, herniation, death
Cyt
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
Evaluation
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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
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National Institute of Health & Clinical
Excellence (NICE):
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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
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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)
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Retrospective cohort study
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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
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In light of pt’s hx
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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
Bibliography
Krug et al. The global burden of injuries. Am J Public Health 2000;90:523
Langlois et al. Traumatic brain injury in the US: ED visits, hospitalizations, & deaths. Atlanta
(GA): CDC&P, Nat’l Center for Prevention & Control;2006
Schneier et al. Incidence of pediatric traumatic brain injury & associated hospital resource
utilization in the US. Pediatrics 2006;118:483
Dunning et al. The implications of NICE guidelines on the management of children presenting
with head injury. Arch Dis Child 2004; 89:763
Mayer et al. Causes of morbidity & mortality in severe pediatric trauma. JAMA 1981; 245:719
Mayer et al. The modified injury severity scale in pediatric multiple trauma patients. J Pediatr
Surg 1980; 15:719
Langlois et al. The incidence of traumatic brain injury among children in the US:differences by
race. J Head Trauma Rehabil 2005;20:229
Walker et al. Modern approaches to Pediatric Brain Injury Therapy. Journal of Trauma, Injury,
Infection, & Crit Care. 67,2:S120-127
Martin et al. Pediatric traumatic brain injury: an update of research to understand and improve
outcomes. Curr Opin Pediatr. 2008. 20:294-299
Chung et al. Critical score of GCS for pediatric traumatic brain injury. Ped Neurol 2006. 34;379387
Durham et al. Utility of serial computed tomography imaging in pediatric patients with head
trauma. J Neurosurg (5 Suppl Pediatrics) 105:365-369. 2006
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D.V. 8 month old female
Transferred from G.B.M.C. to Sinai
Pediatric Ward on 12/17/09
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Bacteremia
Fever
Refusing to bear weight on right leg
l
12/14
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Fever for 4 days
Seen by PMD and placed on Amoxicillin for O.M.
12/15
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Increasingly febrile and irritable
Emesis
Taken to G.B.M.C.; partial septic work-up
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WBC = 22
CXR = normal
Blood culture done, Ceftriaxone
12/16
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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
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Birth hx
Meds
NKDA
Imm
G&D
Family hx
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Soc hx
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FT, SVD, Breastfed
No medications
No immunizations
Appropriate
Older sister (3 y.o.) with
seizure activity after vaccination
(fully Hib immunized); older brother
(2 y.o.) cried for 6 hours after
vaccination
Lives with parents and siblings, no
smokers, no daycare
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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
113
8.8
139
105
5
3.8
21
0.2
490
19.5
26.8
N = 55; Bands = 12; L = 27; M = 3
MCV = 80
CRP = 13.8
CSF = Negative Gram Stain,
Glu = 72; Pro = 12;
WBC = 1, RBC = 2
Bacterial Antigen test negative
Blood Culture (12/15) = H. Influenzae
Blood culture (12/16) = No growth
Albumin = 3.5
Protein = 6.3
Alk Phos = 114
AST = 32
ALT = 17
Total Bilirubin = 0.4
ICa = 5.01
9.6
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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
nd dose
 Hib vaccine 1 month post discharge and 2
after 1 year of age
Neurology
 No evidence of radiculopathy related to spinal tap
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To discuss the Epidemiology of H.
influenzae
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To discuss
To discuss
To discuss
To discuss
refusal
the different vaccine types
the efficacy of vaccines
Herd immunity
AAP guidelines for vaccine
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
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6 serotypes a – f based on polysaccharide capsule
Responsible for invasive disease
 Bacteremia
 Meningitis
 Pneumonia
 Epiglottitis
 Septic arthritis
 Cellulitis
 Pericarditis
 Endocarditis
Non-encapsulated or nontypeable
Mucosal disease
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Sinusitis
Otitis media
Bronchitis
Pneumonia
Conjunctivitis
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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
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1985
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Hib capsular polysaccharide –
polyribosyl-ribitol phosphate (PRP)
Licensed for children 18-59 months
Efficacy 41-88%
Ineffective in infants 3-17 months
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Did not activate T-cell response
Limited, short antibody response
1987-1989
PRP – protein conjugate
PRP – T
HbOC
: Hib and tetanus conjugate
: Hib and diphtheria CRM197
conjugate
PRP – OMP : Hib and meningococcal conjugate
Licensed 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
1993
Incidence of Hib invasive disease declined > 95%
1995
>90% of infants in US were covered by vaccine
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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.
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Prior to vaccine, carriage at 2-5% of
healthy pre-school and school aged
children
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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
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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 vaccine
Lack of knowledge
Low priority
Religious/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.”
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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.
2.
3.
Parents are free to make choices regarding
medical care unless those choices place their
child at substantial risk of serious harm
Restrictions may be placed upon individual
choices when there is a potential threat to
the community as a whole
Continued refusal after adequate discussion
should be respected unless the child is put at
significant risk of serious harm
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WBC – 19 → 16.8 → 12.2
Platelets – 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
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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.
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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.