Case Management Richard Lirio, M.D. PGY-3 & Rachel Gast, M.D PGY-3 26 th January 2010.
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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.
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