Case Management Richard Lirio, M.D. PGY-3 & Rachel Gast, M.D PGY-3 26th January 2010 November Cases HV GS 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 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: HEENT: 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 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: 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 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 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 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 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 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 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 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 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 Meds NKDA Imm G&D Family hx Soc hx 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 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 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 To discuss the Epidemiology of H. influenzae 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 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 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 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 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 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.” 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 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 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.