Problem Rounds

1
Problem Rounds August 31, 2006
15 year-old Hispanic male with dizziness and
neck pain for 3 days
2
CC Dizziness and neck pain x 3 days HPI 15
year-old Hispanic male was in his usual state of
health until 15 days prior to admission, when
patient had severe right ear pain and was brought
to the ER at Hollywood Presbyterian. Per
hospital records, he was diagnosed with R otitis
media, and given amoxicillin, phenergan and
motrin. CBC and UA were sent and showed WBC 15.7
PMN88, L6, M6 Hct 39 Plt 396 UA with pH 5,
SG 1.017, ketones 40 mg/dL, otherwise
negative. 4 days later (11 days PTA), the
patient complained of headache and continued R
ear pain. Mom brought him back to the same
hospital in the early evening. He complained of
pain at his forehead, and at the back of his neck
that worsened with movement. Per mom, a head CT
and lumbar puncture were performed at this time
and were normal.
3
HPI Continued Per hospital record, vital signs
were T 97.6, P50, R24, BP 122/67, SaO2 99 on
RA, pain 8/10. Patient was noted to be in
moderate distress, with a resolving ear
infection. CT head was done, showing bilateral
mastoiditis. LP was performed opening pressure
was 24, with clear CSF showing 1 RBC, 2 WBC (100
monocytes), glucose 59, protein 16.8. Blood
culture and CSF culture showed no growth. He
received Toradol 30 mg, Rocephin 2 g, and Versed
4 g, and was discharged home 5 hours after his
arrival in the ER with a diagnosis of R otitis
media, mastoiditis, and headache (per discharge
papers). No written record could be found
regarding discharge medications or follow-up
care. However, it was noted that treatment and
aftercare were explained to the family.
4
HPI Continued 1 day later (10 days PTA),
patient still had headache. Mom then brought him
to an herbal medicine doctor who said that the
patient did not have an ear infection and did not
need to take any medication. He gave some
natural herbal medicine and vitamins. Mom agreed
with the suggestion and stopped the
antibiotics. The patient continued to have mild
headache, but no ear pain. 3 days PTA, the
patient started to have dizziness and neck pain.
He would not move his neck secondary to the pain.
Mom said he was dizzy with getting up and
walking, so he mostly sat in a chair. He
reported no ear pain, headache, URI, or change in
PO intake. On the day of admission, his older
sister noted that the patient looked ill, had a
tactile fever and was sweating with chills. He
was brought to the Peds ER.
5
Take a moment to consider your differential
diagnosis
6
PMH History of kidney stones diagnosed in Mexico
1 year ago. No h/o any recurrent OM. No h/o
frequent HA. PSH none ALL NKDA Meds
vitamins and herbal meds post-amoxicillin for 10
days and one dose of Rocephin Imm Per card,
needs Hepatitis A 2, hepatitis B 3 last PPD
was 01/2006 and was negative PMD none
7
FH Dad is 44 years old, Mom is 43 years old.
Patient has 3 older siblings and 2 younger
sisters. No family h/o HTN, DM, CA. Older
brother also had renal stones about 1 year
ago. Birth Hx Born in Mexico, full-term, NSVD.
No complications. Social Hx Patient moved to
Los Angeles from Durango, Mexico 8 months ago.
He lives in a 1 bedroom apartment with his
parents, older sister and her husband, and 2
younger sisters. He denies any recent travel,
sick contacts, or visitors in the home. There
are no pets, guns, tobacco, alcohol, or domestic
violence in the home. Patient feels safe at
home. He is in the 9th grade, but does not speak
English yet. He is not employed. He likes to
watch TV, play video games and football. Other
HEADDS exam was negative.
8

• Peds ER
• VS _at_ presentation T 102.8, BP 140/68, P 80, RR
  20,
• SaO2 100 on RA, pain 0/10
• On exam noted to be
• toxic-appearing WDWN, poorly interactive,
  uncomfortable-appearing, holds his neck stiff,
  sweaty and pale
• Red bulging R tympanic membrane with R mastoid
  tenderness, no fluctuance
• PERRL R eye ptosis, and unable to look up and
  laterally on R
• Neck stiff, unable to forward flex/turn head
• Negative Kernig and Brudzinski
• No rash/petechiae
• Grade 1-2/6 systolic murmur over precordium
• Increased tone with clonus normal DTRs slow
  speech

9

• Peds ER
• Patient was started on NS_at_80 cc/hr Tylenol 650
  mg PO Cefotaxime 2g IV decadron 10 mg IV
  Vancomycin 1g IV
• Neurosurgery and ENT were called for
  consultation.
• Labs were drawn and CT head was done.
• 96 7 101 CRP 23.7 Ca 9.3 Mg 2.4
  Phos 4.4 UA 3.3
• 4.4 27 0.6 AP 144 tprot 7.6
  Alb 3.9 CK 71 LDH 302
• AST 255 ALT 412 Tbili 0.5
  Dbili 0.2
• 12.7
• 14.5 406 N80 L8 M13
• 37.8 PT 16.6 PTT 38.3
• UA pH 7.0, SG 1.022, trace prot o/w neg
• VBG 7.4/50/28/30

Labs
10
Take a moment to consider your differential
diagnosis
11
CT
12
CT
13
CT Head R post parietal osteo, mastoiditis,
otitis media, sm fluid in L mastoid air cells
possible thrombosis of R sigmoid sinus. Also,
e/o dural enhancement of the tentorium which may
suggest underlying meningitis. CT Temporal R
mastoiditis with erosion of inner table of bone
and underlying transverse sinus thrombosis fluid
in R middle ear but ossicles intact CT Neck No
abscess seen ?ENT placed right PET and sent
ear drainage for culture
14
Take a moment to consider your differential
diagnosis
15
Physical Exam in PICU Wt 82 kg (90-95) Ht
180 cm (75-90) BMI 25 (90) VS T99, BP
124/62, P61, RR 16, Pain 0/10 Gen Awake,
calm, NAD HEENT NCAT, PERRL Left eye with
left lateral gaze defect with nystagmus No
proptosis, no diplopia Visual acuity 20/200
with card b/l B/l optic disc edema
Left TM normal, R TM bulging/red nl pinnas
b/l. TTP and sl. red at R mastoid but no
fluctuance Nares nl Clear OP with no
lesions, MMM Neck No lymphadenopathy, limitation
of neck movement secondary to pain
at R mastoid CVS Systolic murmur 1-2/6 _at_ LLSB
good pulses, cap refill Lungs CTAB, good air
movement
16
Physical Exam in PICU Abd Soft, obese, NTND,
no HSM, no masses GU Tanner 4, uncircumcised
male with b/l descended testes Ext No
c/c/e Skin No rash Neuro CN showed L lateral
gaze paresis Good tone Normal strength at all
extremities Normal sensation Patellar reflexes
1 b/l No clonus Negative Kernig and Brudzinski
signs Unable to assess gait due to patient
dizziness Pt with slow responses to questions,
but normal orientation
17
Take a moment to consider your differential
diagnosis
18

• PICU Assessment/Plan
• Pt with R acute OM/mastoiditis/osteomyelitis by
  head CT
• s/p myringotomy and PET placement on night of
  admission by ENT Cultures sent
• Pt started on Vancomycin, Cefotaxime, Flagyl IV
• Floxin otic drops to R ear BID
• 2. Pt with R sigmoid sinus thrombosis by CT head
  on DOA
• MRI/MRV was ordered for hospital day 1
• IV Abx started at meningitic dose as could not
  r/o meningitis
• Continue to c/o dizziness ? intracranial process
  (increased ICP from thrombosis) vs ear process as
  explanation
• IVF at 2/3XM
• 3. Pt with transaminitis
• Hepatitis panels sent
• RUQ ultrasound was ordered

19
MRI

20
MRI

21
MRV

22

• Hospital Course
• MRI/MRV showed acute R sigmoid sinus thrombosis
  and transverse sinus thrombosis R otomastoiditis
  with adjacent thickening and enhancement no e/o
  extra-axial (epidural) fluid collection/abscess
• Pt was started on Lovenox on HD 1 for
  thrombosis. Patient continued to have
  neurological findings of increased ICP with
  dizziness, L lateral gaze palsy, worsening visual
  acuity with decreased color perception, and
  unchanged optic disc edema. Started on Decadron
  on HD 3. Lovenox was then discontinued on HD5
  as plan was for therapeutic LP at this time to
  decrease ICP, but parents would not consent.
  Patient was then started on Diamox per Optho
  recs.

23

• Hospital Course
• Pt remained on IV Abx Vancomycin, Cefotaxime,
  and Flagyl. ID was consulted and recommended
  treatment for 6 weeks. PPD was placed and was
  negative. Fluid Cultures from R ear grew out 1
  coag negative Staph and 2 microaerophilic Strep
  Negative AFB smear
• Abdominal US was normal. Hepatitis A, B, and C
  titers were negative EBV and CMV IgM levels were
  negative. AST and ALT levels decreased to 42 and
  205, respectively, by HD10
• Thrombophilia work-up was initiated including
  ANA, antiphospolipid Ab, Factor V Leiden,
  Antithrombin III, Prot C,
• Prot S, and prothrombin III mutation. He was
  found to be a heterozygote for G20210A
  Prothrombin mutation Lovenox was restarted while
  on the ward.

24

• Hospital Course
• On HD10, pt with microscopic hematuria and flank
  pain. Abdominal US done, showing b/l stones.
  Renal service signed on. CT A/P done on HD11
  showing R hydronephrosis with 10 mm stone in
  inferior collecting system and 3.3 mm stone in
  proximal ureter L kidney with moderate renal
  pelvis dilation, 8.5 mm stone in lower collecting
  system

25

• Otogenic Intracranial Complications
• Otitis media (acute gt chronic) can cause a
  variety of intracranial complications, although
  their incidence has been dramatically reduced
  with the use of antibiotics.
• They include meningitis, extradural abscess,
  brain abscess, subdural abscess (empyema),
  sigmoid sinus thrombosis, thrombophlebitis, and
  otitis hydrocephalus.
• Incidence of complications is low in the
  antibiotic era (0.36).

26

• Otogenic Intracranial Complications
• In a retrospective chart review by Migirov et al,
  28 patients developed a complication out of 7792
  patients admitted for OM over 18 year study
  period
• Meningitis 46, brain abscess 21, epidural
  abscess 18 were most common
• Underlying cholesteatoma assoc with thrombosis
  and abscess
• Meningitis had equal frequency in adults and
  children
• Brain abscess 3x more common in adults
• Epidural abscess 2x more common in children
• High morbidity rate (71) related to hearing
  impairment for patients who recovered from
  otogenic complications

27

• Otitic Hydrocephalus
• In the case presentation, the patient was
  unsuccessfully treated for acute OM, which
  progressed to mastoiditis and osteomyelitis, with
  the further complication of R sigmoid and
  transverse sinus thrombosis.
• He also had signs/symptoms of increased ICP,
  including papilledema, headache, gaze palsy, and
  decreasing visual acuity and color perception.
• These signs of increased ICP can be explained by
  otitic hydrocephalus? a non-obstructive
  hydrocephalus that does not demonstrate
  ventricular dilation that occurs as a result of
  decreased venous return secondary to cerebral
  venous thrombosis.

28

• Cerebral Venous Sinus Thrombosis
• In general, the incidence of cerebral venous
  sinus thrombosis is very low in children (0.67
  per 100,000 children/yr)
• In children, CBST is most commonly associated
  with regional infections (OM or mastoiditis) and
  chronic systemic illness (leukemia or its
  treatment, sickle cell)
• According to De Schryver et al, who studied the
  long-term neuropsychological sequelae in 12
  survivors of CBST, all children had average or
  high intelligence scores.
• One had impairment of skilled movement
• 2 had mild cognitive deficits (difficulty with
  written language decreased attention)
• The group concluded that children had a fair
  prognosis, although mild cognitive deficits can
  occur

29

• Role of Anticoagulation for Sinus Thrombosis?
• It is generally accepted that sigmoid sinus
  thrombosis occurring as a complication of OM is
  managed with antibiotics and possible surgical
  drainage
• Literature regarding the recommendations for
  anticoagulation in relation to SST is from
  neurology and hematology patients, who often have
  underlying trauma, neoplasm, autoimmune DO,
  hypercoaguable state, or surgical intervention
  that influences this indication
• Anti-coagulation is considered when there is
  concern for embolization, venous infarction, or
  persistent septic thrombophlebitis.
• Potential risks of anticoagulation include
  bleeding, drug interactions, thrombocytopenia,
  osteoporosis, and hemorrhagic skin necrosis.

30

• Role of Anticoagulation for Sinus Thrombosis?
• In a retrospective review of 9 patients with
  otogenic SST, Bradley et al found that all
  patients were treated with broad spectrum
  antibiotics, 5 were anticoagulated with LMWH, and
  1 with heparin-coumadin.
• HA, otalgia, otorrhea, and imbalance were more
  common in non-anticoagulated group at 6 mo.
• They concluded that thrombus confined to sigmoid
  sinus did not necessarily require
  anticoagulation.
• Criteria to consider use of anticoagulation e/o
  thrombus progression, thrombus extension to
  adjacent sites at presentation, neurological
  changes, persistent fevers, embolic events.

31

• Prothrombin Mutation
• Pt is positive for one copy of the G20210A
  (prothrombin/factorII) mutation
• Per lab report, heterozygotes for this mutation
  are at elevated risk for venous thrombosis. This
  mutation is the 2nd most common inherited risk
  factor for thrombosis. Individuals who have one
  copy of the mutation are 3-6 fold increased risk
  for thrombosis. Other family members may also be
  carriers, and should consider genetic counseling
  and DNA testing to determine their status.
• Studies have shown a higher prevalence of
  prothrombin G20210A mutation in patients with
  cerebral vein thrombosis than healthy controls
  (OR 5.7-10.2)

32

• References
• Bradley DT, Hashisaki GT, Mason JC. Otogenic
  sigmoid sinus thrombosis what is the role of
  anticoagulation? Laryngoscope. 2002
  Oct112(10)1726-9.
• De Schryver EL, Blom I, Braun KP, Kappelle LJ,
  Rinkel GJ, Peters AC, Jennekens-Schinkel
  A.Long-term prognosis of cerebral venous sinus
  thrombosis in childhood. Dev Med Child Neurol.
  2004 Aug46(8)514-9.
• Migirov L, Duvdevani S, Kronenberg J. Otogenic
  intracranial complications a review of 28 cases.
  Acta Otolaryngol. 2005 Aug125(8)819-22.

33

• References
• Reuner KH, Ruf A, Grau A, Rickmann H, Stolz E,
  Juttler E, Druschky KF, Patscheke H. Prothrombin
  gene G20210--gtA transition is a risk factor for
  cerebral venous thrombosis.Stroke. 1998
  Sep29(9)1765-9.
• Sztriha LK, Voros E, Vecsei L. Endovascular
  thrombolytic treatment of extensive dural sinus
  thrombosis in a heterozygous carrier of
  prothrombin gene G20210A mutation. Eur J Neurol.
  2004 Mar11(3)214-5.
• Villa G, Lattere M, Rossi A, Di Pietro P. Acute
  onset of abducens nerve palsy in a child with
  prior history of otitis media a misleading sign
  of Gradenigo syndrome.Brain Dev. 2005
  Mar27(2)155-9.