Transcript 15 year-old Hispanic male with dizziness and neck pain for 3 days

Problem Rounds
August 31, 2006
15 year-old Hispanic male with dizziness
and neck pain for 3 days
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.
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.
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.
Take a moment
to consider your differential diagnosis
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
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.
Peds ER:
VS @ 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, uncomfortableappearing, 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
Labs ER:
Peds
Patient was started on NS@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.
136 96 7 101
4.4 27 0.6
CRP 23.7 Ca 9.3 Mg 2.4 Phos 4.4 UA 3.3
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
Take a moment
to consider your differential diagnosis
CT
CT
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
Take a moment
to consider your differential diagnosis
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 @ LLSB; good pulses, cap refill
Lungs: CTAB, good air movement
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
Take a moment
to consider your differential diagnosis
PICU Assessment/Plan:
1. 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
MRI
MRI
MRV
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 HD#5 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.
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 HD#10
• 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.
Hospital Course:
•On HD#10, pt with microscopic hematuria and flank pain.
Abdominal US done, showing b/l stones. Renal service signed on.
CT A/P done on HD#11 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
Otogenic Intracranial Complications:
•Otitis media (acute > 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%).
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
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.
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
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.
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 heparincoumadin.
•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.
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)
References:
• Bradley DT, Hashisaki GT, Mason JC. Otogenic sigmoid sinus
thrombosis: what is the role of anticoagulation? Laryngoscope. 2002
Oct;112(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
Aug;46(8):514-9.
•Migirov L, Duvdevani S, Kronenberg J. Otogenic intracranial
complications: a review of 28 cases. Acta Otolaryngol. 2005
Aug;125(8):819-22.
References:
•Reuner KH, Ruf A, Grau A, Rickmann H, Stolz E, Juttler E,
Druschky KF, Patscheke H. Prothrombin gene G20210-->A transition
is a risk factor for cerebral venous thrombosis.
Stroke. 1998 Sep;29(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
Mar;11(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 Mar;27(2):155-9.