a “bounceback” with cephalgia: case report
TRANSCRIPT
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Clinical Pathologic Case Competition October 12, 2014
A “Bounceback” with Cephalgia:
Case Report
Neeraja Murali, DO, MPH PGY-3, Mclaren Oakland Hospital
Pontiac, Michigan
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September 23, 2200 hours CC:
Headache
HPI:
20 yo Caucasian female, headache x 8 days
Seen 9/18 and 9/19 for same
Headache improved significantly after second visit
Over past 2 days, headache worsening with inability to eat , new symptoms of photophobia and neck pain
Constant sharp 10/10 pain, band-like distribution
No relief with OTC meds or hydrocodone/acetaminophen
No aggravating or relieving factors
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HPI Continued
Denied new medications, changes in diet, or environmental exposures
Did stop taking oral contraceptives on 9/20/13
G1P1, NSVD occurred ~14 months prior
Lethargic, drifted off mid-sentence, but easily arousable to verbal stimuli
Per mother patient had become confused and lethargic over past two days with increased sleep and decreased activity
Stated patient had stumbled and fallen frequently while ambulating, no head trauma or LOC
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PMH:
IDDM, Fetal Alcohol Syndrome, GERD, pregnancy-associated migraines, pregnancy-associated hypertension
PSH:
Caesarian section (7/2012), Cholecystectomy (2/2013)
All:
NKDA
+ Latex Allergy
Meds:
metoclopromide 10 mg po q 12 h; hydrocodone acetaminophen 5/325 mg po q 4-6 h prn pain; insulin glargine 28 units sq q hs, metformin 1000 mg po q 12 h, simvastatin 40 mg po q hs
FH:
Unknown, patient is adopted
SH:
Never smoker, no alcohol or illicits; engaged, stays home with son
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ROS:
Constitutional: +lethargy, decreased appetite and intake
Eyes: + photophobia and blurred vision
Ear, Nose, Throat: -
Cardiovascular: -
Respiratory: -
Abdominal: + decreased PO intake
Genitourinary: LMP 8/27/13
Musculoskeletal: + neck pain with motion
Integumentary: -
Neuro: + headache and confusion
Psych: -
Endocrine: blood sugars typically 150-250 mg/dL
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Physical Exam
Vitals:
BP 137/84 mmg Hg, P 59 bpm, R 16/min, T 97.4 F, O2 Sat 100%/RA, 63”, 187#, 10/10 pain
General:
Caucasian female, overweight, appears stated age, lethargic but arousable to verbal stimuli
HEENT:
NC/AT, PERRLA, EOMI bilaterally
Fundi with sharp disc margins, no AV nicking or papilledema
NP patent; OP clear with airway intact, dry oral mucosa
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Neck:
Supple, no lymphadenopathy, thryomegaly or bruits
Pain with neck flexion; no Kernig's or Brudzinski's sign
Neuro/Psych:
Slow response to commands, intermittently follows commands based on level of somnolence, easily arousable
Oriented to person, place, month, and year, but not passing of time
CN 2-12 intact, cerebellar function slow but intact by finger-to-finger testing
Moves all extremities spontaneously with normal patellar and brachial reflexes; pinprick sensation intact
Generalized muscle weakness with good tone and 4/5 strength against gravity; no pronator drift
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Respiratory:
Respirations unlabored, lungs CTA in all fields
Cardiovascular:
RRR, S1/S2 noted, no murmurs, clicks, or rubs. 2+/4 distal pulses noted in B/L UE and LE
Abdomen:
Soft, NT/ND, normal bowel sounds; no tympany or organomegaly
Skin:
Intact, warm and dry with good color and turgor; no rashes or lesions
Extremities:
Nontender; normal spontaneous range of motion of all 4 extremities; no edema
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ED Course
After initial interview and exam, prior visits were reviewed and labs and studies were ordered
CBC with diff, BMP, Serum Osm, BCx, lactic acid, ammonia, Liver Enzymes, Coags, EtOH, Tylenol, Salicylates, UA, UDS, Ucx, UHCG, CXR, EKG
Head CT with and without contrast had been performed on 9/19/13 (4 days prior)
Due to worsening headache and lethargy, a lumbar puncture was planned
Risks and benefits of repeat CT before LP explained to patient and mother; declined repeat CT despite being aware of potential concerns
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Image 1. CT Head w/o Contrast, 9/19/13
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Image 2. CT Head w/o Contrast, 9/19/13
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Image 3. CT Head w/ Contrast, 9/19/13
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Image 4. CT Head w/ Contrast, 9/19/13
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ED Course Continued
~2300 hours: labs and results reviewed
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CBC with differential
Result Name Value Ref Range & Units
WBC Count 11.37 4.80-10.80 x 10^3/uL
RBC Count 4.96 4.20-5.40 x 10^6/uL
Hemoglobin 14.9 12.0-16.0 g/dL
Hematocrit 42.8 37.0-47.0%
MCV 86.3 81.0-99.0 FL
MCH 30 27.0-31.0 pg
MCHC 34.8
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Result Name Value Ref Range & Units
Platelet Count 205 150-450 x 10^3/uL
MPV 9.9 6.5-12.0 FL
RDW 12.5 11.0-16.0%
Neuts, Automated 77 36-66%
Lymphs, Automated 12 24-44%
Monos, Automated 11 0-12%
EOS, Automated 0 1-3%
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Result Name Value Ref Range & Units
Basos, Automated 0 0-1%
ABS Neutrophils 8.76 1.73-7.13 x 10^3/uL
ABS Lymphocytes 1.37 1.15-4.75 x 10^3/uL
ABS Monocytes 1.23 0.00-1.29 x 10^3/uL
ABS Eosinophils 0 0.05-0.32 x 10^3/uL
ABS Basophils 0.01 0.00-0.11 x 10^3/uL
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Basic Metabolic Profile
Result Name Value Ref Range & Units
Sodium 138 136-145 mmol/L
Potassium 43 3.5-5.1 mmol/L
Chloride 104 98-107 mmol/L
Carbon Dioxide 17.4 21-32 mmol/L
Anion Gap 16.6 5.0-15.0 mmol/L
BUN 15 7-18 mg/dL
Creatinine 0.9 0.6-1.0 mg/dL
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Result Name Value Ref Range & Units
eGFR (Afr Am) 97 60-240 mL/min
eGFR (non Afr Am) 80 60-240 mL/min
BUN/Creat Ratio 17 6.0-20.0
Glucose 234 65-139 mg/dL
Calcium 8.5 8.5-10.1 mg/dL
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Result Name Value Ref Range & Units
Point of Care Glucose 269 70-130 mg/dL
Ethanol 3 0.00-3.0 mg/dL
Acetaminophen <2.0 0.00-20.00 ug/mL
Salicylates 2.3 0.00-20.0 mg/dL
ALT 33 30-65 U/L
AST 8 15-37 U/L
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Result Name Value Ref Range & Units
Osmolarity 304 275-305 mOsm/L
Prothrombin Time 11.6 10.5-12.9 sec
INR 1 1.00-1.23
Activated PTT 22 25.0-33.0 sec
Venous Lactic Acid 1.9 0.4-2.0 mmol/L
Venous Ammonia 7 11-31 umol/L
Blood Cultures (2) Pending No Growth
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Urinalysis with microscopy
Result Name Value Ref Range & Units
UA Color Red Yellow
UA Appearance Hazy Clear
UA Specific Gravity >=1.030 1.003-1.035
UA PH 6 4.0-8.0
UA Protein 100 Negative
UA Glucose 600 Negative
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Result Name Value Ref Range & Units
UA Ketone >=80 Negative
UA Bilirubin Negative Negative
UA Blood Large Negative
UA Urobilinogen 0.2 0.2-1.0
UA Nitrites Negative Negative
UA Leukocytes Esterase Negative Negative
UA WBCs 0-5 None Seen,0/HPF
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Result Name Value Ref Range & Units
UA RBC >180 None seen,0/HPF
UA Epithelial Cells 0-5 None seen/LPF
UA Bacteria 1 None seen/HPF
UA Mucus None seen None seen/LPF
Urine Culture Pending No growth
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Urine Drug Screen
Result Name Result Cut Off Level
Urine Amphetamine Negative 1000 ng/mL
Urine Benzodiazepne Negative 200 ng/mL
Urine Cocaine Negative 300 ng/mL
Urine Opiates Positive 300 ng/mL
Urine Cannabinoid Negative 50 ng/mL
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Result Name Result Cut Off Level
Urine Phencyclidine Negative 25 ng/ml
Urine Barbiturate Negative 200 ng/ml
Urine Ecstasy Negative 500 ng/ml
Urine Methadone Negative 300 ng/ml
Urine Pregnancy test (Qualitative): Negative
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Image 5. Portable CXR, 9/23/14 2230
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Image 6. EKG, 9/23/13 2245
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ED Course Continued
LP performed in R Lateral decubitus position
Opening pressure 44 cm H2O
~15 ml of clear CSF obtained
Patient instructed to lay flat for 1 hour
Neurology contacted, agreeable with acetazolamide 250 mg po q 12 h
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ED Course Continued
~0000 hours: patient reassessed. Lethargic but arousable, no change in mentation from prior. Pain improved from 10/10 to 7/10
Patient and family agreeable with admission
~0100 hours: LP results available
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CSF Results
Tube 1
Appearance: Clear
Volume: 1.5 mL
Total RBC: 78/mL
Tube 3
Appearance: Clear
Volume: 2 mL
Total RBC: 102/mL
WBC: 0/mL
Result Name Value Ref Range & Units
CSF Culture Pending No growth
CSF Gram Stain No organisms No organisms
CSF Glucose 165 40-70 mg/dL
CSF Total Protein 34.3 15.0-45.0 mg/dL
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ED Course Continued
~0100 hours: patient reassessed and had no further relief of symptoms
Increasingly groggy and difficult to arouse
On repeat exam, pt noted to have profound R hemideficit with inattention and neglect
Localized and withdrew on L; no motor response on R
Able to follow commands on L only
Firm pressure to RUE and RLE nailbed resulted in patient turning head contralaterally and saying “ouch”
~0145 hours: repeat Head CT obtained
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Image 7. CT head w/o contrast, 9/24/13 0200 hours
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Image 8. CT head w/o contrast, 9/24/13 0200 hours
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Image 9. CT head w/o contrast, 9/24/13 0200 hours
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Image 10. CT head w/o contrast, 9/24/13 0200 hours
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ED Course Continued
~0215 hours: CT results communicated to neurology
– Advised MRA/MRV in morning, no other recommendations at this time
~0330 hours: MRI, MRA, MRV of brain obtained emergently.
– No further change in patient's mentation
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Image 11. MRA Circle of Wills w/o Contrast, 9/24/13 0400
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Image 12. MRA Circle of Wills w/o Contrast, 9/24/13 0400
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Image 14. MRV Brain w/o Contrast, 9/24/13 0400
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Image 15. MRV Brain w/o Contrast, 9/24/13 0400
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Image 16. MRV Brain w/o Contrast, 9/24/13 0400
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Image 14. MRV Brain w/o Contrast, 9/24/13 0400
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Image 18. MRI Brain T1 pre-contrast, 9/24/13 0400
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Image 18. MRI Brain T1 post-contrast, 9/24/13 0400
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Image 20. MRI Brain, T2, 9/24/13 0400
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Image 21. MRI Brain, T2, 9/24/13 0400
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Image 23. MRI Brain, Diffusion-Weighted Image, 9/24/13 0400
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Image 24. MRI Brain, ADC Map, 9/24/13 0400
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ED Course Continued
~0615 hours: Patient returned from MRI in stable condition and transported to ICU
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What's the diagnosis?
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Clinical Pathologic Case Competition October 12, 2014
A “Bounceback” with Cephalgia:
Case Solution
Neeraja Murali, DO, MPH PGY-3, Mclaren Oakland Hospital
Pontiac, Michigan
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Final Diagnosis
Cerebral infarction secondary to extensive cerebral venous thrombosis
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Diagnostic Clues
Patient admitted to very recent discontinuation of oral contraceptives
Exogenous estrogen is a well-established risk factor for thrombosis
Noncontrasted head CT from 9/19/13: asymmetric hyperdensity of left transverse sinus without evidence of matching defect on contrasted study (likely hemoconcentration)
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Image 25. Noncontrast Head CT with “cord sign” (thrombosed cortical veins)
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May see “delta sign” on non-contrast CT
Image 26. Contrasted Head CT with “empty delta” sign (fresh clot)
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Continued
Opening pressure on LP 440 mm H2O, well above accepted range of 50-170 mm H2O
Acetazolamide started for intracranial hypertension
Neurologic deterioration led to repeat CT, which showed bilateral subarachnoid hemorrhages and increased attenuation of dural sinuses
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MRI brain
“...increased signal on diffusion-weighted images with associated decreased signal on ADC involving high left frontoparietal and right parietal lobes. There is associated mild T2/FLAIR hyperintensity in these regions. Susceptibility is seen along the superficial veins overlying the bilateral cerebral hemispheres as well as along the straight sinus, superior sagittal sinus, right transverse sinus, left transverse sinus, left sigmoid sinus, and proximal left IJ vein.”
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MRA Circle of Wills
“...intracranial segments of ICA and vertebral arteries are normal in course and caliber. The ACA, CA, and PCA are patent without evidence of occlusion or aneurysmal dilatation.”
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MRV
“...lack of contrast opacification of the superior sagittal, straight, right transverse, left transverse, and left sigmoid sinuses. Lack of contrast opacification of the proximal aspect of the left IJ as well as the superficial veins overlying the bilateral cerebral convexities. Contrast is seen within the right sigmoid sinus and proximal right IJ.
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Continued
Impression:
Extensive cerebral dural venous sinus thrombosis as described above
Diffusion restriction involving the high left frontoparietal and right parietal lobes which may represent ischemia secondary to the cerebral venous sinus thrombosis”
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Epidemiology and Clinical Presentation
Incidence <1.5 per 100000 annually
More often seen in young adults, and more often in men than women
Pathology still not well understood and has a highly variable clinical presentation
Incidence of neurologic findings from 25-71%
2 known mechanisms: thrombosis or occlusion of dural sinuses
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Why the SAH?
Obstruction of venous structures leads to increased venous and capillary pressure
This disrupts BBB and causes vasogenic edema
As pressure continues to increase, hemorrhage can result due to venous or capillary rupture
SSS is the most frequently thrombosed, and presents with infarct in bilateral frontal, parietal, or occipital lobes
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Image 10. CT head w/o contrast, 9/24/13
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Why the ICH?
Dural sinus occlusion also impedes CSF absorption
Arachnoid granulations normally drain CSF into the SSS
With SSS thrombosis, absorption was impaired and thus ICH was seen
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Image 15. MRV brain without contrast lack of high-flow signal = direct sign of thrombus
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Image 17. MRV brain without contrast
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Image 27. Hypointensity at confluens of sinuses on MRI with T2 signal (seen in acute thrombus due to
deoxyhemoglobin)
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Image 28. Heterogenous signal on T2-weighted MRI (hyperintensity from subacute thrombus due to methemoglobin)
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Image 23. MRI Brain, Diffusion-Weighted Image
High signal in areas of ischemia due to cytotoxic or vasogenic edema
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Image 24. MRI Brain, ADC Map
Apparent diffusion coefficient mapping will be reduced in areas of edema and ischemia
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Treatment & Prognosis
Anticoagulation is the first line of therapy
Arrests thrombosis and prevents extension of thrombus via antithrombin activity
In patients with extensive thrombus and deficits, interventional procedures such as thrombectomy and thrombolysis can be used
Clinical trials currently underway comparing these techniques
Overall prognosis is better than previously thought and continues to improve as technology advances
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Our patient
Started on a heparin drip
Seizure like activity was witnessed in ICU
Neurology and neurosurgery recommended antiepileptics and neurointervention
Patient underwent thrombectomy and returned home after several weeks of rehab, later found to have multiple coagulopathies
Continues to be on oral anticoagulation, reports some mild weakness but is able to work and care for family independently
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References Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD, editors.
Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill Medical; 2012.
Ferro JM, Canho P. UpToDate [Internet]. Waltham, MA: UpToDate. 2014. Etiology, clinical features, and diagnosis of cerebral venous thrombosis; [updated 2013 Jan 02; cited 2014 June 09]. Available from http://www.uptodate.com/
Marx J, Hockberger R, Walls R, editors. Rosen's Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philadelphia: Mosby/Elsevier; 2010.
Sahin N, Solak A, Genc B, Bilgic N. Cerebral venous thrombosis as a rare cause of subarachnoid hemorrhage: case report and literature review. Clinical Imaging. 2014;38:373-379.
Wasay M, Azeemuddin M. Neuroimaging of Cerebral Venous Thrombosis. J Neuroimaging. 2005;15:118-128.
Countinho JM, Middeldorp S, Stam J. Advances in the Treatment of Cerebral Venous Thrombus. Curr Treat Options Neurol. 2014;16:299-307.
Countinho JM, Ferro JM, Zuurbier SM, Mink MS, Canhão P, Crassard I, et al. Thrombolysis or anticoagulation for cerebral venous thrombosis: rationale and design of the TO-ACT trial. Int J Stroke. 2013;8:135-40.
Ferro JM, Canhão P, Stam J, Bousser M, Barinagarrementeria F. Prognosis of Cerebral Vein and Dural Sinus Thrombosis: Results of the International Study on Cerebral Vein and Dural Sinus Thrombsosis (ISCVT). Stroke. 2004;35:664-70.
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Thank you!