Spine Trauma

Spine Trauma – Part A
By:Keith Wilkinson MD FACEP
Keith Wilkinson MD FACEP
St. John Hospital and Medical Center

Spinal Cord Injury
* Background:
o 8,000 -10,000 new cases expected annually
o Young men- mean age 33.5
o More frequently on weekends, holidays, during summer months
* Greater than half of cord injuries occur in the cervical spine region, a third in the thoracic region, and the remainder in the lumbosacral area
* Most cases of spine injury do not involve permanent cord injury
* Majority (90%) caused by blunt
trauma
o Majority from MVCs > falls, gunshot wounds, sports/ recreational activities
Bony Anatomy
Vertebral Anatomy
Anatomy
* Spinal cord occupies:
o ~35% of canal at the level of the Atlas
o ~ 50% of the canal in the lower cervical region (C2-7), thoracolumbar spine
Ventral- front
Dorsal- back
Ascending Spinal Cord Tracks
Dorsal column- medial lemniscus
Ipsilateral loss of tactile discrimination, vibration, joint and muscle proprioception
Leg fibers medial, arms lateral
Crosses just below level of medulla
Dorsal spinocerebellar tract
Transmits unconscious proprioceptive information to cerebellum
Fine coordination of posture
An uncrossed tract
Ipsilateral leg dystaxia
Ventral spinocerebellar tract

Unconscious proprioceptive information to cerebellum
Posture of lower extremities
Crossed tract
Contralateral leg dystaxia
Ascending Spinal Cord Tracks
Lateral spinothalamic tract
Pain and temperature
Crossed tract
Contralateral loss of pain and temperature sensation one segment below lesion
Ventral white commissure
Bilateral loss of pain and temperature
Dorsal Horn
Ipsilateral segmental anesthesia and areflexia
Descending Spinal Cord Tracks
Lateral corticospinal tract
Also called pyramidal system
Volitional motion
90% crossed in medulla
Ipsilateral spastic paresis with pyramidal signs
Ventral corticospinal tract
Mild contralateral muscle weakness
Proximal muscles more affected

Ventral horn
Ipsilateral flaccid paralysis
Dermatome Distribution
Spinal Level Muscle Innervation
Muscle Strength Grading
* 0 Flaccid
* 1 Flicker of muscle contraction
* 2 Full range of motion, gravity excluded
* 3 Full range of motion against gravity only
* 4 Full range of motion against gravity and some external resistance
* 5 Normal

Stability of Spine Fractures
* Three columns-Disruption of 2/3 unstable
A.Anterior column- anterior vertebral body, the anterior annulus fibrosus, anterior longitudinal ligament
B.Middle column-posterior vertebral body wall,posterior annulus fibrosus, posterior longitudinal ligament
C.Posterior column-posterior vertebral arch, posterior ligamentous complex
* Degree of compression
+ Vertebral body compressions > 50 %
generally considered unstable

Spine Fracture Types
* Compression fractures
o Result from axial loading and flexion,
o Failure of the anterior column
o Middle, posterior columns intact
o Usually stable unless > 50% height
o Unlikely to be directly responsible for neurologic damage

Burst Fractures
* Axial load
* Both anterior and middle columns fail
* Retropulsion of bone and disk fragments into the canal
* May cause spinal cord compression

Fracture Dislocations
* Fracture-dislocations
o Most damaging of injuries
o Failure of all three columns
o Compression, flexion, distraction, rotation, or shearing forces

Flexion- distraction
* Seat belt–type injuries
o Particularly where lap belts alone are used
* Failure of both the posterior and middle columns
o Intact anterior column prevents subluxation
* Radiographic findings:
o Increased height of the posterior vertebral body
o Fracture of posterior wall of the vertebral body
o Posterior opening of the disk space.


Clinical Clearance of the Cervical Spine
Cervical spine injury is highly unlikely if the patient has

1) No neck pain or tenderness
2) No neurologic signs or symptoms
3) No loss of consciousness
4) Normal mental status
5) No distracting injury

Cervical spine series
* Sensitivities for a cross table lateral demonstrating all 7 cervical vertebra vary (77- 90%)
* Sensitivity of full three view series (lateral, AP and odontoid views) increases to 80% to 100%
o Odontoid 10%, AP 1%
* If cervical fracture found:
o 50% have fx at adjacent level
o 15% have fx in another part of cervical spine
o 10% have fx in thoracic/lumbar spine

Interpreting Cervical Spine X-rays
* True lateral identifies 80- 90% of significant bony or ligamentous lesions
o Adequate films
+ Full visualization of all seven vertebrae
+ C7-T1 injuries are not common, seen with swimmer's view
* Open-mouth odontoid view identifies most of the remaining 10% of significant lesions
o Look for normal alignment and equal spacing between C2 and the lateral masses of C1
* AP or oblique views rarely identifies injury not already suspected

Cervical Spine Radiographs
* Most missed fractures due to inadequate films of the cervico-cranium, C7- T1 junction
* Cervical CT should be used to assess C1-C2 in victims of severe head trauma (GCS < 10, intracranial hemorrhage, skull fractures), when unable to obtain an open mouth or anteroposterior odontoid view
* The open mouth odontoid view is unreliable in unconscious intubated patients missing nearly 16% of injuries
* Up to 15% of cervical spine injuries are missed when the lateral view alone is used to clear patients
* Addition of CT increases sensitivity to 95-100%

Cervical Spine Radiology and the Unconscious Patient

Cervical Spine Radiology
Dens view
Fuchs view
Cervical Spine Radiology
Swimmer’s View
Cervical Spine Radiology
* Look for
o Normal atlanto-occipital alignment
o Predental space 3 mm or less
o Prevertebral soft tissue space less than 5 mm anterior to C3
o Spinal canal plain film anteroposterior diameter 13 mm or greater
o Any horizontal translation of one vertebra on the next
o Fanning of the space between spinous processes
o Fracture of any bone

3 Rules of 3
* The predentate space should be < 3mm
* The prevertebral soft tissue at C3 is usually 3 mm
* Anterior wedging of 3mm or more suggests a fx
Flexion/ extension views
o Used carefully to demonstrate spinal column stability if the initial three views raise a question but would predict a stable spinal column
+ Small chip fracture of the anterior-inferior margin of the vertebral body
+ 1 to 2 mm with no other noted abnormalities
o Used when the initial three views are normal but the pain seems out of proportion, suggesting greater occult ligamentous damage
o Requires awake, cooperative patient
o Abnormal if there is more than a 3.7-mm step-off of one vertebra on the next or if there is an 11° or greater angulation between vertebral segments
* Flexion-extension views
o No urgency
o Fluoroscopic examination of the unconscious patients has a specificity of about 99% and a sensitivity of 92%
o 625 patients with two suffering neurological deterioration, one with complete quadriplegia

Spine Imaging
* CT/ MRI
o The incidence of unstable spinal injury in the unconscious intubated patient is about 10%
o MRI not as sensitive as CT for imaging bone injuries
o MRI- Superb at defining neurologic, muscular, and soft tissue injury
+ MRI may also be used to identify ligamentous injury
+ Indicated in all patients with neurologic symptoms or physical findings but no clear explanation on plain films and/or CT
CT
* Excellent for upper spine anatomy, rotational injuries, degenerative vs. acute subluxations, subtle compressions
o High incidence of upper cord injury with ICH, GCS < 8
* 3-d reconstructions add improved detail

MRI
Unstable Cervical Spine Fractures
* Jefferson fracture
* Hangman’s fracture
* Teardrop fracture
* Bilateral locked facets

C spine Mechanism of Injury
HYPERFLEXION INJURY (46-79%)
* odontoid fracture
* simple wedge fracture (stable)
* tear drop fracture
* anterior subluxation
* bilateral locked facets (unstable)
* anterior disc space narrowing
* widened interspinous distance
* clay shoveler’s fracture
HYPEREXTENSION INJURY (20-38%)
* anteriorly widened disc space
* prevertebral swelling
* tear drop fracture
* neural arch fracture of C1
* subluxation (anterior/posterior)
* hangman’s fracture
Unstable Cervical Spine Fractures
* FLEXION:
o bilateral interfacetal dislocation
o flexion teardrop fracture (usually C5 or C6)
* EXTENSION:
o extension teardrop (usually C2 or C3)
o hangman’s fracture
o extension-dislocation
o extension-fracture-dislocation
o odontoid fracture
* VERTICAL COMPRESSION:
o Jefferson burst fracture

Spine Trauma – Part A
Spine Trauma – Part B

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Morbidity and Mortality

Morbidity and Mortality
by:Randy Hoover MD

Eponyms: Livedo reticularis associated with stroke-like episodes is known as?
* Sly’s Syndrome
* Sneddon’s Syndrome
* Riley-Day Syndrome
* Shwachman’s Syndrome
* Richter’s Syndrome
73 year old woman presents to an outside acute care clinic with a chief complaint of back pain.
* Upper-thoracic region
* Described as a “bunch,” mild in severity
* Constant, no radiation or change with position, not respirophasic
* Similar to recent transient episodes

History of Present Illness
* Associated with fatigue and malaise
* Night prior to presentation, unable to get comfortable; sweats and nausea
* Recent nose bleeds
* No fevers or rigors
* No chest pain, SOB or abdominal pain
* No bowel or bladder symptoms

Past Medical History
* Chronic A.Fib
o Anticoagulated on warfarin
* H/O Atypical Chest Pain
o Cath 12/00, normal
* Chronic Low Back Pain
* HTN
* CRI
o Baseline Creatinine 1.5
* COPD
* Chronic Diarrhea
* Temporal Lobe epilepsy
* S/P Appendectomy, herniated bowel repair

Medications
* Diltiazem CD 360 mg po qd
* Losartan 50 mg po qd
* Triamterene 50 mg po qd
* Warfarin 5 mg po qhs
* Metoprolol XL 50 mg po qd
* Amlodipine 5 mg po qd

ADR’s: Morphine, ACE Inhibitors
Social History
* Widowed mother of 2
* Consumes a glass of sherry and of cognac daily
* Current 2 ppd smoker
o Approx 100 pk year history
* Lives alone and functions independently

Physical Exam
Gen: 73 yowf, pleasant, NAD, who appeared older than her stated age
T=97.9 P=89 R=18 BP=126/90
Heent: EOMI, PERLA, OP pink and moist. Sclera anicteric
Neck: Supple, JVP =6 cm
Lungs: Poor air movement but otherwise clear
CV: Irreg Irreg no MRG and variable S1
AB: + Bs, soft, non-tender, non-distended, no masses, no hepatosplenomegaly
Back: Tender in the mid-dorsal region. Pain could be reproduced. No paravertebral or bony tenderness. No muscular spasm
Ext: No c/c/e
Labs
Initial Radiology
* RUQ Ultrasound: Multiple gallstones, no
wall thickening, no free fluid or dilated ducts
* CT Abdomen: Gallbladder is distended, no gallstones, slightly enlarged common hepatic and common bile ducts

Further Evaluation
* 2 weeks later: Seen by general surgery at DHMC for possible symptomatic cholelithiasis
o Pt extremely reluctant to undergo surgery
o “ I’ve not been significantly bothered by this”
o Referred to GI for possible ERCP
* 1 month later: Seen by GI
o Persisently elevated alk phos and amylase
o Thought secondary to etoh vs stone passage

-Management Options-
What would you do next?
* Ursodeoxycholic acid
* HIDA scan
* MRCP
* ERCP
* Recommend Surgery
* Watchful waiting

-Test Characteristics-
Magnetic Resonance Cholangiopancreatography (MRCP)
MRCP (Thin Slab)
* ERCP
o Could only cannulate pancreatic duct
o Dye injected into pancreatic duct showed local dilatation
o Brushings of pancreatic duct
o Sent to IR for transhepatic cholangiogram
* Percutaneous Transhepatic Cholangiogram
o Mildly distended intra/extrahepatic ducts
o Narrowing of distal common bile duct
o No dye spilling into duodenum, cholecystostomy tube placed

Admitted for monitoring
Physical Exam
Labs
Assessment and Plan
* Hypertensive urgency
o EKG without signs of ischemia. Pt with lethargy and + proteinuria
o IV Labetalol PRN until SBP decreased < 180
o Restart oral antihypertensive agents: diltiazem, losartan, metoprolol, and amlodipine
* Ductal dilatation s/p ERCP and PTC
o Hydrate
o Monitor LFTs and for signs of post-ERCP pancreatitis
o Cefotetan for prophylaxis
o F/U on Brushings
Post-ERCP Pancreatitis
* Serum amylase elevated in 75% of patients
* 5% have clinical pancreatitis
* MOST mild/moderate, rarely (0.4%) severe
* Usually with therapeutic (versus diagnostic)
* Prediction rules
o Amylase < 276, lipase < 1000 @ 2 hours
* Prevention
o Technical, stents, pharmacologic
+ Antibiotics, calcitonin, glucagon, nifedipine, C1-inhibitors, secretin, anticoagulation, corticosteroids, somatostatin, octreotide, gabexate mesilate, IL-10
Hospital Days 2-4
* Hypertension/A.fib
o Improved with oral agents
* Post ERCP pancreatitis
o Amylase 600
o Lipase 3780
o NPO, pain control, continue IV Hydration
* Cholecystostomy tube falls out
o IR contacted: recommend monitoring LFTs
* Day 4
o Feeling much better, tolerating clear liquids, LFTs stable at baseline
Hospital Day 5
* C/o Increasing RUQ pain, worsening abdominal distention, and nausea
* Labs:
* Plan: NPO, adequate pain management, follow LFTs, place PICC line and begin TPN
Hospital Day 6
* Worsened abdominal pain and distention.
* New rhonchi bilateral lung bases
* Labs:
* CT Abdomen and Pelvis

Hospital Day 7
* Worsening abdominal pain and distention
* Return to IR
o Attempted to drain bile pool around liver, but unable to do so
o Replace cholecystostomy tube
* Somnolent and short of breath
o ABG: 7.25/50/77 on 2 L, oxygen increased to 4 liters
o CXR: CHF
o Lasix 20 mg IV
o Appeared to stabilize

Hospital Day 8
* Somnolent and unarousable
* Acute Abdomen
o Absent bowel sounds, + guarding and rebound
o Urgent surgical consultation
* Exploratory Laparatomy
o Bile Leak from right medial lobe of liver at previous puncture site, cultures sent
o Cholecystectomy: gallbladder full of stones, signs of chronic cholecystitis
o T-Tube inserted
o No masses noted
* Transferred to ICU on ventilator

Hospital Day 9-13
* Fever spikes
o Peritoneal fluid growing Enterococci
o Hospital acquired pneumonia
* Brushings Returned:
Bile Duct: negative for malignancy, + inflammation
Pancreatic Duct: ATYPICAL; atypical ductal epithelial cells. Metaplastic and benign mucosal cells present
Hospital Day 14
* Defervesced
* Oliguric, rising BUN/CR
* Increased ventilatory requirements
* Increasing LFTs
Family Meeting
* Family Meeting
o Daughter indicated that her mother would not want her life prolonged by aggressive measures
o Family requested to withdraw support
o Pt made DNR/DNI
* Support withdrawn
o Pt died peacefully 3 hours later
* Family refused autopsy
Haunting Questions
At what point did this go wrong?
What was her diagnosis?

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Lupus Anticoagulant

Lupus Anticoagulant
By:Jennifer Kirkland (Lambe)

Antiphospholipid
Antibody Syndrome
* Antibodies to phospholipids or plasma proteins bound to phospholipids
o Lupus anticoagulant antibodies
o Anticardiolipin antibodies
o Anti-ß2- glycoprotein I antibodies
* Other antibodies: prothrombin, annexin V, phosphatidylserine, phosphatidylinositol
o These antibodies are not standardized for clinical use and their clinical utility is not well characterized

Lupus anticoagulant
* Lupus anticoagulant
o Describes a group of antibodies which react with cardiolipins, other phospholipids, ß2-glycoprotein I, or proteins other than ß2-glycoprotein I
-AND-
o possess “lupus anticoagulant” activity

What is lupus anticoagulant activity?

* Ability to interfere with coagulation testing (in particular, the tests which are phospholipid dependent) leading to prolonged values
* Despite the “anticoagulant effect” in vitro, these antibodies actually cause coagulation in vivo, in the form of arterial and venous thromboses

Lupus anticoagulant:
Actually a Misnomer
* Associated with clotting, not anticoagulation
* More than one antibody is associated with lupus anticoagulant activity
* Only about 50% of individuals with a lupus anticoagulant meet the American College of Rheumatology criteria for the classification of lupus (SLE)

Definitions
* Cardiolipin= mitochondrial phospholipid
o Causes a biologic false positive test for syphilis
* ß2-glycoprotein I -(not a phospholipid but a plasma phospholipid binding protein)
o In early 1990s, discovery that some anticardiolipin antibodies require the presence of ß2-glycoprotein I in order to bind to cardiolipin
o Patients with SLE or the antiphospholipid syndrome require ß2-glycoprotein I in order to bind to cardiolipin
o Most ß2-glycoprotein I-dependent anticardiolipin antibodies recognize ß2-glycoprotein I equally well whether bound to cardiolipin or bound to other anionic phospholipids

Additional info on LAs
* Anticardiolipin antibodies and Anti-ß2- glycoprotein I antibodies may not possess lupus anticoagulant properties
* Specificity of anticardiolipin antibodies for antiphospholipid syndrome increases with titer and is higher for the IgG than for the IgM isotope
* There is no definitive association between specific clinical manifestations and particular subgroups of antiphospholipid antibodies


Effects of antiphospholipid antibodies on coagulation
* Actually has opposing effects on coagulation
Procoagulant Effects
* Inhibits activated protein C pathway
* Up-regulates TF pathway
* Inhibits antithrombin III activity
* Disrupts annexin V shield on membranes
* Inhibits anticoagulant activity of ß2-glycoprotein I
* Inhibits fibrinolysis
* Activates endothelial cells
* Activates and degranulates neutrophils
* Enhances expression of adhesion moleculres by endothelial cells and adherence of neutrophils and leukocytes to endothelial cells
* Potentiates platelet activation
* Enhances platelet aggregation
* Enhanced binding of ß2-glycoprotein I to membranes
* Enhanced binding of prothrombin to membranes
Anticoagulant Effect
* Inhibits activation of factor IX
* Inhibits activation of factor X
* Inhibits activation of prothrombin to thrombin
o “Microenvironment of cell membranes in vivo may promote greater inhibition of anticoagulant pathways and therefore thrombosis.”
o Ultimately, we don’t really know the mechanism by which thrombosis is promoted over anticoagulation

Criteria for detection of lupus anticoagulant antibodies
* Lupus anticoagulant
1. Must prolong coagulation in at least one phospholipid-dependent coagulation assay with the use of platelet poor plasma
+ Extrinsic (dPT)
+ Intrinsic (aPTT, dilute aPTT, KCT, colloidal silica clotting time)
+ Final common pathway (dRVVT, Taipan venom time, Textarin and Ecarin time)

2. Failure to correct the prolonged coagulation time by mixing the patient’s plasma with normal plasma (1:1)
3. Correction of the prolonged coagulation time after addition of excess phospholipid or platelets that have been frozen and then thawed (they release phospholipids)
4. Rule out other coagulopathies with the use of specific factor assays if the confirmatory test is negative or if a specific factor inhibitor is suspected

To rule out a lupus anticoagulant antibody
* Two or more assays that are sensitive to these antibodies must be negative (one should be based on low phospholipid concentration and they should evaluate distinct portions of the coagulation cascade)

Diagnosis of antiphospholipid antibody syndrome
* Clinical Criteria
o Vascular thrombosis (Venous or arterial: blood vessels, brain, kidneys, lung GI tract, placenta etc)
o 1 or more deaths of normal fetuses at or after 10th week of gestation,or 1 or more premature births at or before the 34th week of gestation; or 3 or more unexplained consecutive spontaneous abortions before the 10th week of gestation

* Laboratory criteria
o Anticardiolipin antibodies
+ Anticardiolipin IgG or IgM antibodies present at moderate or high levels in the blood on two or more occasions at least 6 weeks apart
o Lupus anticoagulant antibodies
+ LA detected in the blood on 2 or more occasions at least 6 weeks apart (?12 weeks)

Antiphospholipid syndrome
* Primary
o No other evidence of another autoimmune disease
* Secondary
o Associated with autoimmune or other diseases, most commonly SLE
* Sneddon’s syndrome: clinical triad of stroke, livedo reticularis, and hypertension may represent undiagnosed antiphospholipid syndrome.


Epidemiology
* Antiphospholipid antibodies are found among young, apparently healthy control subjects at a prevalence of 1 to 5% for both anticardiolipin antibodies and lupus anticoagulant antibodies
o Meta-analysis
+ LA= 11.1 Odds ratio for venous thrombosis compared with 3.21 with anticardiolipin Ab
o Multivariant analysis
+ Odds ratio for venous and arterial thromboembolism is 4.4 with LA and 1.2 with anticardiolipin
* Prevalence increases with age

Prevalence of LAs in patients with SLE
* Anticardiolipin antibodies= 12-30%
* Lupus anticoagulant antibodies= 15-34%
* B2glycoprotein I antibodies=20%
o Antiphospholipid syndrome may develop in 50 to 70% of patients with both SLE and antiphospholipid antibodies after 20 years of follow-up
o Up to 30% of patients with SLE and anticardiolipin antibodies lacked any clinical evidence of the antiphospholipid syndrome over an average follow-up of seven years

Prospective study
* In a recent prospective study involving individuals with antiphospholipid antibodies, the incidence of thrombosis per year was:
o 1% in individuals with no history of thrombosis
o 4% in patients with systemic lupus erythematosus
o 5.5% in patients with a history of thrombosis
o 6% in individuals with high titer IgG anticardiolipin antibody (>40 units).

Functional Assays of Lupus Anticoagulants
* aPTT
o Some manufacturers offer aPTT reagent which contains a low amount of phospholipid, therefore it is more sensitive for lupus anticoagulant
o Conditions causing acute phase reactants associated with increased fibrinogen and factor VIII, may shorten the aPTT and mask a weak LA
* Prothrombin Time:
o patients with LA will have a normal PT unless they are receiving oral anticoagulants or they develop an inhibitor to prothrombin (PT reagents contain more phospholipids than PTT reagents)

* DRVVT (screening)
o Activates factor X which in the presence of PL, calcium, and factor V activates prothrombin, leading to the formation of a fibrin clot
o Dilution of the venom yields a clotting time in which concentration of the PL reagent is the rate limiting step (there is low amount of phospholipids)
o Inhibition by LA leads to prolongation
o After positive screen, perform the mixing study- if does not correct then:
* DRVVT (confirm)
o Adds a higher amount of phospholipids to neutralize the lupus anticoagulant
o Ratio is derived from the screen clotting time divided by the confirmatory clotting time
o If ratio exceeds the established cutoff, then lupus anticoagulant is in the specimen

Tissue thromboplastin inhibition test (TTI)
o Modified PT assay
o Thromboplastin, which is rich in phospholipid, can be diluted so that its concentration becomes the rate limiting step
o Inhibition of prothrombinase by a LA will cause prolongation of the PT assay
o Due to the various PL and its concentration in the reagent, the test varies in its sensitivity and specificity

STACLOT LA: Hexagonal II Phase Phospholipid Assay
* Two part aPTT screening assay for LA
* Patient’s plasma is mixed with buffer (screening test) or hexagonal phase phosphatidyl ethanolamine (confirmatory test) to neutralize any lupus anticoagulant present
* Mixtures are incubated with normal plasma to correct any coagulation factor deficiency
* Measure aPTT in both mixtures
* If specimen contains LA, the aPTT of the confirmatory test will be significantly shorter than that of the screening test

Staclot-LA
* Phospholipid antibody positive= difference in the clotting times between the two tubes is greater than + 8.0 seconds.
* The aPTT reagent in this assay contains a heparin inhibitor which makes the test system insensitive to heparin levels up to 2.0 U/mL.
* False positive results may occur in patients with high titer Factor VIII inhibitors

Summary
* Lupus anticoagulant causes thrombosis
* Lupus anticoagulant is a group of antibodies that bind to phospholipids or phospholipid binding proteins
* Due to the heterogeneity of the phospholipid antibody, there is no single test that is confirmatory for all phospholipid dependent antibodies.

References

* Kaolin clotting time
o Sensitive for LA when no additional PL is used
o LA is identified when the KCT fails to correct after the addition of even large amounts of plasma
o Problems with the KCT, owing to the particular nature of kaolin, is that it is unsuitable for some photo-optical devices, which makes full automation difficult
* Taipan (Oxysuranus scutellatus) venom activates prothrombin in the presence of PL and Ca2+
* Textarin (Pseudonaja textiles) acts similarly but requires the presence of factor V
* Specificity of both of the above tests can be improved by mixing tests and/or confirmation with the use of ecarin, an enzyme purified from the venom of Echis carinatus, in conjunction with the Textarin test

Lupus Anticoagulant.ppt

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