11/10/2014 Antiplatelet and anticoagulation ICH

After an amazing resting weekend, I am back to learn more about stroke particularly hemorrhagic stroke. So lets keep going in our journey ... again, the best part of it is that we will be able to help people while walking our travel. 

1) When assessing ICH always keep in mind dysfunctional platelets in renal disease and intrinsic coagulopathy as in hemophilia and von Willebrand disease

2) ICH secondary to vitamin K inhibitor accounts for about 10-15% of ICH. With bleeds mostly multifocal including cerebellar vermis and hemorrhages into previously ischemic tissue.

3) The annual rate of ICH in pts tx with warfarin is 1%.

4) The main risk factors for warfarin associated ICH are HTN, age, intensity of anticoagulation, concomitant aspirin use, cerebral amyloid angiopathy, and leukoaraiosis.

5) Risk factors for hemorrhagic conversion of an ischemic stroke are: large infarct size, older age, hyperglycemia, sustained hypertension, thromboembolic mechanism, and preexisting micro hemorrhages on MRI.

6) Hemorrhagic conversion of an infarct

7) Warfarin and liver failure reversal: Vit K 10mg IV  in 10 min + PCC 50 u/kg IV. ( also aPCC, Kcentra) 

8) Unfractionated heparin reversal: protamine 1mg IV 

per 100u of heparin given in the first 30 min then 0.75mg per 100u for the next 30 min and 0.50mg per 100u of heparin given in the second hour. 

9) Low molecular heparin reversal: protamine 1mg IV per 1mg LMWH given in the last 8 hrs. 

10) Aspirin , NSAID or platelet aggregation inhibitors (clopidogrel/ticlopidine), uremic platelets, GP IIb/IIIa inhibitors reversal: DDAVP (desmopressin acetate) 0.3 ug/kg vi X 1 (20 ug in 50 ml NS over 15-30 min) and transfuse 5-6 units of platelets. 

Today we will do an extra one !!...

11) Thrombolytic induced coagulopathy reversal: 12 units of cryoprecipitate (to replace fibrinogen and factor VIII). 6-8 units of platelets. 

11/6/14 ICH 2

We will continue learning about ICH today. Hopefully this will amplify our knowledge about it. 

1) Dural sinus thrombosis with associated bleed is associated with hyper coagulable states, dehydration, Crohn's disease, and post partum period.

2) Dural sinus thrombosis with associated bleed requires full dose anticoagulation, even with hemorrhage present.

3) Most common primary tumors associated with ICH are GBM, oligodendroglioma, pituitary adenoma. The most common metastatic tumors associated with ICH are pulmonary, melanoma, thyroid, renal and choriocarcinoma.

4) Vasculopathy associated bleed are usually preceded by months of headaches, seizures, cognitive decline, psychiatric symptoms, and multiple strokes.

5) Ischemic stroke with hemorrhagic transformation is typically heterogenous on arterial distribution, commonly associated with an embolic strokes with repercussion.

6) About 38% will have a 33% increase in ICH size within 3 hours of onset of ICH

7) ICH pattern in MRI T1 - T2 "I Bleed, I Die, Bleed Die, Bleed Bleed, Die Die" Bleed: Bright. Die=Dark

8) Angiography is indicated for ICH with SAH, vascular malformations, isolated IVH, abnormal calcifications, and blood in unusual locations 

9) ICP monitoring may be helpful in patients with decreased LOC, or IVH (particularly IVH in the third or fourth ventricle)

10) Patients with cerebellar ICH > 3cm who are deteriorating neurologically or have brainstem compression and/or hydrocephalus from ventricular obstruction should have surgical removal as soon as possible. 

11/5/14 ICH

Well, day by day ... learning 10 things at a time, each day we are more knowledgeable about stroke and hopefully this will translate in saving more lives and providing better medical care to our patients. 

1) Intracerebral hemorrhage (ICH) has the highest mortality rate among stroke types (30-50%) 

2) ICH is more common among men, the elderly, AA, Japanese, and people with low low density LDL cholesterol. 

3) Hypertension is the most modifiable risk factor. 

4) Hypertensive bleed

• Basal ganglia (40-50%), lobar regions (20-50%), thalamus (10-15%), ponds (5-12%), cerebellum (5-10%) 
• IVH occurs in 1/3 of cases commonly related to thalamic or caudate ICH that ruptures into the ventricle.

5) Amyloid angiopathy

• Age >60 yo, b-amyloid deposition, may have history of Alzheimer's dementia, 
• Apo E2 and E4 alleles are more commonly associated with CAA
• Multicompartmental bleeds (ICH + SAH, ICH+SDH)
• Recurrent ICH

6) Coagulopathy related ICH usually causes multifocal bleeds. Cerebellar vermis is a common location.

7) AVM bleed rate is 2-4% per year with a recurrent bleeding of 6-18%. 

8) Cavernous hemangioma bleed rate is 0.25-1.1% per year in the anterior circulation with a rebleeding rate of 4.5% year. In the posterior fossa, the year bleeding rate is 2-3% with a 21% rebleeding rate. 

9) Cavernous hemangioma is associated with CCM-1, CCM-2 and PDCD-10 mutations.

10) Cavernous hemangioma has a multiple "popcorn" gradient echo appearance. 

11/4/14 SAH 2

Lets continue on our stroke journey, learning today about SAH and vasospasm...

1) Symptomatic vasospasm occurs in 20-40% patients and is defined as a clinical deterioration due to vasospasm when other causes (seizures, hydrocephalus, edema) have been excluded.

2) Delayed cerebral ischemia: symptomatic vasospasm or new infarct on CT or MRI due to vasospasm.

3) Risk factors for vasospasm:

1. Thick blood on CT (SAH/IVH) 
2. Fever
3. Admission hypertension
4. Sentinel bleed
5. Ultra-early angiographic spasm
6. Volume depletion
7. Low cardiac output
8. Smoking

4) Cerebral angiogram is the gold standard to dg cerebral vasospasm

5) Transcranial doppler ultrasound shows elevated velocities that may precede clinical symptoms by 34-48 hrs.

6) TCD positive predictive value of MCA mean flow velocity >200 cm/s IS 87% and the negative predictive value for MCA <120 cm/s is 94%

7) Hypercalcemia can cause or exacerbate vasospasm and should be avoided or corrected

8) Nimodipine is the only medication proven in large clinical trials to improve outcome after SAH

9) Nimodipine tx: 60mg q4 hrs for SBP > 140, 30mg q 4 hrs for SBP 120-140 mmHg, and held if SBP <120 mmHg. Therapy for 21 days.

10) Treat fever aggressively and maintain normovolemia.

11/3/14 - SAH

Nothing much to say... this will be my stroke diary to help myself remember that I can learn everyday at least 10 new things and try to keep track on it. It will also help me to go back and quickly review what I have written and learned recently. Hopefully if you want to join me in my journey may help you to learn something new everyday about stroke.

Thanks,

The Fellowship of The Stroke

11/3/14

1) Non traumatic hemorrhagic stroke accounts for about 1-7% of all strokes. The peak age range for aneurysmal SAH is 50-60 years and it is more common in woman and blacks. Patients more than 50 yo with large posterior circulation aneurysms are at the greatest risk for both rupture and repair complications

2) Modifiable risks factors: Cigarette smoking, HTN, moderate to heavy ETOH use, cocaine use and endocarditis.

3) The 2 gradient scales for subarachnoid aneurysms are: Haunt and Hess grading scale for SAH and the World Federation of Neurological Surgeons Subarachnoid Grade. See below

4) The lifetime risk for AVM bleed is 105 minus the patient age. 

5) The Spetzler-Martin AVM grading scale assess surgical risk: < 3cm= 1 point, 3 to 6 cm= 2 points, > 6cm= 3 points; eloquent location= 1 point, non eloquent location= 0 point; deep venous drainage = 1 point, superficial venous drainage= 0 point. Increasing points correlate with a higher risk for resection. 

6) In SAH sensitivity of CT scan drops to 60% 5 days after ictus. 

7) The modified Fisher scale incorporates the risk of vasospasm due to both SAH and IVH 

8) Seizures occur in 10% of pts at ictus, 4% during hospital stay and another 7% have late seizures

9) Hyponatremia following SAH is usually due to CSW (cerebral salt wasting) more than SIADH. Volume status will be normal or high in SIADH. Daily inputs and outputs can help determine the etiology.

10) Vasospasm typically occurs between 3-14 days after SAH ictus.