HEMORRHAGIC STROKENovember 2, 2012
Presented By: Raymond Chow, Yen Nguyen, Maryam Shirmohamadali
Goals & Objectives
Recognize the epidemiology, pathophysiology, risk factors, and clinical presentation of hemorrhagic stroke
Describe the pharmacological and non-pharmacological options for treatment of hemorrhagic stroke
Evaluate benefits and risks of different treatment options
Understand the importance of risk factor mitigation and management after hemorrhagic stroke
Design a pharmacological plan for patients presenting with acute hemorrhagic stroke
Patient Case
CC: “This headache is killing me!”
HPI: GQ is a 60-yo male who presents to the ED with rapidly progressing numbness of his right arm and a headache that started early in the morning and has been getting progressively worse since. He has grown more incoherent in speech at home with his wife, prompting her to bring him to the hospital.
He smokes 5 packs a week, and drinks 3-4 cans of beer every night. History of hypertension, atrial fibrillation, and states that he has not been taking his BP medications for the last few months.
Patient Case
Allergies: NKDA
Current Meds:1. Ibuprofen 200mg 1-2 tab q6hr PRN headache2. Atenolol 25 mg daily3. Metformin 1000mg BID4. Warfarin 6 mg daily
PMH: 5. DM II x 25 years6. HTN x 20 years7. Hyperlipidemia x 10 years
SH: Smokes 5 ppw x 15 years; drinks 3-4 beers per day
Patient Case
ROS: Gen: patient is an obese male who appears
uncomfortable and in distress. Pt is experiencing right facial drooping and right-sided paralysis
VS: BP 220/155, RR 20, T 38.6, Wt: 120 kg, Ht 180 cm
BG 164 INR 9.4 Skin: cold, dry HEENT: Right pupil dilated and right eye deviated
down and out Heart: RRR, normal S1 and S2 ABD: nondistended, no guarding Neuro: A&O x 1 (oriented to person only)
Epidemiology
Stroke is the leading cause of adult disabilities 2nd leading cause of death worldwide 3rd leading cause of death in the U.S. 800,000 strokes per year resulting in 150,000 deaths
Deaths are projected to increase exponentially in the next 30 years owing to the aging population
The annual cost of stroke in the U.S. is estimated at $69 billion
Stroke can be divided into hemorrhagic and ischemic origins 13% hemorrhagic 87% ischemic
Pathophysiology
Usually occurs spontaneously Caused by vascular rupture
with bleeding into brain Mass effect can further cause
bleeding and hematoma expansion from neighboring vessels
Hematoma growth over several hours following presentation of symptoms is common (30-40%)
Hemorrhages commonly occurs at the basal ganglia, thalamus, pons, or cerebellum
Types Of Hematomas
Epidural hematoma: results from damaged artery risk for bursting (e.g. meningeal artery) Commonly due to head trauma associated with skull
fracture Mass effect may occur after several hours
Subdural hematoma: develops from damaged veins leakage of blood to subdural space (e.g. cortical veins bridging) Commonly due to head trauma Mass effect may occur after several days Common in elderly population
Types Of Hematomas
http://brainandspine.titololawoffice.com/2011/09/articles/brain-injury/subdural-hematoma-and-epidural-hematoma/
Types Of Hemorrhages
Subarachnoid hemorrhage: May result from head injury, rupture of
arterial aneurysm, or spread of blood from different location to subarachnoid space
Most common: berry aneurysm▪ ↑ICP disrupts blood flow in brain generalized
concussion
Berry Aneurysm
http://www.strokesurvivors.ca/new/AneurysmFAQ.php
Types Of Hemorrhages
Intracranial hemorrhage (ICH): Hematomas focal neurologic deficits due to
pressure pushing against nearby brain structures Blood leakage cause damages to
surrounding brain tissues Patients with high blood pressure most
common cause for non-traumatic ICH
Types Of Hemorrhages
Traumatic Non-traumaticHead injury Uncontrolled hypertension
Anticoagulant therapy
Platelet and coagulation disorders
Vascular malformations
Brain tumors
Cerebral amyloid angiopathy
Drug-induced: cocaine, amphetamines
Non-Traumatic ICH
Chronic hypertension structural wall changes of small arteries and arterioles in the brain Fibrinoid necrosis Charcot-Bouchard aneurysms
Idiopathic hypertension (acute) usually younger patients with history of drug abuse Amphetamine, cocaine May occur minutes to hours after drug use
Vascular malformations Arteriovenous malformations (AVM): failure of formation of capillary
beds Saccular (berry): results from developmental weakness of arteriole walls
Hemorrhages can cause compression to nearby brain tissues May result in brain tissue inflammation and edema
http://www.uwmedicine.org/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subId=79
Risk Factors
NON-MODIFIABLE
Age Sex Race
Asians > Afr. Amer. > White
Genetics: Cerebral amyloid
angiopathy, coagulation disorders
MODIFIABLE HTN Cerebral amyloid
angiopathy Cholesterol Anti-coagulation Anti-platelets High EtOH intake Smoking DM Microbleeds Dialysis Drug-Induced (e.g.
cocaine, amphetamines)
Poll Question #1
Which of the following risk factors does patient GQ present with?
a. Ageb. Anticoagulant usec. Smokingd. Elevated BPe. All of the above
Patient Case - Revisit
CC: “This headache is killing me!”
HPI: GQ is a 60-yo male who presents to the ED with rapidly progressing numbness of his right arm and a headache that started early in the morning and has been getting progressively worse since. He has grown more incoherent speech at home with his wife, prompting her to bring him to the hospital.
He smokes 5 packs a week, and drinks 3-4 cans of beer every night. Yes history of uncontrolled hypertension, atrial fibrillation, and states that he has not been taking BP his medications for the last few months.
Subjective
Patient Case - Revisit
Allergies: NKDA
Current Meds:1. Ibuprofen 200mg 1-2 tab q6hr PRN headache2. Atenolol 25 mg daily3. Metformin 1000mg BID4. Warfarin 6 mg daily
PMH: 5. DM II x 25 years6. HTN x 20 years7. Hyperlipidemia x 10 years
SH: Smokes 5 ppw x 15 years; drinks 3-4 beers per day
Objective
DIAGNOSTICS
Test ResultsHead CT • Differentiates hemorrhagic from ischemic
stroke
ECG • Signs of myocardial ischemia, large inverted T waves
Labs • Chem panel – r/o conditions that have similar presentation
• CBC – thrombocytopenia• PT/PTT – w/o coagulopathy as cause
MRI • r/o aneurysm or arteriovenous malformation as a cause of bleeding
• Recommended in all patients <45 years of age and in all patients with intracerebral hemorrhage in lobar brain regions
CT angiograph
y
Invasive angiograph
y
Diagnostics
Head CT
http://www.uwmedicine.org/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subId=79
Glasgow Coma Scale (GCS)Eye Opening (E)
Verbal Response (V) Motor Response (M)
4 = spontaneous3 = to voice2 = to pain1 = none
5 = normal conversation4 = disoriented conversation3 = words, but not coherent2 = no words, only sounds1 = none
6 = normal5 = localized to pain4 = withdraws to pain3 = decorticate postureα
2 = decerebrateβ
1 = none
αabnormal posture that can include rigidity, clenched fists, legs held straight out, and arms bent inward toward the body with the wrists and fingers bend and held on the chestβabnormal posture that can include rigidity, arms and legs held straight out, toes pointed downward, head and neck arched backwards)
Assessment:• Severe: GCS 3-8 (cannot score lower than a 3) • Moderate: GCS 9-12 • Mild: GCS 13-15
General Treatment Approach
Mainstay of ICH therapy is to treat the underlying cause when possible
General treatment approach is always patient specific depending on clinical condition
General Treatment Approach
Stabilization of Vital Signs Neurological exam
Supportive care Management of seizures
Blood pressure control Fever control Anticoagulation correction Blood sugar control Surgical/Invasive Interventions
Patient Case - Revisit
VS: BP 201/155, RR 20, T 38.6, Wt: 120 kg, Ht 180 cm
BG 164 INR 9.4 Skin: cold, dry HEENT: Right pupil dilated and right eye deviated
down and out Heart: RRR, normal S1 and S2 ABD: nondistended, no guarding, Neuro: A&O x 1 (oriented to person only) EEG normal
Other: CT reveals areas of hyperintensity
Objective
Reversal of Coagulopathy Patients with elevated INR due to
anticoagulant use Hold warfarin, give clotting factors , and
vitamin K (IVPB)▪ FFP or PCCs
Patients with a severe coagulation factor deficiency or severe thrombocytopenia Factor replacement therapy or platelets▪ Recombinant Factor VIIa (rFVIIa)
New recommendation; 2010 Guidelines
Reversal of Coagulopathy Replenishment of Clotting Factors:
Note: No difference in clinical outcome with FFP vs. PCC’s but PCCs lead to less complications
FFP PCCsHistorically recommended Rapid reconstitution and
administration
• Increased risk of allergic & infectious rxns
• Processed clotting factors
• Inactivated infectious agents
Large Volumes- Fluid overload
Small volumes
Reversal of Coagulopathy Use of platelet transfusions in ICH patients
with a history of antiplatelet use is unclear May be indicated for patients with severe
thrombocytopenia
Intermittent pneumatic compression recommended
May consider low dose SQ LMWH or UFH for prevention of DVT After 1 to 4 days from onset with lack of mobility
Management of Seizures
Use of prophylatic anticonvulsant therapy in ICH is controversial
Patients with a change in mental status and whose EEG shows electrographic seizures should receive tx Benzodiazepenes Phenytoin/fosphenytoin
Blood Pressure Control
Goal SBP to < 180 mm Hg within 1 hour is and maintain for next 24 hours INTERACT study suggests more
aggressive therapy with goal SBP < 140 mm Hg leads to better outcomes
Managing Elevated BP
Antihypertensive agents for ICH have not been compared in controlled trials
Suggested agents: Labetolol Enalapril
For reftractory hypertension: Nicardipine Hydralazine Nitroprusside▪ Can lead to elevated ICP
Managing Elevated BP
Condition Treatment Approach
SBP > 200 mmHg or MAP is 150 mmHg
Aggressive BP with continuous IV infusion, with frequent BP monitoring Q5 min
SBP is 180 mmHg or MAP is 130
mmHg
and
there is the possibility of ICP
Monitor ICP and BP using intermittent or continuous IV meds while maintaining cerebral perfusion pressure 60 mmHg
SBP is 180 mmHg or MAP is 130
mmHg
and
there is no evidence of ICP
Modest BP (eg, MAP of 110 mm Hg or target BP of 160/90 mm Hg) using intermittent or continuous IV meds to control BP and clinically reexamine the patient Q15 min
Treatment of Increased ICP Elevate head of bed to 30 degrees
Analgesia and sedation as needed Aggressive therapies:
Osmotic therapy▪ Mannitol▪ RCT failed to demonstrated difference in disability or
death at 3 months
▪ Hypertonic Saline▪ Barbituate anesthesia
Hyperventilation and glucocorticoids not recommended
Ventriculostomy
CSF drainage may be appropriate in setting of obstructive hydrocephalus High rates of complication : bacterial
meningitis
Endoscopic hematoma Evacuation May improve long-term prognosis
Management Of Glucose
High blood glucose on admission predicts an increased risk of mortality and poor outcome in patients with and without diabetes and ICH Use of insulin is controversial.
Hypoglycemia should be avoided.
Poll Question #2
Which of the following regarding PCCs and FFP is correct?
a. FFP has historically been used because it results in better overall clinical outcome for patients
b. Use of FFP leads to more fluid overload compared to PPC’s
c. More allergic reactions occur with PCCs than FFP
d. FFP use is generally safer than treatment with PCCs
Surgical Intervention
Coil embolization Occlusion of aneurysm Gaining preference
Neurosurgical clipping More invasive
Poll Question #3
Which of the following is true?
a. FFP has historically been used because they result in better overall clinical outcome for patients
b. Use of FFP can lead to fluid overload but PCCs don’t run this risk
c. More allergic reactions occur with PCCs than FFP
d. FFP use is generally safer than treatment with PCCs
Temperature Management
Fever has been related to worsening outcomes Hypothermia protocol▪ For patients with suspected neurologic
deficits▪ Rigorous monitoring required▪ Core body temp cooled to ~33 degrees▪ Intubation and mechanical ventilation usually
required APAP
Complications
Delirium May be fairly common following ICH Therapy: supportive care, sedatives and neuromuscular
blockade, careful hemodynamic management Deep venous thrombosis
Motor weakness, venous stasis Therapy: anticoagulation, inferior vena cava filter
Infection Nosocomial pneumonia, urinary tract infection, cellulitis
from pressure sores Therapy: appropriate broad-spectrum coverage, then
narrowing for cultured organisms
Complications
Aspiration pneumonia Stroke-related dysphagia Therapy: dysphagia/swallow evaluation before moving
to PO status Hydrocephalus
Elevation of CSF pressure of the brain Cognitive impairment, urinary/fecal incontinence Therapy: external ventricular drain placement,
ventriculoperitoneal shunt Seizures
May complicate treatment for ICH; higher risk in cortical bleeding
Therapy: benzodiazapines, phenytoin, fosphenytoin
Post-Stroke Management
Lifestyle modifications: smoking cessation, refrain from alcohol,
diet/exercise, weight control Control blood pressure Control LDL Clot prevention: Warfarin, Aggrenox,
Plavix
Poll Question #4
Which medications can be used for the prevention of a stroke?
i. Warfarinii. Alteplaseiii. Phytonadione
A. I only B. III onlyC. I and IID. II and IIIE. I, II, and III
Risk Factors For Recurrent ICH
Lobar location of initial ICH Uncontrolled hypertension Older age Ongoing anticoagulation Apolipoprotein E epsilon 2 or epsilon
4 alleles Greater number of microbleeds on
MRI
Poll Question #5
Which of the following factors can directly increase the likelihood for patients to have another intracranial bleeding event?
i. Uncontrolled HTNii. Use of warfariniii. Lifestyle (e.g. smoking, excessive exercising)
A. I only B. III onlyC. I and IID. II and IIIE. I, II, and III
Patient Case - Revisit
1. SBP Above Recommended Value Of < 140 mm Hg Per AHA Stroke 2010 Guideline
Esmolol 30mg IVP, Then 3mg/min Continuous IV
2. Supratherapeutic INR, Likely To Have Contributed To Initial Bleeding Event
Hold Warfarin Give Vitamin K 10mg IV Infusion Give 3 Units FFP or PCCs Goal INR < 1.0 Due To Life-threatening Bleed
Assessment/Plan
Patient Case - Revisit
3. ICP monitoring to goal CPP ≥ 60 mmHg
Appropriate analgesia and sedation Head of bed elevation IV Mannitol
4. Seizure prophylaxis not indicated as no EEG abnormalities
Continue EEG monitoring
Assessment/Plan
Follow-Up
Monitoring by appropriate specialists for rehabilitation Physical therapist, occupational
therapist, speech and language pathologist
Strict management of HTN Antiplatelet/anticoagulation therapy
References Greenberg D.A., Aminoff M.J., Simon R.P. (2012). Chapter 3. Coma. In D.A.
Greenberg, M.J. Aminoff, R.P. Simon (Eds), Clinical Neurology, 8e. Retrieved October 25, 2012 from http://0-www.accessmedicine.com.library.touro.edu/content.aspx?aID=56670556.
Lomen-Hoerth C., Messing R.O. (2010). Chapter 7. Nervous System Disorders. In C. Lomen-Hoerth, R.O. Messing (Eds), Pathophysiology of Disease: An Introduction to Clinical Medicine, 6e. Retrieved October 16, 2012 from http://0-www.accesspharmacy.com.library.touro.edu/content.aspx?aID=5368376.
Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2010;41:2108-2129.
Rordorf G, McDonald C. Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis. UpToDate.
Rordorf G, Colin M. Spontaneous intracerebal hemorrhage: Prognosis and treatment. UpToDate [Internet]. http://uptodate.com/. Accessed October 16, 2012.
Thom T, Haase N, Rosamond W, et al. Heart disease and stroke statistics - 2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2006;113:e85-e151.
Valentine KA, Hull RD. Correcting excess anticoagulation after warfarin. UpToDate [Internet]. http://uptodate.com/. Accessed Oct 16, 2012.
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