Hemorrhagic stroke final final

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

http://www.strokesurvivors.ca/new/AneurysmFAQ.php


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


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


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


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


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


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


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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Hemorrhagic stroke final final