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Presented By: Raymond Chow, Yen Nguyen, Maryam Shirmohamadali
   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
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.
Allergies: NKDA
Current Meds:
1. Ibuprofen 200mg 1-2 tab q6hr PRN headache
2. Atenolol 25 mg daily
3. Metformin 1000mg BID
4. Warfarin 6 mg daily

PMH:
1. DM II x 25 years
2. HTN x 20 years
3. Hyperlipidemia x 10 years

SH: Smokes 5 ppw x 15 years; drinks 3-4 beers per day
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)
   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
   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
   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
http://brainandspine.titololawoffice.com/2011/09/articles/brain-injury/subdural-hematoma-and-epidural-hematoma/
   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
   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-traumatic
Head injury      Uncontrolled hypertension
                 Anticoagulant therapy
                 Platelet and coagulation disorders
                 Vascular malformations
                 Brain tumors
                 Cerebral amyloid angiopathy
                 Drug-induced: cocaine, amphetamines
   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
NON-MODIFIABLE                       MODIFIABLE
   Age                                 HTN
   Sex                                 Cerebral amyloid angiopathy
   Race                                Cholesterol
     Asians > Afr. Amer. > White
                                        Anti-coagulation
                                        Anti-platelets
   Genetics:
                                        High EtOH intake
     Cerebral amyloid angiopathy,
                                        Smoking
      coagulation disorders
                                        DM
                                        Microbleeds
                                        Dialysis
                                        Drug-Induced (e.g. cocaine,
                                         amphetamines)
Which of the following risk factors does patient GQ
present with?

    a.   Age
    b.   Anticoagulant use
    c.   Smoking
    d.   Elevated BP
    e.   All of the above
Subjective




 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.
Objective




 Allergies: NKDA
 Current Meds:
 1. Ibuprofen 200mg 1-2 tab q6hr PRN headache
 2. Atenolol 25 mg daily
 3. Metformin 1000mg BID
 4. Warfarin 6 mg daily

 PMH:
 1. DM II x 25 years
 2. HTN x 20 years
 3. Hyperlipidemia x 10 years

 SH: Smokes 5 ppw x 15 years; drinks 3-4 beers per day
Test          Results
  Head 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
     CT         of bleeding
              • Recommended in all patients <45 years of age and in all
angiography
                patients with intracerebral hemorrhage in lobar brain
  Invasive      regions
angiography
    Head CT




http://www.uwmedicine.org/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subId=79
Eye Opening (E)                  Verbal Response (V)                                    Motor Response (M)
4 = spontaneous                  5 = normal conversation                              6 = normal
3 = to voice                     4 = disoriented conversation                         5 = localized to pain
2 = to pain                      3 = words, but not coherent                          4 = withdraws to pain
1 = none                         2 = no words, only sounds                            3 = decorticate postureα
                                 1 = none                                             2 = decerebrateβ
                                                                                      1 = none

      Assessment:
      • Severe: GCS 3-8 (cannot score lower than a 3)
      • Moderate: GCS 9-12
      • Mild: GCS 13-15




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 chest
βabnormal posture that can include rigidity, arms and legs held straight out, toes pointed downward, head and neck arched backwards)
   Mainstay of ICH therapy is to treat the
    underlying cause when possible

   General treatment approach is always patient
    specific depending on clinical condition
   Stabilization of Vital Signs
     Neurological exam
   Supportive care
     Management of seizures
   Blood pressure control
   Fever control
   Anticoagulation correction
   Blood sugar control
   Surgical/Invasive Interventions
Objective




     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
   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
       Replenishment of Clotting Factors:
    FFP                                    PCCs
    Historically recommended               Rapid reconstitution and
                                           administration
    •      Increased risk of allergic &    •   Processed clotting factors
           infectious rxns                 •   Inactivated infectious agents
    Large Volumes                          Small volumes
    - Fluid overload



       Note: No difference in clinical outcome with FFP vs. PCC’s but PCCs lead
        to less complications
   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
   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
   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
   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
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   Monitor ICP and BP using intermittent or
                                     continuous IV meds while maintaining cerebral
and
                                     perfusion pressure 60 mmHg
there is the possibility of ICP

SBP is 180 mmHg or MAP is 130 mmHg   Modest  BP (eg, MAP of 110 mm Hg or target
                                     BP of 160/90 mm Hg) using intermittent or
and
                                     continuous IV meds to control BP and clinically
there is no evidence of ICP         reexamine the patient Q15 min
   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
   CSF drainage may be appropriate in setting
    of obstructive hydrocephalus
     High rates of complication : bacterial meningitis


   Endoscopic hematoma Evacuation
     May improve long-term prognosis
   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.
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
   Coil embolization
     Occlusion of aneurysm
     Gaining preference


   Neurosurgical clipping
     More invasive
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
   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
   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
   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
   Lifestyle modifications:
     smoking cessation, refrain from alcohol,
     diet/exercise, weight control
   Control blood pressure
   Control LDL
   Clot prevention: Warfarin, Aggrenox, Plavix
Which medications can be used for the prevention
of a stroke?
     i. Warfarin
     ii. Alteplase
     iii. Phytonadione

A.    I only
B.    III only
C.    I and II
D.    II and III
E.    I, II, and III
   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
Which of the following factors can directly increase the
likelihood for patients to have another intracranial
bleeding event?
     i.     Uncontrolled HTN
     ii.    Use of warfarin
     iii.   Lifestyle (e.g. smoking, excessive exercising)

A.    I only
B.    III only
C.    I and II
D.    II and III
E.    I, II, and III
Assessment/Plan




   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
   Monitoring by appropriate specialists for
    rehabilitation
     Physical therapist, occupational therapist, speech
     and language pathologist
   Strict management of HTN
   Antiplatelet/anticoagulation therapy
   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

  • 1. Presented By: Raymond Chow, Yen Nguyen, Maryam Shirmohamadali
  • 2. 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
  • 3. 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.
  • 4. Allergies: NKDA Current Meds: 1. Ibuprofen 200mg 1-2 tab q6hr PRN headache 2. Atenolol 25 mg daily 3. Metformin 1000mg BID 4. Warfarin 6 mg daily PMH: 1. DM II x 25 years 2. HTN x 20 years 3. Hyperlipidemia x 10 years SH: Smokes 5 ppw x 15 years; drinks 3-4 beers per day
  • 5. 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)
  • 6. 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
  • 7. 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
  • 8. 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
  • 10. 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
  • 12. 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
  • 13. Traumatic Non-traumatic Head injury Uncontrolled hypertension Anticoagulant therapy Platelet and coagulation disorders Vascular malformations Brain tumors Cerebral amyloid angiopathy Drug-induced: cocaine, amphetamines
  • 14. 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
  • 16. NON-MODIFIABLE MODIFIABLE  Age  HTN  Sex  Cerebral amyloid angiopathy  Race  Cholesterol  Asians > Afr. Amer. > White  Anti-coagulation  Anti-platelets  Genetics:  High EtOH intake  Cerebral amyloid angiopathy,  Smoking coagulation disorders  DM  Microbleeds  Dialysis  Drug-Induced (e.g. cocaine, amphetamines)
  • 17. Which of the following risk factors does patient GQ present with? a. Age b. Anticoagulant use c. Smoking d. Elevated BP e. All of the above
  • 18. Subjective 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.
  • 19. Objective Allergies: NKDA Current Meds: 1. Ibuprofen 200mg 1-2 tab q6hr PRN headache 2. Atenolol 25 mg daily 3. Metformin 1000mg BID 4. Warfarin 6 mg daily PMH: 1. DM II x 25 years 2. HTN x 20 years 3. Hyperlipidemia x 10 years SH: Smokes 5 ppw x 15 years; drinks 3-4 beers per day
  • 20. Test Results Head 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 CT of bleeding • Recommended in all patients <45 years of age and in all angiography patients with intracerebral hemorrhage in lobar brain Invasive regions angiography
  • 21. Head CT http://www.uwmedicine.org/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subId=79
  • 22. Eye Opening (E) Verbal Response (V) Motor Response (M) 4 = spontaneous 5 = normal conversation 6 = normal 3 = to voice 4 = disoriented conversation 5 = localized to pain 2 = to pain 3 = words, but not coherent 4 = withdraws to pain 1 = none 2 = no words, only sounds 3 = decorticate postureα 1 = none 2 = decerebrateβ 1 = none Assessment: • Severe: GCS 3-8 (cannot score lower than a 3) • Moderate: GCS 9-12 • Mild: GCS 13-15 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 chest βabnormal posture that can include rigidity, arms and legs held straight out, toes pointed downward, head and neck arched backwards)
  • 23. Mainstay of ICH therapy is to treat the underlying cause when possible  General treatment approach is always patient specific depending on clinical condition
  • 24. Stabilization of Vital Signs  Neurological exam  Supportive care  Management of seizures  Blood pressure control  Fever control  Anticoagulation correction  Blood sugar control  Surgical/Invasive Interventions
  • 25. Objective  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
  • 26. 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
  • 27. Replenishment of Clotting Factors: FFP PCCs Historically recommended Rapid reconstitution and administration • Increased risk of allergic & • Processed clotting factors infectious rxns • Inactivated infectious agents Large Volumes Small volumes - Fluid overload  Note: No difference in clinical outcome with FFP vs. PCC’s but PCCs lead to less complications
  • 28. 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
  • 29. 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
  • 30. 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
  • 31. 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
  • 32. 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 Monitor ICP and BP using intermittent or continuous IV meds while maintaining cerebral and perfusion pressure 60 mmHg there is the possibility of ICP SBP is 180 mmHg or MAP is 130 mmHg Modest  BP (eg, MAP of 110 mm Hg or target BP of 160/90 mm Hg) using intermittent or and continuous IV meds to control BP and clinically there is no evidence of ICP reexamine the patient Q15 min
  • 33. 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
  • 34. CSF drainage may be appropriate in setting of obstructive hydrocephalus  High rates of complication : bacterial meningitis  Endoscopic hematoma Evacuation  May improve long-term prognosis
  • 35. 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.
  • 36. 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
  • 37. Coil embolization  Occlusion of aneurysm  Gaining preference  Neurosurgical clipping  More invasive
  • 38. 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
  • 39. 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
  • 40. 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
  • 41. 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
  • 42. Lifestyle modifications:  smoking cessation, refrain from alcohol, diet/exercise, weight control  Control blood pressure  Control LDL  Clot prevention: Warfarin, Aggrenox, Plavix
  • 43. Which medications can be used for the prevention of a stroke? i. Warfarin ii. Alteplase iii. Phytonadione A. I only B. III only C. I and II D. II and III E. I, II, and III
  • 44. 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
  • 45. Which of the following factors can directly increase the likelihood for patients to have another intracranial bleeding event? i. Uncontrolled HTN ii. Use of warfarin iii. Lifestyle (e.g. smoking, excessive exercising) A. I only B. III only C. I and II D. II and III E. I, II, and III
  • 46. Assessment/Plan 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
  • 47. 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
  • 48. Monitoring by appropriate specialists for rehabilitation  Physical therapist, occupational therapist, speech and language pathologist  Strict management of HTN  Antiplatelet/anticoagulation therapy
  • 49. 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.

Notas do Editor

  1. Head CT reveals intracranial hemorrhaging
  2. Arresting hematoma growth is therefore a key objective for medical or surgical therapies.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.Rordorf G, McDonald C. Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis. UpToDate.
  3. 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.
  4. Larger hemorrhages:Global cerebral ischemia  can cause severe impairment to brain and elongated comaFocal ischemia  can result later from vasospasm of arteries near ruptured siteLomen-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.Berry aneurysm: thought to come from a congenital wkness in walls of large vessels at base of brain  becomes symptomatic in adulthood, usually after 3rd decade
  5. 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.http://emedicine.medscape.com/article/1916662-overview#aw2aab6b2b4aaBerry aneurysm: thought to come from a congenital wkness in walls of large vessels at base of brain  becomes symptomatic in adulthood, usually after 3rd decade
  6. 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.Pts with liver dz, coagulation factorsDrug-induced: common in young adults, since meds can cause rapid increase in BPOBerry aneurysm: thought to come from a congenital wkness in walls of large vessels at base of brain  becomes symptomatic in adulthood, usually after 3rd decade
  7. Greenberg D.A., Aminoff M.J., Simon R.P. (2012). Chapter 13. Stroke. In D.A. Greenberg, M.J. Aminoff, R.P. Simon (Eds), Clinical Neurology, 8e. Retrieved October 26, 2012 from http://0-www.accessmedicine.com.library.touro.edu/content.aspx?aID=56675112.Acute HTN: The role of acute—as opposed to chronic—hypertension in the pathogenesis of intracerebral hemorrhage is uncertain. Most patients with intracerebral hemorrhage are hypertensive after the event, but this may be explained by baseline hypertension, the vasopressor response to increased intracranial pressure (Cushing reflex), or both. In addition, large intracerebral hemorrhages are an uncommon feature of acute hypertensive encephalopathy. Nevertheless, the fact that some patients with spontaneous intracerebral hemorrhage have no history of hypertension and lack signs of hypertensive end-organ disease suggests that more acute hypertensive episodes might be involved, as does the occurrence of intracerebral hemorrhage in young patients after amphetamine or cocaine abuse.
  8. *most commonRordorf G, McDonald C. Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis. UpToDate.Grysiewicz RA, Thomas K, Pandey DK. Epidemiology of ischemic and hemorrhagic stroke: incidence, prevalence, mortality, and risk factors. NeurolClin. 2008 Nov;26(4): 871-95, vii. PMID: 19026895
  9. Cerebral T waves
  10. http://www.uwmedicine.org/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subId=79
  11. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974; 2:81.
  12. Patients undergoing treatment with OACs constitute 12% to 14% of patients with ICH,34,35 and with increased use ofwarfarin, the proportion appears to be increasing.36 Recognition of an underlying coagulopathy thus provides an opportunity to target correction in the treatment strategy
  13. Notept very disoriented during admission
  14. Endotracheal intubation in patients with decreased level of consciousness and poor airway protection
  15. No difference in clinical outcome between FFP’s and PCC’s but PCC use associated with fewere complications.Although rFVIIa can reverse INR in OAC-ICH, it doesn’t replenish all the vit K dependent factors and therefore may not restore thrombin generation as well as PCCsStudies may suggest use of rFVIIa can limit hematoma enlargement – however benefit in ICH patients remains unproven. Risk for clot increased – use is not recommended
  16. Up to 28% of patients with ICH experience seizures – often nonconvulsive in nature
  17. BP generally falls spontaneously within several days after ICH, but high BP persists in many patientsHTN can lead to expansion of hematoma, edema, and rebleeding; it’s vital to decrease BP. SBP &gt;140-150 associated with double the risk of mortality CCB’s acutely lower DBP and associated with worse outcomesINTERACT STUDY – Target SPB goal of 140 vs 180 w/in 1 hour
  18. Class C recommendations (weak)
  19. Hyperventilation not recommended b/c its effects are transient, it decreases CBF and it may lead to rebound increases in ICPGlucocorticoids are not effective and result in higher rates of complications and poorer outcomes
  20. Hyperactive, hypoactive, mixed--decrease in mortality from ARDS probably due to several factors, including improved supportive care and a more thoughtful approach to mechanical ventilation. --Key components of supportive care include intelligent use of sedatives and neuromuscular blockade, careful hemodynamic management, nutritional support, control of blood glucose, expeditious evaluation and treatment of nosocomial PNA, and prophylaxis against (DVT) and (GI) bleeding. FASTHUG-------Data suggest conservative fluid management strategy that aims to minimize or eliminate positive fluid balance — for example, by aiming for a CVP &lt;4 mmHg or a PAOP &lt;8 mmHg — offers clinical advantages, including improved oxygenation--VAP is a frequent complication of ARDS. Empiric abx coverage should be sufficiently broad. Strategies include avoiding: the supine position, excess sedation, unnecessary antibiotics, and unnecessary ventilator circuit changes. Additional strategies include providing good mouth care, weaning patients from the ventilator in a timely manner, and perhaps use of continuous subglottic aspiration. --Patients with hypoxic respiratory failure may benefit from strategies that decrease oxygen utilization, such as antipyretics to control fever and sedatives to control agitation. NMB may be required, particularly when asynchrony with the ventilator persists despite adequate sedation. 
  21. Sz: acute treatments
  22. A
  23. Rordorf G, Colin M. Spontaneous intracerebal hemorrhage: Prognosis and treatment. UpToDate [Internet]. http://uptodate.com/. Accessed October 16, 2012.
  24. Esmolol250mcg/kgRate of Vitamin K – DNE 1mg/min, at least 20 min