ENLS Version 5.0 Subarachnoid Hemorrhage Content:

Published  . 0 views
↓ Download
ENLS Version 5.0 Subarachnoid Hemorrhage Content:
1 / 1
ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 1 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 2 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 3 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 4 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 5 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 6 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 7 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 8 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 9 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 10 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 11 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 12 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 13 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 14 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 15 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 16 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 17 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 18 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 19 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 20 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 21 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 22 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 23 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 24 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 25 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 26 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 27 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 28 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 29 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 30 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 31 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 32 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 33 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 34 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 35 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 36 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 37 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 38 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 39 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 40 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 41 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 42 of 43 ENLS Version 5.0 Subarachnoid Hemorrhage Content: - slide 43 of 43
Description: ENLS Version 5.0 Subarachnoid Hemorrhage Content: Shraddha Mainali, MD; Brian Appavu, MD; Sayona John, MD; Slides: Sayona John, MD Editors Note: Global Considerations The intent of the editors, authors, and reviewers of this ENLS topic was

Related Topics

Download Presentation

"ENLS Version 5.0 Subarachnoid Hemorrhage Content:" is the property of its rightful owner. Permission is granted to download and print the materials on this website for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.

Presentation Transcript

slide2. ENLS Version 5.0 Subarachnoid Hemorrhage Content: Shraddha Mainali, MD; Brian Appavu, MD; Sayona John, MD; Slides: Sayona John, MD<br>
slide3. Editors’ Note: Global Considerations The intent of the editors, authors, and reviewers of this ENLS topic was not to address all the variations in international practice for the different diseases. We have discussed major practice variances (e.g., the availability of diagnostic testing, or the type of medications used) and encourage learners to use the ENLS algorithms as a framework on which any relevant local practice guidelines can be incorporated.<br>
slide5. ENLS: Subarachnoid Hemorrhage Learning Objectives:
Recognize the signs and symptoms of SAH
Implement clinical and diagnostic assessment of suspected SAH
Initiate initial assessment, early treatment and resuscitation of the SAH patient<br>
slide6. Case 39-year-old woman presents with severe headache associated with nausea that started an hour back
PMH: migraines
Meds:
Took ibuprofen prior to presentation, with moderate improvement of headache
Taking warfarin for a pelvic DVT diagnosed 3 months back during pregnancy
Exam: sleepy but follows commands, left eye droop+ with dilated pupil, moving all extremities equally
BP 170/95 mmHg, RR 24/min, HR 98/min
Breathing pattern is shallow and rapid<br>
slide8. Clinical Features<br>
slide9. Clinical Features Key Exam Features:
GCS
Pupillary exam
Fundoscopic exam for vitreous/retinal hemorrhages
Neck exam for meningismus (versus neck pain)
Hunt and Hess and/or WFNS score<br>
slide10. Clinical Severity Hunt & Hess Clinical Grading Scale World Federation Neurological Scale<br>
slide11. Case 39-year-old woman presents with severe headache and nausea which started one hour prior
PMH: migraine
Meds:
Reports taking ibuprofen prior to ED, with moderate improvement of headache
Taking warfarin for a pelvic DVT three months prior during pregnancy
Exam: sleepy, yet follows commands, left eye droop and dilated pupil, moving all extremities
BP 170/95 mmHg, RR 24/min, HR 98/min
Breathing pattern is shallow and rapid<br>
slide12. Case: 39-year-old woman with HA What’s the first step?
STAT head CT
STAT brain MRI
Assess ABC’s
Start IV nicardipine drip
Order FFP and vit K<br>
slide13. Case: 39-year-old woman with HA What’s the first step?
STAT head CT
STAT brain MRI
Assess ABCs
Start IV nicardipine drip
Order FFP and vit K<br>
slide16. Non-contrast CT imaging of the brain is the gold standard for identifying SAH with sensitivity of 95-100% if:
Classic presentation with thunderclap HA
CT completed within six hours of HA onset
The CT is read by an attending radiologist
Sensitivity of CT decreases with time*
False negative CT: time, anemia (hct <30) low volume SAH, a technically poor scan Brain Imaging<br>
slide17. CTA → ACOM aneurysm Adjunct Brain Imaging CTA
Some advocate for a CTA at the time of the CT scan to look for an intracranial aneurysm.
Caution regarding renal function and contrast administration.
Although CTA is helpful if an aneurysm is seen, the negative predictive value is less clear.
Sensitivity for aneurysm detection using multi detector CT scanner: 98% with 100% specificity (McCormack RF, Acad Emerg Med, 2010)
A negative CTA alone should not be used to rule out aneurysmal SAH.<br>
slide18. MR SWI Sequence Brain Imaging MRI may be useful in patients who are imaged ≥12 hours following the SAH
Specific sequences can be used to image subarachnoid blood even several days later<br>
slide19. Head CT (-) Lumbar Puncture Must perform LP if CT is negative and history suggests SAH
Rationale for LP is to identify xanthochromia of CSF by heme breakdown products
Presence of xanthochromia is time dependent - takes >12 hours to develop<br>
slide20. Lumbar Puncture<br>
slide21. Diagnosis of SAH Confirmed Once SAH is confirmed, the goal is to prevent aneurysm re-rupture and expedite treatment of the aneurysm while preventing or minimizing medical and neurologic complications<br>
slide22. Management<br>
slide23. Initial Orders Once SAH is diagnosed, initial orders should include:
Bed rest
Obtain pre-intervention labs: CBC, platelets, PT/PTT, INR, electrolytes, BUN, Cr, cardiac enzymes
12-lead ECG
Cardiac telemetry
Nimodipine 60 mg (PO/NG) q4h x 21 days (watch for hypotension)
Antiseizure medication until aneurysm is secured
Consult Neurosurgery/NCC<br>
slide24. Seizure Prophylaxis & Management Prophylactic Antiseizure Meds - Controversial
Pro: seizures following SAH and prior to definitive treatment has been associated with re-rupture and can raise ICP.
Con: classically used drug phenytoin has been associated with worse cognitive outcomes in SAH.
Regardless, seizure prophylaxis can be stopped once aneurysm is secured
Although frequently used by many centers, there is limited data on use of alternative anticonvulsant agents such as levetiracetam.
Active Treatment of Seizures
Administer lorazepam for acute seizure management
Administer loading dose of 2nd line therapy
More recently, many centers have started using levetiracetam due to its safety profile<br>
slide25. Coagulopathy Correct underlying coagulopathies
Goal INR < 1.4
Goal platelet count > 50,000
Consider platelet transfusion for those on anti-platelet medication(s)
See ENLS Pharmacology manuscript<br>
slide26. Treat Pain & Anxiety It is important to minimize straining, writhing or Valsalva, as they can potentially contribute to re-rupture of an aneurysm
One must also be careful not to over-sedate the patient as it may mask neurological sings and symptoms
Preferably use IV medication with short half-life (eg: fentanyl)
Use of adequate anti-emetics especially if vomiting occurs
BP control can improve with adequate analgesia
If anxiety seems to be the major issue, may consider small doses of an anxiolytic such as lorazepam<br>
slide27. BP Management Precise guidelines for BP management in SAH unfortunately do not exist
Retrospective data suggest higher rates of re-bleeding with SBP > 160 mmHg
Overzealous BP correction can potentially lead to hypoperfusion - especially if hydrocephalus or vasospasm is present.
Pre-morbid BP should be taken into considerations
Guidelines recommend SBP < 160 mm Hg as a reasonable control, keeping above principles in mind
Preferable to use low dose or titratable IV medications such as nicardipine to avoid large fluctuations in BP.
Avoid long-term nitroprusside due to concern of raising ICP<br>
slide28. Initial CT Case: 39-year-old woman with SAH Back to our patient:
Patient’s level of consciousness abruptly declined
Blood pressure spiked to 220/115 mmHg<br>
slide29. Case: 39-year-old woman with SAH What’s the next step?
Assess ABCs, intubate if necessary
Give IV dose of antihypertensive to achieve goal, add drip if needed for sustained BP control
STAT head CT
A and C
A, B and C<br>
slide30. Case: 39-year-old woman with SAH What’s the next step?
Assess ABCs, intubate if necessary
Give IV dose of antihypertensive drug to achieve goal, add drip if needed for sustained BP control
STAT head CT
A and C
A, B and C<br>
slide31. CT Following Neurologic Deterioration Case: 39-year-old woman with SAH Patient’s level of arousal abruptly declined:
Required immediate intubation
Both pupils transiently dilated
Head CT demonstrated re-bleeding associated with acute hydrocephalus
Upon return from CT, patient had a generalized seizure, requiring treatment with intravenous lorazepam<br>
slide32. Re-rupture estimate 12-15% in the initial 24 hours Decline in Neurological Status Causes of decline in neurological status:
Acute re-rupture of the aneurysm


Acute hydrocephalus
Seizure
Cardiopulmonary complications
Neurogenic pulmonary edema
Neurogenic stress cardiomyopathy
Note: cardiovascular collapse may be a sign of cerebral herniation Risk of re-rupture is 4-14% in the first 24 hrs<br>
slide33. EVD Hydrocephalus Hydrocephalus is caused by blockage of CSF circulation and absorption within the ventricular system and can occur in about 30% of patients within the first 3 days.
If a patient is obtunded or comatose, a ventricular drain (EVD) can be placed. This treats the hydrocephalus and provides monitoring of ICP
If a neurosurgeon is not available:
Transfer immediately to a facility with NS capabilities
Consider mannitol 1 gm/kg or hypertonic saline in the interim<br>
slide34. Anti-fibrinolytic Agents Preventing re-rupture of the aneurysm is a goal of initial SAH management
Antifibrinolytic agents such as ε-aminocaproic acid and tranexamic acid can be used to reduce risk of hemorrhage
These agents also raise the risk of thrombosis such as DVT, PE, and ischemic stroke, if they are continued beyond the acute SAH period
If there is an unavoidable delay in treating the aneurysm and the patient has not had a recent MI, DVT/PE, or any known hypercoagulable state, many centers administer a time-limited course (< 72 hours) of antifibrinolytic agent until the aneurysm can be secured
Early and LIMITED use (<72 hours) of these agents appear to be safe<br>
slide35. Pediatric Considerations Saccular aneurysmal SAH is uncommon in children
Dissecting and fusiform aneurysms associated with other medical co-morbidities (sickle cell, moya-moya, connective tissues diseases) are more common than adults. Also, given wide differential of potential etiologies in children with SAH, in appropriate clinical context, may consider workup for abusive head trauma.
Infectious aneurysms from congenital or rheumatic heart conditions are more common than in adults
In pediatric patients, CT remains the primary imaging modality for SAH evaluation, but if time permits, may consider obtaining an MRI to limit radiation to developing brains<br>
slide36. Pediatric Considerations Perform LP if imaging negative and clinical concern for SAH
Once the diagnosis of aSAH is established, standard four-vessel angiography should be performed
Adequate analgesia and sedation should be balanced with the need to obtain appropriate neurologic examinations
Reasonable to aim for blood pressure as close to normal for age. IV nicardipinemay be used for adequate control
Use of nimodipine has not been well studied in the pediatric population but given the available evidence in adults, may warrant usage if hemodynamically tolerated (1mg/kg q4h)
Normative values for TCD mean flow velocities are available in children and trending may help screen for vasospasm although it tends to occur with lower frequency in children
After stabilization, transfer to a center with experience for definitive managment<br>
slide37. Nursing Considerations Vigilant monitoring for signs and symptoms of hydrocephalus and aneurysmal rebleed
Pain should frequently be monitored and treated, with an effort to use non-opioid medications to preserve level of consciousness
Patient should remain on bedrest when the aneurysm is unsecured, with head of bed at 30°
In the presence of increased ICP, unsecured aneurysm or signs of DCI, nursing evaluation should be performed at frequent intervals
Strict intake and output should be measured in patients who have had an SAH, with efforts to maintain euvolemia
Close BP monitoring is needed to maintain goal and vigilance should be maintained for any significant drop with nimodipine<br>
slide38. Clinical Pearls (presenting symptoms) Typical –sudden onset severe headache, often described as the ‘worst headache of my life’.
Patient may present with any or a combination of nausea, vomiting, photophobia, neck stiffness, focal neurological deficits, cranial nerve palsies, lethargy, impaired consciousness, syncope or coma
Severity of clinical presentation is a determinant of poor prognosis<br>
slide39. Clinical Pearls (Management) CT is highly sensitive if done within the first few days of symptom onset
LP should be done if CT is negative, and history is strongly suggestive for SAH
Xanthochromia and elevated RBC count (>2000 x 106/L RBCs) in CSF is pathognomonic for SAH
CT angiogram is sensitive and helpful for detection of aneurysm, however digital subtraction angiography is the gold standard imaging modality for diagnosis and surgical planning<br>
slide40. Clinical Pearls (Management) Control blood pressure to target SBP <160 mmHg in adults
Correct coagulopathy if present
Treat hydrocephalus if present
Monitor for re-bleeding
Definitive treatment is recommended within 24 hours of SAH
Initiate enteral nimodipine within 24 hours of admission
Monitor for cardiorespiratory complications
Vasospasm/delayed cerebral ischemic typically occur between days 3-14 but early and delayed DCI is possible<br>
slide41. Clinical Pearls (Risk factors for SAH) Increased incidence with age but peaks ~50s.
Female sex
Personal or family history of SAH
Hypertension
Smoking
Alcoholism
Use of illicit simulants/sympathomimetic drugs
Aneurysm size and location (larger aneurysms ~≥7mm and posterior circulation aneurysms are more prone to rupture)<br>
slide43. Questions?<br>