How To Be A Clinical Rock Star Managing Subarachnoid Hemorrhages
- Oct 21st, 2014
- Francesca Civitarese
How To Be A Clinical Rock Star Managing Subarachnoid Hemorrhage
Author: Francesca Civitarese, DO (Attending EM Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) // Editors: Alex Koyfman, MD (@EMHighAK) & Justin Bright, MD
A 62 year old female with a history of hypertension, diabetes, and migraines presents to your ED complaining of headache and dizziness. She states her headache started 3 hours prior to arrival. The pain is right-sided and sudden onset. The patient does state that she has had headaches in the past that were in fact worse than this one, and this current episode is somewhat improved compared to the pain at onset. She took 605mg of Tylenol prior to her arrival.
On questioning, the patient denies photophobia, phonophobia, focal neurologic deficit, weakness, or tingling. She describes her dizziness as being worse when she walks or stands, and that she feels off balance when walking. The rest of her review of systems is negative.
You consider her physical exam to be notable only for a wide based gate. The rest of her neurologic exam is normal top-to-bottom, and her cardiopulmonary exam is also normal.
A New Way to Think About Subarachnoid Hemorrhage:
It is helpful to remember that while a subarachnoid hemorrhage is in fact a “bleed”, it is also a stroke. When compared to ischemic strokes, hemorrhagic strokes tend to have an increased risk death in the acute phase, but for those patients that don’t die, their overall prognosis for return-to-baseline is somewhat better than ischemic events. Why is this? During hemorrhagic strokes (i.e. bleeds), an artery bursts, bathing brain cells in blood. The cells become “stunned”, but there is rarely significant cell death surrounding these events. If the total volume of hemorrhage is small, a patient has a chance at making a full, or near-full recovery (depending on extent of injury and any herniation symptoms).
In ischemic events, lack of blood flow to brain cells causes cellular destruction, and a watershed “penumbra” effect can cause large swaths of brain cell death relative to the small area of initial ischemia. In ischemic cell death, brain cells don’t remodel or regain function, which is why ischemic stroke patients have a high likelihood of residual neurologic deficit. This terminal cell death is also why there is such a push for early identification of ischemic stroke, and why thrombolytics and other neurologic intervention procedures have gained such momentum.
Patients presenting with headaches are worrisome because it can be difficult to sift through so many associated symptoms to determine who has benign pathology and who has a catastrophe brewing in their brain. It is my goal to give you the needed strategy to be a rock star when it comes to evaluating headache patients.
The Two Flavors of Subarachnoid Hemorrhage: Spontaneous versus Traumatic
–Leading cause of SAH overall
–Tend to occur on the side of the injury, but also can be seen with significant contrecoup forces on the opposite side of injury.
Spontaneous – due to three main causes:
1. Ruptured aneurysm (majority of atraumatic SAH cases)
Aneurysms preferentially blossom in the Circle of Willis, with the anterior communicating artery (Acomm) being the most common location for rupture. The posterior communicating artery (Pcomm) is the second most common site. Saccular aneurysms are more likely than fusiform
2. Leaking AVM (about 10% of atraumatic cases)
Arterial-venous malformations (AVMs) are often located in the brain parenchyma. You can be tipped off to the possibility of this diagnosis by looking for a “blush” of blood in the cortex parenchyma that is infiltrated by cluster of “stippling” of calcifications within the area of the bleed.
3. The Duck Factor (approx 10% of atraumatic cases)
The “perimesencephalic bleed”. They look like a duck, talk like a duck, walk like a duck, and even leave little duck droppings…but no one can find the duck. These are bleeds that are in the vascular territories of the typical aneurysms or “deep bleed” locations around the midbrain, but on subsequent imaging studies, no definitive aneurysm can be identified. These patients often do very well, with little intervention required.
Other Causes of Subarachnoid Hemorrhage:
Venous sinus thrombosis
Vasculitis (Behcet’s disease, Churg-Strauss, Wegener’s granulomatosis)
Sickle cell disease
Drugs (cocaine abuse, anticoagulant therapy)
–Headache is the chief complaint in 2% of all ED visits
–1 in 100 Headaches presenting to the ED will be a SAH
–Incidence of severe, abrupt onset headaches with normal neuro exam who have SAH is 10-15%
–approximately 70% of SAH presentations are headache alone, without having any focal complaints or findings.
-Estimates of missed diagnosis range from 15-25%
Aneurysm Fun Facts:
–Average population incidence of cerebral aneurysms? 2%
–25% of patients with ONE aneurysm will have multiple
–Most aneurysms are in the anterior cerebral circulation (70-80%)
–Aneurysms <10mm have very low (<1%) risk of rupture
So How Do We Make Sure We Don’t Miss a Subarachnoid Hemorrhage?
Step One: Define who is a prime candidate for bleeds? What is our classic presentation?
–Peak age of rupture @ 50
–Heavy ETOH users
–Prior personal or family history of SAH or aneurysm (first degree relatives of people with aneurysm history have 5x the risk of having their own aneurysm)
–OCPs (evidence not definitive at this point, but some studies suggest this is a risk factor)
What are some genetic disorders associated with higher likelihood of aneurysm?
-*Polycystic kidney disease* – common board/inservice exam association!
–Neurofibromatosis type I
The Classic Presentation:
–Worst headache of my life
–Headache with associated nausea/vomiting
–Sudden headache during exercise/sex/valsalva
–Seizure at onset of headache
–Syncope with subsequent seizure
–Transient syncope with headache +/- nausea or vomiting
–Any neurological focal exam findings such as weakness/numbness
–Evidence of meningismus
Step 2: Don’t Screw Up the History Taking
Why do ED doctors miss Subarachnoids?
Failure on multiple levels…
- Failure to consider the diagnosis or obtain the history
- Failure to order a CT if you are suspicious
- Failure to complete an LP if the CT is normal
- Failure to recognize that improvement of symptoms does not equal benign pathology
Three important things you need to know from your patient
–Acuity of onset?
–Was the pain at its worst at time of onset?
–Similarities and differences relative to prior headaches?
A word of advice: Don’t ask the patient if it’s the “worst headache of your life”. Very few people presenting to the ED will say to you that it isn’t.
Remember: Phrase your questions openly
- How did the headache start? If they need more specific examples: Did the headache come on ALL OF A SUDDEN (snap your fingers or clap your hands together) like this? Or did it start slowly and gradually build and get worse?
- Has your headache changed at all since it started? Has it gotten better or worse?
- Have you had headaches like this before? How does this one compare?
- Are you having any other symptoms? (Remember that in addition to the obvious “focal weakness or focal sensory deficits, you have to ask about any vision changes, gait/balance issues/speech problems/strange facial sensations?)
Remember: Response to therapy DOES NOT rule out a SAH (or other badness)
Patients can have a headache that was worse when it started, and that got better with Tylenol at home and this could actually be the harbinger of their initial bleed. Anyone bleeding from aneurysmal rupture is at risk for the dreaded “re-bleed”. A positive response to a typical headache “cocktail” has been reported with nearly every category of headache badness, including carotid artery dissection, carbon monoxide (CO) exposure, brain tumor, SAH, meningitis, and venous sinus thrombosis.
Step 3: Achieve Rock Star Status by Your Physical Exam Skills
7 Key Exam Findings to Know
1. Basal Ganglia – responsible for fine motor movement adjustments, and refines the motor activity of the pyramidal system. The basal ganglia functions similarly to the cerebellum.
2. Look for: cerebellar type issues, but also watch for Dystonic postures – unusual, uncoordinated movements such as choreoathetosis (involuntary jerky movements), hemiballismus (slow bizarre movements of half the body), or simply loss of harmony of refined movements.
3. Internal Capsule – location of the lacunar infarcts/bleeds typically associated with HTN/DM. Bleeds/strokes in this area of the brain can easily be confused with cortical lesions, particularly ACA or MCA lesions.
Look for: motor and sensory deficits ONLY, no findings with mental status/thought deficits. Pure motor findings are likely secondary to an isolated lesion to the internal capsule, but can be confused with cortex lesions.
*Clues* that it may be CORTICAL as opposed to isolated to the Internal Capsule:
–Gaze preference or deviation
–Expressive or reactive aphasia
–Visual field deficits
–Visual or spatial neglect
4. Thalamus – relay point for the brain to convey and receive sensory information from the body
Look for: Sensory deficits, loss of pain/touch in the face or extremities
5. Pons – Relays information between hemispheres of the cerebellum and cortex; also plays a key role in your sleeping/dreaming.
Look for: PINPOINT PUPILS; also watch for altered mental status, drowsiness
6. Cerebellum – refines motor activity, gait, and balance. Check coordination.
Take Home Message: Get your patient up, and walk them! Often, a non-focal exam on the gurney is VERY different once someone is up and about!
–Check finger-to-nose: abnormality (past-pointing) is called “dysmetria”
–Check rapid alternating movements: flip hands back and forth fast, tap feet on ground quickly. Abnormalities (slow/uncoordinated) are called “dysdiadochokinesia”
–Nystagmus: the “fast phase” will be towards the side of the cerebellar lesion
–Scanning speech: separated enunciation of syllables: EX: the “American government” will become “Am-er-i-can Gov-ern-ment”
–Gait: may be wide-based/staggering
*Remember that a classic finding of cerebellar dysfunction is ataxia, and that this can be in either the upper extremities, lower extremities, or both. The ROMBERG test assesses proprioception, and is, in isolation, not an adequate evaluation of the cerebellum.
7. PComm Aneurysm – look for a 3rd nerve palsy (anisocoria >2mm)
Posterior Circulation Clues – nystagmus, ataxia, dizziness
BONUS: A simplified summary of the Function of the Lobes
Frontal Lobe: reasoning, planning, parts of speech, movement, emotions, and problem-solving
Parietal Lobe: movement, orientation, recognition, perception of stimuli
Occipital Lobe: visual processing
Temporal Lobe: perception and recognition of auditory stimuli, memory, and speech
CONFIRMING YOUR DIAGNOSIS:
- Decoding the CT Slices
BADNESS IN THE BRAIN — SUBARACHNOID HEMORRAGE WITH DECOMPRESSION INTO VENTRICLES
FOR MORE BASIC RADIOLOGY HELP:
IF YOUR CT IS NEGATIVE?
It is currently recommended to proceed with an LP to “rule out” SAH.
–Get an opening pressure; will be elevated in about 60% of SAH
–Collect 4 tubes, with cell counts on Tube 1, and also in Tube 4. You should hypothetically see “clearing” of the RBCs (approaching zero) in order to “rule out” SAH.
–If you initially see FRANK blood, let it drip a bit before collecting the sample. It may simply represent a traumatic tap and the cell counts in the tubes will be more accurate
–Traumatic taps are likely caused by puncture of the venous plexus located dorsally and ventrally to the spinal sac or vessels that accompany the cauda equina.
–Some literature suggests any number >100 RBCs in tube 4 is positive. There is NO DEFINITIVE STANDARD for what constitutes SAH versus traumatic tap at this point. For Example: if you start out in Tube 1 @ 5,000 RBCs, and Tube 4 “clears” to 700, there is no definite way to tell if this is traumatic tap or SAH.
–Xanthochromia: hemoglobin breakdown products; considered diagnostic for SAH (although controversial).
STEP 4: Be Aware of Common “Mistaken Diagnoses” that end up being an SAH
Acute MI/myocardial ischemia signs – Have been associated with SAH; thought to be related to vasospasm and sympathomimetic effects of SAH (see articles below for further reading)
Cerebral venous sinus thrombosis – Can have variable presentations, but symptomatically can be very hard to distinguish from SAH
Syncope – Not all syncope is cardiogenic or vasovagal. Keep in mind that sudden blood in the brain can induce syncope followed by a temporary recovery that could precede a re-bleed
Vertigo – All nystagmus is not BPPV, use a careful history and clinical judgement on this
Recurrent migraine – Don’t be fooled! Always ask about new/different HA symptoms, different aura, new neurological findings not usually associated with their migraines.
STEP 5: Other than freak out, what do I do?
- Reverse any coagulopathies (FFP, aminocaproic acid, Factor VII, etc.)
- Decrease ICP if patient has evidence of herniation (i.e. mannitol)
- Pain control (helps with BP management as well)
- BP/vasospasm control with nimodipine
- Antiemetics/stool softeners (any straining/valsalva = bad for bleeding in the brain!)
- Surgery with ventriculostomy (bleeds above cerebellum typically) vs craniotomy (more often in cerebellar lesions as this is more of a closed compartment and risk of herniation increases)
- Seizure prophylaxis: since seizures originate in the CORTEX, and most spontaneous subarachnoids are deeper in the midbrain and do not cause seizures, it is up for debate as to whether or not we need seizure prophylaxis on every patient. Consult with your neurosurgeons.
NIMODIPINE: calcium channel blocker used in SAH that inhibits contraction of vascular smooth muscle. Lipophilic, so easily crosses the blood-brain barrier, and has greater effect on cerebral arteries, thus preventing/mitigating effects of cerebral vasospasm
– given orally or via NGT
-needs q4 hour dosing due to 1-2 hour half-life
-dose: 30-60mg q4 hours (differs, literature mostly shows no dose-related improvement, so I would defer to neurosurgery preferences at your institution)
The current up-for-debate topics:
-When can (or should) we start seizure prophylaxis?
-Is CTA, with a negative non-contrast CT, enough to rule out SAH?
-What is the definition of a negative LP result for SAH?
-If tap and CT head are non-diagnostic (ie LP doesn’t clear to near-zero), do we consult neurosurgery? Pursue different imaging studies like a CTA or MRI? Change our approach to consider cerebral venous sinus thrombosis?
Sources for Further Reading:
- Edlow, Jonathan A., and Louis R. Caplan. “Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage.” New England Journal of Medicine 342.1 (2000): 29-36.
- Suarez, Jose I., Robert W. Tarr, and Warren R. Selman. “Aneurysmal subarachnoid hemorrhage.” New England Journal of Medicine 354.4 (2006): 387-396.
- van Gijn, Jan, Richard S. Kerr, and Gabriel JE Rinkel. “Subarachnoid haemorrhage.” The Lancet 369.9558 (2007): 306-318.
- Edlow, Jonathan A., et al. “Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache.” Journal of Emergency Nursing 35.3 (2009): e43-e71.
- Edlow, Jonathan A. “Diagnosis of subarachnoid hemorrhage.” Neurocritical care 2.2 (2005): 99-109.
- Perry, Jeffrey J., et al. “Clinical decision rules to rule out subarachnoid hemorrhage for acute headache.” Jama 310.12 (2013): 1248-1255.
- Perry, Jeffrey J., et al. “High risk clinical characteristics for subarachnoid haemorrhage in patients with acute headache: prospective cohort study.” BMJ 341 (2010).
- Vermeulen, Marian J., and Michael J. Schull. “Missed diagnosis of subarachnoid hemorrhage in the emergency department.” Stroke 38.4 (2007): 1216-1221.
- Diringer, Michael N., et al. “Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference.” Neurocritical care 15.2 (2011): 211-240.
- Edlow, Jonathan A., Adel M. Malek, and Christopher S. Ogilvy. “Aneurysmal subarachnoid hemorrhage: update for emergency physicians.” The Journal of emergency medicine 34.3 (2008): 237-251.
- Byyny, Richard L., et al. “Sensitivity of noncontrast cranial computed tomography for the emergency department diagnosis of subarachnoid hemorrhage.” Annals of emergency medicine 51.6 (2008): 697-703.
- Perry, Jeffrey J., et al. “Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage?.” Annals of emergency medicine 51.6 (2008): 707-713.
- Bederson, Joshua B., et al. “Guidelines for the management of aneurysmal subarachnoid hemorrhage a statement for healthcare professionals from a special Writing Group of the Stroke Council, American Heart Association.” Stroke 40.3 (2009): 994-1025.
- Shah, Kaushal H., and Jonathan A. Edlow. “Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage.” The Journal of emergency medicine 23.1 (2002): 67-74.
- Diringer, Michael N. “Management of aneurysmal subarachnoid hemorrhage.” Critical care medicine 37.2 (2009): 432.
- Le Roux, Peter, et al. “Race against the clock: Overcoming challenges in the management of anticoagulant-associated intracerebral hemorrhage.” Journal of neurosurgery 121.Suppl (2014): 1-20.
- Boesiger, Brian M., and Joseph R. Shiber. “Subarachnoid hemorrhage diagnosis by computed tomography and lumbar puncture: are fifth generation CT scanners better at identifying subarachnoid hemorrhage?.” The Journal of emergency medicine 29.1 (2005): 23-27.
- Mark, Dustin G., and Jesse M. Pines. “The detection of nontraumatic subarachnoid hemorrhage: still a diagnostic challenge.” The American journal of emergency medicine 24.7 (2006): 859-863.
- Asplin, Brent R., and Roger D. White. “Subarachnoid hemorrhage: atypical presentation associated with rapidly changing cardiac arrhythmias.” The American journal of emergency medicine 12.3 (1994): 370-373.
- Benabu, Yves, et al. “Cerebral venous thrombosis presenting with subarachnoid hemorrhage: case report and review.” The American journal of emergency medicine 27.1 (2009): 96-106.
- Seder, David B., and Stephan A. Mayer. “Critical care management of subarachnoid hemorrhage and ischemic stroke.” Clinics in chest medicine 30.1 (2009): 103-122.
- Yamada, Tetsuhisa, and Yoshihiro Natori. “Evaluation of Misdiagnosed Cases of Subarachnoid Hemorrhage and Causal Factors for Misdiagnosis.” Journal of Stroke and Cerebrovascular Diseases 22.4 (2013): 430-436.
- Friedman, Benjamin W., and Richard B. Lipton. “Headache emergencies: diagnosis and management.” Neurologic clinics 30.1 (2012): 43-59.
- MacKinnon, A. D., A. G. Clifton, and P. M. Rich. “Acute subarachnoid haemorrhage: Is a negative CT angiogram enough?.” Clinical radiology 68.3 (2013): 232-238.
- Nomura, Jason T., et al. “A randomized controlled trial of ultrasound-assisted lumbar puncture.” Journal of Ultrasound in Medicine 26.10 (2007): 1341-1348.
- Czuczman, Amanda D., et al. “Interpreting red blood cells in lumbar puncture: distinguishing true subarachnoid hemorrhage from traumatic tap.” Academic Emergency Medicine 20.3 (2013): 247-256.
- Naredi, S., et al. “Increased sympathetic nervous activity in patients with nontraumatic subarachnoid hemorrhage.” Stroke 31.4 (2000): 901-906.
- Wijdicks, E. F. M., H. Kerkhoff, and J. van Gijn. “Long-term follow-up of 71 patients with thunderclap headache mimicking subarachnoid haemorrhage.” The Lancet 332.8602 (1988): 68-70.
- Tung, Poyee, et al. “Predictors of neurocardiogenic injury after subarachnoid hemorrhage.” Stroke 35.2 (2004): 548-551.
- Naidech, Andrew M., et al. “Cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage.” Circulation 112.18 (2005): 2851-2856.
- Stam, Jan. ”Thrombosis of the cerebral veins and sinuses.” New England Journal of Medicine 352.17 (2005): 1791-1798.