Subarachnoid Haemorrhage

Subarachnoid Haemorrhage

Subarachnoid Haemorrhage and Thunderclap Headache Tom Heaps Consultant Acute Physician Lesson Outline Clinical Case Why is this topic important? Thunderclap Headache (TCH): definition SAH: diagnosis, management and pitfalls Clinical Case Other Causes of TCH New SAH/TCH Clinical Guidelines Summary Readmitted to ED 03/07/14

with collapse/seizures and GCS 10/15 Why is this topic important? 3x Serious Untowards Incidents (SUIs) at HEFT in the last 5 years NCEPOD Managing The Flow 2013 (national audit of 427 SAH cases) room for improvement or unsatisfactory care in 42% of cases 32% of hospitals had no policy for Ix/Rx of acute onset headache 18% of patients had no documented neurological examination diagnosis initially overlooked in 32/75 (may have affected outcome in 23) 49/383 did not have a timely diagnosis of SAH (affected outcome in 10) 68% of patients did not receive CT within 1h of admission 46% of patients with confirmed diagnosis of SAH did not receive nimodipine Acute Medicine Audit July 2014 (n=54)

no current guideline/pathway for the assessment and management of thunderclap headache/SAH at HEFT nearly 1/3 of patients did not have a full neurological examination documented in the medical notes only 28% of patients had CT within 1h of presentation 1/3 of patients with normal CT did not have LP for xanthochromia 39% of patients waited >12h (unnecessarily) for LP following ve CT report no confirmed case had a WFNS grade documented in the notes nimodipine was only commenced in 52% of confirmed cases hourly obs not performed in 30% of cases accepted for neurosurgical transfer delays in transfer >12h in 38% of patients accepted by UHB Thunderclap headache Any severe headache (usually >7/10) with sudden onset

(reaches maximal intensity within seconds to minutes, usually <1 minute) Often (but not necessarily) described as the worst headache of my life SAH in 11-25% Subarachnoid Haemorrhage 5-10% of all strokes peak age 35-65 female > male

85% due to ruptured saccular aneurysm headache is primary symptom in 70% (thunderclap in 50%) headache is the ONLY symptom in ~1/3 of cases often occipital but may be frontal/generalized and lateralizes in 30%

sentinel headache (warning leak) recalled in 10-43% 6-20 days prior Other clinical features of SAH precipitated by exertion (including intercourse) or valsalva in 50% vomiting at headache onset (75% but not specific) syncope/dizziness at headache onset (53%)

meningism 6h after onset (35%) paucity of lateralizing neurological signs (absent in >85% of cases) seizure at headache onset (7%) reduced conscious level (67%) and/or confusion

hypertension history of smoking retinal or subhyaloid haemorrhage ECG changes mimicking ACS (ST elevation) Utility of clinical features of SAH

features highlighted in bold increase the odds of SAH in patient with TCH HOWEVER NO clinical features are sensitive or specific enough to allow the diagnosis of SAH to be made clinically AND the absence of these clinical features, improvement in headache with simple analgesia/triptans or prior history of headaches (including migraine) CAN NOT BE USED TO EXCLUDE SAH CLINICALLY

patients may appear deceptively well at time of first presentation CT FOLLOWED BY LP (if CT negative) IS MANDATORY IN ALL PATIENTS PRESENTING WITH Investigation of TCH CT head is MANDATORY in all patients with TCH (ideally within 1h of presentation) sensitivity for SAH declines with time: 98% at 12h from headache onset, 93% at 24h, 74% at 72h, 50% at 1 week

sensitivity ~100% 6h using modern CT scanners removing need for LP not accepted practice currently in UK LP is MANDATORY in all cases of TCH where CT is negative (and does not show CI to LP) spectrophotometry for xanthochromia ~100% sensitive between 12h and 2w of headache onset additional pick-up rate for SAH very low in practice may detect other pathologies: MEASURE OPENING PRESSURE Inform patient at presentation of the need/rationale for the above diagnostic pathway Reasons for declining CT/LP need to be fully explored and risks carefully explained Discussions need to be fully documented (together with assessment of patient capacity) CONSIDER NEED FOR ADDITIONAL Ix (e.g. MRI/MRA, CTA) in CT/LP ve cases

Initial misdiagnosis of SAH is common 12% in one case series (20% in patients with normal mental status at time of presentation) initial diagnosis overlooked in 32/75 patients in NCEPOD audit (may have affected outcome in 23) failure to obtain CT head at initial contact most common error (>70%)

failure to appreciate spectrum of clinical presentation of SAH (false reassurance provided by absence of associated symptoms/signs etc.) Delays in diagnosis are common 25% in one case series 13% of patients in NCEPOD audit did not have a timely diagnosis of SAH outcome adversely affected in 10/49 of these patients

51/383 patients experienced delay in obtaining CT scan (outcome affected in 4) Management of SAH REFER IMMEDIATELY TO NEUROSURGEONS @ UHB (NORSe or via phone) airway protection bed-rest, analgesia, stool softeners, TEDS

reverse anticoagulation, stop antiplatelets +/- transfuse platelets cardiac monitor, hourly BP/neuro-obs IV fluids (0.9% NaCl), correct hypotension cautious control of hypertension (IV labetalol) aiming sBP <160mmHg

control fever and hyperglycaemia PO nimodipine 60mg/4h (monitor for hypotension) ? high-dose statin (may reduce vasospasm/mortality) no evidence for routine AEDs, steroids, anti-fibrinolytics Case 1 41-year-old male PMHx of migraine with aura during adolescence

Admitted 14/7 ago with severe post-coital headache CT and LP normal (xanthochromia negative) Discharged with PRN indomethacin Presents to AEC with recurrent post coital headache 10/10 severity, like being hit around the head with a baseball bat Associated numbness of left face/arm for 2h No fever/meningism MEWS = O Neurological examination (including funduscopy) NAD Routine bloods and ECG normal

Case 1 cont. Further investigations? Repeat CT/LP?? Possible Diagnoses? Coital Headache/Cephalalgia 30% pre-orgasmic (dull, bilateral, gradually increases) excessive contraction of neck/jaw muscles usually benign 70% orgasmic (sudden onset thunderclap headache at point of orgasm) may be benign but can be associated with underlying pathology SAH (4-12%)

haemorrhage into cerebral tumour ischaemic stroke/cervical arterial dissection spontaneous intracranial hypotension phaeochromocytoma reversible cerebral vasoconstriction syndrome (RCVS) may account for

up to 60% Benign Sex (Primary Coital) Headache Diagnosis of exclusion Pathophysiology unclear rapid increases in blood pressure and heart rate during orgasm? possible migraine variant? Preventative management Indomethacin 25-150mg 30-60min prior to intercourse Propanolol 40-200mg OD (first line if history of migraine) Acute management Sumatriptan or zolmitriptan 5mg intranasal spray Prognosis Single attack or single bout of attacks in 75% More chronic course in 25% (69% remission at 3 years) Case 1 cont.

CT angiography requested Reversible cerebral vasoconstriction syndrome (RCVS) Benign angiopathy of the CNS (BACNS), Call-Fleming syndrome, primary/benign thunderclap headache, crash migraine Recurrent thunderclap headaches +/- transient focal neurological deficits, seizures, altered conscious level, vomiting, ataxia, dysarthria May be triggered by sexual activity, exertion, coughing, straining/Valsalva, emotion, bathing/showering Pathophysiology unclear transient disturbances in regulation of cerebral arterial tone and/or endothelial dysfunction? Associated with:

Migraine Pregnancy, pre-/eclampsia, postpartum angiopathy Vaso-constrictive medications (nasal decongestants, triptans, SSRIs, SNRIs, cocaine, amphetamines, ecstacy, cannabis, nicotine) Reversible cerebral vasoconstriction syndrome (RCVS) CT and LP usually normal Diagnosis made by CTA/MRA arterial beading Occasionally may result in infarction (posterior/watershed), convexity SAH, lobar ICH, PRES, SDH

Symptoms and angiographic vasoconstriction resolve <12w (often <4w) Stop vasoactive drugs Avoid other triggers Some evidence for nimodipine 60mg/4h (avoid hypotension) Thunderclap headache: is CT/LP sufficient? Vascular Non-Vascular Primary Headaches SAH/sentinel headache

Spontaneous intracranial hypotension Thunderclap migraine Symptomatic aneurysms PDPH Cluster headache CVST Pituitary apoplexy Primary cough headache

Cervical carotid/vertebral arterial dissection Arnold-Chiari type 1 / aqueductal stenosis / acute hydrocephalus Primary exertional headache Ischaemic stroke Intracranial infection Primary coital headache ICH/SDH/EDH

Acute sinusitis Primary thunderclap headache Vasculitis/angiitis/GCA Colloid cysts of 3rd ventricle RSVCS Posterior fossa tumours Hypertensive encephalopathy/PRES HaNDL syndrome

MI Aortic dissection CTA/MRA after negative CT/LP? Unrealistic for all cases of thunderclap headache in the NHS Consider in selected cases: persistent severe unexplained headache recurrent admissions with thunderclap headache abnormal neurology/GCS/confusion/seizures raised CSF opening pressure at LP neck pain (?dissection) strong clinical suspicion for cerebral aneurysm risk factors for CVST e.g. post-partum (CTV/MRV) New

SAH/TCH Guideline Coming soon TCH/SAH: Key messages Misdiagnosis and delays in diagnosis of SAH common often with catastrophic results History and examination CANNOT be relied upon to rule out SAH URGENT CT +/- LP MANDATORY IN ALL PATIENTS WITH ACUTE SEVERE HEADACHE (TCH) IRRESPECTIVE OF: presence/absence of associated symptoms/neurological signs

previous headache/migraine history improvement in headache with simple analgesia Medical management often suboptimal pending neurosurgical transfer Negative CT/LP does not necessarily rule out other serious pathology in TCH Any Other Questions?

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