review - oapublishinglondon.comture (lp) and radiographic imag-ing help to clinch the diagnosis. the...

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For citation purposes: Simpson VM, Deshaies EM. Diagnosis and initial management of subarachnoid haemorrhage. OA Emergency Medicine. Co

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Diagnosis and initial management of subarachnoid haemorrhage

VM Simpson, EM Deshaies*

AbstractIntroductionAneurysm subarachnoid haemorrhage is a leading cause of mortality occur-ring in about 10 per 100,000 persons annually. It is characterised by three commonly occurring complaints: ‘worst headache of my life’, photopho-bia and meningismus. It is imperative that emergency department and pri-mary care physicians understand how to diagnose and initially manage aneu-rysm subarachnoid haemorrhage. DiscussionThis review details cerebrospinal flu-id analysis and the current imaging techniques for identifying aneurysm subarachnoid haemorrhage and in-tracranial aneurysms. It will cover the initial management and treat-ment options along with considera-tions in delayed SAH presentation.ConclusionA high suspicion for SAH during the initial evaluation increases the pa-tient’s chance for early intervention and reduces mortality and disability.

IntroductionAneurysm subarachnoid haemor-rhage (SAH) is a leading cause of mortality (40%–50% of SAH), occur-ring in about 10 per 100,000 persons annually; 30,000 SAH in the United States alone each year. SAH is char-acterised by three commonly occur-ring complaints: ‘worst headache of my life’, photophobia and meningis-mus. These symptoms often can be confused with bacterial or viral men-

ingitis and migraine headaches. As a result, aneurysm SAH is initially mis-diagnosed in nearly 12% of patients, a potentially lethal mistake. Misdiag-nosis increases the risk of re-bleeding and subsequent death1. The rule of thirds dictates that one-third of the patients with SAH die before reaching the hospital, another third present with irrecoverable neurological defi-cits and the last third make it to treat-ment; half of the last third will have long-term disabilities (Figure 1)2. In short, only about 16% of patients will be left with minimal or no permanent neurological sequelae after SAH.

A high suspicion for SAH during the initial evaluation in the Emer-gency Department or by the Primary Care Physician increases the patient’s chance for early intervention and re-duces mortality and disability. Stand-ardised protocols for the evaluation of patients with ‘headache’ in the Emer-gency Department currently does not exist, further complicating the initial evaluation and disposition of these patients; such a protocol may save lives. Here, we review the diagnosis and initial management of suspected aneurysm in patients with SAH.

DiscussionAetiologyTrauma is the most common cause of SAH, followed by ruptured intracra-nial aneurysm (75%–80%) and arte-riovenous malformations (4%–5%). Other causes to consider include: central nervous system vasculitis, cerebral artery dissection, coagu-lopathy, dural venous sinus throm-bosis, spinal cord arteriovenous mal-formation or dural fistula, sickle cell disease and sympathomimetic drugs such as cocaine. In 14%–22% of SAH,

no cause can be identified on angi-ography even with multiple modes of imaging. In this case, the aetiol-ogy may be from a venous bleed (perimesencephalic haemorrhage) or small aneurysm that auto-throm-bosed and no longer fills with blood; this is referred to as angiographic negative SAH3. Patients with SAH who are suspected of having a rup-tured aneurysm should be evaluated for risk factors associated with brain aneurysm formation, a spinal tap to look for blood in the cerebrospinal fluid and radiographic imaging.

Risk FactorsMany risk factors for brain aneurysm formation and haemorrhage are mod-ifiable with medication or behaviour-al changes; cigarette smoking and hy-pertension being the most important (Table 1)4. Identification of risk fac-tors in men and women aged 18–49 years concluded that SAH in this age group is mostly associated with ciga-rette smoking, illicit drug use and hy-pertension5. A 70%–75% of patients with SAH had a prior history of smok-ing and 50%–60% are current smok-ers. Other independent risk factors in this study included a low Body Mass Index, family history of haemorrhagic stroke, and low educational achieve-ment; the increased risk of SAH per-sists even after cessation of cigarette smoking6. The odds ratio (OR) of SAH in previous smokers (OR, 4.1; 95% confidence interval (CI): 2.7–6.0) and current smokers (OR, 5.4; 95% CI: 3.7–7.8) suggests that the haemody-namic, but not structural changes in-duced by smoking, may resolve after smoking cessation6.

Genome linkage studies observing 104 siblings affected with intracranial

* Corresponding author Email: [email protected]

Department of Neurosurgery, SUNY Upstate Medical University, Syracuse, NY, USA

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to as the ‘worst headache’ of a per-son’s life. Photophobia, meningismus, vomiting and syncope soon ensue. If severe headache is the only symp-tom, the chance of SAH is only 10%10. Other causes of similar headaches in the differential diagnosis include se-vere acute paroxysmal headache, be-nign thunderclap headache (or crash migraine), reversible vasoconstric-tive syndrome and benign orgasmic cephalgia. In 30%–60% of patients presenting with SAH, a transient head-ache may occur briefly for a day or so before clearing; these are called warn-ing headaches from a sentinel haemor-rhage. Warning headaches may occur without SAH and be due to aneurys-mal enlargement or haemorrhage con-fined within the aneurysm wall.

The hallmark symptoms of SAH are the result of blood in the subarach-noid space irritating the meninges and spinal nerve roots, which may produce Kernig’s or Brudzinski’s sign. Fundoscopic examination often unveils ocular haemorrhages (20%–40%) classified into three categories: subhyaloid or preretinal haemor-rhage (11%–33%), vitreous haemor-rhage also called Terson syndrome (4%–27%), and intra-retinal hemor-rhage11. Other less specific and less commonly found symptoms include transient loss of consciousness, cra-nial nerve palsies, diffuse weakness, diplopia, ptosis and seizures. When aneurysm SAH is suspected based on these symptoms and findings from physical examination, lumbar punc-ture (LP) and radiographic imag-ing help to clinch the diagnosis. The initial clinical severity of acute SAH should be determined rapidly by us-ing simple validated scales, including the Hunt and Hess Grading Scale12 (Table 2) and Fisher Scale13 (Table 3), due to their usefulness as an indica-tor of potential outcome.

Lumbar Puncture for cerebrospinal fluid analysisAnalysis of the cerebrospinal fluid (CSF) for suspected SAH can be

Nord-Trondelag Health Study and the Tromos Study in Norway exam-ined a potential synergism between cigarette smoking, hypertension and regular alcohol consumption. There was an additive relative excess risk between hypertension and current smoking (6.40; 95% CI: 0.88–11.92) in 122 cases of SAH followed for 977,895 person-years9. These popu-lation studies suggest that screening and preventive treatment of patients with a family history of SAH will cause a modest reduction in the in-cidence of SAH. Reducing the preva-lence of modifiable risk factors such as ethanol ingestion, smoking and hypertension will also reduce the in-cidence of SAH.

Warning Signs and SymptomsThe hallmark symptom of SAH is a thunderclap headache, often referred

aneurysms mapped the occurrence of brain aneurysms to chromosome 7q117. The best evidence for linkage was detected at D7S2472 in the vi-cinity of the elastin gene (ELN). The haplotype between the intron-20 and intron-23 polymorphisms of ELN was strongly associated with brain aneurysms (P < 0.000) and homozygous patients were at high risk (OR = 4.39, P = 0.002) suggest-ing a genetic placement near the ELN locus on chromosome 77. Ethanol ingestion may also be an important contributor to SAH. Drinking 100–299 g of ethanol per week account-ed for 11% of the SAH cases while >300 g per week accounted for 21% and smoking for 20%. An additional 17% of the cases were attributed to hypertension, 11% to a positive fam-ily history of SAH8. A prospective population-based cohort from the

Figure 1: The rule of thirds dictates patient outcome after subarachnoid haemorrhage (SAH). Only 16% of people experiencing SAH recover with minimal or no permanent disability.

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helpful in making the diagnosis of brain aneurysm bleeding. Various methods can be used to obtain CSF but the simplest, fastest and saf-est way typically is with an LP. An LP can be performed at the bedside with local analgesia. Generally ac-cepted guidelines dictate that an LP should be performed at least 6 h after symptom onset; this timing has been suggested because circulation of the blood cells in the CSF from the brain to the lumbar region will not be im-mediately present and can be missed if performed too early. The CSF should be collected in four separate sterile tubes and sent for analysis specifically looking for red blood cell (RBC) count in the first and fourth tubes to help distinguish between blood from SAH and a traumatic tap; spectrophotometric analysis is also performed to test for the presence of xanthochromia. RBCs lyse in the CSF, releasing haemoglobin. Heme-oxyge-nase-1 then degrades the haemoglo-bin into bilirubin in the CSF and this can be identified as a yellowish dis-coloration of the CSF, or xanthochro-mia. Sometimes xanthochromia can be seen with the naked eye against a white background, but spectropho-tometric analysis is more sensitive and more reliable. Spectrophotom-etry has a specificity of 97% (95% CI: 92%–99%) but only 29% speci-ficity with visual inspection (95% CI: 23%–35%)14.

Xanthochromia will not be appar-ent until the second to fourth hour af-ter SAH and is not seen with a single traumatic tap. It is present in almost 100% by12 h after the SAH, 70% at 3 weeks, and is still detectable at 4 weeks15. A traumatic tap would result in a large number of RBCs in the first CSF tube and far fewer in the fourth tube once the blood from the tap has cleared through the needle. Charac-teristic findings of CSF analysis with SAH include xanthochromia and a high number of RBCs in all four col-lection tubes. Critical to note is that lowering the CSF pressure during

Table 1 Risk factors for aneurysm formation (Reproduced with permission from Frontera4)

Modifiable risk factors Non-modifiable risk factorsCigarette smoking (dose-dependent effect on aneurysm formation)

Previous subarachnoid haemorrhage (new aneurysm formation rate 1%–2% per year)

Hypertension Polycystic kidney diseaseModerate to heavy ethyl alcohol use

Connective tissue disease (Ehlers–Danlos syndrome, Marfan syndrome)

Cocaine use Aortic coarctationEndocarditis (mycotic aneurysm) Pseudoxanthoma elasticum

Moyamoya diseaseArteriovenous malformationFibromuscular dysplasiaDissection w/pseudoaneurysmVasculitisNeurofibromatosis 1Glucocorticoid remediable hyperaldoster-onismFamily history (two first to third degree relatives with IA; 8% risk of having an unruptured aneurysm)

Table 3 Modified Fisher and Fisher Scale for subarachnoid haemorrhageGrade Modified Fisher % with

vasospasmFisher % with

vasospasm0 No SAH or intraventricu-

lar haemorrhage (IVH)— —

1 Thin SAH, no IVH 24 No SAH or IVH 212 Thin SAH w/IVH 33 Diffuse or vertical lay-

ers <1mm thick25

3 Thick SAH, no IVH 33 Local clot and/or ver-tical layer≥ 1mm

37

4 Thick SAH w/IVH 40 Intracerebral or IV clot with diffuse or no SAH

31

Table 2 Hunt and Hess Grading Scale for subarachnoid haemorrhageGrade Clinical exam Assoc.

mortality (%)Mean Glascow Outcome score

1 Asymptomatic, mild headache, slight nuchal rigidity

1 4

2 Cranial nerve palsy, mod-severe headache, severe nuchal rigidity

5 4

3 Mild focal deficit, lethargy, confusion 19 34 Stupor, mod-severe hemiparesis,

early decerebrate rigidity40 2

5 Deep coma, decerebrate rigidity, moribound appearance

77 2

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Other studies report that CT sensitiv-ity is slightly lower, between 95% and 100% on the first day, falling to about 58% at 5 days and less than 50% af-ter 1 week17. By day 10, the blood may have been totally resorbed. Some con-troversy exists about the utility of LP if CT scans are negative for SAH within 6 h of ictus18. A more recent study com-pleted in 2012 found that the sensitiv-ity of head CT within 6 h of ictus was 98.5% (95% CI: 92.1%–100%), diag-nosing all patients with aneurysmal and perimesencephalic SAH; sensitiv-ity of CT performed after 6 h was only 90.0% (95% CI: 76.3–97.2)19. Thus, this group concluded that there was no added value of CSF analysis in patients presenting with acute headache and normal head CT within 6 h after ictus. In patients with an atypical presenta-tion however, it is still recommended that CSF analysis be performed to look for RBCs and xanthochromia. It is our opinion that patients presenting with hallmark signs of aneurysm SAH and a negative CT scan of the brain get an LP for CSF analysis, as this remains the standard of care.

CT Angiography The accuracy of CT angiography (CTA) for identifying brain aneu-rysms, particularly helical CTA, is ap-proaching that of catheter-based dig-ital subtraction angiography (DSA). DSA remains the gold-standard study for the radiographic diagnosis and pre-treatment planning for patients with brain aneurysms. Advantages of CTA over DSA include its non-in-vasive nature, fewer resources, lower risk of complications and morbidity, and suitability for critically ill or un-stable patients20.

The negative predictive value of CTA for detecting aneurysm ranges from 82% to 96% on a multi-detec-tor CT scanner with sensitivity and NPV approaching 100% on a ‘per aneurysm’ basis17. The lower sensi-tivity is associated with aneurysms measuring less than 3 mm but may be improving with newer techniques

Imaging AnalysisCT for SAHCT is a very sensitive radiographic means of detecting acute SAH but should not be relied on as the sole investigational tool (Figure 2). Older generation CT scanners detected acute SAH 93%–95% of the time within the first 24 h after onset of symptoms. The sensitivity of CT scans for SAH decreases with time as the blood prod-ucts disperse within the CSF, clots dis-solve and blood gets reabsorbed from the spinal fluid. Modern CT scanners are more sensitive detectors of SAH with reports of 100% sensitivity up to 5 days after symptom onset and an overall sensitivity of 99.7% (95% CI: 98.1%–99.9%) and specificity of 100% (98.2%–100%)16. Despite the high sen-sitivity and specificity, suspected SAH with a negative CT scan still requires LP to confirm the absence of SAH16.

an LP can precipitate re-bleeding by increasing the transmural pressure across the aneurysm dome. A second cautionary measure is to confirm ra-diographically that there is no con-traindication to spinal tap such as non-communicating hydrocephalus from blood in the fourth ventricle or early signs of brainstem herniation, both of which could result in fur-ther neurological compromise and death. Therefore, it is recommended that only a small amount of CSF be removed and a small (≤20G) spinal needle be used to avoid post-LP CSF leakage and delayed herniation. Pa-tients arriving to the hospital later than day three after symptom on-set should always have an LP even if computed tomography (CT) scan does not show SAH; CT scan loses its sensitivity for SAH detection beyond this time period.

Figure 2: Non-contrast enhanced computed tomography (CT) reveals subarachnoid haemorrhage. Arrows indicate blood in the left sylvian fissure.

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and the 64-slice multi-detector CT scanner. The introduction of spiral CTA has led to improved resolution and prompted some claims that CTA achieves equivalent diagnostic ac-curacy to that of DSA for brain aneu-rysms. However, the sensitivity for the detection of aneurysms smaller than 3 mm is still felt to be less than 90%21. Depending on the history and pattern of blood on the non-contrasted brain CT scan, a negative result on CTA still warrants further investigation.

Magnetic Resonance Imaging and AngiographyIn cases of proved SAH where CTA and DSA are negative magnetic resonance imaging (MRI) is used to search for other causes of SAH. MRI is useful for detecting cavernous angio-mas of brain or spinal cord and cer-ebral venous sinus thrombosis. MRI is more sensitive than CT in detecting SAH (91%–100%) after day five us-ing a gradient echo sequence17. Mag-netic resonance angiography (MRA) is used mainly to monitor already diagnosed aneurysms and those treated with surgical clip ligation and endovascular embolisation. It has a sensitivity of about 94% when the aneurysm is greater than 3 mm in size but only 38% for smaller ones;17 gadolinium-enhanced MRA may in-crease the sensitivity22. For medium- and large-sized aneurysms, the sen-sitivity of MRA is comparable to CTA. CTA remains superior to MRA for aneurysms smaller than 5 mm, with MRA sensitivity dropping to 56% for aneurysms of this size range23.

Catheter-based DSADSA remains the gold-standard radi-ographic test for detecting pathology of the intracranial vasculature (Fig-ure 3). If SAH is confirmed and CTA is negative, then DSA should be con-sidered depending on the blood pat-tern on plain CT. DSA is minimally in-vasive and associated with <1% risk of complications. More specifically, it carries up to a 0.8% risk of serious

Figure 3: Digital subtraction angiography: right internal carotid artery injection shows anterior communicating artery aneurysm.

non-neurological complications and a 0.5% rate of transient neurological complications. In addition, one study reported a 2.6% risk of a second haemorrhage from a ruptured aneu-rysm during DSA performed within 6 h after initial SAH24.

The risk associated with DSA, though minimal, has been the impe-tus for further evaluation of the effi-cacy of three-dimensional (3D)-CTA compared with DSA for aneurysm di-agnosis of brain aneurysm after SAH. 3D-CTA was found to have an overall sensitivity of 96.3%, specificity of 100% and accuracy of 94.6%, com-parable to that of DSA. However, DSA is better for detecting smaller aneu-rysms. Aneurysms less than 3 mm in diameter were more likely to be detected on DSA (90.9% sensitivity)

than with 3D-CTA (81.8% sensitiv-ity)22. In a comparative study on diag-nostic validity of cerebral aneurysm by CTA vs. DSA after SAH, CTA was 89% sensitive and 100% specific, whereas DSA was 74% sensitive with the same specificity. The positive predictive value of both methods was 100%, but the negative predictive value was higher for CTA (85%) than DSA (69%)25. If the surgery is carried out based on CTA alone, aneurysms less than 4 mm may be missed and not repaired during surgery.

Evaluation of Radiographically Negative SAH Previous studies suggest that the overall incidence of DSA-negative SAH ranges from 10% to 20%26. A definitive diagnosis in this sub-

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longer term re-bleed rate for unse-cured brain aneurysms is 15%–20% in 2 weeks, 50% in 6 months and then drops to ~3%/year with a mortality rate of 2%/year. About 50% of the patients who re-bleed will die3. A re-cent retrospective review found that there was a higher risk of re-bleeding in patients with intracerebral or in-traventricular haematoma, high se-rum glucose level (>113.8 mg/dl) on admission, posterior circulation an-eurysms, male gender, hypertension and worse clinical status28. The best method for preventing aneurysm re-bleeding is early treatment of the aneurysm with surgical clip ligation (Figure 4) or endovascular embolisa-tion (Figure 5)26.

Antifibrinolytic agents have been used to reduce the incidence of early

nicardipine, labetalol and esmolol be-cause of their short half-life, reliable dose response and favourable safety profile. They recommend avoiding ni-troprusside in neurological emergen-cies because of its tendency to raise intracranial pressure and cause toxic-ity with prolonged infusion26. A ret-rospective study evaluated the use of nicardipine or labetalol for blood pres-sure control in patients with SAH and concluded that nicardipine was supe-rior27. After the aneurysm has been secured, less stringent blood pressure parameters are tolerable.

Re-bleedingFor untreated ruptured aneurysms, the re-bleed rate is 4% on the first day then 1%–1.5% everyday thereaf-ter until the aneurysm is secured. The

group is only obtained 2%–21% of the time. Some possible causes of a confirmed SAH on CT or LP with negative radiographic imaging in-clude auto-thrombosed aneurysms, venous perimesencephalic haem-orrhage, venous sinus thrombosis, vascular lesions of the spine, spinal neoplasms, pregnancy-induced hy-pertension, sympathomimetic drug abuse, bleeding dyscrasias, antiplate-let agents and anticoagulants. Failure to detect a vascular lesion places the patient at risk for recurrent haemor-rhage. Strategies for managing these patients with radiographically nega-tive SAH include subsequent DSA ap-proximately 1 week after the ictus in an effort to detect missed vascular le-sions such as thrombosed aneurysms that may recur, micro-arteriovenous malformation (AVM), and dural or pial arteriovenous fistula (AVF)11. Further outpatient vascular imag-ing should be performed when the index of suspicion remains high de-spite previous negative studies. Con-trasted MRI of the brain and cervical spine, diffusion weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) of the brain, should be considered to look for subtle in-tracranial lesions such as neoplasms, vascular and cavernous malforma-tions. Laboratory analysis should also be considered to evaluate for vasculitis, coagulopathies, drug use, and pregnancy-related hypertension.

Initial Management and TreatmentBlood PressureControl of hypertension is very impor-tant to lower the risk of re-bleeding from the tenuous aneurysm wall26. Maintaining normotension, systolic blood pressure (SBP) < 130 in patients presenting with SAH can be performed quickly with calcium-channel blockers or β-blockers. We commonly use nica-rdipine or labetalol, sometimes as a combined therapy in difficult-to-man-age situations. The American Heart and Stroke Associations recommend

Figure 4: Aneurysm clip on the base of a posterior communicating artery aneurysm. The arrow points to the neck of the aneurysm pinched closed by the clip. The filled arrow-head indicates the location of the right optic nerve.

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is more prominent in those of in-creased age, poor clinical grade and more extensive blood on CT scan. For symptomatic hydrocephalus, an external ventricular drain (EVD) may be needed emergently to drain CSF and reduce intracranial pres-sures that would otherwise result in brainstem herniation syndrome. Care must be taken not to overdrain the CSF, because this would change the transmural pressure across the aneurysm dome and increase the risk of re-rupture; EVDs are adjusted to maintain intracranial pressures at 15–20 cm of H2O31.

SeizuresThe incidence of seizure activity at the time of SAH is 25%, most com-monly seen after an MCA aneurysm rupture. A seizure at the onset of aneurysm rupture is a predictor of poor outcome. Seizures increase the risk of aneurysm re-rupture in a pa-tient with an unsecured aneurysm32.

of the significant prothrombotic side effects of antifibrinolytic agents and the advent of endovascular therapy, these drugs are rarely used today.

HydrocephalusAcute hydrocephalus can result from SAH blood obstructing the flow of CSF through the ventricular system or by altering reabsorption by the arachnoid granulations. Radiograph-ic evidence of hydrocephalus will occur in 15% of patients with SAH, 40% of these will become sympto-matic (Figure 6)30. Hydrocephalus

re-bleeding when early definitive treatment is not available. Because antifibrinolytics can cause vasos-pasm, their use should be limited to within 72 h of ictus and should not be used in patients with coagulopa-thy, history of myocardial infarction, ischemic stroke, pulmonary emboli or deep venous sinus thrombosis4. The antifibrinolytic, tranexamic acid can reduce early re-bleeding rates and adverse outcomes (from 10% to 2%) when the drug was administered immediately after the diagnosis of SAH29. However, because

Figure 5: Arrowhead points to a basilar tip aneurysm occluded with coils after subarachnoid haemorrhage. Arrow indicates narrowing of the basilar artery indicative of severe cerebral vasospasm.

Figure 6: Computed tomography slice reveals subarachnoid haemorrhage with hyperintense areas in the centre corresponding to blood in the subarachnoid basal cisterns. Laterally, there is a discrete widening of the temporal horns of the lateral ventricles, indicating that the patient has hydrocephalus.

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Figure 7: CT perfusion demonstrating left posterior cerebral artery spasm with reduced cerebral blood flow in the left posterior parietal lobe (blue); notice the difference in cerebral blood flow between the right (60.9) and left (31.1) lobes.

Prophylactic use of antiepileptic drugs in patients with SAH is contro-versial. A retrospective study inves-tigating the impact of prophylactic phenytoin use in SAH patients result-ed in worse cognitive outcomes at 3 months after SAH33. However, the de-velopment of safer drugs with fewer side-effects may be beneficial in high risk patients with SAH suffering from intraparenchymal bleeds or those who are comatose and close neuro-logical monitoring is not possible.

Considerations in Delayed SAH Presentation Hyponatraemia The most common electrolyte im-balance in patients with SAH is hy-ponatraemia. The reported incidence of hyponatraemia after SAH ranges from 10% to –30%. It is more com-mon in patients with poor clinical grade, anterior communicating ar-tery aneurysms and hydrocephalus; and it may be an independent risk factor for poor outcome26. Both syn-drome of inappropriate antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) are common causes of hyponatraemia in the setting of SAH. These electrolyte imbalances usually do not occur immediately af-ter SAH and are not dealt with during the initial assessment. However, pa-tients who present in a delayed fash-ion may have hyponatraemia need-ing correction with hypertonic saline solution. It is important to recognise the aetiology of hyponatraemia be-cause SIADH represents positive wa-ter balance while CSW is associated with a negative total body water bal-ance, the latter of which can exacer-bate cerebral vasospasm (CV) and cerebral ischaemia if treated inap-propriately34. Current guidelines rec-ommend avoidance of large volumes of hypotonic fluids and intravascular volume contraction.

Cerebral VasospasmCV is a constriction of the cerebral vasculature that results from blood

products circulating in the CSF from SAH. It is believed that the SAH causes an inflammatory reaction in the ba-sal cisterns of the brain inducing CV, the most common cause of delayed cerebral ischaemia and neurologi-cal deficits after SAH. The risk of CV increases with the amount of blood in the subarachnoid space and typi-cally does not begin before the fourth day after SAH and can last for 14–21 days10,35. CV can be detected on radio-graphic imaging and also by bedside transcranial Doppler studies (TCDs). Although the specificity and sensi-tivity of TCDs are operator depend-ent, severe CV can be identified with fairly high reliability26. DSA remains the gold standard for the diagnosis of CV and it assesses vessel calibre and cerebral blood flow (Figure 5).

Other ancillary tests that may aid in the diagnosis of CV include static ra-diographic studies such as CTA and MRA. Cerebral blood flow evaluation with CT and MR perfusion (Figure 7), and SPECT scans may be more use-ful for clinical management, but most important is continuous neurological assessment with careful neurological examinations.

Treatment OptionsTreatment options for ruptured brain aneurysms consist of cranioto-my with surgical clip ligation and en-dovascular embolisation. A detailed discussion of the benefits and risks of each treatment option are beyond the scope of this text. In brief, howev-er, a neurosurgeon must be consulted to assess the patient with SAH and

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discuss treatment options and per-form immediate intervention to sta-bilise the patient’s intracranial pres-sures and secure the aneurysm. If no neurosurgical services are available at the institution, the patient should be stabilised for transfer to a facility that can provide all treatment op-tions and post-treatment intensive care unit services (Figure 8). Early aneurysm treatment significantly re-duces the risk of lethal rebleeding26. When deciding surgical or endovas-cular treatment of a ruptured an-eurysm, sac morphology, aneurysm location, presence of an intraparen-chymal clot, medical co-morbidities and experience of the treating neu-rosurgeon or endovascular specialist are all important factors.

ConclusionIt is imperative that emergency de-partment and primary care physi-cians understand how to diagnose and initially manage aneurysm SAH. Recent evidence-based literature recommends non-contrasted head CT scan as the initial first step in evaluation of SAH followed by LP if radiographic imaging is non-diag-nostic. CSF analysis with spectro-photometry provides a specificity of 97% for xanthochromia. Advanc-ing technology has improved the sensitivity and specificity of CTA for detecting brain aneurysms and approaches that of DSA. However, DSA remains the gold-standard and serves as an important tool for plan-ning treatment. It is important to control hypertension immediately following SAH to reduce the risk of an aneurysm re-bleed. A high suspi-cion for SAH during the initial evalu-ation increases the patient’s chance for early intervention and reduces mortality and disability.

Abbreviations list3D, three-dimensional; CI, confi-dence interval; CSF, cerebrospinal fluid; CSW, cerebral salt wasting; CTA, CT angiography; CV, cerebral

vasospasm; DSA, digital subtraction angiography; DSA, digital subtraction angiography; EVD, external ventricu-lar drain; LP, lumbar puncture; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; OR, odds ratio; RBC, red blood cell; SAH, subarachnoid haemorrhage; SIADH, syndrome of inappropriate antidiuretic hormone; TCD, transcra-nial Doppler studies.

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Figure 8: Modifications to current diagnostic protocols arranged according to the distribution of haemorrhage on admission CT scans. (a) Proposed diagnostic algorithm for patients with classic haemorrhage distribution. Detailed follow-up testing is recommended given the likelihood of finding a causative lesion. (b) Diagnostic algorithm for patients with perimesencephalic haemorrhage. Delayed follow-up vascular imaging is performed to detect posterior circulation aneurysms. Laboratory studies (e.g. inflammatory markers) and MRI are of low yield in this subgroup and have been excluded. (c) Diagnostic algorithm for patients with an abnormal lumbar puncture. Laboratory studies (e.g. inflammatory markers) are of low yield in this subgroup and have been excluded. †Follow-up MRI of the brain with FLAIR could be considered in patients in whom the lumbar puncture is non-diagnostic or to confirm a positive result; *follow-up MRI of the cervical spine is recommended in patients with signs and symptoms of spinal pathology. (Reproduced with permission from Little et al36.)

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