Neurology
Question 289 of 300
A 54 year old man presents to the Emergency Department with a 2 hour history of a sudden onset headache. A CT head has been performed which confirms a subarachnoid haemorrhage. What treatment is now indicated?
Answer:
- Consider enteral nimodipine (60 mg orally every 4 hours) for people with a confirmed subarachnoid haemorrhage. This is to prevent delayed cerebral ischaemia and improve outcomes such as survival and being independent in activities of daily living. Nimodipine should be given for 14 to 21 days. If potentially contraindicated (e.g. after recent myocardial infarction), seek specialist advice.
Subarachnoid Haemorrhage
Neurology
Last Updated: 9th January 2024
The most common cause of non-traumatic subarachnoid haemorrhage (SAH) is intracranial aneurysm, accounting for approximately 80% of cases. The remaining 20% are attributed to non-aneurysmal perimesencephalic SAH, arteriovenous malformations, arterial dissections, use of anticoagulants, and other rare conditions. This topic focuses on aneurysmal SAH.
Pathophysiology
Cerebral aneurysms arise at the bifurcation of major arteries that form the circle of Willis. The majority are located at the anterior communicating/anterior cerebral artery junction (Acom/ACA), distal internal carotid artery/posterior communicating artery junction (ICA/Pcom), and middle cerebral artery bifurcation (MCA).
The risk of aneurysm rupture depends on its size, location, the presence of symptoms, the presence of multiple aneurysms, and whether previous aneurysms have ruptured.
When a cerebral aneurysm ruptures, blood flows into the subarachnoid space, sometimes seeping into brain parenchyma and/or ventricles. The sudden increase in intracranial pressure, as well as the destructive and toxic effects of blood on brain parenchyma and cerebral vessels, accounts for most complications.
Risk factors
- Hypertension
- Smoking
- Family history
- Autosomal dominant polycystic kidney disease
- Alcohol use
- Cocaine use
- Marfan syndrome
- Ehlers-Danlos syndrome
- Pseudoxanthoma elasticum
- Neurofibromatosis type I
Clinical features
When carrying out an initial assessment in a person who presents with unexplained acute severe headache:
- have a high index of suspicion for subarachnoid haemorrhage
- take a careful history to establish the rate of onset and time to peak intensity of the headache.
Bear in mind that:
- A 'thunderclap' headache (a sudden severe headache, typically peaking in intensity within 1 to 5 minutes) is a red-flag symptom of subarachnoid haemorrhage.
- Thunderclap headache is associated with other conditions or causes such as migraine, cough, coitus or exertion. Most people with a thunderclap headache do not have a subarachnoid haemorrhage, but this should not deter further investigation if subarachnoid haemorrhage is suspected.
- People with subarachnoid haemorrhage can present with a range of non-specific symptoms and signs and are at greater risk of a diagnosis being missed. Other symptoms and signs of subarachnoid haemorrhage include, but are not limited to:
- neck pain or stiffness
- photophobia
- nausea and vomiting
- new symptoms or signs of altered brain function (such as reduced consciousness, seizure or focal neurological deficit)
- limited or painful neck flexion on examination.
Diagnosis
- Non-contrast CT head:
- Refer the person for an urgent non-contrast CT head scan if review in secondary care by a senior clinical decision-maker confirms unexplained thunderclap headache, or other signs and symptoms that suggest subarachnoid haemorrhage. Be aware that the diagnostic accuracy of CT head scans is highest within 6 hours of symptom onset.
- SAH is confirmed by the presence of the hyperdense appearance of blood in the subarachnoid space/basal cisterns.
- If a CT head scan done within 6 hours of symptom onset and reported and documented by a radiologist shows no evidence of a subarachnoid haemorrhage:
- do not routinely offer a lumbar puncture
- think about alternative diagnoses and discuss with a senior clinical decision-maker
- seek advice from a specialist.
- LP:
- If a CT head scan done more than 6 hours after symptom onset shows no evidence of a subarachnoid haemorrhage, consider a lumbar puncture.
- Allow at least 12 hours after symptom onset before doing a lumbar puncture to diagnose a subarachnoid haemorrhage (this is to allow sufficient time for haemoglobin to degrade into oxyhaemoglobin and bilirubin so that it can be detected on cerebrospinal fluid).
- Diagnose a subarachnoid haemorrhage if the lumbar puncture sample shows evidence of elevated bilirubin (xanthochromia) on spectrophotometry.
- Think about alternative diagnoses if the lumbar puncture sample shows no evidence of elevated bilirubin (xanthochromia) on spectrophotometry.
- CT angiography
- Offer CT angiography of the head without delay to people with a confirmed diagnosis of subarachnoid haemorrhage to identify the cause of the bleeding and to guide treatment.
- Diagnose an aneurysmal subarachnoid haemorrhage if:
- CT angiography of the head shows an intracranial arterial aneurysm and
- the pattern of subarachnoid blood is compatible with aneurysm rupture.
- If CT angiography of the head does not identify the cause of the subarachnoid haemorrhage and an aneurysm is still suspected, consider digital subtraction angiography (DSA), or magnetic resonance angiography (MRA) if DSA is contraindicated.
Initial management
Subarachnoid haemorrhage (SAH) is an acute life-threatening condition. Securing the aneurysm within 48 hours is associated with a lower risk of rebleeding and lower disability rates than delayed aneurysm treatment.
- Assess the patient's level of consciousness. In patients with GCS score ≤8 or falling, use an ABC approach:
- Protect the airway with simple airway manoeuvres and adjuncts (e.g. oropharyngeal or nasopharyngeal airways).
- If indicated, give oxygen to maintain target oxygen saturations >94%. Target saturation of 88% to 92% if the patient is at risk of hypercapnic respiratory failure (e.g. patients with COPD).
- Call the anaesthetist. These patients require intubation, deep sedation, and sometimes paralysis. Cerebroprotective induction is required to protect against laryngoscopy-induced increases in intracranial pressure.
- Use isotonic saline as fluid resuscitation to restore normovolaemia if required. Start with 3 L/day (isotonic/normal saline 0.9%), and adjust infusion for oral intake and supplement other electrolytes as necessary.
- Check pupils for size, shape, and reactivity to light. Fixed and dilated pupils in comatose patients are associated with poor prognosis, especially when present bilaterally.
- Monitor for arrhythmias that can cause haemodynamic instability.
- Nimodipine
- Consider enteral nimodipine (60 mg orally every 4 hours) for people with a confirmed subarachnoid haemorrhage. This is to prevent delayed cerebral ischaemia and improve outcomes such as survival and being independent in activities of daily living. Nimodipine should be given for 14 to 21 days. If potentially contraindicated (e.g. after recent myocardial infarction), seek specialist advice.
- Monitoring
- Observe continuously for signs of deterioration. Monitor (at least until occlusion of aneurysm):
- Neurological status and examination at least every hour
- If the patient is acutely deteriorating (e.g. new focal neurological deficit, seizure, or sudden drop in the patient's level of consciousness) have a high suspicion for rebleed or acute hydrocephalus. Arrange an urgent rescan and consult with the neurosurgeon.
- Consult with a neurologist or neurosurgeon for any patient with clinically apparent seizures. The choice of anticonvulsant depends on patient characteristics.
- BP via arterial line continuously
- BP instability occurs due to the loss of normal cerebral autoregulation as a result of the acute brain injury; BP can also fluctuate after nimodipine and should be monitored to prevent hypotension and decreased cerebral perfusion.
- ECG continuously
- Consult immediately with a cardiologist about any ECG changes. Common cardiac findings in SAH include:
- Arrhythmias and ischaemic changes
- Prolonged QTc
- ST segment/T-wave abnormalities
- Patients with SAH may have ECG changes that mimic acute coronary syndrome and ST-elevation myocardial infarction. Seek specialist advice when deciding whether to perform a CT head scan before or after coronary angiography. Use your clinical judgement alongside specialist input to weigh up the likelihood of the patient having SAH versus acute coronary syndrome.
- Aneurysm rupture can lead to cardiac complications, such as left ventricular subendocardial injury and takotsubo cardiomyopathy (even in the absence of acute coronary disease) leading to treatment delays. SAH can also cause cardiac arrest.
- Consult immediately with a cardiologist about any ECG changes. Common cardiac findings in SAH include:
- Temperature continuously
- Investigate any fever but be aware that in around 20% of patients no infection is found. Give routine antipyretic medication (e.g., paracetamol) and apply cooling blankets to aim for normothermia.
- Neurological status and examination at least every hour
- Observe continuously for signs of deterioration. Monitor (at least until occlusion of aneurysm):
- Initial supportive care (to minimise risk of rebleed until aneurysm is secured)
- Advise bed rest
- Provide analgesia in conscious patients
- Ensure that people with a suspected or confirmed subarachnoid haemorrhage are given effective pain relief.
- Start with paracetamol. Avoid aspirin and non-steroidal anti-inflammatory drugs before aneurysm occlusion.
- For severe pain, give codeine or tramadol. If patient is still in pain give morphine or oxycodone.
- Consider a stool softener and an anti-emetic in conscious patients
- Seek advice from a haematologist for urgent drug-specific reversal strategies
- Stop and where possible reverse all anticoagulation (e.g. warfarin, direct oral anticoagulants). Stop all antiplatelet agents; platelet transfusions are not usually necessary.
- Maintain normovolaemia and avoid hypovolaemia
- Avoid hypotension and hyponatraemia
- Stop any antihypertensive medication and do not treat hypertension unless it is extreme. Maintain systolic blood pressure <180 mmHg until occlusion of aneurysm.
- Treat moderate to severe hyponatraemia (sodium levels <131 mmol/L) with hypertonic saline 3%. Hyponatraemia is the most common electrolyte imbalance in SAH.
- VTE prophylaxis
- Use compression stockings and intermittent compression by pneumatic devices in high-risk patients before occlusion of the aneurysm for the prevention of deep vein thrombosis and pulmonary embolism.
- Avoid hyperglycaemia
- Aneurysm rupture itself can cause stress hyperglycaemia. Follow your local protocol in case of hyperglycaemia.
Referral and further management
- Urgently discuss with a specialist neurosurgical centre the need for transfer of care of a person with a diagnosis of subarachnoid haemorrhage to a specialist neurosurgical centre.
- When referring the patient to a neuroscience unit, specify the following as these will inform management:
- Time from onset of symptoms
- Age
- Comorbidities
- Conscious level
- Any neurological deficit
- An interventional neuroradiologist and a neurosurgeon should discuss the options for managing the culprit aneurysm, taking into account the person's clinical condition, the characteristics of the aneurysm, and the amount and location of subarachnoid blood. They should document a proposed treatment plan based on the following options:
- endovascular coiling
- neurosurgical clipping
- no interventional procedure, with monitoring to check for clinical improvement and reassess the options for treatment.
- If interventional treatment is planned, ensure that it is carried out at the earliest opportunity to prevent rebleeding. Be aware that the risk of rebleeding is highest within 24 hours of the onset of symptoms.
Management of neurological complications
-
- Rebleeding
- A rebleed may substantially alter the prognosis and may even influence the decision whether to treat actively. Consult with a neurosurgeon and arrange an urgent rescan. Do not give antifibrinolytic agents.
- Acute hydrocephalus
- Consult with a neurosurgeon and arrange an urgent rescan. Neurosurgeon may perform a ventriculostomy to drain the excess cerebrospinal fluid.
- Seizures
- Consult with a neurologist or neurosurgeon for any patient with clinically apparent seizures. The choice of anticonvulsant depends on patient characteristics. Levetiracetam and sodium valproate are commonly used.
- Vasospasm and delayed cerebral ischaemia
- Vasospasm is a delayed, focal or diffuse narrowing of large capacitance vessels of the circle of Willis. It accounts for 23% of deaths related to SAH.
- Vasospasm (as seen on angiography) develops between days 3 and 14 after SAH in up to 70% of patients and, of these, around 30% have clinical symptoms.
- Check for the development of new neurological symptoms/signs that may indicate cerebral ischaemia and consult with a neurosurgeon immediately for advice on treatment.
- Clinical pointers to the presence of vasospasm/DCI:
- A drop in GCS score of 2 or more
- A new focal neurological deficit (e.g. unilateral motor or sensory loss, speech disturbance, or visual fields loss) not attributable to rebleeding, hydrocephalus, hyponatraemia, seizures, or any other cause.
- Current available treatments such as triple-H (uses hypertension, hypervolaemia, and haemodilution) or endovascular strategies (e.g. balloon angioplasty or intra-arterial vasodilators) aren’t supported by good-quality clinical trials. Hypertensive therapy alone is, however, still widely practiced.
- Rebleeding
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
