A 31-year-old man with sudden onset headache and vomiting

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Problem 46 A 31-year-old man with sudden onset headache and vomiting

Andrew Zacest

You are working in the emergency department and a 31-year-old man is brought in after collapsing and vomiting while watching television at home the previous evening. It was reported that he had a generalized seizure. When he awoke he was complaining of a severe headache. He is known to drink alcohol excessively and has a 20 pack-year smoking history. He had been binge drinking over the weekend. There is no known history of hypertension.

Q.1

What is the differential diagnosis?

Q.2

What are the key features of the neurological examination in this patient?

On arrival he is alert but agitated, disorientated to time and obeying commands. He is afebrile, but has marked neck stiffness. His heart rate is 52/min and blood pressure 130/80 mmHg. Neurological examination shows no cranial nerve or focal neurological deficit. On investigation his haemoglobin is 127 g/L, white cell count 8.4 and platelets 111 000. His serum biochemistry (including calcium and glucose) is within normal limits and a serum troponin is negative. His chest X-ray is normal and an ECG shows sinus bradycardia with T-wave inversion.

Q.3

What is the next appropriate investigation and what difficulties might be encountered in obtaining this?

The patient required intravenous morphine and midazolam for the radiological investigation.

Q.4

What does the CT head scan (Figure 46.1) show?

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Figure 46.1

On the advice of the consulting neurosurgeon, the patient was retrieved to the nearest neurosurgery centre and had further investigations to determine the cause of the subarachnoid haemorrhage.

Q.5

What are the two investigations shown in Figures 46.2 and 46.3 and what do they show?

image

Figure 46.2

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Figure 46.3

Q.6

What treatment options are available for a patient with a ruptured cerebral aneurysm?

Endovascular coiling was attempted in the patient but was technically unsuccessful.

The patient underwent craniotomy and clipping of the aneurysm which was successful. The patient was making good progress until the third postoperative day when he became progressively confused, verbally abusive and drowsy.

Q.7

What are the diagnostic possibilities and what investigations would be helpful?

The patient’s blood pressure was 140/80 mmHg, temperature 38.6°C and oxygen saturation 100% on room air. A CT head showed no new intracerebral haemorrhage, no hypodensity consistent with infarction or hydrocephalus. The angiogram did not show any evidence of vasospasm. The serum sodium was 121 mmol/L, potassium 4.6 mmol/L, osmolality 266 mmol/kg (270–300), urine osmolality 116, urine sodium 177 mmol/L (40–100).

Q.8

Discuss the diagnosis, pathophysiology and treatment.

The patient was transferred to the high dependency unit for administration of hypertonic saline, monitoring of arterial blood pressure and fluid balance monitoring and oral sodium replacement. The patient progressively improved and was transferred back to his local hospital 3 weeks following his haemorrhage. He was reviewed 3 months following surgery and was doing well. He was smoking again.

Q.9

What are risk factors for aneurysm formation and subarachnoid haemorrhage and what advice should be given to this patient?

Answers

A.1 This is a young man who has suddenly collapsed with vomiting and headache and therefore subarachnoid haemorrhage (SAH) should be considered the diagnosis of exclusion in this patient. Primary intracerebral haemorrhage, secondary to an arteriovenous malformation or hypertensive haemorrhage should also be considered, given the young age. The possibility of a traumatic intracerebral haemorrhage, e.g. subdural haematoma, particularly in a patient with unclear history and a history of alcohol abuse, needs to be considered. Intracranial infection, e.g. meningitis, would be less likely to present with such an acute ictus.

A.2 The neurological examination of any patient has two key aims – to establish the diagnosis and to determine the site of the lesion.

Focus on:

• The level of consciousness (alert or drowsy).
• Glasgow coma score (GCS) (see Table 42.1).
• Cranial nerve examination, particularly the pupillary size and reactivity and external ocular movements, suggests brainstem compression.
• Signs of meningeal irritation suggesting meningeal blood or infection.
• Signs of head trauma – e.g. scalp bruising, laceration or tenderness, CSF leak.
• Limb weakness, e.g. hemiparesis, indicates a contralateral supratentorial lesion usually.
• Vital signs especially HR, BP and temperature.

A.3 A CT head scan with and without contrast needs to be performed urgently in any patient in whom subarachnoid haemorrhage is in the differential diagnosis. If the CT cannot be performed at the receiving facility then the patient should be retrieved to an appropriate facility as soon as possible. Patients who are agitated may require intravenous sedation and even intubation to facilitate or even safely perform this test. It is preferable to avoid intubation to allow careful neurological assessment to be made.

A.4 The CT head shows diffuse subarachnoid haemorrhage around the brainstem.

A.5 The first is a CT angiogram and shows a left terminal internal carotid artery aneurysm. The second test is a cerebral angiogram (digital subtraction angiogram) which shows the aneurysm at the termination of the left internal carotid artery – at the point where it bifurcates into the middle and anterior cerebral arteries.

A.6 Endovascular coiling and craniotomy and surgical clipping of the aneurysm are the two choices. Both techniques can be effective in securing the aneurysm and preventing rebleeding and death. Important variables that may favour one technique over the other include the relative neck to dome ratio (coiling more favourable with a narrow neck), ease of access to the aneurysm location (posterior circulation aneurysms are more difficult surgically), and the presence of active vasospasm and brain swelling (surgical retraction may be more hazardous).

A.7 For 3 weeks following aneurysmal SAH the patient is at potential risk for a rebleed (if the aneurysm is not secured), cerebral vasospasm, fluid and electrolyte disturbance and postoperative surgical and medical complications, including seizures, wound or systemic infection. The history should determine when the deterioration occurred (vasospasm unlikely before 3 days, peaking at 7–10 days and less likely after 2 weeks), whether the deterioration occurred gradually (electrolyte disturbance or progressive ischaemia from vasospasm) or suddenly (acute vascular events or seizures). Vital signs, wound review and a detailed neurological exam will establish important changes from prior baseline. Electrolytes, cardiac enzymes, full blood count, ECG, CXR would be appropriate. An urgent CT with angiography is essential.

A.8 The patient has hyponatraemia. Following SAH hyponatraemia is most commonly due to either cerebral salt wasting (CSW) or the syndrome of inappropriate antidiuretic syndrome (SIADH). The former is currently believed to be due to release of atrial natriuretic (ANF) following SAH which results in the loss of urinary sodium and also water through the kidneys. The distinction can be made by examining the urinary sodium excretion which is well above normal in CSW as well as there being clinical and biochemical evidence of hypovolaemia (reduced CVP, elevated haematocrit). The treatment of CSW is sodium and volume replacement together and for SIADH, volume restriction. A potential hazardous situation may arise if an erroneous diagnosis of SIADH is made, the patient is fluid restricted and hypovolaemia is exacerbated resulting in inadequate cerebral perfusion and ischaemia. If in doubt treatment for CSW with volume and sodium replacement is safer.

A.9 Risk factors for the formation of aneurysms include a prior aneurysm, smoking, cocaine use, hypertension, a family history of aneurysms and some inherited connective tissue disorders, e.g. Marfan’s syndrome. Up to 20% of patients who have one aneurysm may have another at some point in the future. The most modifiable of all the patient’s risk factors will be to cease smoking.

Revision Points

Subarachnoid Haemorrhage

Although spontaneous SAH has a number of potential causes, rupture of a cerebral aneurysm is the most common (75–80%) and the most important cause clinically because untreated the 30-day mortality is 46%. The most important management step for the non-specialist is early recognition (by taking an appropriate history and thinking of the diagnosis) and immediate referral to a neurosurgical centre for specialist treatment. As in this case, a differential diagnosis may exist; however, if SAH is in the differential diagnosis there should be no delay. Delay may be life-threatening and/or may compromise the possibility of good-quality survival.

The newest developments in the diagnosis and treatment of cerebral vascular lesions are radiological. CT and MRI angiography, which can be performed non-invasively and reformatted in multiple planes, is now readily available and has improved the resolution of vascular imaging. However, conventional angiography (DSA) still remains the gold standard investigation after a suggestive history, particularly if intervention is planned. Endovascular therapies, including coiling with or without stenting, are rapidly evolving, are available in most neurosurgical centres and can be an effective treatment for aneurysms (ruptured and unruptured); however, each case should be judged on its own merits by the treating neurovascular team.

Issues to Consider

• What measures might be undertaken to reduce the risk of cerebral vasospasm in a patient with subarachnoid haemorrhage?
• What is the role of lumbar puncture in cases of suspected subarachoid haemorrhage?

Further Information

Bederson J.B., Awad I.A., Wiebers D.O. Recommendations for the management of patients with unruptured intracranial aneurysms. Circulation. 2000;102:2300-2308.

Inagawa T., Kamiya K., Ogasawara H., Yano T. Rebleeding of aneurysms in the acute stage. Surgical Neurology. 1987;28(2):93-99.

Rinkel G.J., Djibuti M., Algra A., van Gijn J. Prevalence and risk of rupture of intracranial aneurysms: a systemic review. Stroke. 1998;29:251-256.

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