PRACTICE EASILY MISSED?
Subdural haematoma in the elderly Elizabeth A Teale,1 Steve Iliffe,2 John B Young1 1
Academic Unit for Elderly Care and Rehabilitation, Leeds Institute of Health Sciences, Bradford BD9 6RJ, UK 2 Department of Primary Care and Population Health, University College London, London NW3 2PF, UK Correspondence to: E A Teale [email protected] Cite this as: BMJ 2014;348:g1682 doi: 10.1136/bmj.g1682
This is one of a series of occasional articles highlighting conditions that may be more common than many doctors realise or may be missed at first presentation. The series advisers are Anthony Harnden, university lecturer in general practice, Department of Primary Health Care, University of Oxford, and Richard Lehman, general practitioner, Banbury. To suggest a topic, please email us at [email protected].
bmj.com Previous articles in this series ЖЖIntestinal malrotation and volvulus in infants and children (BMJ 2013;347:f6949 ЖЖLisfranc injuries (BMJ 2013;347:f4561) ЖЖSpontaneous oesophageal rupture (BMJ 2013;346:f3095) ЖЖPelvic inflammatory disease (BMJ 2013;346:f3189) ЖЖColorectal cancer (BMJ 2013;346:f3172)
An 84 year old woman with a history of postural hypotension and frequent falls presented with a two week history of confusion and wandering. Her general practitioner diagnosed delirium secondary to a urinary tract infection on the basis of a positive urinary dipstick test for white blood cells and nitrites. She failed to improve with oral antibiotics and was admitted to hospital for further assessment. Clinical examination showed a lack of focal neurological signs but cranial computed tomography revealed a left sided chronic subdural haematoma.
What is a subdural haematoma? A subdural haematoma results from tearing of the veins linking the cerebral cortex and the dural sinuses, causing blood to accumulate between the dura and arachnoid maters. Brain atrophy associated with ageing or dementia stretches these fragile veins such that they are more prone to tearing after relatively trivial (and often forgotten) head injury1; in up to half of cases there is a history of fall without head trauma.1‑3 Over time, there is fibrin deposition and organisation of the haematoma, resulting in a chronic subdural haematoma. Neovascularisation processes within the subdural haematoma increase the propensity for acute or chronic bleeding.4 Anticoagulation increases the risk of subdural haematoma and the likelihood of fresh bleeding into an established haematoma.4 Why is it missed? Only about half of people presenting with a subdural haematoma give a history of a direct head trauma or a fall with a head injury. A fall without head injury may account for a further 33-54% of cases.3 5 There may be a long delay between the fall or trauma and the onset of symptoms (mean 49 days, range 15 to 751 days).10 Cranial imaging performed shortly after a fall or head trauma can be normal in individuals who go on to develop a chronic subdural haematoma and may falsely reassure.11 12 The clinical features of a subdural haematoma can easily be misinterpreted. Subdural haematoma can mimic alcohol excess.13 A presentation with behavioural or personality changes may be mistaken for a psychiatric disorder14 15 or dementia,16 especially in patients where these conditions pre-exist.14 Delirium (acute confusion) is a common feature of subdural haematoma, especially in older people (52% of 56 patients aged >60 with subdural haematoma in one case
KEY POINTS Many patients with a confirmed subdural haematoma have no history of fall or head injury Chronic subdural haematomas can present with confusion, behavioural or personality changes, or neurological features that may be mistaken for delirium falsely ascribed to another cause (such as infection), psychiatric illness, or transient ischaemic attack. The absence of neurological signs does not exclude the possibility of a chronic subdural haematoma The diagnosis of a chronic subdural haematoma is made by non-contrast cranial computed tomography (CT) imaging. 36
HOW COMMON IS SUBDURAL HAEMATOMA? • The incidence of chronic subdural haematoma increases with age1 • Case series data from 1996 to 1999 estimate the incidence of chronic subdural haematoma in over 65 year olds at 8.2/100 000/year.5 A recent retrospective case series study from Japan reports the incidence of chronic subdural haematoma in older people to be 76.5/100 000/year in 70-79 year olds and 127/100 000/year in those aged ≥80.6 These higher estimates may reflect better access to diagnostic imaging • Two high quality randomised controlled trials estimate absolute rates of chronic subdural haematoma for patients aged >75 years taking warfarin as 0.2-0.31% per annum7 8 • In a large randomised controlled trial, dabigatran was associated with a lower absolute risk of subdural haematoma than warfarin for patients with atrial fibrillation. This seemed to be dose dependent (absolute annual risk of subdural haematoma with warfarin 0.31%, with 110 mg twice daily dabigatran 0.08%, with 150 mg twice daily dabigatran 0.20%)7 • A recent meta-analysis of published and unpublished data from nine randomised controlled trials did not find a statistically significant association between aspirin therapy and subdural haematoma (odds ratio 1.6 (95% confidence interval 0.8 to 3.5) v placebo)9
series),17 and may be falsely ascribed to other, more common causes of delirium such as infections or medicines. Transient neurological deficits are the presenting feature in 1-21% of chronic subdural haematomas,1 2 5 leading to the potential for a mistaken diagnosis of transient ischaemic attack.18 In patients presenting to hospital with a subdural haematoma, two case series found that the diagnosis was not suspected before imaging in 62-80% of cases.2 5
Why does this matter? There is evidence that cognitive, gait, behavioural, focal neurological, extra-pyramidal, and psychiatric disturbances can improve or be reversed following neurosurgical intervention to treat a chronic subdural haematoma.4 14 16‑ 21 Continued expansion of a chronic subdural haematoma, or fresh bleeding into an established haematoma, can result in deterioration, over hours, days, or weeks that may result in persistent neurological deficit13 or death. How is subdural haematoma diagnosed? Clinical features Consider the diagnosis of chronic subdural haematoma as cause or consequence of new onset falls or increased fall frequency (74% in one series2). Other common features are behavioural or cognitive disturbances (present in 34-55% of patients)1 5 10 22 and transient (1-21% of patients), persistent or progressive focal neurological deficits (24% to 88% of patients).1 2 5 10 22 Headache is the presenting feature in 14-27% of patients,2 5 10 22 reduced consciousness is present in 2.9-35%,2 5 22 and a seizure is the presenting event for BMJ | 15 MARCH 2014 | VOLUME 348
PRACTICE Onset of symptoms in patients treated with anticoagulants is generally more rapid than in the general population (80% present within a week26), and features of raised intracranial pressure or focal neurological deficit are prominent (headache, nausea and vomiting, reduced consciousness, hemiparesis, ataxia),26 even in older people.
Crescentic right side high attenuation subdural collection (arrow), suggesting acute subdural haematoma. There is substantial mass effect and oedema with effacement of the ventricle and midline shift
10-14%.2 10 Features of raised intracranial pressure such as nausea, vomiting, headache, or altered consciousness and neurological features are less common in older people because brain atrophy provides space to accommodate the haematoma. The indolent course of chronic subdural haematoma should prompt reconsideration of the diagnosis in the presence of persistent symptoms, neurological deficit, or features of raised intracranial pressure even if initial imaging is normal. There should be a particularly high index of suspicion for a diagnosis of subdural haematoma in patients treated with anticoagulant drugs. Case series have reported that 9-21% of patients presenting with subdural haematomas are treated with anticoagulants.10 23‑ 25 The absolute annual risk of subdural haematoma in patients taking warfarin has been estimated at 0.2% with a therapeutic international normalised ratio (INR) of 2-3,8 and risk increases substantially with a supratherapeutic INR.26 A large randomised controlled trial has shown that, compared with warfarin, dabigatran is associated with a lower absolute risk of subdural haematoma (see box “How common is subdural haematoma?”).7
ANSWERS TO ENDGAMES, p 38
Investigations The diagnosis of a subdural haematoma is made by noncontrast cranial computed tomography. The clot appears as a crescent shaped opacity around the cerebral hemisphere (see figure).4 An acute subdural haematoma appears as a hyperdense lesion. As the subdural haematoma matures, there is transition through isodensity to the hypodense appearance of a chronic subdural haematoma.27 Features of midline shift may help to alert to the presence of unilateral subdural haematoma in the isodense phase,27 but in bilateral chronic subdural haematomas (16-20% of cases28) where midline shift may not be apparent, more subtle radiological features such as effacement of the sulci suggest the diagnosis.27 28 A high index of clinical suspicion is therefore required reliably to interpret the CT scan findings. How is subdural haematoma managed? Rapid reversal of anticoagulants and discontinuation of antiplatelet therapy are required for patients presenting with a subdural haematoma on these medications. Small subdural haematomas that are asymptomatic and without radiological features of raised intracranial pressure may be managed conservatively4 with follow-up by clinical assessment and repeat CT scanning if deterioration is apparent. However, if there is neurological compromise, or features of brain compression on imaging, evacuation of the clot via craniostomy (drilling a hole through the skull) or craniotomy (where a piece of the skull is removed and then replaced) is indicated.4 Older patients with large haematomas and midline shift have particularly poor outcomes, particularly without surgical intervention.2 10 We thank Dr Samad Punekar for help in preparing the image. Competing interests: None declared. Provenance and peer review: Commissioned; externally peer reviewed. Consent obtained from a relative. References and contributors are in the version on bmj.com. Accepted: 20 December 2013
For long answers go to the Education channel on bmj.com
CASE REPORT Airway obstruction after the development of Hashimoto’s thyroiditis 1 Thyroid swelling (goitre) can be caused by a variety of benign or malignant conditions. The most common cause of thyroid swelling worldwide is iodine deficiency goitre. 2 Thyroid function tests, thyroid antibody tests, and imaging of the neck are necessary investigations. Fine needle aspiration cytology should also be considered for the diagnosis of benign and malignant thyroid disorders. 3 Airway obstruction can be caused by benign and malignant tumours of the thyroid gland, as well as haemorrhage into a thyroid nodule. Neck tumours of non-thyroid origin can also compromise the airway. Because our patient was diagnosed earlier as having Hashimoto’s thyroiditis, a thyroid tumour is the most likely cause. 4 Emergency computed tomography of the neck and fine needle aspiration cytology or core biopsy from the mass are essential for diagnosis. 5 The management of patients with thyroid lymphoma and airway compromise includes management of ABC (airway, breathing, and circulation) and urgent administration of multiagent chemotherapy or radiotherapy.
BMJ | 15 MARCH 2014 | VOLUME 348
STATISTICAL QUESTION Randomised controlled trials: evaluating and communicating treatment effects Statements a and b are true, whereas c is false.
37
Copyright of BMJ: British Medical Journal is the property of BMJ Publishing Group and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Subdural haematoma in the elderly Elizabeth A Teale,1 Steve Iliffe,2 John B Young1 1
Academic Unit for Elderly Care and Rehabilitation, Leeds Institute of Health Sciences, Bradford BD9 6RJ, UK 2 Department of Primary Care and Population Health, University College London, London NW3 2PF, UK Correspondence to: E A Teale [email protected] Cite this as: BMJ 2014;348:g1682 doi: 10.1136/bmj.g1682
This is one of a series of occasional articles highlighting conditions that may be more common than many doctors realise or may be missed at first presentation. The series advisers are Anthony Harnden, university lecturer in general practice, Department of Primary Health Care, University of Oxford, and Richard Lehman, general practitioner, Banbury. To suggest a topic, please email us at [email protected].
bmj.com Previous articles in this series ЖЖIntestinal malrotation and volvulus in infants and children (BMJ 2013;347:f6949 ЖЖLisfranc injuries (BMJ 2013;347:f4561) ЖЖSpontaneous oesophageal rupture (BMJ 2013;346:f3095) ЖЖPelvic inflammatory disease (BMJ 2013;346:f3189) ЖЖColorectal cancer (BMJ 2013;346:f3172)
An 84 year old woman with a history of postural hypotension and frequent falls presented with a two week history of confusion and wandering. Her general practitioner diagnosed delirium secondary to a urinary tract infection on the basis of a positive urinary dipstick test for white blood cells and nitrites. She failed to improve with oral antibiotics and was admitted to hospital for further assessment. Clinical examination showed a lack of focal neurological signs but cranial computed tomography revealed a left sided chronic subdural haematoma.
What is a subdural haematoma? A subdural haematoma results from tearing of the veins linking the cerebral cortex and the dural sinuses, causing blood to accumulate between the dura and arachnoid maters. Brain atrophy associated with ageing or dementia stretches these fragile veins such that they are more prone to tearing after relatively trivial (and often forgotten) head injury1; in up to half of cases there is a history of fall without head trauma.1‑3 Over time, there is fibrin deposition and organisation of the haematoma, resulting in a chronic subdural haematoma. Neovascularisation processes within the subdural haematoma increase the propensity for acute or chronic bleeding.4 Anticoagulation increases the risk of subdural haematoma and the likelihood of fresh bleeding into an established haematoma.4 Why is it missed? Only about half of people presenting with a subdural haematoma give a history of a direct head trauma or a fall with a head injury. A fall without head injury may account for a further 33-54% of cases.3 5 There may be a long delay between the fall or trauma and the onset of symptoms (mean 49 days, range 15 to 751 days).10 Cranial imaging performed shortly after a fall or head trauma can be normal in individuals who go on to develop a chronic subdural haematoma and may falsely reassure.11 12 The clinical features of a subdural haematoma can easily be misinterpreted. Subdural haematoma can mimic alcohol excess.13 A presentation with behavioural or personality changes may be mistaken for a psychiatric disorder14 15 or dementia,16 especially in patients where these conditions pre-exist.14 Delirium (acute confusion) is a common feature of subdural haematoma, especially in older people (52% of 56 patients aged >60 with subdural haematoma in one case
KEY POINTS Many patients with a confirmed subdural haematoma have no history of fall or head injury Chronic subdural haematomas can present with confusion, behavioural or personality changes, or neurological features that may be mistaken for delirium falsely ascribed to another cause (such as infection), psychiatric illness, or transient ischaemic attack. The absence of neurological signs does not exclude the possibility of a chronic subdural haematoma The diagnosis of a chronic subdural haematoma is made by non-contrast cranial computed tomography (CT) imaging. 36
HOW COMMON IS SUBDURAL HAEMATOMA? • The incidence of chronic subdural haematoma increases with age1 • Case series data from 1996 to 1999 estimate the incidence of chronic subdural haematoma in over 65 year olds at 8.2/100 000/year.5 A recent retrospective case series study from Japan reports the incidence of chronic subdural haematoma in older people to be 76.5/100 000/year in 70-79 year olds and 127/100 000/year in those aged ≥80.6 These higher estimates may reflect better access to diagnostic imaging • Two high quality randomised controlled trials estimate absolute rates of chronic subdural haematoma for patients aged >75 years taking warfarin as 0.2-0.31% per annum7 8 • In a large randomised controlled trial, dabigatran was associated with a lower absolute risk of subdural haematoma than warfarin for patients with atrial fibrillation. This seemed to be dose dependent (absolute annual risk of subdural haematoma with warfarin 0.31%, with 110 mg twice daily dabigatran 0.08%, with 150 mg twice daily dabigatran 0.20%)7 • A recent meta-analysis of published and unpublished data from nine randomised controlled trials did not find a statistically significant association between aspirin therapy and subdural haematoma (odds ratio 1.6 (95% confidence interval 0.8 to 3.5) v placebo)9
series),17 and may be falsely ascribed to other, more common causes of delirium such as infections or medicines. Transient neurological deficits are the presenting feature in 1-21% of chronic subdural haematomas,1 2 5 leading to the potential for a mistaken diagnosis of transient ischaemic attack.18 In patients presenting to hospital with a subdural haematoma, two case series found that the diagnosis was not suspected before imaging in 62-80% of cases.2 5
Why does this matter? There is evidence that cognitive, gait, behavioural, focal neurological, extra-pyramidal, and psychiatric disturbances can improve or be reversed following neurosurgical intervention to treat a chronic subdural haematoma.4 14 16‑ 21 Continued expansion of a chronic subdural haematoma, or fresh bleeding into an established haematoma, can result in deterioration, over hours, days, or weeks that may result in persistent neurological deficit13 or death. How is subdural haematoma diagnosed? Clinical features Consider the diagnosis of chronic subdural haematoma as cause or consequence of new onset falls or increased fall frequency (74% in one series2). Other common features are behavioural or cognitive disturbances (present in 34-55% of patients)1 5 10 22 and transient (1-21% of patients), persistent or progressive focal neurological deficits (24% to 88% of patients).1 2 5 10 22 Headache is the presenting feature in 14-27% of patients,2 5 10 22 reduced consciousness is present in 2.9-35%,2 5 22 and a seizure is the presenting event for BMJ | 15 MARCH 2014 | VOLUME 348
PRACTICE Onset of symptoms in patients treated with anticoagulants is generally more rapid than in the general population (80% present within a week26), and features of raised intracranial pressure or focal neurological deficit are prominent (headache, nausea and vomiting, reduced consciousness, hemiparesis, ataxia),26 even in older people.
Crescentic right side high attenuation subdural collection (arrow), suggesting acute subdural haematoma. There is substantial mass effect and oedema with effacement of the ventricle and midline shift
10-14%.2 10 Features of raised intracranial pressure such as nausea, vomiting, headache, or altered consciousness and neurological features are less common in older people because brain atrophy provides space to accommodate the haematoma. The indolent course of chronic subdural haematoma should prompt reconsideration of the diagnosis in the presence of persistent symptoms, neurological deficit, or features of raised intracranial pressure even if initial imaging is normal. There should be a particularly high index of suspicion for a diagnosis of subdural haematoma in patients treated with anticoagulant drugs. Case series have reported that 9-21% of patients presenting with subdural haematomas are treated with anticoagulants.10 23‑ 25 The absolute annual risk of subdural haematoma in patients taking warfarin has been estimated at 0.2% with a therapeutic international normalised ratio (INR) of 2-3,8 and risk increases substantially with a supratherapeutic INR.26 A large randomised controlled trial has shown that, compared with warfarin, dabigatran is associated with a lower absolute risk of subdural haematoma (see box “How common is subdural haematoma?”).7
ANSWERS TO ENDGAMES, p 38
Investigations The diagnosis of a subdural haematoma is made by noncontrast cranial computed tomography. The clot appears as a crescent shaped opacity around the cerebral hemisphere (see figure).4 An acute subdural haematoma appears as a hyperdense lesion. As the subdural haematoma matures, there is transition through isodensity to the hypodense appearance of a chronic subdural haematoma.27 Features of midline shift may help to alert to the presence of unilateral subdural haematoma in the isodense phase,27 but in bilateral chronic subdural haematomas (16-20% of cases28) where midline shift may not be apparent, more subtle radiological features such as effacement of the sulci suggest the diagnosis.27 28 A high index of clinical suspicion is therefore required reliably to interpret the CT scan findings. How is subdural haematoma managed? Rapid reversal of anticoagulants and discontinuation of antiplatelet therapy are required for patients presenting with a subdural haematoma on these medications. Small subdural haematomas that are asymptomatic and without radiological features of raised intracranial pressure may be managed conservatively4 with follow-up by clinical assessment and repeat CT scanning if deterioration is apparent. However, if there is neurological compromise, or features of brain compression on imaging, evacuation of the clot via craniostomy (drilling a hole through the skull) or craniotomy (where a piece of the skull is removed and then replaced) is indicated.4 Older patients with large haematomas and midline shift have particularly poor outcomes, particularly without surgical intervention.2 10 We thank Dr Samad Punekar for help in preparing the image. Competing interests: None declared. Provenance and peer review: Commissioned; externally peer reviewed. Consent obtained from a relative. References and contributors are in the version on bmj.com. Accepted: 20 December 2013
For long answers go to the Education channel on bmj.com
CASE REPORT Airway obstruction after the development of Hashimoto’s thyroiditis 1 Thyroid swelling (goitre) can be caused by a variety of benign or malignant conditions. The most common cause of thyroid swelling worldwide is iodine deficiency goitre. 2 Thyroid function tests, thyroid antibody tests, and imaging of the neck are necessary investigations. Fine needle aspiration cytology should also be considered for the diagnosis of benign and malignant thyroid disorders. 3 Airway obstruction can be caused by benign and malignant tumours of the thyroid gland, as well as haemorrhage into a thyroid nodule. Neck tumours of non-thyroid origin can also compromise the airway. Because our patient was diagnosed earlier as having Hashimoto’s thyroiditis, a thyroid tumour is the most likely cause. 4 Emergency computed tomography of the neck and fine needle aspiration cytology or core biopsy from the mass are essential for diagnosis. 5 The management of patients with thyroid lymphoma and airway compromise includes management of ABC (airway, breathing, and circulation) and urgent administration of multiagent chemotherapy or radiotherapy.
BMJ | 15 MARCH 2014 | VOLUME 348
STATISTICAL QUESTION Randomised controlled trials: evaluating and communicating treatment effects Statements a and b are true, whereas c is false.
37
Copyright of BMJ: British Medical Journal is the property of BMJ Publishing Group and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
