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Intracranial infective aneurysms : angiographic evaluation with treatment.
Correspondence Address:
Infective intracranial aneurysms are relatively uncommon. They develop due to septic embolisation of the vasa vasorum or lumen of the artery, with resultant focal arteritis and necrosis, leading to aneurysm formation. They are an important cause for intracranial haemorrhage. Six cases of infective aneurysms are described. A focus of infection could be detected in all the patients. Surgery was done in three cases, out of which two patients made significant recovery, while one patient died in the immediate postoperative period. Out of the three cases, treated conservatively with antibiotic therapy, there was total resolution on follow up angiogram in two, while one patient was lost to follow up.
Church described the first infectious intracranial aneurysm in 1869, when he established a relationship between intracranial aneurysm and infective endocarditis. Osler described aneurysm associated with bacterial endocarditis as mycotic aneurysm.[1] Currently preferred terminology is infectious aneurysm. The term bacterial and mycotic aneurysm is only used when bacteria or fungus respectively can be demonstrated as the causative organism.[2] Infective intracranial aneurysms make up 2-6% of all intracranial aneurysms in adults. The incidence rises to 10% in paediatric age group.[1],[3] The true incidence of intracranial infectious aneurysms is probably underestimated, because many go undiagnosed and are asymptomatic or remain undetected due to early institution of antibiotic treatment. Untreated infectious intracranial aneurysms carry a high mortality. Kojima et al reported 31.8% mortality in bacterial intracranial aneurysms and 90% mortality in patients with mycotic aneurysms.[4] Incidence of rebleed in infectious intracranial aneurysms is unknown.
Case 1 : A 45 year old man presented to the casualty with history of acute onset headache, giddiness, and fall, followed by altered sensorium. Plain CT scan of brain showed evidence of blood in the right temporal lobe and in the right sylvian fissure, ambient and suprasellar cisterns [Figure. 1a]. There was no abnormal enhancement noted on contrast enhanced CT scan. A diagnosis of subarachnoid haemorrhage (SAH) with intracerebral haemorrhage due to right middle cerebral artery territory aneurysm was made. Fourvessel angiogram [Figure. 1b] showed an aneurysm of the right middle cerebral artery. The wall of the aneurysm was irregular and the aneurysm was directed posteromedially with no definite neck. No additional aneurysm was detected. His routine blood count and biochemistry were normal. Blood culture showed no growth. Urine examination showed 8-10 pus cells, bacteria (1+) on high power field. The culture yielded Klebsiella species and Morganella morgavii. Chest radiograph and B-mode and M-mode echocardiogram were normal. The angiographic features, a wide necked rounded aneurysm arising at vessel branching on the peripheral branch of middle cerebral artery, were suggestive of an infective aneurysm although no definite focus of infection could be detected. He was, thus, managed conservatively with antibiotics and anti-oedema measures for 3 weeks. The patient progressively improved in his level of sensorium and became fully conscious and ambulant. Repeat cerebral angiogram [Figure. 1c] done at this stage showed total resolution of the aneurysm. Case 2 : A 24 year old, non-hypertensive, non-diabetic male presented to emergency department with sudden onset of global throbbing headache followed by right motor seizures with secondary generalisation. Ten days prior to this, the patient had a boil on the back for which he had incision and drainage. The patient, on examination, was drowsy but arousable. [Signs] of meningeal irritation were present. Tone was normal in all the 4 limbs with plantars were bilaterally equivocal. CT head showed blood in the right sylvian fissure with diffuse cerebral oedema. Four-vessel angiogram [Figure. 2a] showed evidence of aneurysm in distal middle cerebral artery branch on right side. Echocardiogram showed no evidence of vegetations. Blood and wound swab culture did not yield any growth. He was treated with antibiotics for 6 weeks. Follow up angiogram at this time showed shrinkage of aneurysm to almost 1/4th of its original size. Antibiotic was continued for another one month and subsequent follow up angiogram [Figure. 2b] showed total resolution of the aneurysm with no evidence of any fresh aneurysm. Case 3 : A 40 year old man, a known case of rheumatic heart disease since one year, on procaine penicillin presented to the casualty with 20 days history of headache and sudden onset of altered sensorium. On examination, neurologically he was in altered sensorium, opening eyes to pain and had purposive movement on the left side. There was no verbal response. Pupils were 3mm, equal and reacting. He had right upper motor neuron 7th cranial palsy and right hemiparesis with neck stiffness. Echocardiography showed mitral and aortic regurgitation with vegetations attached to the anterior mitral leaflet. Anti-nuclear antibody was positive, but rheumatoid factor was negative. Blood culture did not yield any growth. CT head [Figure. 3a] showed evidence of left parietal haematoma with intraventricular and subarachnoid extension. Cerebral angiogram [Figure. 3b] showed a wide necked saccular aneurysm arising on the peripheral branch of left middle cerebral artery. Since the angiographic features were consistent with infective aneurysm, patient was treated with antibiotics and anti-oedema measures. Left temporo-parietal trephine and evacuation of intracranial haematoma was done since the haematoma was large. Aneurysm could not be located at surgery. Post-operatively, the patient worsened and died after 6 days. Repeat CT showed decompression of the intracranial haematoma. Case 4 : A 24 year old lady with rheumatic heart disease and mitral regurgitation presented with recurrent history of fever for one month and acute onset of headache, vomiting, altered senorium, left facial weakness and left hemiplegia. On examination, fundus showed bilateral papilloedema. CT head showed right parietal lobe haematoma. Cerebral angiogram showed bilobed aneurysm directed upwards and laterally from the bifurcation of frontal opercular branch of right middle cerebral artery. Routine blood, urine and CSF examinations including cultures were negative. Echocardiography showed vegetations on the mitral leaflets. She was put on antibiotic treatment. Since she did not improve in her neurological status, on the third day of admission, right temporal craniotomy and excision of right middle cerebral artery opercular branch mycotic aneurysm was done. Postoperatively, she improved in power, and level of conciousness. Repeat cerebral angiogram did not show any evidence of aneurysm. Case 5 : A 25 year old man, a known case of rheumatic heart disease presented with history of fever for 1 month, vomiting, acute onset of weakness of left upper and lower limbs and difficulty in speaking for one day. On examination, he had motor aphasia, neck stiffness, left upper motor neuron 7th cranial nerve palsy, hypotonia of left sided limbs with power of 0/5. A mid-diastolic murmur and a loud 2nd pulmonary valve sound were heard. Routine haemogram, urine examination and blood and urine cultures were normal. Echocardiography showed mitral valve stenosis and regurgitation, pulmonary valve hypertrophy and aortic valve regurgitation with no evidence of any vegetation. CT of head showed right frontoparietal intracerebral haematoma with intraventricular extension. Cerebral angiogram showed right middle cerebral artery parietal branch aneurysm. Case 6 : An 8 year old boy, with history of exanthematous fever for 20 days, presented with acute onset of headache, vomiting followed by loss of consiousness. On examination he was moving limbs to deep painful stimuli, hypotonia in all limbs, paucity of movement in right upper and lower limbs. CT of head showed left parietal intracerebral haematoma with midline shift. Routine haemogram, urine examination and blood and urine cultures were normal. Cerebral angiogram showed a large saccular aneurysm arising from temporal brach of left middle cerebral artery distal to bifurcation. He was put on broad spectrum antibiotics. He improved in his level of conciousness. But since he again deteriorated with expressive aphasia and focal motor seizures of right sided limbs with right UMN facial palsy; and repeat CT head showed rebleed, surgical clipping of the aneurysm was done. Post operatively, child became conscious, alert and moving all the four limbs. Repeat angiogram before discharge did not reveal any evidence of aneurysm. The summary of the relevant findings is shown in [Table I].
Bacterial intracranial aneurysms develop due to septic embolisation to the vasa vasorum or lumen of the artery. This leads to infection and stasis in the vasa vasorum. The bacteria escape the lumen of the vessel through occluded origins of the thin walled penetrating vessels, to the Virchow-Robin space and then to the adventitia of the parent vessel. This produces intense inflammatory reaction, which is most intense in the adventitial layer. Late recanalisation or secondary distal migration of emboli after establishing a segmental arterial infection may account for the chronic course usually observed in clinical mycotic aneurysms. Another factor may be low virulence of the organism. Dilatation of the infected segment to aneurysmal proportion and eventual rupture may occur when blood pressure and flow through the occluded segment is established.[3] These aneurysms can be divided into 3 types: aneurysm of embolic origin secondary to bacterial endocarditis affecting mainly the middle cerebral artery; aneurysm of extravascular origin secondary to extension of infection from a neighbouring septic focus affecting mainly the large arteries, such as intracavernous internal carotid artery; and primary or cryptogenic bacterial aneurysm occuring in the absence of obvious inflammatory focus elsewhere in the body.[5] The increasing use of prosthetic valves, intravenous drug abuse and degenerative valve disease have made detection of these aneurysms important.[6] The true prevalence of these aneurysms is unknown with reported incidence ranging from 2-6%[5] and it may be probably higher, because some aneurysms remain totally asymptomatic and are undetected and resolve on antibiotic therapy.[7] They are usually associated with endocarditis and can present with various neurological complications.[8] Bacterial intracranial aneurysm occur most frequently on the middle cerebral artery or its distal branches, less commonly on the posterior and anterior cerebral arteries.[5] In a study of 35 patients with neurologic complications arising from endocarditis, Corr et al,[8] found infective intracranial aneurysm in 31% of patients. Multiple aneurysms occurred in 18.28% of cases. These aneurysms were most commonly located on the peripheral branches of middle cerebral artery (55%), usually at vessel branching. Patients with unruptured single peripheral aneurysm had the best outcome while patients with ruptured aneurysms, multiple aneurysms or acute endocarditis had the worst outcome. In their series patients presented with stroke, seizures and SAH, while in our series, two of our patients presented with stroke while one patient presented with seizure.[8] A focus of infection could be detected in all our patients. Surgery was done in three patients out of which two patients made significant recovery, while one died in the immediate postoperative period. In three cases, where conservative treatment with antibiotic therapy was used, two gave total resolution on follow up angiogram, while one patient was lost to follow up. Bacterial intracranial aneurysm present with variable neurological features. Angiography helps in the diagnosis and follow up after antibiotic therapy, to demonstrate total resolution. MR angiography may prove to be a good initial screening investigation to detect infective aneurysms in asymptomatic patients with endocarditis.[8] Follow up angiogram is required in all cases of suspected infective intracranial aneurysm. If the aneurysm remains unchanged or enlarges despite prolonged antibiotic therapy, surgical management[1],[5] or endovascular management is required.[9],[10],[11]
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