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Vasif Mayan M CGMKMCH
A CASE OF VENTRICULAR SEPTAL
DEFECT
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HISTORY
• 26 year old male presented with a 4 day history of
fever headache
Left focal
seizures
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• No h/o vomiting
• No h/o stiffness of neck
• No h/o Visual blurring
• No h/o sensory or speech abnormalities
• No h/o any focal neurological deficits
• No h/o syncopal attacks
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HISTORY OF PAST ILLNESS
• Known case of ventricular septal defect diagnosed 10 years back
• Not on any treatment
• No prior history of cardiac failure
• No history of Intravenous drug abuse
• Occasional alcoholic
• Non smoker
• Betel nut chewer
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EXAMINATION
• Moderately built and nourished
• Afebrile, conscious, oriented
• No pallor/icterus/cyanosis/clubbing/LNE/pedal edema
• PR 90/mt, regular rhythm, normal volume, character , vessel wall nonplaplable, no radioradial or radiofemoral delay
• BP – 120/80mm measured in right upper limb in supine position
• JVP not raised
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EXAMINATION
• CVS• S1, S2 heard• S1 soft aortic area• Harsh pansystolic murmur of 3/6 intensity heard in left parasternal area with
maximal intensity at 3rd and 4th ICS• P2 component loud in pulmonary area
• RS : NVBS, clear• NS : Conscious , oriented, NFND
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INVESTIGATIONS
• TC 3500cells/mm3
• DC N 60 L 38 E 2
• ESR 30mm/ 1st Hr
• Hb 9 gm%
• RBC 3.5million/mm3
• Platelets 2 lakh/mm3
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ECHOCARDIOGRAM
• Global hypokinesia of LV , Dilated LV
• Small Subaortic Perimembranous VSD ( Left Right shunt)• Ejection Fraction 43%
• Moderate Pulmonary hypertension
• Severe AR
• TRPG 45mm
• 2 VEGETATIONS ATTACHED to AORTIC valve
• Imp : INFECTIVE ENDOCARDITIS
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ELECTROCARDIOGRAM
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IMPRESSION
• Ventricular septal defect
• Infective endocarditis
• Severe AR
• Moderate Pulmonary hypertension
• ? BRAIN ABSCESS
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TREATMENT
• Inj CEFTRIAXONE 2gm iv OD
• Inj GENTAMICIN 60mg iv tds
• Tab Sodium Valproate 200mg tds
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CT BRAIN PLAIN
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Tiny calcific focus with adjacent hyperdense hemorrhagic focus with surrounding edema in right temporoparietal region
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BLOOD C/S
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• Proceeded with MRI Brain with MR angiogram and Venogram
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MRI BRAIN
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MRA
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DISCUSSION
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MODIFIED DUKE’S CRITERIA
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PREDICTORS OF POOR OUTCOME IN IE
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INVESTIGATION OF RARE
CAUSES OF I.E.
BLOOD CULTURE -VE
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ANTIBIOTIC TREATMENT OF BLOOD CULTURE NEGATIVE INFECTIVE ENDOCARDITIS
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NEUROLOGICAL COMPLICATIONS OF IE
• Transient ischaemic attacks
• Intracerbral hemorrhages
• Sub arachnoid hemorrhages
• Brain Abscess
• Meningitis
• Toxic encephalopathy
• Seizures
• Personality changes
• ICMA (intracranial mycotic aneurysms)
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CNS EMBOLIZATION• Neurologic complications, dramatically changes the prognosis in IE• Such complications are clinically apparent in 20% -40% of cases• True incidence of acute brain embolization is not actually known.• Clinically silent embolisations occur in 35- 60% of the cases.• In general CNS takes up to 65% of the systemic embolization in IE • Mostly involve MCA• CNS emboli are mainly caused by Staph aureus• Early surgery is main treatment in embolism prevention• Antithrombotic drugs have no role
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CEREBRAL ISCHEMIC INFARCTION
• Stop anticoagulation in S aureus infection and with large infarctions• At least for 2 weeks• Better only if not life threatening to postpone surgery for 2
weeks• Cerebral dehydrating measures if needed
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INTRA CRANIAL MYCOTIC ANEURYSMS
• Relatively small, but extremely dangerous subset
• True incidence of ICMAs is not known• ICMA contribute to 2- 5% of all intracranial aneurysms• 80% of these are identified in the setting of Infective endocarditis
• Overall mortality 60-80% in patient with ruptured ICMA
30% in patient with unruptured ICMA
• Most of ICMA remain silent until rupture
• Treating ICMA before rupture might change prognosis among these patients
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ICMA
• Result from septic arterial embolism to the intraluminal space or vasa vasorum.• Typically thin walled and friable
• Very high likelihood to RUPTURE and cause hemorrhage
• Size is NOT a predictor of potential rupture
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ICMA
• Due to the lack of randomized controlled trials , there are no definite guidelines/ protocols as yet to treat the patients
• Treatment Individualised
• In intracranial infectious aneurysms, ruptured aneurysms must be treated immediately by surgical or endovascular procedures
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UNRUPTURED ANEURYSM
• Must be serially followed up with imaging studies whilst on antibiotic therapy
• If size decreases with antibiotic therapy, surgical treatment is unnecessary.
• If size increases , surgical intervention is needed
• Persistently symptomatic and large aneurysms need endovascular therapy
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• if early cardiac surgery is required, preoperative endovascular intervention might be considered before the procedure
• depending on • associated cerebral lesions• haemodynamic status• risk of the procedure
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