Vasif Mayan M CGMKMCH

A CASE OF VENTRICULAR SEPTAL

DEFECT

HISTORY

• 26 year old male presented with a 4 day history of

fever headache

Left focal

seizures

• 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

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

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

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

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

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

ELECTROCARDIOGRAM

IMPRESSION

• Ventricular septal defect

• Infective endocarditis

• Severe AR

• Moderate Pulmonary hypertension

• ? BRAIN ABSCESS

TREATMENT

• Inj CEFTRIAXONE 2gm iv OD

• Inj GENTAMICIN 60mg iv tds

• Tab Sodium Valproate 200mg tds

CT BRAIN PLAIN

Tiny calcific focus with adjacent hyperdense hemorrhagic focus with surrounding edema in right temporoparietal region

BLOOD C/S

• Proceeded with MRI Brain with MR angiogram and Venogram

MRI BRAIN

MRA

DISCUSSION

MODIFIED DUKE’S CRITERIA

PREDICTORS OF POOR OUTCOME IN IE

INVESTIGATION OF RARE

CAUSES OF I.E.

BLOOD CULTURE -VE

ANTIBIOTIC TREATMENT OF BLOOD CULTURE NEGATIVE INFECTIVE ENDOCARDITIS

NEUROLOGICAL COMPLICATIONS OF IE

• Transient ischaemic attacks

• Intracerbral hemorrhages

• Sub arachnoid hemorrhages

• Brain Abscess

• Meningitis

• Toxic encephalopathy

• Seizures

• Personality changes

• ICMA (intracranial mycotic aneurysms)

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

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

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

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

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

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

• 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