DR.ANIRUDH J .SHETTY PROF.DR.G.ELANGOVAN ‘S UNIT

A 24 yr old patient came with the c/o breathlessness – 10 yrs fever – 5 days seizure -1 episode

Breathlessness – increased for the past one month ;initially it was grade 1 progressed to grade 3 this breathlessness had been

there for the past 10 yrs on & off

Fever for - 5days sudden in onset continuous in nature assoc. with chills & rigors no night sweats

h/o seizure – 1 day back 1 episode sudden in onset involved R UL first progressed on to involve other limbs post ictal confusion present no h/o tongue bite no bladder /bowel incontinence no h/o chest pain , palpitations. no h/0 cough with expectoration.

Past history : Patient was told to have heart disease but no records available

ANTENATAL H/o-no h/o fever, rashes,jaundice or drug intake. No h/o similar complaints in other family members.

PERINATAL H/O –Baby cried immideately after birth

no h/o failure to thrive

Childhood h/o- mother noted bluish discolouration of lips at 8 yrs of age.

No h/o recurrent RTI or hospitalisationCyanotic spells n equivalents present.

o/E- Pt conscious, oriented

Afebrileno pallor ,icterus, cyanosis presentclubbing grade -3

pan-digital ,no pedal edema B.P -120/80 mmHg P.R-80/minRR -16/minHT-160cmsWt-47 kgs

JVP NOT RAISED CVS- Mild precordial bulge present Apical impulse in the 5th intercostal space at the

MCL S1S2 Present in Mitral area. S1S2 PRESENT IN Pulmonary area Single second heart sound,Short systolic

murmur present S1S2 Present in the AA n TA

RS –NVBS present no added sounds P/A- soft CNS- Higher functions –normal

CN –WNLspinomotor system –wnlNo cerebeller, sensory,

meningeal signs

DIAGNOSISCongenital cyanotic heart disease- most

probably TOF? Cerebral Abscess.

INVESTIGATIONSCBC RFTTC – 6,000 Urea-20 DC-P 77,L 20,E 3 Creatinine-0.6RBC- 3.2 MILLIONPLT-1.2 LAKHSHb-13mgPCV-33%

Chest X-Ray

RT VENTRICULAR APEXPULMONARY OLIGEMIA

ECG

Peaked P wavesRight axis deviationTall monophasic R waves in V1 with an

abrupt change to Rs pattern in V2

CT- SCAN

NEUROSURGERY DEPT took over the case Bur hole with aspiration of abscess was done20 ml of frank pus was drained.Patient was put on INJ CEFOTAXIME GENTAMYCIN METROGYL DEXA EPSOLIN

PUS C/SPSUEDOMONAS Spp GrownSensitive to imepenem

ECHO SUBAORTIC PERIMEMBRANOUS VSD BIDIRECTIONAL SHUNTAORTIC OVERRIDING >50%

Cyanotic heart disease is the most commonly identified risk factor for development of brain abscess in immunocompetent patients.

The incidence of brain abscess in patients with cyanotic heart disease has been reported to range between 5 and 18.7%.

Tetralogy of Fallot is the most common cardiac anomaly associated with brain abscess.

Transposition of great vessels Tricuspid atresia Pulmonary stenosis Double-outlet right ventricle have also been

reported as predisposing factors. Most of these abscesses are supratentorial in

location

WHY ARE THEY PREDISPOSED?

In patients with cyanotic heart disease, there is a right-to-left shunt of venous blood in the heart, bypassing the pulmonary circulation. Thus, bacteria in the bloodstream are not filtered through the pulmonary circulation, where they would normally be removed by phagocytosis.

Patients with cyanotic heart disease could have low-perfusion areas in the brain due to chronic severe hypoxemia and metabolic acidosis as well as increased viscosity of blood due to secondary polycythemia.

These low-perfusion areas commonly occur in the junction of gray and white matter, and they are prone to seeding by microorganisms that may be present in the bloodstream.

The hematogenous mode of spread accounts for the subcortical location as well as the multiple number of abscesses often encountered in these patients.

COMMON ORGANISMS Streptococcus milleri was the most common

organism isolated from the abscess in patients with cyanotic heart disease in one series.

Staphylococcus, other Streptococcus spp, and Haemophilus have also been isolated.

The isolation of gram-positive cocci is higher than that of gram-negative bacilli. With the advent of broad-spectrum antibiotic therapy, sterile cultures are being reported more often. Multiple organisms have also been isolated in some patients

Patients with cyanotic heart disease have compromised cardiopulmonary systems and exhibit a variety of coagulation defects, rendering them poor candidates for general anesthesia.

Moreover, these abscesses are often deep seated in location, in proximity to the ventricular system and they are often multiple.

TREATMENTThe treatment of choice in these patients is

thus aspiration of the abscess through a bur hole or twist-drill craniostomy performed after induction of local anesthesia.

Any coagulopathy, if present, should be corrected before the surgical intervention.

In one series, the mortality rate following craniotomy and excision was as high as 71%.

Even with aspiration, nearly 17% of patients can develop cyanotic spells that could lead to life-threatening complications.

Intravenous antibiotics should be administered for 6 weeks in these patients, with regular CT scans obtained to monitor the size of the abscess. Repeated aspirations may be required.

Craniotomy should be restricted to patients with abscesses resistant to antibiotic therapy.

IMPORTANCE OF CT-SCANThe advent of CT scans and their use in the

management of these abscesses has resulted in a 4 fold decrease in the mortality rate in patients with brain abscesses; from 40–60% in the pre-CT era to ∼ 10%.

This could be attributed to early detection, availability of image guidance for aspiration (particularly in small lesions), and better radiological follow-up during the course of the antibiotic therapy.

Intraventricular rupture of brain abscess has been reported to be a poor prognostic factor in these patients.

The advent of stereotaxy has aided in avoiding empirical therapy in patients with brain lesions, particularly so in patients with brain abscesses secondary to cyanotic heart disease.

Stereotactic intervention can also help in obtaining a histological diagnosis of lesions mimicking a brain abscess in these patients.

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