Infective Endocarditis Resulting in Septic Cerebral Infarction

Dr. Nakouzi *, Dr. Kathrine Smith ¹, Dr. Youssif Mohammad ²

1.Acute Medicine Consultant.

2.Senior Clinical Fellow.

*Correspondence to: Dr. Nakouzi, MTW/ Maidstone and Tunbridge wells NHS trust/ UK.

Copyright

© 2024 Dr. Nakouzi. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: 13 March 2024                    

Published: 08 April 2024

-> 66 years old male IW admitted to A&E for 2/52 Hx of lethargy and generally unwell. Mild drossiness and reduced oral intake and mobility.

->Initial blood results showed Leucocytosis (WBC=22,000, CRP=97, NEU= (20.18), and PCT= 1.07), furthermore, AKI on CKD secondary to dehydration( Urea= 26.7).

->Initial diagnosis was sepsis, and Vasculitis-IgA=4.71,ANCA=negative, Complements= normal ( Blood Cx were taken 3 sets as per micro, and Vancomycin was initiated), with Positive Flu A

->ABG showed mild hypocapnia.

->U/A Proteinuria.

->66 years old male IW admitted to A&E for 2/52 Hx of lethargy and generally unwell. Mild drossiness and reduced oral intake and mobility.

->Initial blood results showed Leucocytosis (WBC=22,000, CRP=97, NEU= (20.18), and PCT= 1.07), furthermore, AKI on CKD secondary to dehydration( Urea= 26.7).

->Initial diagnosis was sepsis, and Vasculitis-IgA=4.71,ANCA=negative, Complements= normal ( Blood Cx were taken 3 sets as per micro, and Vancomycin was initiated), with Positive Flu A

->ABG showed mild hypocapnia.

->U/A Proteinuria.

-> PMH: SAH(coiling 3years ago)

• AVR 2018
• TIA 10 years ago
• Dyslipidemia
• OA
• Rt.Adrenal adenoma
• Lung Granolomatosis

->Physical examination: GCS=12/15, Mild drowsiness, Power 4/5 upper and lower extremeties, no Nystagmus. Vital signs= acceptable, Afebrile.

-> CVS= No CP, No SOB , Blowing diastolic murmur, prominent at left sternal edge, equal pulses, no carotid bruits, no murmur radiation. Normotensive, HR=70-75 , Rt. hand palmar erythema, and mild splinter haemorrhage. Upper and Lower extremities pulses equal, with no delays. EKG= no RVH strain, LVH, no signs of STEMI or NSTEMI ( although trop was= 250, most probably high trop due to sepsis)

->Abdomen= soft, no bowel habit changes

->LL= No swelling, preserved peripheral pulses.

->Resp= GBAE, no crackles or any end-expiratory wheezes.

->MRI= Imaging shows extensive abnormality of mixed age. There is background multifocal haemorrhage which would suggest an angiopathy however there are areas of more acute abnormality with apparent acute/subacute infarcts identified on the diffusion weighting.

CT Intracranial Angio:

He has known previous aneurysm with coiling He presented with lethargy over 10-days. No report of sudden onset headache He has a few small patches of SAH but no blood in basal cisterns. This can happen with delayed presentation due to redistribution of blood. He has a cerebellar infarct CTA in first instance to look for recurrence or new aneurysm Also needs MRI as per your radiologist to look for vasculitis.

Echocardiogram:

MRI Image:

QUICK Reflection:

->General lethargy for two weeks.

-> Decreased mobility.

-> History of AVR.

-> Diastolic murmur , with mild dermatological manifestation.

-> Positive Blood cultures ( Staphylococcus Epidermidis ) 2: Staphylococcus epidermidis ranks as one of the most common species to cause infective endocarditis in both the prosthetic valve and the native valve. Up to 40% of cases of prosthetic valve endocarditis (PVE) are due to coagulase-negative staph.

-> HIGH risk of Endocarditis , with positive echo of AV vegetation. 2

-> Positive MRI for Ischaemia.

-> Splinter haemorrhage. 1

Primary Diagnosis : IE

Definition:

A condition in which the tissues lining the inside (the endocardium)  of the heart and the heart valves become inflamed (red and swollen). Endocarditis was first described by William Osler in 1885. Developments in medical science and research in microbiology have contributed to a better understanding of the disease. The most common risk factors for infective endocarditis are previous heart damage, recent heart surgery or poor dental hygiene.

No race or ethnicity is more affected than others.?Prognosis of infective endocarditis remains poor despite advances in diagnosis and therapies. Mortality rates are approximately 25% even with the best therapies available. Female sex is less common in patients diagnosed with IE ( unknown reason ), but mortality is higher.

Risk factors :

-> Although the heart is usually well protected against infection, it may be easier for bacteria to bypass the immune system in people who have:

-> An artificial (prosthetic) heart valve

-> Valve replacement surgery congenital heart disease – where a person is born with heart defects

-> Hypertrophic cardiomyopathy – where the heart muscle cells have enlarged and the walls of the heart chambers thicken

-> Risk factors that contribute to the onset of Infective Endocarditis include:

-> Intravenous drug use with a needle contaminated with bacteria or fungi

-> Presence of an artificial (prosthetic) heart valve or other valve repair material

-> Presence of a cardiac pacemaker lead

-> Previous infective endocarditis

-> Mitral valve prolapse with valve leakage

-> An aortic valve with only 2 (instead of the normal 3 valve leaflets). This condition, called a bicuspid aortic valve, is present in about 1% of people.

-> Narrowing (stenosis) of the aortic valve due to age-related calcification

-> Other abnormal valves caused by rheumatic fever and degenerative conditions

-> Congenital heart disease, especially if repaired with artificial material.

Endocarditis can be broken down into the following categories :

Native valve endocarditis (NVE), acute and subacute: gram-positive bacteria such as Staphylococcus aureus, viridans group streptococci, Streptococcus bovis, and enterococci (Gould et al, 1975; Chambers & Bayer, 2020).

-> Prosthetic valve endocarditis (PVE),  early and late: Prosthetic valve endocarditis (PVE) can occur early or late after surgery, and the bacteria causing early vs late infections tends to differ (Karchmer, 2017). Early infections ( S aureus and S epidermidis)  are caused by bacteria that are able to stick to surfaces that are not endothelialized (e.g. sutures, valve sewing ring), but have become coated with host proteins such as fibronectin and fibrinogen. Late infections ( streptococci ) are more commonly caused by bacteria that adhere to tissues that have become endothelialized after several months following valve replacement. These pathogens more closely resemble those causing native valve endocarditis (Karchmer, 2017).

-> Intravenous drug abuse (IVDA) endocarditis, (right side of the heart) : S. aureus is the most common cause of IDU-IE (accounting for more than half of all cases). Streptococci and enterococci are the next most common pathogens (Sexton & Chu, 2017).

-> Acute infective endocarditis develops suddenly and may become life threatening within days. Subacute infective endocarditis (also called subacute bacterial endocarditis) develops gradually and subtly over a period of weeks to several months but also can be life threatening.

-> The tricuspid valve is most commonly affected (50%), whereas involvement of the mitral and aortic valves is less common (20% each).

Organisms in IE :

IE has a large number of causative organisms :

-> Streptococci. These account for 50%–80% of IE cases. ...

-> Staphylococci. Staphylococcus aureus and Staphylococcus epidermidis account for 20%–30% of subacute cases of IE and 50% of the acute forms. ...

-> Enterococci. Enterococci account for 5%–15% of IE cases. ...

-> HACEK  (Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae) organisms. Negative blood Cx

-> Marantic endocarditis is characterized by the presence of sterile vegetations in the heart valves, and is associated with hypercoagulability states (cancer, autoimmune diseases, HIV). Its main complications are stroke, pulmonary thromboembolism, acute intestinal ischemia and splenic, renal and hepatic infarcts. Marantic endocarditis, Libman-Sacks endocarditis, NBTE, typically associated with cancer and collagen vascular diseases: should be considered in patients with culture-negative endocarditis and elevated inflammatory markers.

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