The recommended pre-operative workup for patients taking anticoagulants involves stratifying both thromboembolic & bleeding risk, determining appropriate timing for medication interruption, & deciding whether bridging therapy is needed. Specific approach depends on the type of anticoagulant, renal function, and procedure-related bleeding risk. • Direct Oral Anticoagulants (DOACs) o For apixaban, rivaroxaban, and Edoxaban, the American College of Chest Physicians recommends stopping these agents 1-2 days before low-to-moderate bleeding risk procedures and 2 days before high bleeding risk procedures. • For dabigatran, interruption timing depends on renal function. o With normal renal function (CrCl ≥50 mL/min), stop 1-2 days before low-risk procedures and 2 days before high-risk procedures. o With impaired renal function (CrCl <50 mL/min), extend interruption to 3-4 days before high-risk procedures due to predominantly renal clearance. #apixaban #rivaroxaban #Edoxaban #dabigatran #DOACs #preoperative #perioperative #Warfarin #CHA₂DS₂-VASc #antithrombotic #anticoagulant #guidelines

Urinary Tract Infections (UTI) 1. Women have a lifetime risk of 53% of experiencing UTI. 2. Men prior to age 50, have lifetime risk is 14%. 3. Risk of experiencing a UTI increase with age in both sexes. Classification: Uncomplicated UTI Infection confined to the bladder in afebrile women or men. Complicated UTI: Infection beyond the bladder in women or men. 1. Pyelonephritis 2. Febrile or bacteremic UTI 3. Catheter-associated (CAUTI) 4. Prostatitis. Catheter- Associated UTI (CA-UTI) 1. CAUTIs are one of the most common healthcare-associated infection (HAI). 2. About 75% of UTIs developed in hospitals are associated with a urinary catheter. 3. 15-25% of hospitalized patients receive urinary catheters during their hospital stay. 4. CAUTIs are associated with increased morbidity, mortality, healthcare costs & LOS. 5. They are preventable. #UTI #CAUTI #IDSA #KIDNEYS

The diagnosis of UC is best made with endoscopy and mucosal biopsy for histopathology. Laboratory studies are helpful to exclude other diagnoses and assess the patient's nutritional status, but serologic markers can assist in the diagnosis of inflammatory bowel disease. Radiographic imaging has an important role in the workup of patients with suspected inflammatory bowel disease and in the differentiation of UC from Crohn disease by demonstrating fistulae or the presence of small bowel disease seen only in Crohn disease. #UC #IBD #ulcerativecolitis

Invasive Fungal Infection (IFI) Invasive fungal infections are severe infections in which fungal pathogens invade normally sterile body sites. They predominantly affect immunocompromised patients, including those with neutropenia, hematologic malignancies, solid organ or stem cell transplants, and prolonged corticosteroid or broad-spectrum antibiotic use. Common Pathogens Candida species (most frequent cause of bloodstream infections) Aspergillus species (primarily pulmonary infections) Cryptococcus species (commonly CNS involvement) Emerging molds and rare fungi in high-risk populations Risk Factors Immunosuppression (neutropenia, chemotherapy, transplant) Indwelling catheters or prosthetic devices Prolonged ICU stay and broad-spectrum antibiotic exposure Clinical Presentation Symptoms vary by site of infection and may include fever, organ dysfunction, respiratory distress, or neurological deficits Diagnosis Culture and microscopy from sterile sites Antigen/antibody testing (e.g., β-D-glucan, galactomannan, cryptococcal antigen) Imaging studies (CT, MRI) for organ involvement Histopathology when feasible Management Early initiation of targeted antifungal therapy Source control, including removal of infected catheters or drainage of abscesses Selection of therapy guided by species identification and antifungal susceptibility Multidisciplinary approach with infectious diseases consultation Prognosis Dependent on timely diagnosis, host immunity, and pathogen virulence Delays in treatment significantly increase morbidity and mortality #candida #candidemia @invasivefungal #fungemia

Orbital cellulitis is what happens when your sinuses throw a tantrum and decide to drag your eyeball into the mess. It starts innocently enough, just a stuffy nose, maybe a little sinus infection and then, BAM! The bacteria stage a prison break and march straight into the orbit like, “We live here now.” The eyelid swells up like it lost a boxing match, the eye starts bulging like it’s trying to escape the drama, and suddenly you’ve got a look that says, “I’ve seen things.” Pain with eye movement? Naturally. Your eye muscles are basically shouting, “We did not sign up for this nonsense!” Vision might blur a bit, because apparently the bacteria want to direct their own action movie from inside your face. The emergency room staff take one look and go, “Yep, that’s not conjunctivitis, that’s DEFCON 1.” Then come the IV antibiotics, biochemical superheroes, charging in to clean up the microbial chaos. Radiologists join the scene with their CT scanners, narrating the plot twist: “Ah, the infection’s gone orbital!” And if the pus really sets up camp, a surgeon might need to swoop in for a cleanup mission, like the final episode of a very dramatic season. Don’t ignore that sinus infection, it might be plotting an invasion. And if your eye ever looks like it’s trying to call for backup, it’s time to get to the hospital before the bacteria win an Oscar for Best Infectious Performance. #orbitalcellulitis #postseptalcellulitis

Tale of Two Staphylococci: Methicillin-Sensitive Staphylococcus aureus (MSSA) and Methicillin-Resistant Staphylococcus aureus (MRSA). MSSA arrived quietly, without unnecessary drama. Predictable and courteous, he followed the usual clinical trajectory of fever, positive blood cultures, appropriate management, and steady improvement. The team appreciated his transparency; he respected the rules of engagement and left promptly once his source was addressed. There were no consult wars, no prolonged discussions but just a clean resolution and a satisfied discharge summary. MRSA, however, was a different story altogether. He entered the bloodstream with confidence and defiance, fully aware of his reputation. The moment his name appeared on the microbiology report, the atmosphere changed. The primary team sighed, pharmacy frowned, and infection control started whispering about isolation protocols. MRSA thrived on attention and turning every simple bacteremia into a multidisciplinary production involving ID, nursing, infection prevention, and sometimes even hospital administration. He lingered longer than anyone wanted, testing the limits of patience, policy, and resource allocation. With coordinated teamwork, careful management, and more meetings than anyone cared to count, MRSA was finally cleared from the bloodstream. #MSSA #MRSA #ID #bacteremia #staphylococcus

Picture MRSA-PCR as the hospital’s ultimate crime-fighting superhero team, but instead of capes and laser eyes, it wields test tubes and genetic scanners. MRSA the notorious “bad boy” of bacteria, likes to sneak into hospitals, pick fights with antibiotics, and then hide in plain sight like a germy ninja. Old-school tests stumble around like detectives in a black-and-white movie, muttering “the culture will be ready in a few days,” while MRSA laughs and throws confetti in the background. But PCR? Oh no, PCR doesn’t waste time. It storms in like a caffeinated detective on double espresso, grabs a swab, and yells: “Aha! There’s the MRSA DNA, hiding in your nose like it pays rent!” In just hours, the mystery is solved, the bacteria is busted, and the lab gets to feel like it just solved the medical equivalent of a bank heist. Fast, flashy, and way more reliable than waiting around for Petri dishes to gossip, MRSA-PCR is basically the hospital’s drama-filled reality show where the germs always get exposed. #mrsa #PCR #Methicillin-ResistantStaphylococcusaureus

Think of sodium as the ultimate event planner in your body, the one who keeps everything orderly, balanced, and running on time. Sodium knows how to keep water in the right places: not too little, not too much, just the perfect hydration vibe. It’s like that one responsible friend who prevents the party from getting out of control. Now, here’s where the drama starts: certain medications like thiazide diuretics, SSRIs, carbamazepine, and their buddies decide they know better. Instead of appreciating sodium’s years of experience, they “reassign” it, often flushing it away or silencing its role in water regulation. It’s like firing the competent manager and hiring an overenthusiastic intern. With sodium out of the picture, water seizes the opportunity. It floods the party like uninvited guests crashing a wedding buffet pouring into cells, especially in the brain. At first, the brain cells are polite, trying to squeeze in a little extra water. But soon they swell like overfilled balloons, and the nervous system throws a fit: headaches, confusion, unsteady gait, seizures and in severe cases, a medical emergency that’s about as fun as a power outage during surgery. The irony? This whole watery rebellion isn’t caused by an exotic tropical disease or some rare genetic mutation it’s often the very “helpful” medications prescribed to make life better. That’s drug-induced hyponatremia: when well-meaning pills accidentally kick sodium out of its leadership role, and water runs the show like a toddler hyped on sugar. So, the moral of the story? Respect sodium, it may be small, but it’s mighty. And always keep an eye on those meds, because sometimes the cure sneaks in with a side hustle as the troublemaker. #hyponatremia #sodium

Mitral valve regurgitation is the heart’s version of a plot twist — just when you think everything’s flowing forward, boom, blood decides to moonwalk back into the left atrium. Picture the mitral valve as a pair of elegant French doors between the left atrium and ventricle: they’re supposed to swing shut with precision and class. But in MR, one or both of those doors get a little loose, floppy, or just plain defiant — thanks to degenerative disease, ischemic insults, or the occasional rheumatic meddler still hanging around like it’s the 1940s. The result? Blood backflows during systole, the atrium gets flooded like a poorly planned basement, and the ventricle starts pumping harder than a med student during exam week just to keep up. Clinically, it’s a delicious mix of holosystolic murmurs, volume overload, atrial fibrillation auditions, and left ventricular eccentric hypertrophy trying to make it all work. And let’s not forget the symptoms — fatigue, dyspnea, and that glorious pulmonary congestion that says, “I’m leaking but fabulous.” Diagnosis by echocardiography turns into a cardiac detective story, and treatment spans the spectrum from medical finesse to surgical drama, complete with valve repair or replacement. So while MR might sound like just another leaky valve, in the world of internal medicine and cardiology, it’s a charismatic troublemaker — dramatic, unpredictable, and never boring. #mitralvalve #MR #Mitralvalveregurgitation #cardiology

"Imagine you're running airport security, screening passengers (tests) to catch dangerous items (diseases). Now meet your two star agents: Sensitivity and Specificity. Sensitivity is your overachiever. It’s all about catching every possible threat. If a test has high sensitivity, it correctly identifies most people with the disease—it rarely misses anyone. In other words, it’s great at picking up true positives. The downside? It might sometimes flag innocent travelers (false positives), just to be safe. Specificity, on the other hand, is cool and precise. If a test has high specificity, it correctly clears people without the disease—it rarely calls someone sick if they’re actually healthy. That means fewer false alarms (false positives), but if it’s too strict, it might miss some real cases (false negatives). In short: High sensitivity = fewer false negatives. High specificity = fewer false positives. #medicine #specificity #sensitivity