Tasty Morsels of Critical Care

Welcome back to the tasty morsels of critical care podcast. This is part 2 of infective endocarditis, this time covering the highlights of endocarditis management from the ICU perspective. Once the diagnosis is made and checked that the diagnosis is solid (remember there are published criteria about how to reach the diagnosis) then you should be reaching for some antibiotics. The guidelines have multiple, tedious tables describing antibiotic combos for native and prosthetic valves all guided by knowing what bug you are dealing with. If you are at the stage where you know what bug it is you will almost have a specialist in infection giving advice so I think this is somewhat beyond the scope of the ICU exam setting. Having a broad overview that of what bugs are gram +ve and gram -ve I think is key and will allow you to put together an appropriate reigime in any septic scenario, not just IE. As such i’m not going to go into detail. I suspect the more relevant scenario for us will be the crashing patient with an eaten out valve lesion at 2am and we’re the first person to be considering the diagnosis and have no micro to guide us. If you find yourself in such a situation then ceftriaxone and amoxcillin and some vancomycin will cover all the bases included prosthetics for the first 12 hours till help is available. This will cover all the commonest bugs of staph, strep, e faecalis and prosthetics. If you want to cover the weird culture -ve bugs then I have one, somewhat predictable word for you – doxycycline. If they’re in crit care they’ll almost undoubtedly be septic and any of your arsenal of sepsis interventions is probably appropriate and again beyond the scope of this post. The major modifiable part of your sepsis resus here will be determined by the echo. Are you dealing with severe, torrential AR then keeping the BP a little lower and diastolic period a little shorter with a tachycardia might be in your benefit. Have you got torrential MR from a perf or flail – then a balloon may be helpful. Again, the physiological management of a bad valve pending surgery is great fun but also beyond the scope of this post. So perhaps time would be better spent thinking about surgical indications in IE. The guidelines again have fairly clear indications here but many patients fall foul of the usual problem of having surgical disease when they are not surgical candidates. You can split surgical indications into 3 categories heart failure – this is the commonest indication and is driven by the degree of valve destruction and the heart’s ability to compensate for this. Cardiogenic shock and pulmonary oedema are obvious signs here. control of infection – the guidelines suggest surgery indicated if cultures not clear at 7-10 days or appropriate therapy. But these surgeries are often sensibly deferred to avoid putting what should be a life long valve into an infected patient. Persistent septic shock (even if cultures cleared) is another similar indication control of emboli – the guidelines would suggest very large vegetations (>30mm) should be operated on, even smaller veg (>10mm and other indications) could have surgery. However the risk of surgery is highest in few days before and after starting antibiotics and tails off signficantly at 2 weeks. As such you can imagine that many feel more comfortable with conservative management in this scenario. Be aware that the guidelines use the words “urgent” and “emergency” differently from what we might expect with “emergency” not meaning “right now” but “within 24 hrs”. There are often multiple good reasons for deferring theatre when there is the opportunity to optimise someone for a challenging bypass run. Intracranial emboli with bleeds also pose a big challenge when you’re proposing giving someone 30000 units of heparin. Lots of painful but necessary MDT discussion needed. Finally a common question appears regarding whether or not you anticoagulate to prevent the emboli causing strokes. . We do it when we find clot in the heart so why not veg (which inevitably have clot and infection in them). The guidelines give a reasonably clear answer with anticoagulation not recommended as a prophylaxis strategy.  To give a direct quote from the ESC guidance “To date, no data support initiation of either antithrombotics nor anticoagulants for treatment or prevention of stroke in IE.” In distinction  continuing anticoagulation in someone on it for pre existing reasons (eg a fib) does not seem especially high risk. Reading: – Fowler, V. G. et al. The 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria for Infective Endocarditis: Updating the Modified Duke Criteria. Clin. Infect. Dis. 77, 518–526 (2023). – Delgado, V. et al. 2023 ESC Guidelines for the management of endocarditis. Eur. Hear. J. 44, 3948–4042 (2023).

A focused dive into how infective endocarditis can present to critical care teams. Short sections cover sepsis presentations, embolic events like strokes and splenic or renal infarcts, and heart failure from valve destruction. The diagnostic framework is reviewed, plus microbiology pitfalls and the roles of TOE, CT and PET in imaging.

Welcome back to the tasty morsels of critical care podcast. Today we look at blunt cerebrovascular injury or BCVI. I added this to my list to cover for unclear reasons as when i looked back at my notes i had about 8 bullet points and a couple of referenced articles. So this will be shorter than usual I suspect. Effectively this refers to injuries to the carotids and vertebral arteries in the context of trauma. The pathology here is typically a pinch, twist or stretch of the vessel leading to an intimal tear in the vessel. The exposed endothelium then is a nidus for thrombus formation. The main downstream consequence is stroke and it’s a real shame to have a successful haemostatic and surgical resus of a major trauma patient only to have them suffer a life changing stroke 3 days into their hospital stay. They’re also pretty tricksy injuries as there are rarely obvious clinical signs to indicate their presence until they you find the dense hemiplegia, so this is one of those things were the term “index of suspicion” comes into play. It is especially important seeing as we have now effectively outsourced all diagnosis to the radiologists and these injuries are not picked up on the typical trauma pan scan that we so love. Given that I described the pathology of the injury as pinching, twisting and stretching we can probably get a sense of the mechanism of injury associated with these injuries. Top of the list here are c-spine injuries – if the neck has moved enough to break it you should think about the delicate blood vessels beside the c-spine. This is particularly pertinent to the vertebrals whose course, evolution in her wisdom, placed inside the tiny little vertebral foramen transversarium of the c spine itself. To make life more difficult for the poor little vertebrals they have to navigate a few 90 degree turns to get between C1 and the skull to get into the foramen magnum. This is reflected in the higher incidence of BCVI in high spine injuries. Obvious other associations are with severity of TBI and complex facial fractures (remember the carotid has to navigate its way past these). You might get some pointers to diagnosis from your clinical exam. Horner’s syndrome would be a classic (disruption to sympathetic neurons in the carotid) but if you’re diagnosing a Horner’s syndrome in your primary survey then you’re either over achieving or doing it wrong or possibly both. They may have stroke features on arrival which would be an obvious trigger for imaging. A bruit is also listed as a sign of injury but I think that’s a sign for better clinicians than you or I. Most of the time you will have an injured patient without specific symptoms of BCVI. Who do we pursue further imaging on given that I’ve already noted the initial trauma pan scan will often not pick up this? Enter stage left the geographically titled criteria each named after the academic centre that developed it. Denver, Memphis and Boston have all contributed a published criteria. The Denver criteria appear to be the most commonly used and referenced. I think listing the individual components is probably beyond the scope of the post but I’d emphasise the main headlines c-spine injuries facial fractures complex base of skull severe TBIs hanging Once you’ve decided the patient needs imaging then you should be reaching for our trusty friend the CT scanner. in this case a well done CT angiogram of the neck vessels extending into the intracranial vessels. It is not (unsurprisingly) a perfect test but it is a very good test and certainly where you should start. If you do find a BCVI you may even have the joy of seeing it classified I to V according to the wonderfully named Biffl classification system. It covers things like intimal tears and degrees of narrowing and occlusion. once you’ve found a BCVI it’s unclear who your go to specialist might be and I have seen vascular, neurosurgery and stroke all give opinions on treatment. Overall risk of stroke in BCVI is ~8% but changes significantly depending on grade with higher grades having higher stroke risk. For the vast majority of patients your treatment options come down to heparin vs aspirin. There does not appear to be a clear proven superiority of one strategy over the other. Some form of antithrombotic does, in observational data, seem to reduce stroke rate and is probably worth doing. Aspirin is generally easier delivered and seems to be the most common choice in our region. Many of the injuries would actually be amenable to surgical repair but the vast majority are surgically inaccessible hence the antithrombotic treatment as next best thing. The decision to give something that makes clotting more difficult in a patient who is either still bleeding or at risk of major bleeding is not an easy one. Hence there is typically a day or two of hand wringing amongst several specialties till we are all comfortable giving it. Observational work suggests that we’re likely a little overcautious on this in a similar way to our reluctance to commence VTE prophylaxis in TBI. Reading Doctor’s Little Helper Radiopaedia      

They dig into when to give blood and why transfusion targets matter in critical care. Storage lesions and how donated red cells change over time get a clear rundown. Important transfusion reactions and complications are reviewed. Evidence from trials across sepsis, surgery, GI bleed, and cardiac care is traced to practical haemoglobin targets and noted exceptions for massive bleeding and brain injury.

They explore why putting critically unwell adults on their tummy can change lung inflation and make the lungs more homogeneous. Listeners hear about CT evidence showing recruitment and better ventilation–perfusion matching. The conversation covers potential benefits beyond oxygenation, key trial evidence that shifted practice, and practical safety and contraindication considerations.

Delve into the fascinating world of oesophageal balloons, innovative devices that aid in measuring pressures in critical care. Learn how these devices function like fancy NG tubes, providing crucial insights into pleural pressure. Discover their clinical applications, from titrating PEEP to assessing muscle contributions in respiratory injuries. Despite their potential, barriers like cost and compatibility keep them from routine use. Tune in for practical insights and a look at emerging research in respiratory mechanics.

Dive into the complexities of managing pulmonary embolism, focusing on high-risk cases. Explore the critical interventions like thrombolysis and anticoagulation strategies, as well as the nuances of using inotropes and fluids. Learn about the role of CPR, the risks of intubation, and the controversial nature of catheter therapies. Discover the potential of VA ECMO as rescue support and the challenges of surgical embolectomy. Insightful discussions highlight the importance of swift decision-making in critical care!

A focused dive into how to risk stratify pulmonary embolism in critically ill patients. It contrasts PEs found in the ICU with ED referrals and argues CT pulmonary angiography is key. It flags that many ICU PEs are small and clinically insignificant. It highlights the value of echocardiography, RV dysfunction markers, and rising lactate when deciding who needs aggressive treatment.

Dive into the intriguing world of hypertriglyceridemia-induced pancreatitis, where strikingly lipemic blood samples can be a diagnostic clue. Learn when to suspect this rare cause and how triglyceride levels directly correlate with the severity of pancreatitis. The discussion covers the toxic mechanisms of fatty acids and dives into acute management strategies, including nutrition adjustments and insulin use. Plus, explore plasmapheresis as a rapid triglyceride-lowering option, even as guidelines caution against its routine use in acute scenarios.

Dive into the critical world of acute liver failure, where understanding the distinction from acute-on-chronic liver failure is crucial for diagnosis and management. Discover the main presentations like coagulopathy and encephalopathy, and explore various causes, including toxins and viral infections. The conversation also navigates through complications, such as intracranial hypertension, and highlights cutting-edge treatments like high-dose CRRT and urgent transplant referrals. It's a whirlwind through life-saving critical care insights!