Confessions of an ICU Physician with a terrible memory Accessing the Right Information < Back Confessions of an ICU Physician with a terrible memory Training in medicine starts with textbook learning. But the art of caring for patients can’t be learned in a textbook. Higher-order thinking is essential to understand the interaction between multiple conflicting disease processes, identify nuisances of atypical presentations and find solutions for clinical conundrums. As the field of medicine grows exponentially, the volume of information is too much for one person to keep track of. I find that understanding clinical concepts is much easier than rote memorization of pharmaceutical brand names with their associated generic name, recalling the dose of a paralytic, or identifying the ideal antibiotic for a multi-drug resistant bacteria. After several years of learning and studying mechanical ventilation and how it interacts with and affects a patient's respiratory physiology, I now understand the principles of how to optimize oxygenation and ventilation. As an ICU physician, I can't re-read the basic textbook of mechanical ventilation every time I care for a patient with respiratory failure. I must be able to make decisions relatively quickly and must be able to explain my rationale to residents and bedside nurses while we are working to manage a patient with severe lung disease. But I can pause to look up the recommended dosing of a medication for a patient on dialysis or identify the best anti-microbial for a particular bacteria or fungi. What do I do about important information that I need immediate access to but that doesn't reside in the forefront of my mind? Smartphones, with access to websites and applications , have revolutionized our ability to bring evidence-based medicine to the bedside. Clinical practice guidelines can be accessed on society websites. Deployed Medicine is a resource that provides access to Tactical Combat Casualty Care and Joint Trauma System Clinical Practice Guidelines. There are apps for a wide number of clinical programs that were initially web-based, such as UpToDate. In addition to the resources that are openly available to the public, I have created a database of personal high-yield references. Medication dose ranges, CPGs for our trauma center, AAST Injury Scales, sedation/ pain scores, TEG parameters, and a wide variety of other information that I refer to on a relatively routine basis are now in the palm of my hand. I use the Trello app. I created a dedicated workspace with a group of lists (titles such as trauma, medication, ICU, etc) which each contain multiple individual cards (titles such as A-F bundle, CAM-ICU/ RASS/ CPOT, TEG). I'm not saying you have to use this. But I highly recommend finding a tool that works for you. TL;DR • Take the time to understand processes and concepts- learn one physiology concept from each pt • Have an external tool for storing “rote memorization” facts that you can readily access Previous Next

< Back Pneumonia...pending Pneumonia Previous Next

< Back Respiratory Failure- it hurts to breathe A 47-year-old male sustains multiple traumatic injuries after being struck by a vehicle while on the side of the road. He had severe thoracic trauma (bilateral pulmonary contusions), bilateral femur fractures and a liver laceration. He also had a severe TBI, requring intubation shortly after his arrival. 10 days into his hospital stay, he still requires ventilatory support. What are some of the potential causes of the patients ongoing requirement for mechanical ventilatory support? Pain from rib fractures, pneumonia, ARDS, pulmonary embolism, fat embolism, pulmonary contusions, loss of chest wall stability due to severe thoracic trauma, hypomagnesemia, volume overload, retained hemothorax, poor nutrition from inadequate protein delivery. He is undergoing a trial of spontaneous ventilation, but he develops tachypnea and hypoxemia and appears to be struggling on the ventilator. What are some of the initial steps in evaluating this patient? Physical exam (pulmonary exam, assess for edema), bedside ultrasound (pleural effusion, pneumothorax). Chest x-ray- look for infiltrates. ABG, EKG, review volume status. His chest x-ray is shown below. What do you see? Trachea midline, no effusions. Bilateral fluffy infiltrates. His current ventilator settings and ABG results are shown below. Ventilator settings: RR 12, TV 450, PEEP 10, FiO2 50. Arterial blood gas: pH 7.34, PaCO2 42, PaO2 64, HCO3 24 What does this tell you about his oxygenation? PaO2:FiO2 ratio is an indicator of oxygenation. This patients P:F ratio is 182. See below for explanation. What diagnosis is this consistent with? Acute respiratory distress syndrome. What are the management principles when caring for a patient with ARDS? What are your initial ventilator management strategies? ARDS is not a primary diagnosis, so it is important to treat the underlying cause (pancreatitis, pneumonia, etc). Minimize further insults to the lungs. Optimize ventilator strategies- low tidal volume, target PEEP/FiO2 combination to target SpO2 88-95% Diagnosis and Management of ARDS Etiologies of ARDS Pneumonia, pulmonary contusions, aspiration, inhalation Trauma, burn Pancreatitis Transfusion-related acute lung injury (TRALI) ARDS diagnostic criteria: The Berlin Definition [1] Onset of respiratory failure within 1 week of an insult that is known to cause ARDS Bilateral fluffy infiltrates on CXR not explained by effusions/ infiltrates/ contusions/ lung collapse Respiratory failure not related to heart failure or fluid overload Oxygenation PaO2/FiO2 ratio with PEEP ≥5 cm H2O. Mild 200-300, moderate 100-200, severe ≤100. Basic principles of ARDS management [2,3] Low tidal volume ventilation- 4-8 mL/kg predicted body weight. Prevent volutrauma. Permissive hypercapnia- low TV ventilation leads to decreased minute ventilation, which leads to CO2 retention (hypercapnia). Hypercapnia is tolerated as long as pH remains above 7.2. Positive end-expiratory pressure (PEEP)- goal is avoiding overdistension and optimizing recruitment If ↑PEEP→ ↓plateau pressure: recruitmentIf ↑PEEP→ ↑plateau pressure: overdistension Optimizing mean airway pressure (MAP). Prolonged inspiratory:expiratory ratio Target plateau pressure <30, driving pressure ≤15. Recruitment manuevers Advanced strategies for persistent hypoxemia Prone positioning Airway Pressure Release Ventilation (APRV) Neuromuscular blockade Inhaled vasodilators Prostacyclin and nitric oxide ECMO High frequency oscillatory ventilation Open lung ventilation Dexamethasone Extracorporeal carbon dioxide removal (ECCO2R) References Ferguson ND et al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med. 2012;38(10):1573-1582. Narendra DK et al. Update in Management of Severe Hypoxemic Respiratory Failure. Chest. 2017 Oct;152(4):867-879. SCCM Clinical Practice Guideline. Fan E et al. ATS/ SCCM CPG: Mechanical Ventilation in Adult Patients with Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med. 2017;195(9):1253-1263. Basic Principles of Ventilatory Management of ARDS Previous Next

< Back Unusual Case of Peritonitis A 23-year-old male presents to the ED with several days of abdominal pain. He is otherwise healthy and denies any other symptoms. On exam, he has diffuse peritonitis, but no other obvious findings. He is tachycardic with a heart rate in the 110s-120s. His blood pressure is 100s/60s. No significant medical or surgical history. No remarkable events recently. He had plain films of his chest and abdomen. Plain film of the chest and upper abdomen What's going on? Differential diagnosis? Perforated hollow viscus- gastric or duodenal ulcer, bowel obstruction leading to perforation, procedural complication (EGD, ERCP). On further questioning, the patient endorses a recent soccer game during which he blocked a goal and was hit in the stomach. Unsure if it was the soccer ball or a kick to the stomach. He then had a CT of his abdomen and pelvis. CT of the abdomen and pelvis, representative slices What's going on? Diagnosis? Intervention? Free air (pneumoperitoneum) and free fluid are consistent with a perforated hollow viscus. No clear source on the CT. This requires abdominal exploration. We proceeded with exploratory laparotomy. Found liters of succus. There was a single perforation of the small bowel that was resected and anastomosis was performed. The abdomen was closed and a drain was placed. Intraoperative Findings Management of Peritonitis from Perforated Hollow Viscus The hollow viscus refers to the gastrointestinal tract from the esophagus to the rectum. Pain associated with hollow viscus perforation is classically acute onset, constant, severe, and worse with movement. The peritoneal lining of the abdomen becomes inflamed in reaction to the leaking enteric contents. This is a surgical emergency. The diagnosis can be made with the visualization of pneumoperitoneum on an upright chest x-ray (lucency under the diaphragm). A patient with peritonitis and free air requires surgical exploration. A CT scan can help identify the underlying pathology, but is not mandatory and should not delay operative intervention. Non-operative management is reserved for the patient with a sealed perforation (example- retroperitoneal duodenum) or a patient who is a prohibitively high-risk operative candidate (example- patient on palliative or hospice care). Cultural differences Not all cultures have adopted the practice of Western medicine. In some cultures, people still seek advice and medical care from traditional healers. Unfortunately, this can delay treatment if a patient requires operative intervention. Some of the treatments provided by traditional healers can also lead to further injury. This patient with a small bowel injury was seen by a traditional healer several times before he was finally brought to the hospital. The marks on his skin are the result of a practice of cutting the skin to heal the cause of his abdominal pain. Another patient was brought to the hospital for a severe infection of his genitalia. By the time he came to the hospital, his infection was so extensive that he required a debridement of a large portion of the skin in his perineum. He had been seeing a healer who was treating him with a topical solution that had essentially burned his skin, so in addition to the underlying infection, he had severe tissue damage. Previous Next

2 Range Why Generalists Triumph in a Specialized World - Early expertise and overspecialization do not equate to success. Having a breadth of knowledge is key to solving issues that cross different disciplines. - An extensive explanation of the benefit of the breadth of knowledge and the risks of super sub-specialization. Loss of cross-communication between silos of isolated components. - Wicked problems- issues that require outside-the-box thinking, can't be solved by relying on specialization but needs interaction between various contexts. - Capitalize on the varied backgrounds when trying to solve a problem. Gathering 10 specialists who all share the same knowledge and experience to focus on one issue can easily lead to a dead-end- without the benefit of new and fresh ideas, the team ends up in a loop. Diversity can exponentially increase problem-solving by drawing from different perspectives, viewpoints, and thought processes. - Contrasts to the 10,000-hour rule, which asserts the benefits of focused training and specialization. Previous Next

11 Made to Stick Why Some Ideas Survive and Others Die 6 Principles of Sticky Ideas - Simple - Unexpected- crash at the end of the car commercial. - Concrete - Credibility- the ability to test. Before you vote ask yourself if you are better off today than you were 4 years ago- Reagan. - Emotions - Stories Curse of knowledge- we find it hard to imagine not knowing what we have learned. Can’t imagine what it’s like not to understand a certain concept that we accept as fact Previous Next

< Back Pulmonary Embolism...pending Diagnosis and Treatment of Pulmonary Embolism Previous Next

8 Freakanomics A Rogue Economist Explores the Hidden Side of Everything - Hard to include all the different topics under one umbrella. Very controversial topics, such as crime, cheating, the impact of a name. - Correlation versus causation. Does legalized abortion lead to decreased crime? Using broad generalizations, people who grow up with mothers who didn't want them are placed in circumstances that increased their likelihood of involvement in crime. Previous Next

< Back Abdominal Pain- Mesenteric Ischemia A 65-year-old male with 1 week of progressive abdominal pain presented to a small hospital. His medical history is significant for a myelofibrosis with chronic portal vein thrombosis. He underwent CT scan and was urgently transferred to the surgical ICU at the nearby tertiary hospital. CT abdomen and pelvis (coronal) https://video.wixstatic.com/video/3b6ff6_3a044f13731447f68a338b2b814e0d65/480p/mp4/file.mp4 CT abdomen and pelvis (axial) https://video.wixstatic.com/video/3b6ff6_102334b9eba6428f8c132cdcc0aa175e/360p/mp4/file.mp4 The abdomen pelvis CT showed chronic portal vein thrombosis with cavernous transformation as well as distal SMV thrombosis with inflammatory changes of the distal small bowel. There is a moderate amount of intra-abdominal fluid, including around the spleen and liver as well as in the pelvis. There is thickening of the small bowel wall as well as stranding and edema in the mesentery. There was also evidence of a splenorenal shunt. Representative slice from CT, axial Representative slice from CT, axial- labels Representative slice from CT, axial Representative slice from CT, axial- labels Differential diagnosis? Splenic injury secondary to splenomegaly (minor trauma can lead to splenic injury in the setting of splenomegaly). Bowel ischemia. Hollow viscus perforation. On arrival to the ICU, his abdominal exam revealed diffuse rebound tenderness. He became disoriented during our interview. Concurrent with our evaluation, the images with reviewed with radiology who reported that the fluid was not consistent with hemoperitoneum from a splenic injury. Based on our concern for bowel ischemia, he was taken to the operating room for abdominal exploration. He was noted to have a significant length of ischemic and necrotic bowel. This was resected and his bowel was left in discontinuity. He was returned to the ICU with an open abdomen and plan for second look laparotomy within 24 hours. Evaluation and Management of Acute Mesenteric Ischemia Causes Arterial Embolism- from the left atria (atrial fibrillation), left ventricle (decreased function following cardiac ischemia) or heart valves. Arterial Thrombosis- progression of underlying atherosclerotic disease leading to critical stenosis at the takeoff of the celiac or SMA from the aorta. Venous Thrombosis- hypercoagulable states, acute inflammatory process around the SMV (pancreatitis), post-operative following splenectomy or bariatric surgery. Non-occlusive mesenteria ischemia (NOMI)- low-flow through the SMA with vasoconstriction. Often having underying illness or cardiac failure, which is exacerbated by vasoconstrictive medications and hypovolemia. Presentation Severe abdominal pain, "pain out of proportion to exam" (report severe pain but abdominal exam doesn't elicit tenderness). Arterial thrombosis may be acute on chronic, if there is underlying chronic mesenteric ischemia. Diagnosis Etiology can be suspected based on symptoms and medical/ surgical history. Sudden onset is suggestive of arterial embolism. Known hypercoagulable state is suggestive of venous thrombosis. Chronic abdominal symptoms including pain with eating (food fear) and weight loss are suggestive of arterial thrombosis. Imaging Plain films may be non-specific, but may show free air or portal venous gas later in the course. Angiography Arterial thrombosis- often seen right at the takeoff of the celiac or SMA from the aorta. Arterial embolism- typically an occlusion of the celiac or SMA at a branch (versus right at the takeoff). Treatment Volume resuscitation, antibiotics Anticoagulation Surgery consultation for assessment of bowel viability and treatment of vessel occlusion Previous Next

12 Barking Up The Wrong Tree The Surprising Science Behind Why Everything You Know About Success Is (Mostly) Wrong - Good grades in school- likely to be a "rule follower", and less likely to be innovative, think outside the box. - Introverts are more likely to be experts, extroverts tend to make more money (socializing, "networking"). We should look at "networking" as "making friends". This disputes the "nice guys finish last"... - Match your strengths/ passion/ skill to the right context. - Flattery (sucking up to the boss) can work in the short term, but in the end, when people see their colleagues/ neighbors/ etc cutting corners and reaping benefits, this leads to a general collapse into distrust and rule-breaking. - IQ only matters up to a certain point, but then it yields diminishing returns. After that, hard work is what makes the difference. - Tradeoffs- every hour that you spend working is an hour spent away from other things (family, hobbies). In this age of constant accessibility, you have to decide to leave work behind (ignore your emails when you're at your kid's ball game). - Gratitude in relationships- on their deathbed, people regret working too much and not saying thanks to the people in their life. - Some helpful things I learned...please note that tact and delivery matter and these are not appropriate in every scenario. - When someone is getting upset or frustrated and starts yelling, "Please speak more slowly, I want to help." Or try, "What would you like me to do?" - When someone is upset, validate/ name their feeling. "Sounds like you’re angry/ hurt/ frustrated." If you're wrong, give them the chance to correct you. - Gratitude to relationships. Previous Next

6 Tips to Be More Comfortable with Uncomfortable Conversations Giving Bad News < Back 6 Tips to Be More Comfortable with Uncomfortable Conversations It's not fun to tell families (or patients) that there was a complication, that their loved one died, or that their loved one is not going to survive. But it's a fundamental principle of good patient care, especially in the specialties of trauma and critical care. I didn't become truly comfortable with these conversations until my critical care fellowship. After many years and countless conversations in private rooms, here are my tips on how to develop this skill. 1. Experience. It's uncomfortable, but you should take every opportunity to participate in these conversations, starting as a student/ trainee. - As a young resident, I remember walking with my attending to go talk to a family about an intra-operative complication. I'll never forget the sinking feeling in my chest, the shame that I made a mistake. This was a pivotal moment in my training. My attending didn't have to tell me I messed up. But he knew I needed to see how he handled disclosing to the family members. He showed me that this wasn't something that I should allow to crush my self-confidence. - A few years later, during one of my first trauma rotations, I remember sitting in a small room in the ER as one of my co-residents told a family that their child was the victim of a fatal shooting. I didn't have much experience telling families that their loved one had died. In particular, I didn't have any exposure to telling a family that their loved one died in a trauma bay- a family I'd never met, a family who never had a chance to see their loved one before they died from their injuries. I was initially embarrassed that my co-resident, who was one year younger than me, was more comfortable leading the discussion than I was. But then I realized he had much more exposure to that type of conversation because of his previous trauma rotations. So I took it as an opportunity to learn and prepare myself to lead the conversation the next time. - Two years later, in the ICU waiting room of the same hospital where I watched my (younger) co-resident tell a family their son died, I sat with the mother of a young man who was critically injured. Thankfully, I had much better news. But still, it's not easy to tell a single mother that her oldest son was shot through the chest, and was laying in the ICU, intubated, with an open chest and abdomen. 2. Learn from watching experts. - Everyone has a slightly different style of handling these conversations. I joined my attendings for every conversation I had the opportunity to witness. This included conversations about everything from Code Blue incidents to fatal injuries and end-of-life care. It's important to see different styles, which will allow you to develop your style. Some are more blunt, some are more observant of family dynamics, some are overly talkative. There are some you may choose to not replicate, but it's important to see a spectrum of styles to learn what works for you. - I've watched my MICU attending talk with the wife of a man who came to the hospital with acute cardiac arrest, requiring emergent coronary angiography and intervention, then therapeutic hypothermia. I learned how to succinctly describe a complex situation and support a wife make a crucial decision without pressuring her. - I've watched my trauma attending talk to a family of a young male patient who had died on the operating table. I've watched that talk more than once, unfortunately. And it never got more comfortable. But I learned how to convey devastating news while simultaneously expressing compassion. 3. Practice. - As a fellow, I would often have a pre-brief with my attending and we would discuss key points for the meeting, as well as the goals of the discussion (ie deciding about proceeding with surgery, deciding about comfort care, etc). - When I have younger residents who are having family meetings, particularly one's that I haven't worked with before, I have them rehearse their conversations with me before. I did this as a resident and a fellow, and I still do this with my fellows. 4. Get feedback. Positive feedback is always nice, but true constructive feedback is key to improving. - I've had nurses and chaplains who have joined me for multiple family meetings, and it's always reaffirming to hear them compliment my interaction. - My attendings still occasionally joined me in conversations toward the end of my fellowship. It was always helpful to hear feedback about what was well-received and how I could have been more effective. 5. Once you've practiced, developed your style, and absorbed feedback- don't expect it to always be easy. - Towards the end of my fellowship, I had a particularly challenging case. I had already had countless family discussions and had become very comfortable with being uncomfortable. For a variety of reasons, I was emotionally overwhelmed with this patient's situation- I sat and cried at the nurse's station for a long time. Then I went and talked to my attending and told her I couldn't have the conversation, that I couldn't stop crying. I was hoping she would take over and lead the conversation- I should have known I wouldn't get off that easily. She reassured me that I wouldn't have to say much- I had already established rapport with the patient's family the day before, and they'd be able to tell from my non-verbal communication that I didn't have good news. It was (and still is) the hardest conversation I've had. 6. Don't Stifle Your Emotions (within reason) - Some people would criticize me for expressing emotion when having discussions with families. I do think there has to be a healthy separation, and getting emotionally invested with every case would be paralyzing. I don't cry during the majority of these conversations. However, I'm not a robot, and I still occasionally have patients that affect me on a more personal level. For example, I had one family that came to the very difficult decision to transition their mother to comfort care. Their mother was the matriarch of the family and her children didn't want to disrespect her. She had expressed that she would not want to be kept alive if she couldn't continue to have meaningful interactions and care for the family. I told them that giving them the implicit approval to allow her to die peacefully was probably the greatest gift she could have given them, and I reassured them that they were showing her the ultimate level of respect and kindness by honoring her wishes. That hit me differently because I could feel their pain as I imagined myself in their position. Previous Next

< Back Don't mess with the Pancreas A 47-year-old female with epigastric abdominal pain and nausea presents to the ER for evaluation. She is an otherwise healthy female, with no prior surgical history. On further questioning, her pain started 3 days ago and radiates toward her back. It has persisted and wasn't relieved with over-the-counter Tums, Gas-X, and Pepcid. She has had nausea but no vomiting. She has had minimal appetite over the past few days. Her history is otherwise unremarkable with no prior similar symptoms. On exam, she is uncomfortable but not in acute distress. HR 112, BP 112/63, T 99.1, O2 sat 99% on room air. Her abdominal exam is notable for focal tenderness in the epigastrium. What is on your differential and what is your initial workup? Peptic ulcer disease, esophagitis, hepatobiliary pathology (cholecystitis, hepatitis), pancreatitis, bowel obstruction, GERD, and bowel perforation. Labs- CBC, amylase, lipase, lactate. Imaging- acute abdominal series, possibly CT scan. Her labs are notable for a WBC of 11K, markedly elevated lipase, normal bilirubin and normal renal function. Her acute abdominal series shows non-specific bowel gas pattern with minimally dilated loops of small bowel. Right upper quadrant ultrasound revealed gallstones without evidence of acute cholecystitis. Based on the patients clinical presentation and lab findings, she is diagnosed with acute gallstone pancreatitis and was admitted to the surgical service. What are your initial goals of management? Pain control, IV fluid resuscitation. NPO until pain is improving. NGT if nauseated/ vomiting. Monitor vitals and organ function (urine output, labs). On her second hospital day, she developed worsening nausea/ vomiting, so an NGT was placed to decompress her stomach. Over the next few days, she has ongoing low grade sinus tachycardia, and then she developed intermittent low grade fever and mild leukocytosis. At that point, a CT scan is obtained. CT abdomen and pelvis https://video.wixstatic.com/video/3b6ff6_7d78015ba7b5430bb996145d60f8b0d6/360p/mp4/file.mp4 The scan reveals peripancreatic inflammation with peripancreatic stranding, gland edema and hypoperfusion. There is also simple appearing peripancreatic fluid. Over the next few days, the patient developed worsening pain and an uptrend in her leukocytosis. She is mildly hypotensive and she is urinating less frequently. When a Foley catheter is placed, she has a small volume of concentrated urine in the collection bag. She is transferred to the ICU and a Dobhoff tube was placed for post-pyloric enteral feeding. Over the next two days, she develops fevers, an increasingly oxygen requirement and persistent pain. A repeat CT scan was obtained. Follow-up CT abdomen and pelvis https://video.wixstatic.com/video/3b6ff6_e3134e03b3f242a291efd6dbc2e187e2/360p/mp4/file.mp4 There is evidence of progression of her pancreatitis. There are bilateral pleural effusions as well as worsening intra-abdominal free fluid. There is evidence of non-perfusion of the midportion of her pancreas, consistent with pancreatic necrosis. She remained in the ICU over the next several days. She did not clinically deteriorate and her pain slowly resolved. She had persistent high-volume output from her NGT. Why would she have high volume output in her NGT? Gastric outlet obstruction from peripancreatic fluid collection or necrosis. Ileus from ongoing intra-abdominal inflammation. Her distension improved with NGT decompression, and she continued to have bowel function. She was started on post-pyloric enteral feeds via a nasojejunal tube, and this was continued for the next month, awaiting for the acute necrosis to wall-off and develop a rind. Management of Acute Pancreatitis Etiology Gallstones and alcohol account for the vast majority of cases of pancreatitis. Other causes include hypertriglyceridemia, medication, ERCP, and hypercalcemia. Diagnosis Clinical presentation- epigastric pain, sometimes radiating to the back or shoulder. Nausea/ vomiting. Labs- elevated amylase/ lipase at least 3x normal Radiology- peripancreatic inflammation on contrast CT of abdomen. CT scan is not always mandatory on admission, but its commonly obtained for patients who have significant enough disease that they warrant a surgical consult. CT is also useful to rule out other pathology if the diagnosis is unclear. Clinical Course Most patients (about 80%) with acute pancreatitis suffer only mild disease and have resolution of symptoms without sequalae. The remaining 20% progress to moderate or severe pancreatitis, which is defined by the development of peri-pancreatic fluid collections or necrosis (sterile= moderate, infected= severe), or organ failure (transient= moderate, persistent= severe). Patients with organ dysfunction require ICU admission. Initial management Fluid resuscitation and ensuring adequate pain control. Nutritional support is also important, and patients are allowed to eat. Enteral nutrition should be initiated if the patient doesn't have adequate intake over the first few days. Close monitoring for development of sequalae. Patients are at risk for ARDS, abdominal compartment syndrome and infection. Assessment of Disease Severity Ranson's Criteria: Classic criteria for estimating pancreatitis severity[1] Admit data: WBC >16K, age >55, glucose >200, AST >250, LDH >250 48 hours: ↓Hct >10%, ↑BUN >5, Ca <8, PaO2 <60, Base deficit >4, >6L IVF. CT Severity has also been used to grade pancreatitis- inflammation, fluid collections and necrosis.[2] Management of Complicated Pancreatitis- Fluids Collections, Necrosis, Infection Diagnosis and Classification of peri-pancreatic fluid collections and necrosis [3] Acute interstitial edematous pancreatitis Less than 4 weeks, the fluid collection is an acute peripancreatic fluid collection . After 4 weeks, it becomes walled-off/ encapsulated and is a pancreatic pseudocyst . Acute necrotizing pancreatitis [non-enhancing pancreatic parenchyma] Less than 4 weeks, the fluid collection is an acute necrotic collection . After 4 weeks, it becomes walled-off/ encapsulated and is walled-off necrosis . Infected pancreatic necrosis- diagnosed by air in the necrosis, clinical symptoms consistent with infection and confirmed by aspiration and culture. A negative culture does not definitely rule out infection, so in the appropriate setting of clinical deterioration, there must be a high index of suspicion for infection. Indication for Antibiotics Antibiotics are NOT indicated for severe pancreatitis or pancreatic necrosis as a prophylaxis for infection.[4, 5] They are only indicated in known or highly-suspected infected necrosis. The antibiotics chosen must penetrate pancreatic tissue to be effective- quinolones and carbapenems are both broad-spectrum antibiotics (cover gram positive and gram negative) that penetrate pancreatic tissue. Carbapenems also cover anaerobes. Metronidazole covers gram negatives. Regimen: carbapenem or quinolone + metronidazole. Also consider antifungal coverage in severely ill patients.[6] Diagnosis of Infected Necrotizing Pancreatitis Infected pancreatic necrosis can be a challenging clinical diagnosis because the inflammatory state associated with pancreatitis can present with similar signs and symptoms, including fever, tachycardia, leukocytosis and ileus. CT evidence of air in the pancreatic necrosis is highly suggestive of infection, although absence of air does NOT definitively rule out infection. Fine-needle aspiration (FNA) can be used to obtain a sample for culture. There is a risk of infecting a sterile necrotic collection by performing an FNA, so this requires careful clinical decision-making. Management of Infected Necrotizing Pancreatitis These patients need broad spectrum antibiotics. Some patients may improve with antibiotics alone, but a drainage procedure is often needed. Percutaneous IR drain placement has a low rate of complications, but frequently fails to fully resolve the infection. Upsizing the drain or proceeding to more invasive intervention (see below) is required if that patient deteriorates despite drain placement and antibiotics. Previously, open necrosectomy was the standard. This is a highly morbid procedure, that requires maintaining an open abdomen, repeat washouts, and a prolonged ICU stay. Now, the step up approach is being increasingly utilized to manage these patients less invasively with similar or better outcomes (percutaneous retroperitoneal drainage or endoscopic transgastric drainage, endoscopic necrosectomy, followed by retroperitoneal necrosectomy).[7-10] Management of peri-pancreatic fluid collections [11-13] Enteral nutrition and pain control. A trial of a regular diet is appropriate, but if the patient is able to tolerate a regular diet, supplemental nutrition is required. Enteral nutrition is ideal, as it is associated with improved outcomes compared to TPN. Enteral access distal to the 3rd portion of the duodenum may theoretically avoid stimulation of the pancreas, but there is no evidence that jejunal feeds are superior to gastric feeds. However, depending on the location of the fluid collection, gastric outlet obstruction is a potential complication. Ideally, post-pyloric access would be obtained prior to obstruction, and can be used for long-term feeding while the fluid collection is allowed to resolve/ mature. Most resolve without intervention. As long as the patient is not systemically ill, drainage of pancreatic necrosis should be delayed as long as possible, ideally 6-8 weeks. Goal is to avoid procedural intervention until the fluid/ necrosis have become walled off, and then only intervene if the patient remains symptoms (pain, early satiety). However, if the patient clinically worsens, earlier intervention is necessary. Open pancreatic necrosectomy is associated with significant morbidity and mortality. An algorithm starting with least invasive (percutaneous or endoscopic drainage) and progressing to more invasive if the patient continues to do poorly is associated with decreased morbidity and mortality. References Ranson JH et al. Prognostic signs and the role of operative management in acute pancreatitis. Surg Gynecol Obstet. 1974 Jul;139(1):69-81. Balthazar EJ et al. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990;174(2):331-336. Banks PA et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013 Jan;62(1):102-11. Dellinger EP et al. Early antibiotic treatment for severe acute necrotizing pancreatitis: a randomized, double-blind, placebo-controlled study. Ann Surg. 2007 May;245(5):674-83. Leppanieme A et al. Executive summary: WSES Guidelines for the management of severe acute pancreatitis. J Trauma Acute Care Surg. 2020 Jun;88(6):888-890. Howard TJ. The role of antimicrobial therapy in severe acute pancreatitis. Surg Clin North Am. 2013 Jun;93(3):585-93. van Santvoort HC et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010 Apr 22;362(16):1491-502. van Brunschot S et al. Endoscopic or surgical step-up approach for infected necrotising pancreatitis: a multicentre randomised trial. Lancet. 2018 Jan 6;391(10115):51-58. Luckhurst CM et al. Improved Mortality in Necrotizing Pancreatitis with a Multidisciplinary Minimally Invasive Step-Up Approach: Comparison with a Modern Open Necrosectomy Cohort. J Am Coll Surg. 2020 Jun;230(6):873-883. Boxhoorn L et al. Immediate versus Postponed Intervention for Infected Necrotizing Pancreatitis. N Engl J Med. 2021;385(15):1372-1381. Tyberg A et al. Management of pancreatic fluid collections: A comprehensive review of the literature. World J Gastroenterol. 2016 Feb 21;22(7):2256-70. van Dijk SM et al. Acute pancreatitis: recent advances through randomised trials. Gut. 2017 Nov;66(11):2024-2032. Maurer LR et al. Contemporary Surgical Management of Pancreatic Necrosis. JAMA Surg. 2023;158(1):81. Previous Next