< Back Pack the Guts https://video.wixstatic.com/video/3b6ff6_f29c38a601b645459ef002f51792fc87/1080p/mp4/file.mp4 Previous Next

4 Trauma References General Reference GCS .pdf Download PDF • 78KB Injury Severity Scores .pdf Download PDF • 195KB Snakebite Severity Score .pdf Download PDF • 102KB Staplers.Sutures.Mesh .pdf Download PDF • 530KB Hemostatic Agents .pdf Download PDF • 18KB TEG .pdf Download PDF • 12KB TBI Brain Injury Guidelines .pdf Download PDF • 213KB Brain Trauma Foundation .pdf Download PDF • 148KB DVT in TBI .pdf Download PDF • 137KB Spinal Cord ASIA Score .pdf Download PDF • 1.98MB

Common Measurement Conversions < Back Kitchen Hacks #3 Common Measurement Conversions Powdered Milk Reconstitution Use volume of water equivalent to desired milk volume. 1 Cup Milk= 3 Tbsp Powdered Milk= 45 mL 3/4 Cup Milk = 2.25 Tbsp Powdered Milk 2/3 Cup Milk = 2 Tbsp Powdered Milk= 30 mL 1/2 Cup Milk = 1.5 Tbsp Powdered Milk 1/3 Cup Milk = 1 Tbsp Powdered Milk= 15 mL 1/4 Cup Milk = 3/4 Tbsp Powdered Milk Measuring Spoon Conversions 1/2 tsp= 2.5 mL 1 tsp= 5 mL 1 + 1/2 tsp= 1/2 Tbsp= 7.5 mL 2 tsp= 10 mL 3 tsp= 1 Tbsp 6 tsp= 2 Tbsp= 1/8 c Liquid Measurement Conversions 1 fluid ounce= 2 Tbsp= 6 tsp 2 fluids ounces= 4 Tbsp= 1/4 cup 2+2/3 fluid ounces= 5 Tbsp + 1 tsp= 1/3 cup 4 fluid ounces= 8 Tbsp= 1/2 cup 6 fluid ounces= 3/4 cup 8 fluid ounces= 1 cup 16 fluid ounces= 2 cups= 1 pint 4 cups= 2 pints= 1 quart 4 quarts= 1 gallon Substitute dry for fresh spices 1:3 of dry:fresh 1 tsp dry= 1 Tbsp fresh Previous Next

[Editorial inspired by @kari_jerge] Why Don't They Believe Us? < Back [Editorial inspired by @kari_jerge] Seen on Twitter recently: Troll: I demand pictures of your full ICU to prove to me it’s full Female surgeon: None of us owes you a damn thing. Especially not pictures that will get us fired. But I’ll get right on that… What do you do if you accidentally injure yourself while working or making home improvements? Do you call 911 or have someone drive you to the ER? What do you do if you have high blood pressure, or diabetes, or depression? Do you go to a primary care doctor? What do you do if you have severe arthritic hip pain that doesn't resolve with conservative (non-operative) management? Do you consider talking to an orthopedic surgery about a hip replacement? I don't know what portion of the population inherently trust the medical community, but for the remainder of this editorial, I will presume that it's a majority. For those that don't, this doesn't apply. If you don't trust modern medicine, I won't convince you that you should trust our reports about this pandemic. Let's assume you accept modern medicine, including visiting the emergency department, having a primary care doctor, taking prescription medicine, and any of the other various diagnostic tests, consultations, and treatments. If this is the case, why would you think we would voluntarily try to deceive you about the capacity and occupancy of our ICU facilities? Why would so many medical community leaders actively speak out with a nearly singular voice to spread a lie? Ranging from the widely known Dr. Sanjay Gupta to a wide assortment of medical providers in many specialties. We have nothing to gain from building this whole façade. This isn't just a few people speaking up. This is a monumental effort to warn people. Social media has given a voice- and many have worked very hard to dispel the myths spread by many loud voices that continue to spread falsehoods. We have nothing to gain. You trust us to save your life when you have a heart attack, need emergency surgery, or care for you when you're severely ill from any matter of diseases. We haven't changed as a community to collectively spread these myths. It really is as bad as we say. We genuinely don't get paid more for patients who die from COVID. We don't have adequate PPE. We aren't lying. If you continue to deny reality, we will still care for you or your family and friends, in the unfortunate case you become ill, because that's what we do. We are just hoping that we will have the resources you need. And if we stretch our personnel any thinner, we will not have enough nurses and providers to care for you. We are the last hope. Don't make choices you'll regret. Previous Next

< Back Stabbed in the Right Thigh A 42-year-old male is brought to the Emergency Department as a Level 1 trauma activation for a stab wound to the right thigh. He was hypotensive before arrival, with SBP in the 70s-80s. Estimated blood loss of 500 mL on the scene. On arrival, the patient is awake and argumentative. His blood pressure is 90 systolic. On a rapid secondary survey, there is no evidence of any other wounds. There is a tourniquet in place to right upper thigh. When the tourniquet is released, there is arterial bleeding from the wound and there is no palpable distal pulse. What do you need to do before leaving the trauma bay? Replace tourniquet. Call OR to have vascular instrument set available, as well as massive transfusion, cell saver, etc. Type and cross for blood transfusion. After ensuring a type and cross, we proceeded to the operating room. How do you want to prep and drape the patient? Any instructions for anesthesia? Wide prep and drape to ensure adequate access for proximal and distal control- this includes prepping the lower abdomen for possible iliac exposure. Also, need to prep contralateral lower extremity for potential saphenous vein harvest. Ultrasound localization of the saphenous prior to prepping can allow identification of the larger vein. Anesthesia will need to monitor hemodynamics and volume status and be prepared for volume resuscitation with blood. In addition, they will have to be vigilant for the repercussion syndrome, the metabolic disturbance following the re-establishment of arterial flow (washout of toxins following ischemia). We placed a pneumatic tourniquet on the patient's upper thigh. We prepped and draped from the umbilicus to the knees, and also prepped and draped the contralateral thigh to have access in case a saphenous vein harvest was required for repair. We made an incision directly over the wound and dissected down to the artery. There was a single wound in the anterior surface of the distal superficial femoral artery. Proximal and distal control was obtained after circumferentially dissecting and placing vessel loops. The artery was divided and spatulated. It was repaired with an end to end tension-free anastomosis. Following arterial repair, we performed a lower extremity fasciotomy. Management of Penetrating Arterial Trauma WTA Algorithm Diagnostic Workup Hard signs- pulsatile bleeding, thrill, bruit, expanding hematoma, pulse deficit, cold pale limb. These patients require operative intervention. A few exceptions can benefit from preoperative imaging to document the presence and location of associated arterial injuries: wounds in the thoracic inlet, shotgun wounds in the extremities, and segmental fractures or fractures at different levels of an extremity. Soft signs- history of pulsatile bleeding, wound near an artery, non-expanding hematoma, neuro deficit, weak pulse, proximity injury. These patients need further workup to evaluate for the presence of arterial injury. An ankle-brachial index should be performed, and if ≤0.9, CT angiography is indicated. If ABI >0.9- no further w/u needed. ABI <0.9- CTA. Principles of arterial repair 1. Plan incision to facilitate proximal and distal control. 2. Ensure adequate back bleeding. Fogarty to remove distal thrombus. 3. Tension-free anastomosis. Adequate lumen. Clean margins. Don't create more damage to the vessel. 3. Consider risk/ benefit of heparinization. Systemic dose: 70-100 units/kg IV. Regional dose: 50U/ml x50 mL. 4. Completion angiogram to document repair. There are various techniques for creating an anastomosis, but the basic principles must be maintained. Recently, I was taught a useful technique [Dr. Feliciano, AAST 2020 Virtual Conference] that prevents tension at one point along the anastomosis. A parachute technique, starting with loosely approximated sutures on the back wall, followed by parachuting the two ends close to continue the suture on the anterior surface of the artery. Indications for fasciotomy include prolonged limb ischemia (>6 hours), combined arterial and venous injuries. 1. Feliciano DV. Evaluation and Management of Peripheral Vascular Injury. Part 1. Western Trauma Association/Critical Decisions in Trauma. J Trauma. 2011;70(6):1551-1555. 2. Feliciano DV. Pitfalls in the management of peripheral vascular injuries . Trauma Surg Acute Care Open. 2017;2:1–8. Parachute Technique [Feliciano] WTA Algorithm for Peripheral Vascular Trauma Previous Next

< Back Postoperative hypotension A 35-year-old male is in the ICU following emergency surgery for a small bowel obstruction. On arrival to the ICU, he has the following vital signs: HR 115, BP 85/40, SpO2 98. He underwent a 4-hour open lysis of adhesions. He received 2L of crystalloid and made 50 mL of dark urine, and did not require any medication to improve his blood pressure. He remains intubated and sedated. What is the differential for his hypotension? Hypovolemia- under-resuscitation relative to the insensible losses from open abdomen and likely preoperative dehydration Sepsis- bacteremia from gut translocation from small bowel obstruction, pneumonia from aspiration due to obstruction Tamponade, tension pneumothorax- did he have any intra-vascular devices placed in the OR? Pulmonary embolism- lengthy surgery, did he have appropriate mechanical prophylaxis? Cardiomyopathy The surgical team reports that he has not been tolerating a diet, or even liquids, for the previous 3 days. He received perioperative ertapenem for surgical infection prophylaxis. There was no evidence of aspiration during intubation and his admission CXR was unremarkable. He had a right internal jugular central line placed intra-operatively. He had no issues with oxygenation/ ventilation or high airway pressures intra-operatively. How can you diagnose shock and differentiate between the different potential etiologies? Physical exam- evaluation of skin turgor/ color/ temperature and mucous membranes, evaluation of fluid status (open wounds, nasogastric tube output, passive leg raise), examination of urine quality, auscultation of heart/ lungs Labs- cultures, complete blood count, lactate, liver function tests, BUN/Cr Ultrasound- gross evaluation of heart function, lung sliding to rule out pneumothorax, volume and collapsibility of the inferior vena cava Test for fluid responsiveness- based on stroke volume variation (SVV, see below), or response to passive leg raise or a fluid challenge. On exam, he is tachycardic without murmurs, lungs have equal air movement bilaterally. His nasogastric tube remains on suction with ongoing high output of gastric contents. On ultrasound, he has bilateral lung sliding. His cardiac contractility looks grossly preserved. He has normal oxygenation. His inferior vena cava is collapsible. He has a known source of infection (positive blood cultures), leukocytosis, elevated lactate, high fluid losses with evidence of fluid responsiveness. Shock: Undifferentiated Hypotension Hypotension ≠ shock. So what is shock? Inadequate perfusion to maintain end-organ function Pathophysiology: effective perfusion requires adequate cardiac output (CO). CO is the volume of blood that the heart pumps each minute, and it depends on stroke volume (SV; the volume of blood ejected with each heartbeat) and heart rate (HR; the number of heartbeats per minute). SV depends on preload (intra-vascular volume returning to the heart), myocardial contractility, and afterload (systemic vascular resistance). Shock is a disruption of preload, contractility, and/ or afterload. Signs of shock= signs of end-organ hypoperfusion Altered mental status (brain) Decreased urine output (kidney) Change in color/ temperature of extremities (skin) Abnormal liver function tests (liver) Ileus (gastrointestinal tract) Diagnosis of shock + tools for monitoring response to treatment Elevated lactate (global hypoperfusion) Ultrasound- evaluate cardiac function, evaluated IVC to assess volume status Minimally invasive cardiac monitoring (central line or arterial line)- CVP and SVV to assess volume status Invasive cardiac monitoring (pulmonary artery catheter)- cardiac output, ScVO2 (central venous oxygen saturation) Four types of shock Shock is typically categorized as hypovolemic, obstructive, cardiogenic or distributive. However, in order to link the specific category with the associated pathophysiology, I have described each state as it relates to maintaining cardiac output, as described above. Decreased preload: hypovolemic shock- low circulating blood volume→ decreased blood volume returning to the heart. Etiologies: bleeding, inadequate fluid replacement/ maintenance, high output from nasogastric tube or ostomy, insensible losses that aren't appropriately replaced (burn patients, large open wounds). Decreased preload: obstructive shock- disease process that impedes venous return to the heart (tamponade, tension pneumothorax, pulmonary embolism). Decreased contractility: cardiogenic shock- disturbance of the intrinsic function of the heart. Etiologies: heart failure, arrhythmias, valvular insufficiency, or decompensated valvular stenosis. Decreased afterload: distributive shock- dilated peripheral vasculature, sometimes known as vasoplegia. Etiologies: sepsis, anaphylaxis, neurogenic following spinal cord injury (NOTE- this is NOT the same as spinal shock), burns, trauma, pancreatitis. Neurogenic- hypotension with concurrent bradycardia. Vasoplegia is a term used to describe pathologically low systemic vascular resistance- this can be associated with post-cardiac bypass or any of the other causes mentioned here. Management of shock Treat underlying cause (see below). Restore adequate intravascular volume (aka preload). This is part of the initial treatment of hypovolemic shock, obstructive shock, and distributive shock. Fluids in the management of cardiogenic shock depend on the primary cardiac pathology. Treat hypotension/ decreased cardiac output that persists despite fluid resuscitation and treatment of the underlying cause. Septic shock- norepinephrine is the first line vasoactive medication. Monitor end-points of resuscitation (see above, Diagnosis of shock + tools for monitoring response to treatment ) Supportive care- nutrition, respiratory support, venous thromboembolism, etc. Specific Treatments Based on Etiology Hypovolemia from hemorrhage- transfusion, stop the bleeding Hypovolemia from fluid losses- replace fluid via enteral or intravenous route, as appropriate Sepsis- antibiotics, control source of infection (appendectomy, drain placement, etc). Tamponade- drainage of pericardial fluid (pericardiocentesis, pericardial window) Tension pneumothorax- release of tension physiology (needle decompression or finger thoracostomy) Cardiogenic- management of primary cardiac pathology, whether that entails treating acutely decompensated heart failure, resolving acute symptomatic arrhythmias, etc. Previous Next

< Back Abdominal Pain- Renal Disease A 72-year-old male with multiple medical co-morbidities presents with several weeks of right-sided abdominal pain. His family reports he hasn't been eating or drinking much. He has a slightly altered mental status and was unable to provide any more detailed history of his symptoms, such as aggravating/ alleviating factors or the relationship of his pain to meals. His medical history is significant for poorly controlled diabetes with neuropathy and renal insufficiency. He has not seen a primary care provider in over 6 months. On exam, he is uncomfortable but not in acute distress. His heart rate is in the 100s, and his blood pressure is normal. He is febrile to 101. He has dry mucous membranes. He has tenderness in the right upper quadrant with a positive Murphys sign. His exam was otherwise unremarkable. Workup? Imaging- right upper quadrant ultrasound Laboratory evaluation- CBC, basic metabolic panel, AST/ALT, bilirubin His labs are remarkable for mild leukocytosis and an elevated Cr (baseline 1.2, currently 2). Imaging was remarkable for cholelithiasis and gallbladder thickening. The EGS team is consulted and the patient is admitted to the surgical ICU given his acute on chronic renal insufficiency. What are the possible etiologies of his renal insufficiency and the initial treatment strategies based on the underlying cause? Pre-renal causes, such as hypovolemia, lead to decreased renal perfusion. Treatment involves volume repletion. Intra-renal causes, such as medication and acute tubular necrosis from sepsis, requires treatment of the underlying cause concurrent with volume repletion, treatment of electrolyte derangements and avoiding further nephrotoxin exposure. Post-renal causes, such as kidney stones or foley catheter malfunction, require relief of the obstruction. Based on the patient's history of decreased oral intake, he is at risk for acute hypovolemia, which can worsen his baseline chronic renal insufficiency. He was treated with volume resuscitation and close monitoring of his urine output. When should he undergo cholecystectomy? If cholecystitis was the precipitating cause, he would likely continue to worsen if his surgery was postponed. If hypovolemia was the precipitating cause, it would benefit from volume resuscitation, which can be administered throughout the operative course. If his renal insufficiency was not an acute change, and it was a slow decline since his last clinic visit, it was unlikely to significantly improve in a short time. The ICU team, EGS team and anesthesiology discussed the risks versus benefits of proceeding with surgery. Regardless of the etiology, postponing his surgery would be unlikely to improve his operative risk profile. We proceeded with laparoscopic cholecystectomy, and he returned to the ICU postoperatively for ongoing resuscitation and monitoring. Management of Renal Failure The causes of renal failure can be categorized into pre-renal, intra-renal, or post-renal. Acute infection can precipitate renal insufficiency, which is associated with poorer outcomes. Pre-Renal Caused by hypovolemia (dehydration) from decreased intake, nausea/ vomiting, excessive diuresis, third-spacing from acute inflammatory processes (pancreatitis), blood loss, inadequate replacement of insensible losses. The common final etiology in pre-renal causes is decreased renal perfusion. Treatment- volume replacement. Intra-Renal Multiple different intra-renal causes, including vascular or micro-vascular etiologies, glomerular disease, and interstitial disease (acute tubular necrosis, medications, and various precipitates such as myoglobin and crystals). The most common acute causes are medication and ATN from ischemic/ sepsis. Treatment involves management of the underlying etiology and supportive care. Post-Renal Caused by any obstruction from the renal pelvis to the urethra, including kidney stones, malignancy (can obstruct anywhere from the ureter to the bladder), retroperitoneal fibrosis, prostate enlargement, blood clots in the bladder or foley catheter malfunction. Treatment involves relief of the obstruction. Acute Cholecystitis with Renal Dysfunction Diabetes and severe cholecystitis (Grade III- organ dysfunction) are risk factors for increased mortality in patients with acute cholecystitis.[1] As noted in the discussion above, it is crucial to weigh the risks and benefits of operative intervention. If there is a modifiable risk factor, such as an acute cardiac event that is amenable to intervention. Escartin A et al. Acute Cholecystitis in Very Elderly Patients: Disease Management, Outcomes, and Risk Factors for Complications. Surgery Research and Practice. 2019;2019:9709242. Previous Next

And You Really Should be Nice to People It's a Small World < Back And You Really Should be Nice to People The medical community is incredibly small and interconnected. This can be very beneficial, but can also create challenges if interpersonal discord arises. Word travels fast and it's easy to burn bridges. In the medical field, there is a palpable tension between certain specialties. Not every hospital has the same procedure for managing trauma. However, in the countless hospitals I've worked in, clinicians in Emergency Medicine and Trauma Surgery work hand in hand to manage severely injured trauma patients. We have different training experiences and different management styles. When we (Trauma Surgery) come down to the trauma bay to evaluate a patient, we are a visitor. Yes, in a busy hospital, we might be incredibly frequent visitors. But still, we are guests in another department's home. Despite the best intentions, and perhaps even because of varying perspectives on what is "the best" intention, it is not a surprise that the trauma bay can serve as a breeding ground for animosity,(1) unless there are deliberate efforts to prevent conflict. Thankfully, creating a common language and developing standard practices is possible through mutually developed protocols, as well as principles in ATLS. This is crucial to effective patient care. I am grateful that I completed my Acute Care Surgery fellowship at a hospital system with a phenomenal relationship with our Emergency Department colleagues. I won't exaggerate and deny any conflicts, but there was a culture of mutual respect and a common goal of optimal patient care that I had never experienced before. Why Does It Matter? I started this post to share a story of why it's important to be nice to everyone you encounter. I mean, besides the fact that I believe that we should be kind and compassionate to everyone. At one facility that I worked, there was a less than friendly relationship between surgery and the emergency department. Again, I will confess that I likely had several of my own negative interactions. However, my general principle is based on what I described above. I consider my behavior and attitude to be at least a basic level of respect and decency to the providers that I interacted with. In contrast to unpleasant providers, I appeared to be above average. About 5 years ago, I was preparing for a deployment. I had the misfortune of being attacked by several dogs and required a series of rabies vaccines, which delayed my medical clearance. Thankfully, one of the ER providers from my hospital was at pre-deployment with me. He called a senior medical officer and obtained clearance so I could proceed without delay. It would have been easy for me to dismiss this provider during any of our countless interactions. If I had been consistently less pleasant, I suspect that he would have maintained a basic level of decency despite my poor behavior. But it's unlikely that he would have extended himself to advocate on my behalf. You never know what interaction could make the difference, so we should be nice to everyone. 1. Why Can't Emergency Medicine and Surgery Just Get Along? EmCrit Podcast. Previous Next

< Back AKI...pending ​ ​ ​ ​ Previous Next

< Back Pneumonia...pending ​ ​ ​ ​ Previous Next

< Back GI Dysmotility...pending ​ ​ ​ ​ Previous Next

< Back Gunshot Wound to the Leg ​ ​ ​ ​ Previous Next