Intracranial Hematoma Expansion and Reversal of Warfarin and DOACs WITH DR. Walsh
Intracranial Hematoma Expansion
Hematoma expansion is most often diagnosed on a scheduled follow-up CT scan or on an emergent CT scan ordered due to acute change in patient status
When describing an intracranial hemorrhage seen on a head CT it is important to note both volume and location.
Volume can be calculated using the ABC / 2 method.
A: Measure the hematoma at its largest diameter
B: Measure the largest diameter at 90 degrees to point A
C: Measure the number of CT slices. You must account for size of ICH relative to largest slice when counting the slices.
Multiple A by B by C then divide by 2.
Blood Pressure Management in ICH
Elevations in blood pressure is very common following ICH
Conceptually, it make sense that persistently elevated blood pressure would lead to increased hematoma expansion; however, the data is conflicted on this topic.
INTERACT-2 Trial: 2839 patients with SBP 150-220. Showed no benefit for death or disability with aggressive blood pressure.
ATACH-2 Trial: 1000 patients either receiving aggressive blood pressure management (SBP 110-139) for 24 hours or standard management (SBP 140-179). Showed no benefit in death or disability at 90 days with aggressive BP management.
Bottom line: Different institutions use different blood pressure goals with most falling between 140 - 180. There does not seem to be benefit to more aggressive management.
Anticoagulation with ICH
With all patients with suspected ICH it is important to quickly acquire a complete medical and medication history. Often the patient cannot provide this so you must pursue alternative sources such as EMS, family/friends/caregivers, or the electronic medical record.
If you identify that a patient is taking an anticoagulant medication you must clarify the specific agent as well as the time the last dose was administered.
Urgent labs for the these patients include: CBC with platelet count, PT/INR, and PTT.
For patients taking Warfarin:
Immediately withhold additional doses of warfarin, provide vitamin K dependent factors, and provide 10mg Vitamin K IV.
FFP vs. PCC
FFP contains all coagulation factors present in plasma.
PCC: Multiple different formulations (3 vs. 4 factor and activated vs. inactivated).
FFP typically requires larger volumes to be administered over a longer period of time than PCC.
PCC are much more expensive than FFP.
There are not sufficient studies in the literature to directly show that PCC are superior to FFP in patient centered metrics. Conceptually, the faster reversal with lower volume required suggests it would be the superior agent.
For patients taking DOACs:
Common DOACs include direct thrombin inhibitor Pradaxa (Dabigatran) and Factor Xa inhibitors such as Xarelto (Rivaroxaban) and Eliquis (Apixaban).
Lab monitoring for DOACs is challenging. Thrombin time and aPTT show a modest correlation with increasing plasma concentration. Common laboratory tests are even less helpful with the Factor Xa inhibitors. An Anti-Factor Xa assay specifically calibrated against the medication the patient is taking would be ideal. This is both logistically and financially prohibitive for most institutions.
Reversal of DOACs:
FFP has very limited data as almost all studies are focused on PCCs
Data for PCCs is variable.
Activated PCC has more consistent results than inactivated PCC for Dabigatran.
Factor Xa inhibitors has more consistent data suggesting either activated or inactivated PCC work.
R4 Capstone : clinical efficiency WITH DR. summers
System Efficiency vs. Individual Efficiency
System efficiency involves a variety of factors including triage protocols, staffing, technology, access to scribes, lab availability/functionality, etc. These factors are often out of the control of the individual ED physician.
Individual efficiency focuses on the skills and practices that an individual can apply to any work environment to improve the management of their emergency department on any given shift
Bobb et al 2018. used a mixed-methods study design to identify key behaviors associated with efficiency.
High efficiency behaviors identified: using team member names, having conversations with the health care team, running the board, and average patient load.
Inefficient behaviors identified: performing non-work related tasks on shift and documentation of patients no longer present in the ED.
Improving Efficiency During the Three Phases of the Patient Encounter
Arrival: Always work to “Hit the Box”, meaning actively pick up patients quickly as they enter your department. Try to pace your shift so that you quickly pick up many patients early into your shift and then slow down as the shift goes on. This will allow you to use your mental energy early in the day when you are the most fresh and to slow down as you approach shift change.
Work-Up: Setting expectations with your patients upfront, avoiding interruptions, and avoiding bottle-necks will all improve your efficiency.
Setting expectations: Identifying the patient’s goal of the visit and working to come to a shared goal that you both can agree on can limit delays in treatment, need for subsequent labs and imaging, and deterioration in the doctor-patient relationship towards the end of an encounter.
Avoiding interruptions: There are four common strategies employed to avoid interruptions.
Outright reject the interruption: This is not good for team morale and can lead to team members not bringing critical information to your attention.
Multi-task: Many would argue that there is no such ability. Multi-tasking is often just rapid task switching. This can lead to inefficiency and multiple uncompleted tasks piling up.
Immediately stop what you are doing and address the interruption: It often takes 30-60 seconds to resume a task once interrupted if suddenly stopped.
Delay the interruption and then address it: When this is done effectively it is the preferred method. Finding a good stopping point (i.e. completing whatever micro task you are working on) and then quickly addressing the interruption allows for a smoother work flow.
Common bottle-necks include laboratory/urine studies. Discussing priority testing with your nursing staff can help them complete tasks in the order you deem most important. Additionally, identifying team members who are not task saturated to draw labs on a nurse who has multiple complex patients can help alleviate this common bottle-neck.
Disposition: Focus on dispositions whenever possible. This allows you to clear a patient from your board and allow for your mental bandwidth to be directed towards the active work-ups that are still ongoing
R1 Clinical knowledge: Abdominal compartment syndrome WITH DR. irankunda
Recognized first in the early 19th century
Incidence and prevalence are unknown as it is a rare condition
According to the World Society of Abdominal Compartment Syndrome:
Normal abdominal pressure: 0-5 mmHg
Intra-abdominal pressure is 5-7 mmHg in critically ill adults
Intra-abdominal hypertension is greater than or equal to 12 mmHg.
Abdominal Compartment Syndrome is when intra-abdominal pressure exceeds 20 mmHg and is associated with organ dysfunction/failure.
Primary: Intra-abdominal pathology is directly responsible
Secondary: Not caused by intra-abdominal injury but fluids accumulate in sufficiency to cause intra-abdominal hypertension
Chronic: Presence of end organ disease over time such as ascites that progresses to elevated pressure in the abdomen.
At a cellular level abdominal compartment syndrome leads to a decreased perfusion causing reduced oxygen delivery. This leads to anaerobic metabolism and starts a cascade of inflammatory mechanisms leading to endothelial permeability which worsens the ischemia as oxygen transportation is further inhibited.
At an organ level, elevated pressures compress non-solid structures such as the blood vessels and intestines. This leads to decreased blood circulation especially in thin walled vessels such as the veins. When the veins collapse, fluid backs up and edema worsens and pressures keep climbing.
The intestinal tract develops bowel wall edema and collapses under pressure. There is translocation of bacteria from the lumen into the peritoneal space. Mesenteric veins in the GI system easily collapse.
The kidneys are affected as compressed renal veins lead to congestion and impaired perfusion. When the perfusion is decreased to the kidneys secondary to hypovolemia the RAAS system leads to renal vasoconstriction and acute kidney injury.
Patients develop increased ventilatory requirements as the diaphragm is pushed up and thus the lung has poor compliance and increased inspiratory pressures.
ED treatment of abdominal compartment syndrome involves recognition of the disease process and resuscitation of the patient. Recognition of intra-abdominal hypertension before it comes abdominal compartment syndrome is of key importance!
Improve abdominal wall compliance
Correct positive fluid balance
Empiric antibiotic treatment
Organ support such as optimizing ventilation
Surgical management and decompression is the definitive treatment
For more information check on the Annals of B Pod post about Abdominal Compartment Syndrome!
Back Pain management WITH DR. lang
Evidence to help guide the management of acute and chronic low back is limited and varies by modality.
Bed Rest: There is moderate quality evidence suggesting you should resume normal activity as soon as possible for most cases of acute back pain; however, when sciatica is present the evidence is of lower quality.
Heat: Applying heat is thought to help with both acute and chronic low back pain; however, there is a very limited evidence to actually support this practice.
Massage/Manual Therapy: These practices are thought to be effective; however, there is limited evidence to support this practice.
Acupuncture: There is moderate evidence showing acupuncture to be effective in managing acute and chronic low back pain.
Acetaminophen: There is a high amount of evidence showing that that Acetaminophen is not effective in managing either acute or chronic low back pain. Many providers still incorporate acetaminophen into their practice; however, evidence suggests it should never be considered as a mono-therapy due to its low efficacy.
NSAIDs: High amount of evidence showing NSAIDs to be effective; however, with only limited improvement in both acute and chronic back pain. When sciatica is present the limited benefit is even less.
Opiods: Very limited evidence leaving the role of opiods in acute or chronic low back pain very unclear. The general consensus among providers appears to be that they should be avoided in most cases due to the high associated risk profile including addiction. Our current recommendation would be a limited role in severe acute low back pain and to include a pain specialist when using for chronic low back pain.
Steroids: Evidence is limited specifically within the ED population. A small study showed no benefit. Radicular/Sciatica did show a small benefit in other small studies.
Muscle Relaxers: Evidence suggests that they are effective for acute but not chronic low back pain. Most often studied medications include tizanidine, thiocochioside, epersione, carisoprodol. There is no evidence suggesting benefit with benzodiazepines.
R3 taming the sru: penetrating neck trauma WITH Dr. Golden
Penetrating neck trauma, by definition, must violate the platysma; otherwise, it is just a superficial injury
Estimated to represent 5-10% of all traumatic injuries
Often related to GSW and stab wounds
Mortality estimated to be 3-6%, mostly from exsanguination and airway injuries
The neck is divided into three zones:
Zone 1 involves the structures from the clavicles to the cricoid cartilage, including:
Phrenic and vagus nerves
Apex of lung
Zone 2 involves the structures from the cricoid cartilage to the angle of the mandible, including:
Carotid and vertebral vessels
Zone 3 involves the structures from the angle of the mandible to the base of the skull, including:
Carotid and vertebral vessels
Base of skull
Zones 1 and 3 are much more challenging to access surgically
Hemodynamically stable patients or those with “hard signs” should be taken to the OR
Pulsatile or expanding hematoma
Bruit or thrill
Air bubbling from wound
Those with “soft signs” should undergo CTA of the neck
Soft signs with positive CTA should likely go to the OR
Soft signs with negative CTA can be observed with plus or minus EGD/barium swallow study
Asymptomatic patients can be observed with low incidence of missed injuries
Cervical Spine Immobilization
Low incidence of cervical spine fracture or cervical spinal cord injury
Studies have shown increased odds ratio for death in patients with cervical collars in place in penetrating neck injuries
Patients who are GCS 15 and neurologically intact likely don’t need cervical collars placed
Should be tailored to individual patient presentations
If the need to intubate arises, prepare for a bloody airway by having direct laryngoscopy capabilities, suction, and a bougie
Cricothyrotomy is the ultimate definitive procedure if unable to complete orotracheal intubation
Studies have shown that most patients can be intubated with RSI in the setting of penetrating neck injuries
Digestive Tract Injuries
CTA of the neck is insensitive to diagnose these injuries
Have a low threshold for EGD or barium swallow studies
Mortality increases if not repaired within 12 hours
Administer broad spectrum antibiotics. Unasyn and Zosyn have both been shown to be effective