Grand Rounds Recap 11.17.21
/
QI/kt: Acute Kidney Injury WITH drs. finney and diaz
What is the definition of an AKI?
An increase in serum creatinine > 0.3 mg/dL compared to 48 hours prior
An increase in serum creatinine > 1.5 times baseline or presumed creatinine baseline within the last 7 days
Urine output falling to < 0.5 ml/kg/hr for at least 6 hours
Note that a change in urine output may be more sensitive for early kidney injury than an increase in serum creatinine, although this is something that is harder to track in the ED, it can be worth asking the patient about and continuing to monitor in the ED.
AKIN Staging Criteria
Stage 1: an increase in serum creatinine by at least 0.3 mg/dL or to 150-200% of the patient’s baseline OR urine output < 0.5 mL/kg/hour for 6- 12 hours.
Stage 2: an increase in serum creatinine by at least 200-300% of the patient’s baseline OR urine output < 0.5 mL/kg/hour for 12-24 hours.
Stage 3: an increase in serum creatinine by more than 300% of the patient’s baseline OR an increase in serum creatinine to over 4 mg/dL with at least a 0.5 mg/dL from baseline OR urine output < 0.3 mL/kg/hour for more than 24 hours, or anuria for 12 hours, or initiation of renal replacement therapy.
What are the different types of AKI
Previously denoted as prerenal, intrarenal, and postrenal. Now described as functional, structural, and obstructive.
Functional
Essentially this is an AKI due to problems outside of the urinary tract such as hypotension or hypovolemia. This was previously thought of as prerenal.
Structural
Damage to the functional units of the kidney due to nephrotoxic agents or prolonged prerenal insults. Previously thought of as intrarenal.
Obstructive
Distal obstruction causing backup in the excretory system resulting in damage to the kidney. Previously thought of as post-renal.
Trending Creatinine in the ED
Can we give patients with a functional AKI IVF and recheck the serum creatinine?
Studies have shown that creatinine elevation is delayed compared to actual kidney insult. Healthy kidneys may take as little as 4 hours to show a 50% elevation in serum creatinine. Stage 4 CKD kidney can take several days to manifest a 50% change in serum creatinine. Given this, trending creatinine in the ED may not represent a realistic time period to assess for rising serum creatinine.
There are new studies leaning towards measuring various biomarkers which may assist us in detecting early AKI, predicting the severity of an AKI, such as NGAL and assisting with safe discharge in the future.
Recommended Workup for AKI in the ED
Renal panel
Urinalysis
Urine Electrolytes including urine urea
Renal Ultrasound
NGAL (neutrophil gelatinase-associated lipocalin) or other biomarker once available in your emergency department
Managing AKI in the ED
Fluids
Based on a 2019 study in CHEST by Ostermann et. al, the only indication for fluid administration in AKI is intravascular hypovolemia
Oliguria should trigger an assessment of a patient’s volume status.
An additional study in SHOCK demonstrated that increased fluid administration after early acute kidney injury was associated with less renal recovery and had a higher risk of progression to significant AKI and a higher risk of death.
Another study in the Journal of Critical Care by Inkinen et al evaluated overzealous fluid administration and fluid accumulation in patients with AKI . What they found was that patients with an AKI frequently received more fluids but still had lower urine output compared to non-AKI patients. Additionally small volumes of fluid administration and higher urine output were associated with improved renal recovery.
Diuretics
A meta-analysis evaluating the use of lasix in preventing or treating acute renal failure found that although patients treated with diuretics had a lower fluid balance, they typically had worse electrolyte abnormalities and had no significant difference in progression to worsening kidney injury.
Minimizing further damage
Avoid nephrotoxic agents in the ED. Here are some common ones we utilize frequently in the ED
Aspirin, ibuprofen, iohexol, indomethacin, naproxen, ketorolac, lisinopril, losartan, vancomycin, valsartan
The combination of vancomycin + piperacillin-tazobactam has a greater risk for AKI when compared to vancomycin + cefepime or vancomycin alone.
Ketorolac - always has the potential for harm to kidneys but is certainly worse when combined with other potentially nephrotoxic agents.
Dialysis
Indications for dialysis
Acidosis, Electrolyte abnormalities, Ingestion/Tox, volume Overload, Uremia
Is earlier dialysis better?
Early initiation of dialysis did not decrease 90 day mortality in critically ill patients (STAART AKI Investigators).
iHD vs CRRT
There was no significant difference in renal function outcomes between patients started on CRRT vs iHD. CRRT obviously had less hemodynamic instability than patients on iHD, however they had more catheter and thrombotic complications.
Disposition
Functional AKI
Stage 1 AKI
Evaluate fluid status
If volume overloaded, give IV lasix at 1-2x the patient’s usual home dose. If this results in appropriate urine output then the patient may be discharged. If the patient does not start to urinate appropriately then admit them for continued management.
If hypovolemic, administer IV fluids and ensure they are tolerating PO. If the patient is tolerating PO they can be discharged. If not, they should be admitted for IVF hydration.
Stage 2 AKI
If the patient’s serum creatinine is under 2.0 mg/dL and there is a rapidly reversible etiology identified (dehydration), administer IVF and admit to the ED observation unit vs discharge.
If the patient’s serum creatinine is over 2.0 mg/dL, or there is not a rapidly reversible etiology, attempt to correct the suspected underlying cause and admit the patient for further management.
Stage 3 AKI
Attempt to identify and correct the underlying cause and admit the patient for further management.
Structural AKI
Avoid additional nephrotoxic agents while in the ED
All stages of structural AKI should be admitted for further monitoring and management.
Obstructive AKI
Have the patient attempt to urinate independently.
If the patient is unable to urinate, place a foley catheter. If the patient has a stage 1 AKI, they may then be discharged home. If the patient has a stage 2 or stage 3 AKI, they should be admitted to the hospital for further evaluation and management.
If the patient is able to urinate, you should perform a post void bladder volume measurement to assess the post-void residual volume.
If the post-void residual volume is greater than 150mL, you should place a foley. If the patient has a stage 1 AKI they can then be discharged. If the patient has a stage 2 or stage 3 AKI they should be admitted for further evaluation and management.
R1 Clinical knowledge: Blunt cardiac injury WITH Dr. gobble
Following blunt chest trauma, the incidence of blunt cardiac injury ranges from 8 to 75%.
Mechanisms of injury
Direct Injury: Results from a direct blow to the chest with direct force applied to the heart
Indirect Injury: Increased abdominal pressure or systemic venous return which causes a sudden increase in preload, making the heart susceptible to rupture.
Bidirectional Injury: Anterior and posterior compression from the sternum and vertebrae.
Deceleration Injury: When the heart is torn from its attachment points within the mediastinum. These are frequently non-survivable and patients suffering this injury often die in the field.
The spectrum of blunt cardiac injury
Myocardial concussion- a stun response to blunt force that results in no permanent injury but may cause a momentary dysrhythmia.
Myocardial Contusion - cellular hemorrhage resulting in a hematoma of the myocardium.
Myocardial infarction - a more severe myocardial contusion that results in irreversible cellular damage and scar formation.
Myocardial rupture - rupture of any of the chambers of the heart due to sudden compression with intracardiac pressure increase and damage to the integrity of all layers of the heart. This is severe and frequently fatal.
Note that because the right ventricle is the most anterior chamber of the heart, it is most susceptible to suffering from blunt cardiac injury.
Evaluation for BCI
EKG - look for any signs of strain or ischemia as well as dysrhythmias. These will typically manifest within 48 hours of the initial insult.
Findings suggestive of a BCI on EKG can range vastly. At UC we include the following findings:
Unexplained tachycardia over 120
Arrhythmia
Right bundle branch block
New Q waves or ST/T abnormalities
Cardiac Biomarkers (Troponin)
A negative standard sensitivity troponin has been noted to have a negative predictive value for BCI up to 100%. Unfortunately, there is no consensus on the appropriate timing of the initial screening troponin or the frequency of reassessment of troponin.
A study by Kespaik et al in 2020 evaluated the use of high sensitivity troponin in predicting outcomes following blunt chest trauma.
They found that in-hospital mortality was worse in patients with an elevated high sensitivity troponin when compared to patients with a normal high sensitivity troponin. However there was no direct comparison between high sensitivity troponin and conventional troponin.
The EAST guidelines provide a level 1 recommendation that all patients at risk/concern for blunt cardiac injury should receive an admission EKG.
Level 2 recommendations;
Patients with a normal EKG and normal troponin are considered ruled out for BCI.
Patients with either an abnormal troponin or an abnormal admission EKG should be admitted for continuous telemetry monitoring
Any patients with hemodynamic instability or persistent arrhythmias should undergo a comprehensive echo.
A sternal fracture alone is not an indication for admission and continuous monitoring in the setting of a normal EKG and troponin.
Level 3 Recommendations
Elevated troponins should be followed-up serially, although optimal timing is unknown.
Cardiac CT or MRIs can be used to help differentiate acute MI from blunt cardiac injury in trauma patients with abnormal ECG findings, elevated troponins an/or abnormal echo findings to determine the need for cardiac catheterization
Commotio Cordis
Commotio cordis is a primary arrhythmic event that occurs from mechanical energy being applied to the myocardium during the repolarization of the ventricles (the ascent of the T wave), which functionally results in an R on T phenomenon, which precipitates ventricular fibrillation. Given that this is a fatal rhythm the condition has high fatality and is the second most common cause of sudden death in young athletes.
Mortality has recently decreased with increases in bystander CPR and public AED availability which has decreased response times and earlier termination of the fatal rhythm.
r4 case follow-up WITH dr. gawron
A previously healthy male presenting for AMS. The patient’s roommate noted that when he woke up this morning he was confused, but was normal when he went to bed the night before. He was initially seen at an outside hospital prior to this encounter and was diagnosed with a viral URI, was COVID negative and was discharged. Bloodwork from that encounter was notable for an anemia of 9.5, platelets of 109, sodium of 129, and a creatinine of 1.38.
In our ED the patient was febrile, tachycardic to the 130s, tachypneic to the 30s, normotensive, and saturating well on room air. He was found to be normoglycemic. He was confused but intermittently lucid, ill-appearing, and diaphoretic. He had blanching petechiae on his upper and lower extremities including his palms and soles. He was noted to have a previously undocumented murmur.
An EKG was performed which showed impressive ST elevation in the anterior leads with reciprocal inferior depressions. A code STEMI was called and a stat bedside echo was performed. The echo demonstrated an abnormal aortic valve leaflet with severe aortic regurgitation. Blood cultures were drawn and antibiotics were started.
A CT/CTA of the head demonstrated scattered SAH in a non-aneurysmal pattern and a L cerebellar infarct. A CT C/A/P demonstrated borderline enlargement of the main pulmonary arteries and multiple infarcts in the spleen and bilateral kidneys.
The patient was admitted and went to the OR for aortic and mitral valve replacement with reconstruction of the intervalvular fibrosa. During the surgery, the patient was found to have vegetations on the aortic and mitral valve with erosion of the intervalvular fibrosa. The patient was also noted to have a purulent pericardial effusion. He subsequently underwent coronary angiography where he was found to have a 100% LAD occlusion without vessel disease, suggesting an embolic source. The patient was unable to transition off bypass and he was on VA ECMO.
What is the differential diagnosis for myocardial infarction in young patients?
With regards to MI, ‘young’ patients are defined as under 45 years of age
The most common cause is still atherosclerosis (80%). In order, the remaining etiologies include the following:
Coronary artery dissection or coronary vasospasm (6%)
Coronary artery embolism (5%)
PFO and endocarditis
Hypercoagulable states (5%)
OCPs, SLE, procoagulant genetic disorders
Congenital artery anomalies (4%)
ST elevation MI associated with endocarditis
Patients with infective endocarditis and septic emboli to the brain are at an increased risk for intracranial bleeding around those septic emboli. Outcomes are extremely poor in patients with infective endocarditis who receive thrombolytics (43% 30-day mortality in one study), and they should be avoided.
Aircare grand rounds WITH drs. connelly and lane
Proning patients
The lungs are asymmetric front to back, with the bulk of the lung mass being in the dorsal portion of the lungs. The supine position results in cardiac compression of the posterior lung mass and gravity dependent atelectasis of a large portion of the lung mass. Placing the patient in the prone position displaces the heart off of the bulk of the lung and allows for antigravity dependent distention of a larger mass of alveoli.
A multicenter RCT in the NEJM compared 28-day all-cause mortality in ARDS patients who were prone 16 hours a day to patients with ARDS who were left supine for 24 hours a day. This study demonstrated that early prolonged prone positioning of severe ARDS patients decreased all-cause 28- and 90-day mortality. Additionally, the rate of successful extubation was higher in the prone group, and there was no significant difference in the occurrence of adverse events between the groups.
Risks of proning patient
Ventral pressure ulcers - Patients lying in the prone position are, of course, at higher risk to develop anterior pressure ulcers. As such providers need to be mindful of anterior equipment (such as central lines) and irregular surfaces (face) that may increase the potential for pressure injury to skin.
Peripheral neuropathies - Mostly of the brachial plexus due to being maintained in a swimmer’s position or as a result of transitions between the prone and supine position.
Central Line infections - increased risk for central line infections due to dressing disruption with positioning transitions
ETT and other equipment dislodgement - higher frequency for equipment dislodgement with more complex patient positioning transitions.
Bougie first intubation
Bougie first intubation has been demonstrated to increase first attempt intubation in both the ED and in pre-hospital settings (Driver et. al, Latimer et. al)
One study by Angerman et al demonstrated a 98% first attempt success rate in patients intubated with video laryngoscopy assisted by bougie, compared to 86% in the control group.
Statins in STEMIs on Aircare
The SECURE-PCI study is an RCT that enrolled over 4,000 patients undergoing PCI for ACS (although not all STEMI). They found that patients going for PCI who received a loading dose of a statin had a HR of 0.54 for major cardiac events when compared to PCI destined patients who did not receive a loading dose of a statin.
Trauma
Shock index
A study by Vandromme et al demonstrated a stepwise relationship between prehospital shock index and likelihood of needing massive transfusion.
Patients with a shock index of 0.9 -1.1 had a relative risk of 1.61 for needing massive transfusion.
Patients with a shock index of 1.1-1.3 had a relative risk of 5.57 for needing massive transfusion.
Patients with a shock index greater than 1.3 had a relative risk of 8.13 for needing massive transfusion.
Another study by Jehan et al demonstrated that patients with a shock index greater than 1.0 had a higher likelihood of needing massive transfusion (0.01% vs 25.0%) ,needing laparotomy (1.7% vs 12%), dying in the ED (0.8% vs 3.0%), and dying during that hospital admission (5.2% vs 12%).
TXA
An exploratory analysis of the CRASH-2 RCT performed by the CRASH-2 Collaborators in 2011 evaluated the impact of early administration of TXA in bleeding trauma patients.
This analysis showed that there was a decreased risk of death due to bleeding when TXA was administered in under 3 hours (RR of 0.79), and an even greater reduction when administered within 1 hour of trauma (RR of 0.68).
Interestingly, the study found that patients who received TXA more than 3 hours after the traumatic incident actually had an increased rate of death due to bleeding (RR 1.44).
