Kidney Week 2012: AKI in the Trauma ICU
Lecture: Ward Rounds and Acute Kidney Injury
Dr. Sarah Faubel created this 2-hour lecture block. The idea was to look at 4 different theater of operations and do a deep dive on how the causes and treatments of acute kidney injury differ. This is a salute to Bayesian logic and attempts to give doctors a refined view of pre-test probabilities for the etiologies of AKI depending on the clinical scenario. Great idea.
The second lecturer was Lakhmir Chawla, MD of George Washington University, talking about AKI in the Trauma ICU.
Trauma is the leading cause of death for patients aged 1-44 years.AKI occurs in 0.32% (this is dialysis dependent AKI, and his own, unreferenced data). Given the frequency of trauma this represents a significant incidence of acute kidney injury. Dr. Chawla references data from the National Hospital Discharge Survey in 2007 that identified 2.5 million admissions for trauma. If his data on the rate of dialysis dependent AKI holds up, that translates into 8,000 cases of dialysis dependent AKI, compare that to the 2,500 cases due to cardiac surgery. He then pointed to a survey of blunt trauma patients who had an incidence of AKI of 26% by RIFLE criteria:
R = 11%
I = 8.0%
F = 6.9%
Poorly resuscitated patients more commonly suffered from AKI, which was identified as an independent predictor of death in trauma patients.
Abdominal Compartment Syndrome is defined as intra-abdominal pressure >12 mm Hg with organ failure, or an intra-abdominal pressure over 25mm Hg. Intra-abdominal hypertension can develop from:
- Capillary leak from inflammation or ischemia, or
- Aggressive fluid resuscitation causing tissue edema.
Intra-abdominal volume rises gradually because the abdomen is distendable but ultimately reaches a critical volume where the abdomen is maximally distended and then the pressure spikes. This increased pressure results in reduced blood flow and kidney injury.
Look for intra-abdominal compartment syndrome in patients with abdominal or retroperitoneal disease, resuscitation with more than 5 liters in 24 hours (10 pound weight gain) and in patients with low-flow mesenteric ischemia and bowel edema.
An interesting study was shared during this session:
To simulate the consequences of increased intra-abdominal pressure an experimental model was created by placing a 15 liter bag of water on the abdomen. Citerio et al found increased intracranial pressure, internal jugular pressure and increased central venous pressure.
It also may increase the wedge pressure while dropping the cardiac index. Doctors may misdiagnose these indices as an adequate fluid resuscitation with primary cardiac dysfunction.
Renal sequelae include: reduced renal blood flow, decreased GFR, and ATN. The urinary indices look pre-renal, low FENa, oliguria.
Physical exam is no better than a coin flip. Bladder pressure monitoring is needed.
Dr. Chawla outlined a number of different treatment strategies including: optimize fluids, sedation, cathartics and enemas, NG suction, paracentesis and dialysis but ultimately noted that the definitive therapy is decompressive laparotomy. Delaying this may result in intestinal ischemia. Data from De Waele et al shows clear and consistent reductions in intra-abdominal pressure with laparotomy.
Conclusion: Intra-abdominal compartment syndrome is missed in the ICU because it is not considered in the differential for acute kidney injury and the cardiac indices point away from the abdomen and to the heart.
Remember the belly, save the kidneys.
Post written by Dr. Joel Topf and edited by Dr. Kellie Calderon
eAJKD Advisory Board members
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