Background Changing creatinine concentrations during acute renal failure are often confusing to clinicians to interpret and can cloud the patient’s true current state of renal injury. By modifying the formula for kinetic estimate of glomerular filtration rate (KeGFR), a simple bedside clinical tool can be used to identify subtle changes in renal function. Methods The KeGFR was rewritten to instead calculate a predicted peak creatinine after renal injury. By comparing the changes in predicted peak creatinine at two or more subsequent time intervals, the patient’s current state of renal injury can be determined: whether improving, worsening or unchanged from prior. Results Three case examples are provided using the equation for predicted peak creatinine. In each case, the creatinine concentration has continued to rise at three sequentially measured times. The change in predicted peak creatinine is analyzed for each case, demonstrating scenarios involving (i) improving renal injury, (ii) unchanged renal injury continued by unfavorable hemodynamics and (iii) worsening renal injury despite interventions. Conclusions The use of this model may provide clinicians with an easy bedside tool to assess a patient’s state of acute kidney injury. Reassessment of how the creatinine is changing is already a nonquantitative part of a nephrologist's approach to acute kidney injury. Providing an assessment of the patient's changing renal function would be a useful addition to potentially detect early renal recovery or worsening renal injury and appropriately adjust treatment strategies.
The Seraph-100™ is a purification filter that blunts cytokine storm, providing a more favorable environment to establish immune homeostasis. We present a novel case of compassionate use of Seraph filter in a young, healthy active duty service member with heat injury-induced massive inflammatory response. The patient is a previously healthy 26-year-old male with altered mental status, tachycardia, fever to 40.3 °C, and hypotension after losing consciousness during a 4-mile run. He had a history of one heat injury in college and took no medications or supplements. Initial workup demonstrated hemoconcentration, leukocytosis, and hyperkalemia. He was intubated, received isotonic crystalloid fluid, and was admitted to the intensive care unit. The patient developed vasopressor-resistant shock and multiorgan failure with rhabdomyolysis requiring continuous renal replacement therapy. The addition of the Seraph resulted in improved hemodynamic stability, decreased inflammatory markers, and improved organ function. Approximately 1 week after the final Seraph treatment, the patient had an abrupt massive lower gastrointestinal bleed and was transitioned to comfort care by family. We present the novel use of Seraph in the setting of multiorgan failure and hyperinflammatory state due to heat injury. The patient’s vasopressor refractory distributive shock was believed to be secondary to heat stroke-induced massive inflammatory response, leading to a trial of Seraph therapy. This case demonstrates that the Seraph filter has the potential to improve hemodynamic instability and reduce cytokine storm in nonsepsis patients.
Ethylene glycol (EG) toxicity is an important cause of toxic alcohol poisoning in the USA with over 5,000 exposures reported annually. While classically characterized by solitary accidental or intentional ingestions, mass toxic alcohol poisoning outbreaks and more rarely collective consumptions (typically of methanol) have been described. We describe an ethylene glycol poisoning from collective ingestion that involved soldiers presenting at William Beaumont Army Medical Center in El Paso, Texas. Eleven soldiers presented to the emergency department over a 12-h period after ingestion of an unknown substance. The first two patients exhibited severe neurologic symptoms, while the remainder were asymptomatic. As serum EG levels were not immediately available, treatment decisions were based on surrogate laboratory values. Two patients received immediate hemodialysis, and fomepizole (FOM) because of severe acidosis with elevated anion and osmolal gaps. These patients developed acute kidney injury with renal recovery within a 3-week period. Two patients with elevated lactate received bicarbonate-based intravenous (IV) fluids and FOM. Two patients received IV fluids only and required prolonged observation for worsening acidosis and/or acute kidney injury. Five patients with normal laboratory values were treated with IV fluids and observation. All patients received cofactors including thiamine and pyridoxine. All patients survived. The outbreak occurred in the setting of limited dialysis resources, limited FOM availability, and in a resource-limited community. Additional guidelines are needed to determine allocation of limited resources, optimal dialysis and FOM treatment course, and comorbid conditions, which may prolong recovery.
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