Mass Poisoning From Ethylene Glycol at a U.S. Military Base.

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.

Novel Use of Seraph-100™ Blood Purification Therapy in Heat Stroke.

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.

Kidney Disease: Acute Kidney Injury.

Acute kidney injury (AKI) is characterized by an abrupt decrease in renal function or the onset of frank renal failure. Kidney Disease: Improving Global Outcomes (KDIGO) defines AKI as an increase in the serum creatinine (SCr) level of 0.3 mg/dL or more within 48 hours, an SCr level increase of 1.5 times or more of the baseline level within 7 days, or a decrease in urine output to less than 0.5 mL/kg/hour for 6 hours. AKI severity is determined by the degree of SCr increase or decrease in urine output. AKI typically is caused by systemic illness or toxic exposure. Thus, determining the cause is critical when possible. The history should focus on risk factors, including nephrotoxic drugs. The physical examination should include determination of fluid volume status. Urinalysis with microscopy can narrow the differential diagnosis. AKI management includes control of the underlying cause, achievement and maintenance of euvolemia, nutritional optimization, blood glucose control, and pharmacotherapy. Treatment with fluid resuscitation or diuresis is guided by the volume status. Emergent referral to a nephrology subspecialist is recommended for patients with stage 2 or 3 AKI; patients with stage 1 AKI and a concomitant, decompensated condition; or if the etiology of the AKI is unclear. Urgent referral should be considered if the injury does not improve with treatment or if glomerulonephritis is suspected.

Kidney Disease: Chronic Kidney Disease.

Chronic kidney disease (CKD) affects 37 million US adults. It is characterized by damage to the renal glomeruli, vascular supply, and/or tubulointerstitium through complex processes involving inflammation, fibrosis, and hyperfiltration. CKD typically is asymptomatic but may be detected incidentally via urinalysis showing proteinuria or blood test results showing an elevated creatinine level. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation is the most accurate creatinine-based method for estimating glomerular filtration rate (GFR) in routine practice. Cystatin C level measurement can be considered if patients have factors that might make creatinine-based equations inaccurate (eg, high or low muscle mass). CKD is defined as a GFR less than 60 mL/min/1.73 m2 or persistent evidence of kidney damage on imaging, biopsy, or urinalysis that persists for longer than 3 months. CKD is classified into stages based on estimated GFR, degree of proteinuria, and the cause. Screening guidelines vary. Screening should be considered if patients are at high risk of CKD (eg, patients with diabetes, hypertension, cardiovascular disease, family history of kidney failure). After CKD is identified, is it important to identify and reduce or eliminate exposure to nephrotoxic drugs. Management goals include mitigation of CKD risk factors to slow disease progression, including optimizing management of underlying conditions (eg, hypertension, diabetes).

Kidney Disease: End-Stage Renal Disease.

End-stage renal disease (ESRD) affects approximately 745,000 individuals in the United States. Patients with ESRD are dependent on renal replacement therapy (RRT) via dialysis or kidney transplantation. The two dialysis modalities are peritoneal dialysis and hemodialysis. No differences in long-term mortality rates between the two modalities have been shown. Peritoneal dialysis is performed at home. Hemodialysis typically is performed at a dialysis center through vascular access via an arteriovenous fistula (which must mature for several months before use), an arteriovenous graft (which can be used in as few as 24 hours, depending on the graft material), or a central venous catheter (usable immediately but associated with the highest risk of infection). Transplantation is the treatment of choice for patients with ESRD, and referral should be offered to patients who are candidates. However, some patients with ESRD decide against RRT and opt for supportive care. For these patients, and for patients who choose to discontinue dialysis, palliative care and hospice referral are indicated. For all patients with advanced chronic kidney disease or ESRD, treatment includes management of complications, including hyperkalemia, hypervolemia, metabolic acidosis, anemia, mineral and bone disorders, and protein-calorie malnutrition.

Kidney Disease: Kidney Stones.

Kidney stones have a prevalence of 8.8% in the United States, with men affected more than women (10.6% versus 7.1%). Most stones are composed of calcium oxalate (61%). Calcium phosphate (15%) and uric acid (12%) stones are the second and third most common types. Risk factors include renal and ureteral anatomic abnormalities, family history, previous stones, older age, and various drugs. Factors that increase the risk of stone development include obesity, older age, metabolic syndrome, diabetes, and hypertension. Symptoms include renal colic, dysuria, urinary frequency, hematuria, fever, flank pain, and groin pain. Renal ultrasonography is the recommended first-line imaging modality, and is preferred in pregnant patients. Metabolic testing is recommended in high-risk patients (eg, with a family history of stones, one kidney, malabsorption or intestinal disease). A nonsteroidal anti-inflammatory drug is the first drug of choice for pain management. Medical expulsive therapy (MET) is considered first-line therapy if stones do not resolve with observation. MET is recommended for patients with uncomplicated distal ureteral stones 10 mm in diameter or less. If a stone fails to pass, other interventions (eg, extracorporeal shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, ureteral stents, nephrostomy tubes) can be considered, depending on the situation. Increased fluid intake and dietary interventions can reduce the risk of recurrence.

A bedside clinical tool using creatinine kinetics to predict worsening renal injury and early recovery.

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.