Trystan Casey
Acute kidney injury (AKI) is a rare but major complication of burn injuries, with a high mortality rate. The risk of developing AKI increases with the severity of the burn, especially when it affects over 20% of the total body surface area. Electrical burns can cause extensive tissue destruction, leading to the release of myoglobin and free haemoglobin, which can result in the blockage of renal tubules and subsequent kidney damage. Other factors contributing to AKI in burn patients include hypovolemia, cardiac dysfunction, inflammatory responses, and nephrotoxic medications. While acute renal failure in burn patients is less frequent due to advances in cardiovascular management, it remains a significant concern with a complex interplay of physiological changes.
| Characteristics | Values |
|---|---|
| Renal failure complication | High mortality rate |
| Renal failure occurrence | Immediately after injury or later when sepsis develops |
| Renal failure causes | Filtration failure, tubular dysfunction, haemoglobin blockage, sodium retention, sodium-potassium pump impairment, fluid overload, nephrotoxic usage, etc. |
| Renal failure prevention | Aggressive and early fluid replacement |
| Renal failure treatment | Dialysis, hemofiltration, medication, diet, and exercise |
| Acute Kidney Injury (AKI) occurrence | Early (up to 3 days after burn incident) or late (from day 4 after injury) |
| AKI causes | Rhabdomyolysis, muscle breakdown, cardiac dysfunction, tumour necrosis factor-alpha (TNF-α) activation, etc. |
| AKI prevention | Early diagnosis and management, prevention of sepsis and multi-organ dysfunction syndrome (MODS) |
| AKI treatment | Continuous arteriovenous hemofiltration (CAVH), biomarkers identification, etc. |
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What You'll Learn
Rhabdomyolysis and haemoglobin breakdown
Electrical burns can lead to rhabdomyolysis, a condition that causes muscle breakdown. This breakdown releases myoglobin, a relative of haemoglobin, into the systemic circulation. Myoglobin is a protein that can cause tubular obstruction and urine backflow, resulting in acute renal impairment.
Rhabdomyolysis is a well-known complication of electrical burns, with a recent study including 50 patients with trauma and electrical burns showing that 93.33% had CK levels indicative of rhabdomyolysis. Another study found that out of 714 severely burned patients, 1% were diagnosed with rhabdomyolysis, with 75% of those developing acute renal failure.
The release of myoglobin and free haemoglobin results in the blockage of renal tubules, constriction of afferent arterioles, and the generation of oxygen free radicals. Myoglobinuria occurs when serum myoglobin levels exceed 1,500-3,000 ng/ml, and it is typically associated with elevated levels of creatine kinase (CK). CK levels are used to diagnose rhabdomyolysis, and they are often significantly elevated in patients with acute renal failure.
Early detection of acute renal failure due to rhabdomyolysis can be achieved by monitoring biochemical parameters such as serum creatinine, serum CK, and urinary myoglobin. While urinary myoglobin can be useful, it is not as accurate as blood tests for CK levels because myoglobin moves quickly through the body.
The treatment of rhabdomyolysis focuses on preventing acute renal failure. Intravenous fluids are administered to maintain urine production and prevent kidney failure. In some cases, dialysis may be required to support the kidneys in filtering waste products. Additionally, managing electrolyte abnormalities is crucial to protect the heart and other organs.
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Myoglobinuria and hypotension
Renal failure is a major complication of burns, with a high mortality rate. It can develop early (up to three days after the burn incident) or late (starting from day four after injury). Early renal failure is often caused by hypovolemia due to fluid loss, increased inflammatory mediators, and denatured protein release, while late renal failure is associated with sepsis and multi-organ dysfunction syndrome.
Electrical burns can lead to myoglobinuria-induced acute renal failure (ARF). Myoglobinuria occurs when serum myoglobin levels are greater than 1500-3000 ng/ml, resulting in elevated levels of creatine kinase. In a study of 162 patients with electrical injuries, 14% had myoglobinuria, but none developed ARF. Multivariate modelling identified high-voltage exposure, prehospital cardiac arrest, full-thickness burns, and compartment syndrome as risk factors for myoglobinuria.
The pathophysiology of ARF in burn patients is not yet fully understood, making prevention and early diagnosis critical. Aggressive and early fluid replacement can protect against renal failure. Additionally, identifying risk factors and biomarkers can aid in early detection and management of acute renal failure in burn patients.
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Dehydration, acidosis, shock, or endotoxaemia
Renal failure is one of the most common complications of burn injuries, with a high mortality rate. Electrical burns may result in compartment syndrome or rhabdomyolysis, which can lead to acute kidney injury (AKI).
Dehydration, acidosis, shock, and endotoxaemia are all factors that can contribute to renal failure after electrical burns. Dehydration can occur due to fluid loss through the burn wound, which can lead to a decrease in circulatory volume and plasma tonicity, causing reduced renal flow and tubular necrosis. This is further exacerbated by the release of inflammatory and vasoactive mediators, such as histamines, prostaglandins, and cytokines, which cause a systemic capillary leak and intravascular fluid loss, resulting in hypovolemia and hypoperfusion, known as burn shock. Burn shock can be managed with aggressive fluid resuscitation and close monitoring of IV fluids.
Acidosis, a condition where the body's pH levels become imbalanced, can also contribute to renal failure. This is often corrected through anticoagulation therapy, such as antithrombin III and heparin, to prevent the development of renal failure.
Shock, as mentioned earlier, is a result of hypovolemia and hypoperfusion. It can lead to decreased renal perfusion, local and systemic cytokine storms, ischemia, cellular death, and the release of oxygen free radicals. These mediators cause direct tubular damage and disrupt tight junctions, leading to obstructive nephropathy and a further reduction in renal function.
Endotoxaemia, or the presence of endotoxins, can also play a role in renal failure. Endotoxins can activate Tumor Necrosis Factor-alpha (TNF-α), which impairs the response to catecholamine, leading to myocardial suppression, low ejection fraction, and biventricular dilatation.
Overall, dehydration, acidosis, shock, and endotoxaemia are critical factors that can contribute to renal failure after electrical burns, requiring careful management and monitoring to prevent further complications and ensure patient recovery.
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High blood pressure and diabetes
Electrical burns can cause acute kidney injury (AKI), which can lead to renal failure. This is due to a complex interplay of various cellular and neuro-humoral changes affecting burn patients.
Diabetes causes the kidneys to become less efficient at filtering blood. When someone has diabetes, they cannot make or use insulin properly, leading to a rise in blood sugar, which causes complications throughout the body. High blood pressure is the second leading cause of kidney failure in the United States, after diabetes.
People with diabetes and high blood pressure can take steps to prevent chronic kidney disease (CKD) or slow its progression. Maintaining a healthy weight through diet and exercise can reduce blood sugar, blood pressure, and the risk of kidney disease. A healthy diet includes fruits, vegetables, whole grains, and other foods that are good for heart health and lower in sodium. For those with advanced kidney disease, a dietitian can help tailor their diet to their specific needs.
Additionally, new medications for diabetes, such as SGLT2 inhibitors and GLP-1 receptor agonists, can dramatically reduce deaths from kidney disease and lower the rates of heart failure, stroke, and death from cardiovascular causes.
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Tumour necrosis factor and/or oxygen free radicals
Renal failure is one of the most common complications of burn injuries, with a high mortality rate. Burn-induced acute kidney injury (AKI) can develop early (up to three days after the burn incident) or late (starting from day four after injury).
One of the factors implicated in the development of burn-induced AKI is tumour necrosis factor-alpha (TNF-α) activation, which has a direct impact on myocardial suppression. In the presence of endotoxins or thermal injury, the myocytes synthesize TNF-α, which contributes to an impaired response to catecholamine, a low ejection fraction, and even the presence of biventricular dilatation.
Oxygen free radicals are also implicated in the development of AKI following burn injuries. The release of myoglobin and free haemoglobin results in the blockage of renal tubules, constriction of afferent arterioles, and the generation of oxygen free radicals. The free haemoglobin absorbed by the tubular epithelium is degraded into globin and haem, with the latter inducing tubular damage by generating oxygen free radicals via iron ions.
In addition to the above, burn stress and the associated circulatory derangement induce elevated levels of catecholamines, angiotensin II, aldosterone, and vasopressin. These hormonal changes cause vasoconstriction and fluid retention, as well as alteration of regional blood flow, especially in the kidneys.
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Frequently asked questions
Renal failure, also known as kidney failure, is when the kidneys lose their ability to filter blood and regulate fluids, electrolytes, and acid-base status in the body.
Acute renal failure is an uncommon occurrence in burn patients, but it is one of the major complications of burns and is accompanied by a high mortality rate. Renal failure itself is no longer considered life-threatening due to the availability of haemodialysis.
Renal failure in burn patients can be caused by a combination of factors, including decreased cardiac output, high abdominal pressures, and increased levels of tumour necrosis factor, leading to reduced blood flow to the kidneys. Other factors include fluid loss, cardiac dysfunction, rhabdomyolysis, and the release of inflammatory mediators and proteins into the bloodstream. In the case of electrical burns, the release of myoglobin and free haemoglobin can result in the blockage of renal tubules, contributing to renal failure.
Renal failure can develop early (within the first three days after the burn incident) or late (starting from the fourth day after the injury). Early kidney injury is often due to low blood volume, while late-onset renal failure is usually associated with sepsis and multiple organ dysfunction syndrome (MODS).
The treatment for renal failure in burn patients may include aggressive fluid resuscitation to protect against renal failure. In some cases, renal replacement therapy (RRT) and dialysis may be required. Prevention and early diagnosis are key to improving outcomes and avoiding the need for more invasive treatments.
