Disaster nephrology: a new concept for an old problem

Abstract

Natural and man-made mass disasters directly or indirectly affect huge populations, who need basic infrastructural help and support to survive. However, despite the potentially negative impact on survival chances, these health care issues are often neglected by the authorities. Treatment of both acute and chronic kidney diseases (CKDs) is especially problematic after disasters, because they almost always require complex technology and equipment, whereas specific drugs may be difficult to acquire for the treatment of the chronic kidney patients. Since many crush victims in spite of being rescued alive from under the rubble die afterward due to lack of dialysis possibilities, the terminology of 'renal disaster' was introduced after the Armenian earthquake. It should be remembered that apart from crush syndrome, multiple aetiologies of acute kidney injury (AKI) may be at play in disaster circumstances. The term 'seismonephrology' (or earthquake nephrology) was introduced to describe the need to treat not only a large number of AKI cases, but the management of patients with CKD not yet on renal replacement, as well as of patients on haemodialysis or peritoneal dialysis and transplanted patients. This wording was later replaced by 'disaster nephrology', because besides earthquakes, many other disasters such as hurricanes, tsunamis or wars may have a negative impact on the ultimate outcome of kidney patients. Disaster nephrology describes the handling of the many medical and logistic problems in treating kidney patients in difficult circumstances and also to avoid post-disaster chaos, which can be made possible by preparing medical and logistic scenarios. Learning and applying the basic principles of disaster nephrology is vital to minimize the risk of death both in AKI and CKD patients.

Keywords: AKI; acute tubular necrosis; chronic renal failure; dialysis; rhabdomyolysis.

Fig. 1.

Pathogenesis of pressure-induced rhabdomyolysis. When muscles are compressed, permeability of the sarcolemma increases and substances present in the extracellular environment such as calcium, sodium and water move to the intracellular milieu, whereas substances highly concentrated in the muscle cells such as potassium and myoglobin seep out of the muscle cells into the extracellular space. Increased free calcium triggers muscle contraction and depletes ATP stores; mitochondrial damage occurs resulting in oxidative stress; proteases, phospholipases and other enzymes are activated, resulting in myofibril and membrane phospholipid damage. The next step is myocyte lysis and release of toxic intracellular constituents into the extracellular microenvironment, resulting in microvascular damage, producing capillary leak and causing compartmental syndrome. Increased pressure on the capillaries occludes microcirculation and depletes myoglobin oxygen content, resulting in more cell lysis. Most of the damage occurs only after the blood flow into the damaged tissue has been restored due to decompression (reperfusion injury) (adapted from [44]).

Fig. 2.

Pathogenesis of AKI related to the crush syndrome. 1. Muscle necrosis causes dramatic fluid third spacing, leading to intravascular volume depletion, renal hypoperfusion and ischaemia. 2. Myoglobinuria causes intratubular cast formation, which contributes to AKI. 3. Scavenging of nitric oxide by myoglobin and activation of the inflammatory pathways due to severe muscle injury, can aggravate renal hypoperfusion and tissue injury. 4. Nucleosides released from disintegrating cell nuclei, and metabolized to uric acid, may contribute to cast formation and tubular obstruction. 5. Degradation of intratubular myoglobin causes release of free iron, which catalyses free radical production enhancing ischaemic damage. 6. Hyperkalaemia depresses cardiac output potentiating renal hypoperfusion. 7. Hyperphosphataemia may contribute to hypocalcaemia, which can further depress myocardial contractility, and may result in the precipitation of CaPO4 salts that induce inflammation of the kidney tissue. 8. Damaged muscles can release tissue thromboplastin, triggering disseminated intravascular coagulation (adapted from [44]). IVV: intravascular volume; ATN: acute tubular necrosis; AKI: acute kidney injury; DIC: disseminated intravascular coagulation; NO: nitric oxide.

Fig. 3.

Clinical course of a typical case of crush syndrome patient after the 1999 Marmara Earthquake-Turkey: (a) at the disaster field, fluid resuscitation was initiated with a certain delay and the amount of applied fluid was inadequate; thus, crush-related AKI could not be prevented; (b) at the referral hospital, immediate fasciotomy was performed. Although this patient showed an uneventful course, routine fasciotomies are not recommended for treating compartmental syndrome because of high risk of sepsis in disaster victims; (c) very frequent haemodialysis was performed, mainly for treating hyperkalaemia; (d) patient suffered from serious psychological trauma, because of loss of the family members, and finally was lost to follow-up. Both of the latter observations are very frequent among victims of mass disasters.

Fig. 4.

Principal steps in global and local coordination of renal-disaster relief efforts (reproduced from [85] with permission) (the figure is for viewing only and, for any reuse, permission must be obtained from Oxford University Press).

Fig. 5.

Application of the action plan during the acute phase of major disasters. Measures to be taken by the responsible relief coordinator are summarized at the centrum. The substitutes should try to contact the chief disaster relief coordinator and each other even before the 2 h limit shown, so that they know each other's status and availability as early as possible (reproduced from [85] with permission) (the figure is for viewing only and, for any reuse, permission must be obtained from Oxford University Press). RDRTF: renal disaster relief task force.