and hypermagnesemia in ESRD. A patient with a magnesium disturbance may have an arrhythmia or ECG abnormality, often related to QT interval changes. Classically, patients with low magnesium have increased reflexes and weakness with a prolonged Qtc interval. Hypermagnesemia is associated with hyporeflexia, mental status changes, and respiratory depression progressing to cardiac arrest. ECG findings may mimic hyperkalemia with peaked T‐waves, QRS widening, and possibly complete heart block [4,16].
Table 22.1 ECG changes in hyperkalemia
| Peaked T‐waves | Slow atrial fibrillation |
| PR prolongation | Sine wave |
| Wide unusual QRS complexes | Asystole |
| Conduction blocks | Ventricular fibrillation |
| Bradycardia | Wide complex pulseless electrical activity |
Pericarditis
Inflammation of the pericardium with or without effusion is a known complication for dialysis patients. Uremic pericarditis is defined as development of pericarditis before or within 8 weeks of initiating dialysis, while dialysis‐associated pericarditis is thought to occur after the 8‐week mark of dialysis treatment. More classic etiologies such as infectious, postmyocardial infarction, and constrictive are also possible [17].
A patient with both uremic and dialysis‐associated pericarditis may present similarly with fever, chest pain that can be positional in nature, and a friction rub heard on cardiac exam. Classic ECG findings may not be present, as the inflammatory cells associated with noninfectious ESRD pericarditis do not involve the epicardium. The ultimate treatment for ESRD pericarditis is dialysis [4, 17].
Cardiac tamponade is a realistic possibility, and it should be considered in the hypotensive, dyspneic ESRD patient with distant heart sounds, elevated jugular venous pressure, pulsus paradoxus, or electrical alternans on ECG [17]. Focused point of care ultrasound may be used to aid in this diagnosis in the prehospital setting.
Cardiovascular disease
Cardiovascular disease is prevalent in the ESRD and CKD population. Accounting for 39% of deaths among dialysis patients, death from cardiovascular disease is more common in CKD patients than their progression to ESRD. While kidney disease and heart disease have similar causal factors, unique properties of the renal patient’s physiology also impose higher cardiac risk. Such factors as inflammation, oxidative stress, uremia, and metabolic abnormalities contribute to higher coronary artery disease incidence and mortality. Diagnosis of cardiac disease can be more difficult in this patient population. Typical ECG findings of ischemia may be subtle due to baseline ECGs with underlying left ventricular hypertrophy and acute changes related to electrolyte disorders or fluid overload. When present, though, classic ST‐segment changes indicative of acute coronary syndrome are the same in the ESRD patient as the nondialysis patient [18,19].
Stroke is also more common in renal disease patients than the general population. The risk is increased in patients with more advanced CKD, and even higher rates of stroke exist in the first year after dialysis begins. Both hemodialysis and peritoneal dialysis carry elevated stroke risks, although incidence may be slightly lower for the latter [20].
Hematologic
Patients with kidney disease are often anemic. Their red blood cell counts tend to be low, with hemoglobin usually less than 10 g/dL upon starting dialysis [1]. The cause is multifactorial and includes renal undersecretion of erythropoietin, a hormone responsible for red blood cell production [4].
Uremic bleeding is also thought to be multifactorial, though primarily due to platelet dysfunction. The resulting prolonged bleeding time can cause complications in the trauma setting and with routine access of fistulas and grafts during hemodialysis, prompting activation of the EMS system for potentially life‐threatening hemorrhage [21]. When presented with a bleeding dialysis patient, the EMS clinician may need to be more aggressive than usual with regard to direct pressure, hemostatic agents, and tourniquet application.
Infection
Renal patients, especially those with ESRD, have an increased risk for infection, with greater associated morbidity and mortality. Uremia is associated with dysfunction in both innate and adaptive immune systems through complex cellular alterations. Those with indwelling devices for dialysis access have an obvious source for contamination and seeding with bacteria. Transplant patients on immunosuppressive therapy additionally are immunocompromised from the medicines required to reduce risk of graft rejection [22]. With sepsis and bacterial infections being common in ESRD patients, the prehospital clinician must be able to recognize patients with severe sepsis and septic shock and treat them with appropriate fluid resuscitation. Clinicians often are hesitant to initiate administration of 30 mL/kg fluid bolus over the first 3 hours, as suggested by the Surviving Sepsis Campaign, due to concern for triggering pulmonary edema and respiratory failure. Studies, however, have suggested that there is no increased harm among ESRD patients, with the caveat that further prospective studies are needed [23, 24].
Rhabdomyolysis
Rhabdomyolysis is caused by muscle breakdown and release of intracellular material including myoglobin, leading to renal damage. In adults, alcohol and drug intoxication, trauma, prolonged immobility, excessive strenuous activity, toxic ingestions, and infections can lead to this syndrome. Symptoms include weakness, myalgia, mental status change, and darkened urine. Assessment for arrhythmias should be done, as prehospital treatment of hyperkalemia may be required, especially in cases involving prolonged extrication with potential crush syndrome. Specific treatment of hyperkalemia will be discussed later in the chapter. The mainstay of treatment for rhabdomyolysis otherwise is adequate resuscitation with crystalloid IV fluids and transport. Hospital admission is often needed for treatment of resulting metabolic abnormalities [25, 26].
Complications of hemodialysis
Hypotension
Hypotension is common during dialysis, occurring in 10%‐50% of patients. Often, this is a direct result of fluid shifts from the dialysis procedure. At times, there may be calibration issues and the patient has an overzealous removal of fluid, leaving him or her intravascularly depleted. Additionally, the medications and temperature shifts commonly found in the dialysis circuit, combined with the patient’s baseline autonomic irritability, frequently contribute to decreased blood pressures [4]. However, care must be given not to attribute all postdialysis hypotension to hypovolemia, as these patients are at higher risk for septic shock, cardiac tamponade, bleeding, myocardial ischemia, and heart failure.
Treatment of hypotension is directed at the cause. Should dialysis‐related hypovolemia be the likely insult, small boluses (250–500 mL) of isotonic crystalloid IV fluid should be considered, followed by reassessment of the patient for response and any respiratory distress [4]. During any care transitions, EMS clinicians should clearly communicate the volume of any administered IV fluids.
Air embolism
Since the patient’s vascular circuit is violated and connected to the outside world during hemodialysis, concern exists for the introduction of air into the patient’s bloodstream. While small amounts of air into the vascular system can be asymptomatic, larger amounts can cause serious sequelae. It is estimated that 3–5 mL/kg of air is the lethal dose [27]. Air traveling through the vasculature toward the brain can cause cerebral blood outflow obstruction, leading to increasing intracranial pressure, altered mental status, and seizures. If air travels into the right side of the heart and migrates