Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3609_Библиотеки_им_академика_М_И_Перельмана

On admission to our unit his blood pressure was 170/80mmHg and heart rate 96 beats per min. He had oligu­ria and symptoms and signs of pulmonary edema (dyspnea, tachypnea, use of auxiliary respiratory muscles, rales in the lower elds of both lungs). The laboratory investigation showed hematocrit 38.5%, hemoglobin 13.1 g/dL, white blood cell count 10,200/μL, blood urea nitrogen 111mg/dL and serum creatinine 7.8mg/dL.Arterial blood gas examina­tion was consistent with metabolic acidosis and profound hypoxia. Chest X-ray was diagnostic of pulmonary edema. Kidney size was normal (11 cm) on ultrasound examination.

Although well-tolerated, in the vast majority of cases, contrast media can cause discomfort, allergic reactions, kid­ney damage, and thyroid problems. Immediate mild hyper­sensitivity reactions (<3%) have included skin rashes, ushing, urticaria, pruritus, rhinorrhea, nausea, vomiting, diaphoresis, coughing, and dizziness, while more severe reactions (<0.04%) have included facial and laryngeal edema, bronchospasm, angioedema, hypotension and car­diac arrhythmias, pulmonary edema, seizures, and death (<1 death per 100,000 patients). Delayed adverse reactions have included skin rash and redness, sometimes associated with nausea, vomiting, dizziness and either hyperthyroidism or hypothyroidism due to the exposure to iodine material [1, 2].

Iodinated contrast media are excreted via the kidney and can be seen in renal calyces within 2min after intravenous or even earlier after intraarterial administration. Both animal experiments and clinical observations have documented that the contrast material can cause kidney damage leading to decreased kidney function and acute kidney injury (AKI). They exert their cytotoxic effect directly on the proximal tubules of the kidney, and indirectly by enhancing the gen-

0.3 or 0.5 mg/dL from baseline, or a relative increase in serum creatinine by >25 or >50% from baseline value within 48–72h after administration of contrast media. Although no denition of AKI has been designed specically for contrast­associated AKI, both the European Society of Urogenital Radiology and the American College of Radiology have adopted the denition of AKI by the Acute Kidney Injury Network (AKIN) and suggest to dene contrast-associated AKI, as an absolute increase in serum creatinine levels by ≥0.3 mg/dL from baseline or a relative increase in serum cre­atinine by ≥50% from baseline within 48–72h from contrast infusion. Contrast associated AKI is usually non-oliguric, the creatinine peaks within 3–4 days, and often returns to baseline within 7–10 days. It is unusual for patients to develop permanent renal dysfunction.

The risk of AKI has been shown to be signicantly higher with high-osmolar CM compared to low-osmolar contrast media and depends on the volume of contrast media admin­istered during the procedure. For instance, for each 100mL increase in volume of contrast media administered at the time of primary coronary intervention the risk of AKI increased by 12%. Similarly, in a study with 10,065 consecu­tive patients undergoing percutaneous coronary intervention from 2000 to 2008, a gradual increase of the risk for contrast­associated AKI was observed depending on the volume of contrast media above the maximum allowable contrast dose (5mL×body weight [kg])/baseline serum creatinine [mg/ dL]) [10, 11].

By contrast, ultra-low contrast volumes of 27mL reduced rates of contrast-associated AKI in patients with CKD and median serum creatinine of 2.1mg/dL and mean eGFR of 31 ± 10mL/min/1.73m2 [12].

Besides the type (low- vs iso-osmolar agents), volume, frequency of administration in a short time interval (48–72h) and route of administration (intravenous vs intraarterial), many patient-specic factors have been considered as risk factors for the development of contrast induced AKI, most of them associated with the severity of underlying kidney dam­age (number of remaining functioning nephrons) and the adequacy of blood supply and oxygenation of renal paren­chyma (low cardiac output due to either dehydration or heart failure). Thus, the most accepted patient-related risk factors have included advanced age, pre-existing renal insufciency (especially if eGFR <30mL/min/1.73m2), a prolonged his­tory of diabetes mellitus and/or hypertension, multiple myeloma, anemia, proteinuria and hypoalbuminemia, low cardiac output and congestive heart failure with left ventricu­lar ejection fraction less than 40%, the use of diuretics or dehydration from any cause, hypotension, administration of other nephrotoxic medications (non-steroidal anti­inammatory agents, antibiotics etc.) and renal transplantation.

The decision to administer contrast in high-risk patients should always be a matter of clinical judgment and physician needs to clarify if contrast is diagnostically imperative and its administration outweighs the risks of post-contrast AKI and other complications. This is particularly true in patients requiring closely spaced contrast-enhanced studies.

Theoretically, the intravenous route of crystalloid solu­tions should be preferred to the oral route since most of the free water administered per os will move into the cells or remain in the intracellular space and only less than 1/10 of the administered volume will stay in the intravascular space to support the circulation. This notion was proven correct in some, but not all the studies [17, 18]. Isotonic intravenous uids (0.9% normal saline, lactated Ringer’s solution) are preferred and are better than 0.45% half-normal saline [19]. There is no clear superiority of 0.9% normal saline or sodium bicarbonate solutions for prophylaxis in this setting [20].

The usual course of post-contrast acute kidney injury con­sists of a transient asymptomatic elevation in serum creati­nine. Serum creatinine usually begins to rise within 24h of intravascular iodinated contrast medium administration, peaks within 3–4days, and often returns to baseline within 7-10 days. It is unusual for patients to develop permanent renal dysfunction.

because no control group with patients not receiving radio­contrast material was included. It is possible that the increased morbidity and mortality seen in patients with contrast- associated AKI is because the intravascular iodin­ated contrast exposure unmasked some other factors and underlying comorbid diseases present in these patients. At any rate, the possibility of development various damages after contrast administration highlights the importance of

Case Presentation