Israel Medical Association Journal

Background: Iatrogenic illness, defined as a disease that results from a diagnostic procedure or from any form of therapy, is a well-recognized phenomenon in clinical practice.

Objectives: To study and evaluate major car-diac iatrogenic disease as the cause of admission to the intensive cardiac care unit in the modern era.

Methods: We assessed 64 critically ill patients suffering from major cardiac iatrogenic problems among a total of 2,559 patients admitted to the intensive cardiac care unit during 3 years. Iatro-genic illness was defined as any problem that resulted from therapy. Only cardiac problems were included in the study. Complications of interventional cardiovascular procedures, suicide attempts or accidental intoxications were ex-cluded.

Results: There was evidence of a major cardiac iatrogenic problem as the cause for admission in 64 patients (2.5%): 58 (91%) suffered from ar-rhythmias (mainly bradyarrhythmias) secondary to beta-blockers, amiodarone, calcium antago-nists, electrolyte imbalance or a combination, and 6 (9%) had non-arrhythmic events (hypotension, syncope or acute heart failure). In 41 patients (64%) the iatrogenic event was considered pre-ventable

Conclusions: Major cardiac iatrogenic compli-cations are an important factor among patients admitted to the intensive cardiac care unit. Most of the events are bradyarrhythmias related to anti-arrhythmic agents. Almost two-thirds of events are preventable.

Background: Protruding aortic atheromas are a potential source of stroke and systemic emboli. The single modality currently available for their detection has been transesophageal echocardiography. However, TEE does not allow full visualization of the upper part of the ascending aorta and proximal aortic arch.

Objectives: To investigate whether double helical computerized tomography- both with and without contrast injection - may represent a useful technique for noninvasive detection of PAA in stroke patients.

Methods: Forty consecutive patients ≥50 years of age who sustained a recent ischemic stroke and/or systemic emboli (within 15 days after the onset of the event) were enrolled in the study and underwent TEE and DHCT without contrast injection using thin slice acquisition (3.2 mm thickness and 1.5 mm reconstruction increment). In addition, the last eight consecutive patients, after obtaining an unenhanced scan, underwent a contrast-enhanced DHCT following peripheral intravenous injection of a small amount of contrast material (15 ml of diatrizoate).

Results: PAAs were demonstrated by TEE in 18 patients (45%); in 16 of them (89%) the atheromas were recognized by DHCT. Of the 22 patients without PAA on TEE, DHCT confirmed their absence in 18 (82%). DHCT yielded a sensitivity of 89%, a specificity of 82%, and an overall accuracy of 85%. The total number of protruding plaques detected by TEE was 43, of which 41 (95%) were correctly identified by DHCT. The mean thickness of the plaques was 5.6±2.4 mm on TEE, and 5.4±2.3 on DHCT (P=NS), with a good correlation between the modalities (γ=0.84). Contrast-enhanced DHCT scans demonstrated absolute equivalence to TEE in aortic areas defined as "clearly visualized by TEE." DHCT detected PAA between the distal ascending aorta and the proximal arch in seven patients; these atheromas were not included in the comparative analysis. In these "occult" areas, DHCT may be superior to TEE.

Conclusions: DHCT without contrast injection using thin slice acquisition may become a useful modality for rapid noninvasive detection of PAA. Contrast-enhanced DHCT scans significantly improve imaging quality and may be superior to TEE in the upper ascending aorta and the proximal arch (areas not well visualized by TEE).

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TEE= transesophgeal echocardiography

PAA= protruding aortic atheroma

DHCT= dual helical computerized tomography
 

Objectives: To report the characteristics of liver injury induced by nimesulide.

Patients and Methods: We report retrospectively six patients, five of them females with a median age of 59 years, whose aminotransferase levels rose after they took nimesulide for joint pains. In all patients nimesulide was discontinued, laboratory tests for viral and autoimmune causes of hepatitis were performed, and sufficient follow-up was available.

Results: One patient remained asymptomatic. Four patients presented with symptoms, including fatigue, nausea and vomiting, which had developed several weeks after they began taking nimesulide (median 10 weeks, range 2–13). Hepatocellular injury was observed with median peak serum alanine aminotransferase 15 times the upper limit of normal (range 4–35), reversing to normal 2–4 months after discontinuation of the drug. The remaining patient eveloped symptoms, but continued taking the drug for another 2 weeks. She subsequently developed acute hepatic failure with encephalopathy and hepatorenal syndrome and died 6 weeks after hospitalization. In none of the cases did serological tests for hepatitis A, B and C, Epstein-Barr virus and cytomegalovirus, as well as autoimmune hepatitis reveal findings.

Conclusions: Nimesulide may cause liver damage. The clinical presentation may vary from abnormal liver enzyme levels with no symptoms, to fatal hepatic failure. Therefore, monitoring liver enzymes after initiating therapy with nimesulide seems prudent.