Acute severe thrombocytopenia following contrast administration is incredibly rare, but it can lead to significant morbidity. This case details the experience of a 63-year-old male whose diagnostic coronary angiography quickly led to severe thrombocytopenia with cardiovascular compromise in the absence of any immediate symptoms of anaphylaxis. His platelet count normalized within a week, increasing from 2 × 10³/μL to 328 × 10³/μL. A thorough review of the literature along with the present case is being reported.

Severe thrombocytopenia following contrast administration is a rare phenomenon. As per our literature search derived from PubMed, there have been a net fourteen reported cases of acute, severe thrombocytopenia following contrast administration. Due to rarity of this phenomenon, a drastic drop in platelet counts is not anticipated, which could be disastrous in the context of recent femoral access. Platelet count usually responds well to conservative therapy and spontaneously returns to normal within a week.

The patient described here presented for an elective left heart catheterization complicated by severe thrombocytopenia two hours post-procedure leading to a large inguinal hematoma at the access site and life-threatening hemodynamic compromise requiring vasopressors.

A male patient aged 63 years with a history of atrial flutter, smoking and hypertension was referred for a left heart catheterization for further evaluation following abnormal myocardial perfusion stress test. He had no prior cardiac procedures, known drug allergies or contrast exposures. On the day of the procedure, he presented with normal vital signs and a platelet count of 269 × 10³ . 6-Fr access was obtained in the right common femoral artery. During the coronary angiography, the patient received intracoronary (IC) adenosine and nitroglycerin, unfractionated heparin (intra-arterial), intravenous fentanyl, midazolam, phenylephrine and 100mL of Visipaque-320, a non-ionic iso-osmolar contrast medium. Neither Aspirin nor a P2Y12 inhibitor was given before or during the procedure. Coronary angiography showed three-vessel disease with a Fractional Flow Reserve (FFR) positive Right Coronary Artery (RCA) lesion; Percutaneous Coronary Intervention (PCI) was deferred in favor of a potential Coronary Artery Bypass Graft (CABG). Intraoperative hypotension was attributed to nitroglycerin and adenosine rather than anaphylaxis since it was not associated with other symptoms including dyspnea, throat tightness, pruritis or flush. Vascade vascular closure system (Cardiva Medical, Inc.) was used along with ten minutes of manual pressure. Good hemostasis at the access site was achieved.

However, within two hours of the procedure, femoral access site was found to develop a large hematoma complicated by hypotension and supraventricular tachycardia. Resuscitation was done with intravenous normal saline and twenty-five minutes of direct manual pressure applied to the access site. A FemoStop^® plus compression system was then placed. Intravenous vasopressors and amiodarone were initiated to stabilize the condition.

Patient was emergently taken to the catheterization lab for a right iliac and femoral angiogram via contralateral access using an additional 40mL of visipaque which ruled out retroperitoneal hemorrhage. Mild access site active extravasation was noted. Decision was made to perform prolonged manual compression which eventually achieved hemostasis. Immediately afterwards, he was found to have platelets of 2 × 10³ . Peripheral smear confirmed thrombocytopenia and identified rare schistocytes. Doppler studies of all four extremities were preformed to rule out Deep Venous Thrombosis (DVT). Normal INR/PTT, LDH and fibrinogen ruled out DIC. A second peripheral smear found no schistocytes and identified only a single platelet in addition to increased eosinophils. HIT (Heparin Induced Thrombocytopenia) antibodies were negative. Indirect antibodies to platelets detected by flow cytometry were positive. Provisional diagnosis of contrast induced thrombocytopenia was made.

The patient ultimately received four units of platelets and two units of packed RBCs. He had melena for next 48 hours which, on colonoscopy, were found to be due to diffuse mucosal bleeding. This complication was likely due to the severe thrombocytopenia as no focal spot of gastrointestinal hemorrhage was found on esophagogastroduodenoscopy or colonoscopy.

Although a few case reports [1-3] have documented corticosteroid administration in similar situations, there is insufficient literature to support this intervention. Hence, we decided not to use IV corticosteroids. Platelet counts increased to 127 × 10³ by discharge three days later and were 328 × 10³ in one week. Due to prompt improvement in platelet count, marked improvement in patient’s clinical condition and logistic constraints, allergy specialist was not involved in the case.

Patient subsequently underwent successful three-vessel CABG and was reportedly event free since the last clinical encounter. Temporal trend of platelet count is represented in figure 1.

Figure 1: Temporal trend of platelet count.

There are fourteen reported cases of acute, severe thrombocytopenia following contrast administration as per our literature search derived from PubMed (Table 1). Both ionic and non-ionic, low and high osmolar contrast agents have been reported to be associated with this phenomenon. Repeat exposure within weeks of the primary exposure were invariably associated with recurrent thrombocytopenia [1,2,4].

Table 1: Literature review of case reports of intravenous contrast induced thrombocytopenia.
LHC: left heart catheterization; PCI: percutaneous coronary intervention; IVUS: intravascular ultrasound; ADHF: acute decompensated heart failure; CT: Computed Tomography; HIT: Heparin-induced thrombocytopenia

Clinical profile, temporal trend of platelet reduction and recovery noted in these handful of contrast-induced thrombocytopenia cases closely resemble the thrombocytopenia induced by LigandMimetic Fibrinogen receptor antagonists (GpIIb-IIIa inhibitors) [5]. Thrombocytopenia associated with GpIIb-IIIa inhibitors is a wellknown phenomenon where a severe, acute drop in platelet counts occurs within hours of exposure followed by recovery within a week. This can be associated with fever, chills and other systemic symptoms. These antibodies can be naturally occurring, accounting for the observation that platelet destruction can occur within a few hours of the first exposure to one of these medications [6,7].

Maintaining a high clinical suspicion for contrast induced thrombocytopenia is paramount. Thrombocytopenia can be the only manifestation; however, systemic symptoms like fever, chills and hemodynamic instability have been reported. Avoidance of the contrast exposure especially in close temporal proximity with the earlier exposure is of utmost importance. Once established, sensitivity to contrast causing immune thrombocytopenia is usually permanent; hence, patients should avoid future exposure [7]. Glucocorticoids use is controversial, but often administered. It is difficult to attribute the improvement in platelet count to steroid administration as this could be simply due to withdrawal of the sensitizing agent itself. IV immunoglobulin’s and plasma exchange are used for other forms of drug induced thrombocytopenia; however, in the context of contrast induced thrombocytopenia, we found only one reported case of IV immunoglobulin’s [4] while none reported use of plasma exchange. Platelet counts invariably improved within next one to two weeks, regardless of the treatment options.

Contrast induced thrombocytopenia is rare but clinically important entity especially in a busy cardiovascular practice. Awareness of this phenomenon is paramount in avoiding future contrast exposures and management of the patient. Platelet count invariably improve within days, however, supportive care during this interval is critical.

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Citation: Roy DD, Marshall CS, Pham SV, Chilton RJ (2021) Acute Life-Threatening Contrast Induced Thrombocytopenia Following Diagnostic Coronary Angiography: A Case Report and Literature Review. J Clin Case Stu 6(2): dx.doi.org/10.16966/2471-4925.218

Copyright: © 2021 Roy DD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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