Case
The patient was a 40-year-old African American male who presented to the emergency department (ED) for dyspnea. His medical history was significant for coronary artery disease, heart failure with preserved ejection fraction, OSA, hypertension, and medical non-compliance. Social history was significant for alcohol, tobacco, and marijuana use. Family history was significant for an unspecified clotting disorder.
On arrival at the emergency department, the patient was obtunded and lethargic. Vital signs were significant for a heart rate (HR) of 103, blood pressure (BP) of 192/121 mmHg, respiratory rate (RR) of 26, and oxygen saturation of 87% on room air. Physical exam was notable for morbid obesity, diminished breath sounds bilaterally, and 1+ bilateral pitting edema.
Initial serology was notable for hemoglobin of 17.9, hematocrit of 58.7, platelets of 248, and normal renal function based on BUN/Cr. Venous blood gas revealed a respiratory acidosis with a pH of 7.3 and PCO2 of 72.7. Chest x-ray did not reveal an acute cardiopulmonary process. With his hypercapnia and inability to protect his airway, he was intubated and transferred to the intensive care unit. In addition, DVT prophylaxis heparin Subcutaneous was started on day two of admission.
Treatment was started for heart failure exacerbation with intermittent IV diuretics, and therapy was later escalated to continuous infusion due to poor initial response. However, the patient eventually responded to treatment and began to have significant diuresis. Initially, his renal function improved but plateaued and then worsened, prompting a Nephrology consult.
On hospital day seven, a palpable cord was noted along the medial aspect of the left arm. Bilateral upper extremity duplex revealed occlusions of the left brachial, radial, and ulnar arteries (Image 2). The patient’s prophylactic dose of heparin was increased to the therapeutic dose.
The renal injury worsened, and he developed oliguria, prompting hemodialysis (HD). Unfortunately, immediately after starting HD, the HD lines began to clot. Dialysis was again attempted on a different unit with similar results. With this new event and worsening polycythemia and arterial thrombus, Hematology was consulted, and labs were ordered to evaluate possible clotting disorders. Anti-phospholipid was negative, the HIT 4T score was 1-2 with platelets remaining stable at 271 on day seven of heparin administration (Table 2), therefore a low probability.
Additionally, on day nine, the patient developed rectal bleeding. Anticoagulation was held, and CTA of the abdomen revealed no active gastrointestinal (GI) bleeding but found an acute thrombus of the left main renal artery and multiple right renal infarcts. Colonoscopy was performed, but no active bleeding was noted. Anticoagulation was restored after as bleeding was due to rectal tube injury.
With these findings, and the patient requiring mechanical ventilation, a CTA of the chest was ordered, which revealed tiny, distal, bilateral upper lobe non-occlusive pulmonary emboli. Even though thromboses were present, anticoagulation had to be held due to continued GI bleed and polycythemia developing into significant anemia.
On day 14, the patient was found to have a left dilated pupil. CT scan of the head showed large, symmetric infarcts within the occipital poles and retinal artery thrombus. With ongoing thromboses and hemorrhages, and despite no thrombocytopenia and a low 4T score (< 1%) , he was started on Argatroban. Subsequently, a PD4 antibody was ordered and resulted positive; this was confirmed by Serotonin Release assay.