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.