Case Reports

Pain, Anxiety, and Dementia: A Catastrophic Outcome

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The death of a cognitively impaired patient with catastrophic antiphospholipid antibody syndrome showed the importance of avoiding invasive surgery and focusing anticoagulation management on measures that avoid triggers.


 

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Advanced psychiatric illness and dementia create a wide range of barriers to health care. These patients are unable to provide reliable details with respect to their illness or even discuss basic features of their medical history, forcing providers to rely on contributions from caregiver reports and medical records. Confounding the limits on medical information, physical examinations are often abbreviated or completely refused because of the patient’s distrust, discomfort, or delusion. Over time, the involvement of consulting services may amplify the impact of these barriers as the need for diagnostic and therapeutic interventions emerge. Meanwhile, this delay in definitive management opens a window of risk for deterioration, in which patients cannot be relied on to report important clinical changes.

This case report describes a patient with significant cognitive dysfunction who developed a rare and devastating complication of a hematologic disorder. As the case illustrates, transferring a patient from the psychiatric ward to Internal Medicine (IM) can create unique diagnostic and management challenges.

CASE REPORT

A 64-year-old man developed hematochezia after having been hospitalized in a locked psychiatric ward for the preceding 6 months following a suicide attempt. The episode of hematochezia occurred while on anticoagulation treatment with warfarin for chronic lower extremity deep venous thrombosis (DVT), which prompted the IM consultation. The patient’s past medical history was notable for dementia, hypothyroidism, Crohn disease, and primary sclerosing cholangitis.

The IM Consult Service recommended holding anticoagulation therapy and reversing the coagulopathy with vitamin K. The patient’s stool returned hemoccult and toxin positive for Clostridium difficile (C difficile). The hematochezia was attributed to the infection with C difficile in the setting of anticoagulation. Oral metronidazole was started. Hemoglobin remained stable without further episodes of bleeding. Seven days after the episode of hematochezia, the patient experienced worsening generalized pain and new skin findings. He was transferred to the general medical ward for further management.

The patient’s medical records revealed early cognitive decline with recommendations for supervised residential care as early as age 59 years. An extensive neurocognitive assessment indicated a diagnosis of semantic dementia. He also had a history of recurrent DVT with anticoagulation therapy for > 10 years with no prior workup for a hypercoagulable state. A recent baseline mental status report described a childlike demeanor, profound global speech deficits with marked difficulty understanding even basic medical concepts (eg, the need for a peripheral intravenous catheter), and generalized anxiety disorder complicated by hyperesthesia. The patient frequently refused physical examinations and blood draws as a result. He devoted himself to simple puzzles of kittens and puppies.

Vital signs were normal as were the head and neck, pulmonary, cardiac, and abdominal examinations. The patient’s neurocognitive examination was remarkable for his dependence on instrumental activities of daily living, global aphasia, impaired short- and long-term recall, and poor judgment. He scored 21 out of 30 on a recent mini-mental state examination: failure to achieve 3-word recall; disorientation to month, season, hospital, and county; and an inability to write a sentence or identify a pen. Otherwise, he had fluent speech, facial symmetry, intact strength and sensation throughout, and normal reflexes.

A skin examination revealed diffuse tender subcutaneous lesions. The largest lesion was about 5 cm, located in the left anterolateral thigh. Smaller lesions of about 1 cm were noted in the abdominal wall, right thigh, and bilateral upper extremities. An exquisitely tender, well-demarcated 20-cm elliptical lesion with central necrosis and an erythematous border developed in the left axilla the following day (Figure 1A). Pain limited adduction of the left arm.

The initial laboratory evaluation demonstrated a stable hemoglobin level of 11.1 g/dL, a platelet count of 128 k/mL, and no leukocytosis. Electrolytes and renal indexes were normal. D-dimer and fibrin split products were > 10,000 ng/mL and 20 mg/mL, respectively. Fibrinogen level was 351 mg/dL. The prothrombin time and international normalized ratio were 15.1 seconds and 1.4, respectively. The activated partial thromboplastin time (aPTT) was measured at 40 seconds. High sensitivity C-reactive protein was 4.59. Recent head imaging included a brain magnetic resonance imaging (MRI) notable for enlarged sulci and ventricles with temporal predominance. Positron emission tomography (PET) brain imaging was significant for diffuse hypometabolism in bilateral parietal and temporal lobes with preservation of sensorimotor and occipital cortexes. There was no clear radiographic evidence of cerebral embolic phenomenon or focal cerebrovascular events.

Enoxaparin treatment was initiated for a suspected hypercoagulable state. Ceftriaxone was administered for a urinary tract infection (UTI). Despite premedication, the bedside biopsy of his necrotic skin lesion was aborted due to severe anxiety and generalized somatic pain. A surgical excisional biopsy was thus obtained under general anesthesia. Enoxaparin was held the night before and the morning of surgery. There were no immediate complications related to the biopsy, and malignancy was not seen on intraoperative frozen sections.

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