A 71-year-old man accompanied by his wife presented for the evaluation of dementia. His history was significant for hypertension and hyperlipidemia for which he took benazepril and lovastatin. He was healthy until five years previously when he noted word-finding difficulties. He could now only express himself in monosyllables. There were no focal neurological deficits. His behavior, mood, ability to recall recent events and recognize people were intact. He had mild difficulty dressing. Social graces, facial expressions, coordination and gait were normal. He followed commands. He accurately drew a clock and wrote a sentence without spelling errors. His MMSE was measured at 10/30. CBC, metabolic panel, Vitamin B-12, Folate, TSH, Ceruloplasmin levels, and HIV and Syphilis serologies were normal. CT and MRI only showed generalized cerebral atrophy. Neuropsychological testing revealed Primary Progressive Aphasia (PPA).
DISCUSSION: Unlike most common dementias where memory problems are common and an integral part of the diagnosis, PPA is an atypical dementia characterized by a relentless dissolution of language with relative preservation of memory. Patients usually present with word-finding difficulties, spelling errors or abnormal speech patterns. Unlike Alzheimer’s disease, these patients can recall and evaluate recent events despite an inability to express their knowledge verbally. Folstein’s MMSE because of its reliance on verbal expression overestimates the degree of the patient’s cognitive dysfunction in PPA and may lead to inappropriate labeling and ineffective treatment. Neuropsychological testing is the diagnostic modality of choice. There is no effective pharmacological treatment for PPA although speech therapy is useful in exploring alternative communication strategies. Explaining the nature of the condition is one of the greatest benefits in terms of coping with the impairment and recognizing the primary problem to be expressive rather than cognitive.
DEPRESSION AS A RISK FACTOR FOR HYPOGLYCEMIA IN A WELL-CONTROLLED DIABETIC.M.A. Mendiola1; E. Coffey1. 1Hennepin County Medical Center, Minneapolis, MN. (Tracking ID #117183)
LEARNING OBJECTIVES: 1) Recognize that diabetics have a higher incidence of depression than non-diabetics. 2) Recognize that depression is associated with poor glycemic control. 3) Recognize that anorexia associated with depression may put a diabetic a risk for hypoglycemia.
CASE: A 71 year old female with a history of type 2 diabetes presented to her primary physician for routine follow up. She had been maintained on a regimen of NPH and regular insulin with a recent glycohemoglobin of 6.3%. She had previously experienced few hypoglycemic reactions, but the episodes had become more frequent over the previous two months. At this visit, she also described symptoms consistent with depression, including anorexia and poor motivation for meal preparation. Venlafaxine was initiated, and her insulin regimen was switched to Glargine and Lispro, to allow more flexibility. She was specifically instructed not to take her short acting insulin if she was not eating. However, she continued to have frequent serious hypoglycemic events requiring emergent medical care. Her insulin regimen was significantly liberalized until her depression could be brought under better control.
DISCUSSION: It has been shown in a meta-analysis by Anderson et al. in Diabetes Care, 2001, that diabetics are twice as likely as non-diabetics to suffer from depression (14–26% in diabetics vs. 5–9% in non-diabetics, with an overall odds ratio of 1.9). Depression is also associated with poor glycemic control, increased microvascular and macrovascular complications, as well as increased healthcare expenditures. Total healthcare expenditures for people with depression and diabetes were 4.5 times as high as for those with diabetes without depression, in a 2002 study by Egede et al. in Diabetes Care. This case demonstrates the need for close follow up in diabetics diagnosed with depression. Moreover, it may be necessary to tolerate hyperglycemia in the short run to reduce the risk of life-threatening hypoglycemia until the depression can be controlled. Further research is necessary to investigate the risk of hypoglycemia in diabetics with depression.
DIABETES INSIPIDUS COMPLICATING GASTRIC BYPASS SURGERY. D.L. Mercado1; P. Liew2. 1Baystate Medical Center, Wilbraham, MA; 2Baystate Medical Center, springfield, MA. (Tracking ID #116467)
LEARNING OBJECTIVES: To appropriately screen preoperative gastric bypass surgery patients for Diabetes Insipidus
CASE: A 26 year old woman with morbid obesity was admitted for gastric bypass surgery. Her past history was notable only for polycystic ovarian syndrome and depression. On postoperative day 1, she had a high urine output, but had clinical signs of volume depletion. She complained of thirst but was unable to take adequate oral fluids due to intake limits from the postoperative gastric bypass diet. Her initial serum sodium was 151, but her urine specific gravity was 1.006; renal function was normal. IV fluid resuscitation was initiated resulting in urine output of 7 liters in 24 hours. She was suspected of having Diabetes Insipidus. History from the patient’s mother revealed chronic polydipsia and polyuria, which the patient had failed to mention. Further labs showed serum Na 149, urine sodium 140, and serum osms 302. A trial of vasopressin decreased her urine output dramatically from 300 cc/hr to 50 cc/hr with a > 100% increase in urine osms. Work up revealed no specific cause and the condition was deemed idiopathic central DI. With daily vasopressin nasal spray she was able to maintain adequate hydration while adhering to her post-surgical fluid limits, and her polyuria and polydipsia resolved.
DISCUSSION: Central DI is a rare neurohypophyseal disease defined as polyuria of 2–10 L/day with dilute urine (SpGr 1.000–1.005) in conjunction with high serum osmolarity and high serum sodium. The most common causes are trauma or neurosurgery, but 30–50% are idiopathic. Our patient had daily symptoms consistent with DI which she did not think to mention preoperatively because of their chronicity. Postoperatively undiagnosed DI can result in severe volume depletion because of limited access to free water. This is particularly true of gastric stapling and gastric bypass patients, who have limited oral intake allowances, especially during their first few days postoperatively. Preoperative screening for DI is critical in these patients since they would not be able to maintain hydration without IV fluids due to their limited oral intake postoperatively. In fact, the presence of nephrogenic DI, which is poorly responsive to vasopressin, is an absolute contraindication to this type of surgery. Preoperative patients should be questioned about polyuria and polydipsia. If symptoms are present and not due to hyperglycemia, urine and serum osms, and urine and serum sodium should be checked. If the clinical findings and history are suspicious, water deprivation testing can be considered to confirm the diagnosis.
DIAGNOSIS AND MANAGEMENT OF A PREGNANT FEMALE WITH BRUISES AND SPONTANEOUS ABORTIONS: A CATCH 22.J. Cunningham1; M. Panda1; W.P. Caine1. 1University of Tennessee, Chattanooga, Chattanooga, TN. (Tracking ID #115585)
LEARNING OBJECTIVES: 1. Recognize the effect of pregnancy on platelet aggregation disorders 2. Discuss the diagnosis, categorization, and treatment of thrombophilic disorders 3. Recognize the dilemma in the evaluation and treatment of combined hypercoagulable and hypocoaguable disease.
CASE: A 19 year old black female G4P0030, at 9 weeks of gestation presented with spontaneous bruising. She was diagnosed with von Willebrand factor deficiency 3 months ago. She has a history of menorrhagia but denies history of bleeding from other sites. No family history of bleeding disorders. She has had two spontaneous first trimester abortions. No history of alcohol, tobacco, or illicit drug use. Meds include ASA (started during this pregnancy by PCP) and prenatal vitamins. Physical exam revealed new bilateral pretibial bruises and multiple bruises in different stages of healing on legs and arms. Labs revealed a normal CMP, CBC, PT 13 (INR 0.96), aPTT 34, negative ASO &nANA titer, monospot, RPR, HIV, hepatitis panel. Fibrinogen was elevated at 509, D-dimer 0.6. Ristocetin cofactor, Factor VIII, beta-2-glycoprotein and hexagonal antibodies were normal. All vWF multimers were present and normal. Mixing study and dilute Russell Venom Viper Test (dRVVT) were abnormal confirming the presence of a lupus anticoagulant.
DISCUSSION: Thrombophilic disorders can be hereditary, acquired, or both. The antiphospholipid antibody syndrome (APAS) is an acquired disorder associated with arterial and venous thrombosis, recurrent miscarriages and thrombocytopenia due to the presence of anticardiolipin antibodies, lupus anticoagulant, or subgroup of other antibodies. Types of thromboses associated with the APAS are categorized into syndromes with specific treatment. Mixing study and the dRVVT are specific tests to evaluate presence of a lupus anticoagulant. As commonly seen, our patient’s platelet aggregation disorder (vWF def) corrected during pregnancy. Her history of spontaneous abortions prompted an APAS workup.The presence of lupus anticoagulant confirmed our patient had the Fetal Wastage variant of the APAS. Treatment for this is aspirin immediately before conception and heparin immediately after continued till 6 weeks postpartum. In our patient Aspirin exacerbated her vWF def causing bruising. We anticipate that the vWF def will resurface in the postpartum period which together with treatment will increase bleeding. In an attempt to prevent another abortion Aspirin was continued and heparin was added after discussion of the risk and benefits of receiving anticoagulation and antiplatelet therapy with the patient. A team approach by a high risk obstetrician, internist and hematologist for close monitoring during and after pregnancy will be utilized
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