Time for change: Dyslipidemia Management by Internal Medicine Housestaff

Objective: To demonstrate that management of dyslipidemia does not improve with post-graduate level advancement. Methods: Data was extracted by retrospective review of admissions for the primary diagnosis of chest pain, regardless of final diagnosis. Exclusion criteria included the lack of an ordered lipid profile or identification of chest pain as a secondary diagnosis. Data from 150 patients, from the Internal Medicine residency patient lists at our institution from 2006 to 2008, was recorded and compared with the ATP III Guidelines to classify risk factors and lipid profiles. For each patient, we identified whether appropriate treatment measures were followed and the post-graduate level of the house officer involved with the care. Appropriate treatment is defined as lifestyle modification or pharmacologic treatment. Results: Among the 150 randomly selected patients, there were 99 cases (66%, 95%-confidence interval 58%-74%) where lipid profiles were abnormal. Appropriate treatment based on guidelines was not followed in 63 cases (42%, with a 95%-confidence interval 34%-50%). Of these cases where appropriate treatment was not followed, 94 cases were handled by interns (PGY-1) and 56 cases were handled by senior residents (PGY-2 and PGY-3). The error rate among interns was 38/94 (40.4%) and the error rate among senior residents was 25/56 (44.6%). A two sample comparison of binomial proportions resulted in a p-value of 0.614, indicating that the error rates among the two groups were statistically similar. Discussion: Dyslipidemia is associated with increased morbidity and mortality in coronary heart disease (CHD) and its equivalents. ATP III Guidelines recommend treatments depending on major and minor risk factors. As a low Framingham score correlates with a lower 10-year risk of CHD, appropriate lipid management leads to improved outcome and fewer adverse/fatal events. Inadequate appreciation of cardiovascular risk stratification results in suboptimal patient care. Given our study, advancement in Internal Medicine post-graduate level fails to improve dyslipidemia management. Conclusion: Lipid management should be promoted not only at the beginning of PGY-1, but needs to be reemphasized and monitored throughout training to ensure optimal patient care

Does age and gender correlate significantly with Dyslipidemia?.

Objective: Observationally, at our institution, younger individuals paradoxically appeared to have disproportionately higher abnormal lipid profiles, thus we hypothesize that advancing age does not directly correlate with dyslipidemia and subsequent coronary heart disease risk. Methods: Data was obtained by retrospective review of 150 randomly selected admissions with the primary diagnosis of chest pain. Lack of lipid profile and chest pain as a secondary diagnosis was exclusion criteria. Data, obtained from the Internal Medicine residency patient lists at our institution from 2006 to 2008, was recorded and compared with ATP III Guidelines to classify risk factors and determine the degree of dyslipidemia. Selected demographic details (age, gender, etc.) were also obtained. Correlation of age and gender with dyslipidemia was examined by applying a binary logistic regression model. Results: Of the patients selected for review, 66% (99/150) fulfilled the selection criteria. The mean age of the cohort was 59 years (range 29-97) and 51% of the subjects were females. The quartiles were evenly distributed around the age ranges, with Q172. Based on the quartile split, prevalence of dyslipidemia in the four age groups was 73%, 67%, 71% and 53% respectively. Notably, 74% of men and 58% of women had dyslipidemia. Thus it appears that dyslipidemia may be better correlated with gender than age. A logistic regression model demonstrated a one-sided p-value of 0.095 for age and 0.035 for gender, with the usual significance threshold of 0.05. The odds ratios of 0.52 (gender) and 0.99 (age) indicate that women had a 48% reduced risk of dyslipidemia as compared to men, and that the risk goes down by 1% with each additional one year in age. Discussion: Dyslipidemia increases morbidity and mortality related to coronary heart disease (CHD). ATP III Guidelines and Framingham scores determine the risk of CHD and risk factors are presumed to be related to advanced age. Given our study, gender was a greater correlate with dyslipidemia, with men at a significantly higher risk. Interestingly, the eldest patients (age \u3e 72) had the lowest prevalence of dyslipidemia. This may be indicative of better personal care or optimal pharmacologic treatment for these patients. Conclusion: Advanced age fails to demonstrate increased prevalence of dyslipidemia. Patient education and strict treatment regimens should be enforced early on to prevent adverse events in all patients with dyslipidemia

Rapid-onset piperacillin-tazobactam induced thrombocytopenia.

Thrombocytopenia can occur from a variety of etiologies. Drug-induced thrombocytopenia is known to occur with beta-lactam medications, but often in the setting of prolonged use. We describe 2 patients who developed rapid-onset thrombocytopenia from piperacillin/tazobactam. Other causes of immediate thrombocytopenia were excluded. These cases describe a rare presentation of rapid-onset thrombocytopenia in a commonly used medication

A Stroke of Bad Luck

Introduction Unusual case of adrenal masses in a normotensive patient Clinical case A 37 year old female, no significant medical history, presented with sudden onset of right sided weakness and dysarthria. On presentation she was normotensive but exhibited expressive aphasia and complete right hemiplegia. Initial CT Head demonstrated a dense left MCA infarct with no hemorrhage. Echo was normal. Abdominal Ultra sonogram and CT revealed large bilateral cystic and solid adrenal masses, right measured 22x12.5x11cm, weighing 2058g and left measured 16x11.5x7.7cm, weighing 672g; highly suspicious for neoplastic disease. A repeat CT head showed increasing edema and brainstem herniation which necessitated emergent decompressive frontotemporoparietal craniectomy and durotomy. 24-hour urine studies were metanephrine 130,896 µg (35-460 µg), normetanephrine 25,938 µg (110-1050 µg) and vanillylmandelic acid 127.2 mg (1.8-6.7 mg). TSH and serum calcitonin were normal. MEN2 screening for RET proto-oncogene mutation was negative. Hypercoagulable work up was negative. Patient was pretreated with phenoxybenzamine and had exploratory laparotomy and bilateral adrenalectomy. Pathology and immunohistochemical staining confirmed the diagnosis of bilateral benign pheochromocytomas. Patient was discharged with daily hydrocortisone and fludrocortisone. 24-hour urinary fractionated metanephrines measured 2 weeks post-surgery were normal. The triad of episodic headache, sweating and tachycardia is infrequent; pheochromocytomas may present as paroxysmal hypertension, acute pulmonary edema, myocardial infarction or stroke. Plasma metanephrines were normal though urinary metanephrines were elevated. Patient was not on medication that might alter catecholamine metabolism. Conclusion Manifestations of catecholamine hypersecretion are common. Though adrenal masses were found incidentally in our patient, pheochromocytoma should be considered in young patients presenting with acute stroke

An Incidental Pituitary Adenoma with intact LH Hypersecretion

Objective: We present a relatively uncommon case of gonadotroph cell adenoma with elevated FSH and intact LH resulting in supranormal free and total testosterone. Case Presentation: A 52 year old Caucasian male with a history of hypertension, diabetes mellitus, normal pubertal and fertility history presented with head trauma due to assault by his son. He did not have any focal neurological deficit on initial presentation. CT of the head incidentally showed a large rounded mass measuring 4.1 x 4.3 x 6.3 cm. Brain MRI showed a large sellar and suprasellar mass extending to the right anterior cranial fossa with surrounding vasogenic edema. Imaging was most suspicious for a pituitary macroadenoma. His initial labs were FSH 58.3 mIU/mL (0.9-15), LH 9.1 mIU/mL (1.5- 9.3), prolactin 25.3 ng/mL (1.8-14.4), free testosterone 29 ng/dL (7.2-24) and total testosterone 837 ng/dL (193-740). LH was confirmed to be intact by immunoassay. TSH and ACTH were normal, but GH was 0.1 ng/mL (0-6.0) and IGF-1 was 59 ng/mL (87-238). The patient underwent image guided transnasal, transsphenoidal resection of the tumor, right frontotemporal craniotomy and orbital osteotomy for resection of the supratentorial component of the tumor. Pathology returned as pituitary adenoma with expression of only FSH and LH. His postoperative course was complicated by intracranial hemorrhage and Enterobacter encephalitis, eventually requiring tracheostomy and PEG tube placement. Post resection labs showed L

A case of Hypokalemic Hypertension...Primum non Nocere

Objective: We present an uncommon case of surreptitious diuretic usage mimicking Gitelman syndrome. Case Presentation: A 31 year old Caucasian female who works as a pharmacy technician presented with fatigue, polyuria, polydipsia, intermittent leg cramps and tingling in her feet. She reports that she was diagnosed with hypertension two months before admission and was started on metoprolol succinate. This was discontinued several weeks later and she was started on spironolactone as her potassium was noted to be decreased. Her serum potassium had been persistently low for a month prior to admission and was receiving potassium supplementation. Interestingly her serum potassium was noted to be low (2.8 mmol/L) ten years ago but had normal values until one month prior to admission. On admission, the patient was noted to be normotensive with the following lab values: serum sodium 130 mmol/L(136-145); potassium 2.2 mmol/L(3.5-5.3); bicarbonate 35mmol/L(23-33); BUN 42 mg/dL(5-25); creatinine 1.4 mg/dL(0.6-1.3); uric acid 10.4 mg/dL(2.7-6.8); calcium 10.6 mg/dL(8.3-10.1); renin 92.56 ng/ml/hr(1-4) and aldosterone 74.9ng/dL(0.0- 30.0). Twenty four hour urine potassium and calcium were 58 mmol (25-150) and 84mg (42-353) respectively. Serum magnesium was normal. Serum metanephrines, cortisol, TSH and PTH were normal. The patient denied self-induced vomiting and licorice consumption. She persistently denied surreptitious diuretic usage. Renal arteriogram and MRI abdomen ruled out renal artery stenosis and renin secreting tumor respectively. Her potassium normalized with supplementation and she remained normotensive without antihypertensive medications. Urine analysis performed by high performance liquid chromatography showed hydrochlorothiazide 14mcg/ml and furosemide 5.4mcg/ml. Spironolactone was discontinued and was discharged without any potassium supplementation. Discussion: The diagnosis of surreptitious diuretic usage is largely one of exclusion, made in someone who presents with unexplained hypokalemia and metabolic alkalosis with a normal or low blood pressure. This condition mimics Gitelman syndrome except that urine diuretic screen will be positive. High urine chloride variability suggests the possibility of diuretic usage whereas urine chloride persistently greater than 25 meq/L suggests Gitelman syndrome. The diagnosis is usually made with a careful history, physical examination, measurement of the urine chloride concentration, and a urine diuretic screen. Conclusion: In patients who present with unexplained hypokalemia, metabolic alkalosis, and an index of suspicion for surreptitious diuretic use should undergo a urine diuretic screen to provide the most cost-effective care