NOT ALL VOMITING IN PREGNANCY IS HYPEREMESIS. S. Vora 1 , R.O. Powrie 1 ; 1 Brown University School of Medicine, Providence, RI LEARNING OBJECTIVES: 1. Recognize the differential diagnosis of hyperemesis gravidarum and illustrate the role of a general internist in diagnosis and management of medical illness in pregnancy. 2. Demonstrate the clinical presentation of mesenteric thrombosis. 3. Emphasize the fact the pregnancy is a hypercoaguable state and briefly outline the management of thrombosis in pregnancy. CASE INFORMATION: A 37 year-old primigravid Nigerian woman presented in her 19th week of an IVF pregnancy to the emergency room with complaints of two days of fever and constipation and three weeks of malaise, anorexia, and vomiting. She had been treated in the ER on three prior occasions with hydration and antiemetics for hyperemesis gravidarum. On this last presentation, she produced her photograph from one month prior to demonstrate the extent to which her appearance had deteriorated. Her past medical history was significant for only childhood malaria and sickle cell trait. She had not suffered from protracted nausea and vomiting of pregnancy during the first trimester. She was taking only prochlorperazine suppositories at the time of presentation. She had no personal history of smoking, alcohol or recreational drug use. Her examination was significant for a temperature of 101.6 F, a heart rate of 114 per minute, respiratory rate of 12 per minute, and BP 103/60. She was mildly jaundiced with sunken orbits. Her cardiopulmonary examination was normal. Her abdomen was markedly tender in the right upper quadrant with voluntary guarding but no rebound. No fluid wave was present and her rectal examination was normal. Her uterus was gravid and nontender to palpation. Her fetal heart tracing was reassuring. Neurologic examination was unremarkable. Her laboratory examination was remarkable for a leukocytosis of 36.6 with a left shift. Her chemistries revealed a hypochloremic metabolic alkalosis with a serum bicarbonate of 34 mEq/ L. She had a mild elevation of her serum AST to 40 U/L. The remainder of the laboratory data was unrevealing. A malarial blood smear was negative. An abdominal ultrasound revealed absent portal venous flow, but was otherwise normal. A subsequent CT scan of the abdomen demonstrated thrombosis of the portal vein and superior and inferior mesenteric venous branches. The patient was admitted, treated with intravenous unfractionated heparin, gentamycin and piperacillin and achieved significant improvement in pain. She defervesced by the second hospital day. Her liver enzymes normalized. Her hypercoaguable work-up revealed only a relative protein S deficiency. Once therapeutic on intravenous heparin, she was changed to low molecular weight heparin, which she continued until 36 weeks gestation. At that time her therapy was changed to adjusted dose subcutaneous unfractionated heparin until her uncomplicated cesarean delivery of a healthy 2475 g girl. DISCUSSION: Nausea and vomiting occurs frequently during pregnancy, especially during the first 20 weeks, afflicting 70-90% of all pregnant women. Causes can be physiologic, due to progesterone effects on the lower esophageal and pyloric sphincters, or due to mechanical compression of the diaphragm on the enlarging uterus. However pregnant women are also subject to all other causes of nausea and vomiting, such as severe gastroenteritis, cholecystitis, pyelonephritis, hyperthyroidism, primary hyperparathyroidism, liver dysfunction, and rarely, small bowel obstruction, mesenteric thrombosis or mesenteric ischemia. Internists can be instrumental in assisting in these less common medical diagnoses during pregnancy. Portal and mesenteric venous thromboses are rare conditions, even in nonpregnant patients. Most patients present with at least two weeks of abdominal pain, anorexia, vomiting, and change in bowel habits. Many patients are also febrile. In 20% ndash;40% of cases of mesenteric thrombosis no underlying cause can be found. Other investigated cases of mesenteric thrombosis during pregnancy have revealed inherited thrombophilias such as activated protein C resistance, antithrombin III deficiency, and protein C and S deficiency. The latter is a difficult diagnosis in the face of both active thrombosis and in pregnancy, since protein S normally decreases in both of these settings. The treatment of acute thrombosis involves heparin (either low molecular weight or unfractionated), as warfarin is contraindicated in pregnancy. Special care is required in the management of anticoagulation in the peripartum period. Recognize the importance of ductography and fiberoptic ductoscopy, the later being a new technology for nipple discharge. CASE INFORMATION: A 45-year-old woman presented with a 1 day history of a spontaneous amber right nipple discharge. Breast examination revealed fibrocystic changes. A small amount of clear, non bloody fluid could be expressed from one of the right breast ducts. There was no palpable lymphadenopathy. A mammogram revealed fibroglandular densities. Ultrasound (US) of the right breast showed slightly dilated ducts. Ductography was performed as follows: by applying focal pressure a single draining orifice was identified, cannulated and 0.2 cc of Conray 60 were injected. Post-mammographic images showed the presence of a cystically dilated duct that contained a small 3 ± 4 mm intraluminal filling defect, which now could also be visualized by repeat US examination. Multiple core biopsies were obtained under US guidance using a vacuum assisted biopsy (bx) needle. A small clip was deployed in the bx cavity following the procedure. Histology revealed high grade ductal carcinoma in situ (DCIS). The patient was seen in surgical consultation and underwent an attempted wide local excision, which revealed extensive DCIS, 5 cm in greatest extent. There were multiple microscopic foci of invasive cancer. The surgical resection margins were positive for DCIS after multiple re-excisions. After thorough discussion the patient elected to undergo bilateral mastectomies. Two sentinel lymph nodes (blue dye and lymphoscintigram) contained micrometastatic adenocarcinoma. The patient is presently undergoing adjuvant chemotherapy. DISCUSSION: This case exemplifies the importance of an extensive evaluation of a pathologic nipple discharge. While a bilateral, inducible nipple discharge involving multiple ducts is a physiologic finding in many women, patients presenting with a spontaneous, unilateral discharge (bloody or watery) confined to one duct need careful evaluation for an underlying neoplasm (papilloma, carcinoma). A small malignancy, which in our patient had already involved axillary nodes, can be easily missed on physical examination and mammogram. In this setting an US examination in the "trigger zone" may identify an occult lesion. Cytologic evaluation of the discharge or ductal lavage fluid may be helpful. An important diagnostic tool is ductography, as performed in our patient. With the recent introduction of fiberoptic ductoscopy direct, realtime intraductal images, allowing detection of lesions as small as 0.2 mm can be obtained offering a safe alternative to ductography in guiding subsequent breast surgery in the treatment of nipple discharge. (Shen K-W. Breast Cancer Research and Treatment, Vol. 64, No 1, Nov. 2000, p. 30) ACUTE METHEMOGLOBINEMIA SECONDARY TO TOPICAL BENZOCAINE SPRAY. J. Walker 1 , H. Houston 1 , S. Miller 1 , G. Rouan 1 ; 1 University of Cincinnati, Cincinnati, OH LEARNING OBJECTIVES: 1) Define the pathophysiology associated with methemoglobinemia, and 2) Recognize the clinical settings likely to be explained by methemoglobinemia. CASE INFORMATION: JT is an 82-year-old white female with a history of HTN, paroxysmal atrial tachycardia, and hypothyroidism who was admitted for elective laparoscopic left adrenalectomy, which proved to be a benign adenoma. Post-operative course was uncomplicated until POD #3 when the patient developed nausea and vomiting with a distended abdomen and decreased bowel sounds. A diagnosis of paralytic ileus was made and a nasogastric tube was placed, preceded by a 3 second dose of Hurricane spray (20% Benzocaine, approximately 600 ± 885 mg total dose) to the oropharynx. Within several minutes, the patient developed lethargy and confusion. The patient then became dyspneic, syncopal, and developed a cyanotic appearance. She did not respond to 100% O 2 by non-rebreather mask despite an arterial blood gas (ABG) with a PaO2of 310 and an O2saturation of 99.7%. A simultaneous pulse oximetry revealed an O2sat of 86%. The arterial blood was extremely dark in appearance. An ECG revealed supraventricular tachycardia with a rate of 170 ± 180 and ST depression, which converted after 6mg adenosine to sinus rhythm, with a rate of 120 and resolution of the ischemic changes. A diagnosis of methemoglobinemia was confirmed by co-oximetry, which revealed a methemoglobin level of 30.9% (normal = 0%). A 50 mg dose of methylene blue was administered, and over the course of 1 hour, the patient developed dramatic improvement in mental status and cyanosis. Methemoglobin levels decreased to 6.4%, 3.7% and 2.4% over the next 1, 3, and 6 hours, respectively. DISCUSSION: Methemoglobinemia is a condition in which iron in hemoglobin becomes oxidized (Fe 2+ to Fe 3+ ) at an overwhelming rate, resulting in a drastic decline in the oxygen carrying capacity of the RBC. Pharmacological agents, such as benzocaine, are capable of inducing methemoglobinemia by direct or indirect oxidation of the hemoglobin molecule. The ABG is not an accurate indicator of oxygenation status in a patient suffering from acute methemoglobinemia. The treatment of choice is methylene blue (1mg/kg, IVP). This case of benzocaine-induced methemoglobinemia is similar to others that have been reported in the past and indicates the need for a high index of suspicion for this syndrome and a need for close supervision of patients receiving benzocaine spray for clinical signs and symptoms of cyanosis. 1) Recognize the importance of the life narrative in the comprehensive understanding of the adolescent who presents with somatic distress and chronic fatigue. 2) Distinguish between diagnoses that denote a disease process (eg anemia) and those that are strongly influenced by cultural``memes'' (eg chronic fatigue syndrome). CASE INFORMATION: CASE 1: A 17 y/o white teenager developed increasing fatigue beginning at age 15. Other symptoms included daily fever spikes, visual changes, myalgias, and headaches. Her grades suffered greatly as a result of repeated absences from school, & she also had to quit her part-time job. At the age of 5, she witnessed her 3 y/o brother drown in their pool while her mother was in the house. Her parents subsequently divorced when she was 12, & she has a strained relationship with her alcoholic father. The patient received counseling after the drowning and at the time of the divorce. CASE 2: A 18 y/o high school senior was diagnosed with chronic fatigue syndrome (CFS) at the age of 13. She was unable to attend school fulltime because of sleep disturbance, diffuse pain, & disabling fatigue. Both her parents were alcoholic, and her dad was verbally & physically abusive. She served as a caretaker for her wheelchair-bound mother. At the age of 12 she was raped by her half-sister's 29 y/o boyfriend. At the age of 17 while being treated with an antidepressant for depression, her psychiatrist would not allow concurrent oral contraceptives & she became pregnant and had an abortion. DISCUSSION: Many hypotheses have been put forth to explain CFS, an illness in search of an etiology. Characterized by a variety of somatic symptoms, CFS often has an abrupt onset. We postulate that it may be a form of "post-traumatic stress disorder," particularly in young patients. Children with CFS have been reported to exhibit more psychological morbidity, such as anxiety and depression, than those with chronic disease, but these psychological categories are not necessarily helpful in patient management. We have found that the life narrative which will often include antecedent traumatic events serves to illuminate the unique personal issues of the adolescent with CFS. This approach can create a doctor-patient relationship that will engender trust and perhaps lead to better clinical outcomes. LEARNING OBJECTIVES: 1) Recognize Salmonella Hepatitis as a cause of acute hepatitis in a patient with typhoid fever. 2) Mortality rate is as high as 20% particularly with delayed treatment. The prognosis is good if treated early with specific antibiotic therapy. CASE INFORMATION: A 22 year old female ,immigrant from Bangladesh with no past medical history was admitted with complaints of fever, nausea ,vomiting and headache of one week duration. The patient had visited Bangladesh three weeks back. Prior to this presentation she had two visits to the ER in the same week and was diagnosed as viral syndrome. On admission now the patient was delirious and agitated .Her BP was 112/62; Pulse-70; Temperature-105 deg. Farenheit. Physical Examination -Right hypochondriac tenderness, no hepatosplenomegaly, no neck rigidity, no icterus, no skin rash. Lumbar puncture and CT Scan of head were normal. USG Abdomen was normal and HIDA Scan showed no uptake. There was a moderate elevation in the Transaminase level with AST/ALT of 294/205 respectively, LDH 579,Total bilirubin of 1.3 and direct-0.5.Albumin PT/APTT and Reticulocyte counts were normal. WBC count was 8300 with 10% band cells. Blood cultures later came positive for Salmonella Typhi sensitive to ceftriaxone. Hepatitis serology was negative for A,B and C.The patient was started on ceftriaxone .LFT's improved and patient was discharged home after 7 days in stable condition. DISCUSSION: Salmonella hepatitis is a rare condition and 20% of the patients with salmonella hepatitis may not be bacteremic. A diagnosis of salmonella hepatitis was made on the basis of 1)ALT/LDH < 4 (0.35 in this case).This happens to be the best discriminator between Salmonella hepatitis and viral hepatitis as is appreciated in this case.2) Positive blood culture for Salmonella.3) Relative bradycardia. 4) High-grade fever.5) Left shift of WBC and 6) Positive travel history to an endemic area. The prognosis is good if treated early with specific antibiotic therapy, however the clinical course can be severe with a mortality rate as high as 20% particularly with delayed treatment. the malar eminences, neck and trunk with bilateral axillary and submental lymphadenopathy. Neurological exam was normal and no joint deformity was noted. There was generalised abdominal tenderness with no guarding or organomegaly. Investigations revealed Hb-10.6 gm/dl and total WBC-3.4K/ul, BUN-23mg/dl, creatinine-0.9 mg/dl. Liver function tests showed albumin-2.3 g/dl, AST-54, ALT-26, GGT-53U/L, LDH-485 U/L. Serum amylase was 401 and serum lipase 358. Serum calcium was 8.9 with triglycerides of 187mg/dl. Urine analysis showed specific gravity of 1015 with 3+ proteinuria. CT scan of abdomen showed fullness of pancreatic head and ultrasound showed a normal sized CBD with no evidence of cholelithiasis. Biopsy of skin rash showed intravascular thrombi, vasculitis consistent with early lupus with atypical lymphocytic infiltrate. Diagnosis of SLE with acute pancreatitis was made on the the basis of above and ANA of 1:1280 with homogenous pattern and Anti ds DNA positivity. Patient was started on intravenous steroids. Patient's clinical status continued to worsen and required mechanical ventilation. Repeat CTscan confirmed pancreatitis with bilateral pleural effusions and no evidence of necrosis or abscess formation. She improved over the next few days and was successfully extubated. However, two weeks later she developed diffuse and severe abdominal pain accompanied with fever. Repeat CTscan now showed Grade E pancreatitis(multiple fluid collections +/À gas in or adjacent to pancreas)with necrosis. CT guided aspirations of necrotic material was negative for gram stain but culture grew pseudomonas, MRSA and candida. The patient had an exploratory laprotomy with necrotectomy. Despite aggressive antibiotic and antifungal treatment with multiple abdominal explorations the patient's condition deteriorated. She died of multiple organ failure. DISCUSSION: Acute pancreatitis is an uncommon manifestation of SLE. It is even rarer for such patients to present with pancreatitis as the sole major organ affected. The role of corticosteroids in such setting is controversial. Review of literature suggests that corticosteroids do not cause pancreatitis in patients with SLE and they should be used during episodes of pancreatitis if required. He also noted pruritic, non-tender skin lesions on his face and arms. He denied the use of any medications. Review of systems revealed a 10 lb. weight loss, blurry vision, nonproductive cough, hoarseness and mild dyspnea on exertion. He denied any HIV risk factors. Physical examination revealed widespread, small, hyperpigmented, nodular and papular lesions. A 3Â2 cm subcutaneous nodule was noted on the left side of the neck. Breath sounds were decreased bilaterally, with dullness to percussion on the left. The testicles were each twice normal size and tender with enlarged epididymi. Vital signs and the remaining exam were unremarkable. Scrotal ultrasound confirmed the physical exam and showed no discrete masses. Chest x-ray and CT revealed a moderate left pleural effusion with mediastinal and hilar adenopathy but no infiltrates. PFTs were consistent with a mild restrictive pattern. Serum ACE level was elevated at 87. Skin biopsies revealed non-caseating granulomas, negative for AFB or fungi. Follow-up scrotal ultrasound after corticosteroid therapy showed regression of testicular abnormalities. DISCUSSION: Sarcoidosis is a disease of unknown etiology, which can present with a wide variety of symptoms and involve virtually any organ system. In this unusual case, the patient presented for care due to testicular involvement but also had dermatologic and pulmonary manifestations, which he had ignored. While many cases of sarcoidosis spontaneously remit within 5 years and do not need treatment, therapy is indicated in patients such as this one, with symptomatic disease or systemic involvement. The goals of treatment include a reduction in symptoms and the avoidance of systemic complications. Despite attempts with steroid-sparing agents, the mainstay of treatment remains systemic corticosteroids. Monitoring with chest x-ray and PFT's is often warranted and patient education remains essential. SARCOIDOSIS AND STONES. K. White 1 , U. Mason 1 ; 1 Denver Health Medical Center, Denver, CO LEARNING OBJECTIVES: 1) Diagnose renal manifestations of sarcoidosis, and 2) Recognize the need for monitoring calcium levels and renal function in sarcoidosis. CASE INFORMATION: A 43-year-old man with a long history of cystic sarcoidosis presented with acute renal failure. He had chronic renal insufficiency with a baseline serum creatinine of 1.4 mg/dL. He had been treated with prednisone for several years and his dose had been tapered recently because his pulmonary status appeared stable. Review of systems ascertained a 10 ± 15 pound weight loss and decreased energy for 2-3 months. Physical examination was unrevealing. Laboratory data was significant for serum creatinine of 2.5 mg/ dL and calcium of 11.3 mg/dL. Renal ultrasound showed right hydronephrosis and bilateral nephrolithiasis. Computed tomography showed left staghorn calculus with caliectasis and right ureteropelvic junction stone with hydronephrosis, hydroureter and a more distal stone. A right percutaneous nephrostomy was placed and serum creatinine decreased to 1.8 mg/dL. Evaluation of the etiology of hypercalcemia included normal serum PTH, protein electrophoresis and PSA levels. Urinary calcium excretion was 252 mg/24 hours. The hypercalcemia was felt to be secondary to sarcoidosis and therefore the prednisone dose was increased. He underwent right nephrolithotomy, which was successful only for the proximal stone. Bilateral stone removal is planned for the future. Serum creatinine is back to baseline and serum calcium is normal. DISCUSSION: Hypercalcemia -an uncommon complication of sarcoidosis ± results from endogenous overproduction of 1,25 dihydroxyvitamin D. Nephrolithiasis is more common, occurring in about 10% of patients, and more frequently associated with hypercalciuria than with hypercalcemia. Nephrocalcinosis is much less common and is probably related to chronic hypercalcemia. This patient had both nephrocalcinosis and nephrolithiasis, likely due to both long-standing hypercalcemia and hypercalciuria leading to chronic and then acute renal failure. Long-term management of patients with sarcoidosis includes frequent monitoring of calcium levels and renal function.