2002 Clinical Vignette Abstract Winners
First Place
Trim the Fat...STAT!, Maya K. Johnston, MD, R3, Des Moines Internal Medicine Residency Program, Nathan Josephson, MD, Mentor
Case: J.P. is a 65 year-old female with a h/o giant cell arteritis diagnosed eight months prior by temporal artery biopsy. Whenever her steroid dosage was tapered to 15mg daily, she developed severe symptoms of polymyalgia rheumatica with an increase in her sedimentation rate. In an attempt to lower her prednisone below 15mg daily, mycophenolate mofetil was begun. One month later, she presented urgently to her rheumatologist with a complaint of excruciating low back pain and inability to get up from a wheelchair without severe pain. She was admitted to the hospital, at which time prednisone dose was 10mg/day.
Exam: revealed obesity without overt features of Cushing's. She was afebrile. There was no hip or shoulder girdle discomfort, with full range of motion. She had no tenderness to palpation over the spine. She had a positive straight leg raise on the left, and slight weakness was noted in her tibialis anterior and extensor hallucis longus function. No hypoesthesia was noted. Ankle reflexes were 1+ Labs revealed an ESR 18 and CRP 0.7. An MRI was obtained that revealed lumbar spinal stenosis with evidence of lumbar spinal epidural lipomatosis.
During the next 48hrs, J.P.'s lower extremity weakness increased, and she developed urinary retention and noted some incontinence. Because of the progressive nature of her symptoms, she underwent L2-L5 lumbar spinal laminectomy with complete resolution of her pain and neurologic symptoms.
Discussion: Spinal epidural lipomatosis is a recognized but rare complication of chronic steroid treatment. Normal adipose tissue in the spinal canal hypertrophies, causing compression of the spinal cord with resultant pain and, rarely, symptomatic neurologic disease. The hypertrophied epidural fat is usually found in the thoracic and lumbar spinal areas. While it was originally described in patients on high-dose steroids, spinal epidural lipomatosis has also been reported in patients with endogenous Cushing's syndrome and patients with morbid obesity. Diagnosis is made by MRI. Treatment usually consists of surgical decompression and fat debulking, although some patients have also been shown to improve with weight loss and reduction of steroid dosage. Recovery is usually complete.
Conclusion: Spinal epidural lipmatosis should be considered in the differential diagnosis of any patient presenting with back pain and radicular symptoms who is obese or taking corticosteroids.
Second Place
Not Just a Simple UTI, Kelly J. Martens, MD, R3, Des Moines Internal Medicine Residency Program, Daniel P. Allen, MD, Mentor
Case: 65 yo healthy WM referred from LMD for UTI and anemia. Upon admission he described three months of dry cough with intermittent dysuria and mild R flank pain. A month after symptom onset he had progressive fatigue, DOE, and skin yellowing. Pt denied chills, night sweats, or weight loss but had low grade fevers X 4 days prior to presentation. No unusual travels or exposures. Recent h/o numerous cuts and abrasions on his hands from working on a trailer.
PE: Afeb, HR 102, 02 sat 98% RA. Exam was remarkable for scleral icterus, conjunctival pallor, pale MM, moderate jaundice. No LAD, petechiae or skin/nail lesions. Lungs clear, heart RRR w/o murmurs. Abd soft with no hepatosplenomegaly.
Lab: WBC 8.5 (nl diff), Hgb 5.9, MCV 83, plt 244, retic 4.0, basic chemistry wnl, Tbili 3.4, LDH 363, AST/AL wnl. UA neg protein, 4-10 rbc, 11-25 wbc. Coags wnl, fibrinogen 648, FDP>20 (<5), haptoglobin <20 (30-200), direct coomb's +, IgG +, C3 +, cold agglutinins (-), ESR 94, ANA (-). Peripheral smear normochromic normocytic anemia. Blood cx were neg however pt had been on abx from LMD. CXR was unremarkable, bone marrow biopsy with normoblastic erythroid hyperplasia. Urine cx obtained locally grew MSSA. Abd CT showed 5cm R perinephiric abscess and multiple splenic infarcts. Purulent material drained from the abscess also grew MSSA. A TEE discovered a 1.8 cm mitral valve vegetation. Head CT was unremarkable.
Discussion: Normochromic normocytic anemia is a common association with infective endocarditis and is shown to be related to hypersplenism and hypertrophy of the reticuloendothelial system. However, intravascular hemolytic anemia has only been documented in case reports. In all cases, hemolysis was temporally related to the onset of endocarditis and improved with antibiotic administration. In two cases, the hemolysis did not fully resolve until the vegetations were surgically removed. The etiology is thought to be twofold: intravascular fragmentation related to sheer stress produced by large vegetations, and/or production of IgG to RBC antigens. Our patient likely seeded his bloodstream via the numerous cuts on his hands, leading to development of his mitral valve vegetation, perinephric abscess, and splenic infarcts. He had no peripheral stigmata of endocarditis, which is not unusual with Staph aureaus. In fact, it wasn't until the hemolysis created significant dyspnea that the patient sought medical care. His case remained a puzzle until the urine culture growing MSSA prompted further testing and subsequent diagnosis of endocarditis.
Conclusion: Diseases can present insidiously and unusually. It is important to keep searching for answers if the clinical clues do not effectively explain the whole picture.
Third Place
Castleman's Disease: A Rare Manifestation of Lymphadenopathy, Mark C. Erickson, MD, R3, Des Moines Internal Medicine Residency Program, Roscoe F. Morton, MD, Mentor
Case: A 65-year-old white male presented with approximately 5 weeks of fever up to 100.6, occasional rigors, fatigue, night sweats, dyspnea, orthopnea, lower extremity edema, and anorexia. He was recently hospitalized with what was felt to be a UTI, for which he was treated with levofloxacin; however, this did not relieve his symptoms. A series of 3 sets of blood cultures begun 2 days prior to admission revealed gram-negative rods, at which time he was admitted. Past history is significant for SLE, which presented 16 years ago with interstitial pneumonitis, pericarditis, and polyneuropathy. Three years ago he was admitted for seizure and was found to have bilateral subdural hematomas and quinine-induced thrombocytopenia; he subsequently underwent bilateral craniotomies, as well as ventriculoperitoneal shunt placement for obstructive hydrocephalus. New onset of seizure d/o was treated with phenytoin.
Physical Exam: Findings were significant for the patient being afebrile at admission, with a recent weight gain of 14 pounds. He had a left-sided ptosis, inspiratory crackles and scattered expiratory wheezes, and a grade II diastolic murmur of aortic regurgitation without gallop. No hepatosplenomegaly or other abdominal masses were noted. Two to three palpable, mobile lymph nodes measuring 1-1.5 cm were noted in the anterior axilla bilaterally, right greater than left, as well as a right inguinal node measuring 1.5-2 cm, which was slightly tender but mobile, and some small left inguinal nodes. Lower extremities had 2+ pitting edema.
Labs: WBC 7.6, Hgb 9.6, BUN 23, Cr 0.8, Alb 3.1, TSH 2.33, ESR 96, normal UA. One of ten blood cultures revealed Ochrobacterium anthropi. CXR showed mild vascular congestion. CT of abdomen and pelvis indicated prominent lymph nodes in the presacral and iliac chains, as well as the right femoral region. EKG was normal TEE revealed moderate AR, normal LV size and conractility, and no evidence of vegetation or abscess. Right inguinal and axillary biopsy results indicated the hyaline-vascular variant of Castleman's disease.
Discussion: Castleman's disease (angiofollicular lymph node hyperplasia) is just one of many presentations of lymphadenopathy. The differential diagnosis of lymphadenopathey is extensive, and the condition can be the result of either infiltrative or proliferative processes. The diagnostic approach is based on a thorough history and physical examination.
Conclusion: A deliberate step-by-step approach starting with the history and physical exam can eliminate many unnecessary labs and procedures that could result in potential complications and added expenses for the patient.
Third Place
Cutaneous Manifestation of A Systemic Illness: Pyoderma Gangrenosum and Wegener's Granulomatosis, Preethi Srikanthan, MD, R3, University of Iowa Internal Medicine Residency Program, Peter J. Kaboli, MD, Mentor
Background: Wegener's Granulomatosis is a systemic vasculitis that in its classic form involves upper and lower respiratory tracts and the kidney. A "limited" form occurs in one fourth of cases and has no apparent renal involvement at presentation
Case: We report on the case of a previously healthy 69 year-old male with a 3-month history of weight loss, night sweats, and a non-healing right pretibial ulcer. The ulcer was 5 by 10 cm with central necrosis and had a foul smelling green-brown exudate and a fleshy, heaped-up border. This was treated as a venous stasis ulcer. Due to lack of improvement with local wound treatment, he was referred to plastic surgery clinic. Their assessment was that this was a brown recluse spider bite. However, a medicine consult was obtained due to his systemic symptoms. A thorough history and physical suggested this was the cutaneous presentation of a systemic disease. A chest x-ray revealed a cavitary lesion in the left upper lobe. Other lab evaluations included an increased ESR, leukocytosis, and a c-ANCA of 1:160. Lung biopsy showed chronic inflammation with multinucleated giant cells. Re-biopsy of the pretibial ulcer showed areas of leukocytoclastic vasculitis. The pathology and gross appearance were consistent with pyoderma gagrenosum. No renal involvement was present. Cyclophosphamide (125mg/day) and prednisone (70 mg/day) were commenced and 6 months hence, the patient is free from any signs of disease.
Discussion: According to the literature, the frequency of cutaneous lesions in Wegener's Granulomatosis ranges from 16 to 46% and are the presenting feature in only 6% of patients. Pyoderma gangrenosum is the classic cutaneous manifestation. Our case demonstrates an atypical presentation of this condition, which upon correct diagnosis and treatment yielded a positive therapeutic outcome. Also, systemic illnesses often present with cutaneous manifestations requiring strong physical diagnosis skills.
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