A 30-year-old Korean man with a history of gastritis and gastroesophageal reflux disease presented to his primary care physician’s office with exertional chest pain relieved by rest. Because of his underlying gastrointestinal problems, young age, and lack of cardiac risk factors, his physician prescribed pantoprazole, obtained a complete blood count (CBC), and scheduled him for a treadmill stress test later that week. The next day, when the CBC revealed a platelet count of 2,800,000/uL (normal range 150–450,000/uL) the patient was instructed to go to the emergency department. He reported chest pain at rest, but this resolved after 2 sessions of emergent platelet pheresis and treatment with aspirin and nitroglycerin. Cardiac enzyme levels and electrocardiographic findings were normal. Peripheral smear showed numerous platelets, and bone marrow biopsy confirmed the diagnosis of essential thrombocytosis. After the initiation of anagrelide, a platelet-reducing agent, the patient’s platelet count dropped to 1,700,000/uL by the second hospital day. To avoid a positive stress test result attributable only to platelet sludging in the coronary arteries, the physician waited until the platelet count was below 600,000/uL to perform a stress test. When the test was performed, it yielded negative results for ischemia. At 8 months after diagnosis, the patient is asymptomatic and has a platelet count of about 300,000/uL.
DISCUSSION: In young patients, cardiac causes of chest pain can be found in about 16% of cases, noncardiac causes in 68%, and unknown causes in 16%. The common noncardiac causes include musculoskeletal problems (in 36% of cases), gastrointestinal problems (in 19%), psychological problems (in 8%), and pulmonary problems (in 5%). The noncardiac causes that are most serious and require immediate treatment are pulmonary embolus, pneumothorax, and aortic dissection. A thorough history and physical examination and focused laboratory studies usually exclude life-threatening causes of cardiac chest pain. Although the patient in this case was young, his chest pain was typical for angina, so further investigation was initiated. Investigation uncovered essential thrombocytosis, an unusual cause of angina.
A CASE OF WIDE ANION GAP NON-ACIDOSIS. E. Cichowski1; H. Sakowski1; H. Hashish1; R. Baltaro1. 1Creighton University, Omaha, NE. (Tracking ID #117266)
LEARNING OBJECTIVES: 1) Recognize laboratory error in the measurement of serum bicarbonate. 2) Utilize the Henderson-Hasselbach equation to indentify blood gas analysis errors. 3) Identify a previously unrecognized interfering substances as potential causes of laboratory errors.
CASE: A 72 year-old male was admitted for respiratory distress and confusion, and found to have a right upper lobe lung mass and hypercalcemia. He was intubated on the second hospital day due to worsening of his respiratory status. Propofol was initiated for sedation and methylprednisolone and levofloxacin were given for a presumed post-obstructive pneumonia. His initial arterial blood gas after intubation showed a pH 7.38 pCO2 38 pO2 143 on an Fio2 of .60. His measured HCO3 was 26 meq/l. Over the next 4 days, his measured bicarbonate progressively dropped to 8 meq/l despite no change in his arterial blood gas (pH 7.38 pCO2 36 pO2 103 on an FiO2 of .45). His anion gap was calculated at 19. Serum lactate was normal, and serum ketones were absent. Consultation with the pathology department revealed the patient’s serum to be grossly lipemic. A review of the chart revealed the patient did receive lipid infusions with TPN 36 and 18 hours prior to this discovery. A lipid panel was obtained and revealed marked hypertriglyceridemia at 4,426 mg/dl. The lipid infusions were discontinued, and the propofol was weaned off. The bicarbonate level dropped to a low of 3 meq/l approximately 7 hours after the medication was discontinued. Four hours later, the bicarbonate had corrected to 21 meq/l. The serum, however, remained grossly lipemic. The patient’s condition continued to decline with the development of septic shock, multi-organ failure and ventricular arrythmias. Results of a previous bronchoscopy demonstrated small cell carcinoma. The patient’s family requested no further aggressive treatment and he expired later that day.
DISCUSSION: This patient developed marked derangement in his measured bicarbonate levels that did not correspond to his arterial blood gas analysis (according to the Henderson-Hasselbach equation). A laboratory error was hypothesized as the cause. Due to the finding of lipemic serum, the hypertriglyceridemia was initially suspected as the interfering substance. Upon discontinuing the propofol, the serum bicarbonate level normalized, the serum, however remained lipemic. In a review of the literature, neither propofol nor hypertriglyceridemia have been reported as potential causes of this lab error. Further testing is needed to determine the role of propafol as an interfering substance in bicarbonate laboratory analysis.
A CASE REPORT OF OXYGEN EMBOLISM FOLLOWING HYDROGEN PEROXIDE INGESTION.D. Misra1; B. Legere1. 1New Hanover Regional Medical Center, Wilmington, NC. (Tracking ID #116225)
LEARNING OBJECTIVES: Recognize that ingestion of concentrated solution of hydrogen peroxide can result in significant morbidity and mortality owing to venous or arterial oxygen embolization. We intend to share our experience through a case report to emphasize this fact .
CASE: We present the case of an 82 yr old caucasian female with prior history of emphysema who had inadvertently ingested a large quantity of concentrated hydrogen peroxide solution. Following this, she vomited and developed resiratory distress which required intubation and mechanical ventilation. On examination, she was sedated, tachycardic and had hemoccult positive stool. Blood work revealed elevated white cell count and a low hematocrit. Her basic metabolic panel, urine drug screen, liver function tests were within normal limits. Chest xray showed emphysema. CT scan of abdomen/pelvis was significant for portal venous gas and pneumatosis involving duodenal and jejunal wall. Upper endoscopy revealed hemorrhagic gastritis and distal esophagitis. She was started on empiric antibiotics and followed with serial abdominal radiographs. CT scan of the abdomen obtained five days later revealed no free air or pneumatosis. On the sixth day of hospitalization, patient was extubated and at that point of time was noted to have right sided hemiparesis. MRI scan of the brain revealed multiple areas of acute/subacute non-hemorrhagic infarction. Patient was evaluated by a neurologist and it was felt that her neurologic deficits were a result of oxygen embolization. Patient gradually improved with physical and occupational therapy and currently awaits discharge to a rehabilitation facility.
DISCUSSION: Hydrogen peroxide is widely used as an oxidant/disinfectant. It is sold in health food stores also as means of “improving oxygenation” in people with coronary artery disease. Literature search revealed several cases of accidental hydrogen peroxide ingestion. A retrospective review of all exposures reported to a poison control center revealed that 0.34% were hydrogen peroxide related. Although exposure to diluted (3%) hydogen peroxide is benign, ingestion of the concentrated form can be dangerous. Following ingestion, hydrogen peroxide breaks up into water and oxygen in the presence of catalase. When the amount of oxygen produced exceeds the maximum blood solubility, embolization occurs. We emphasize that physicians should be alert to the possibilty of multiorgan embolization in patients presenting with accidental ingestion of concentated hydrogen peroxide.
A CASE REPORT OF RECURRENT COCCIDIOIDES MENINGITIS (CM).S.M. Maiorano1; P. Radhakrishnan2. 1St. Joseph’s Medical Center, Phoenix, Phoenix, AZ; 2Catholic Healthcare West, Phoenix, AZ. (Tracking ID #117418)
LEARNING OBJECTIVES: 1. Recognize that CM recurrence can occur despite prolonged antifungal treatment. 2. Recognize that indwelling CFS shunt can mask the hallmark symptoms of hydrocephalus associated with CM. 3. Recognize that diagnosis of CM can be made on serum serologies without positive CSF cultures.
CASE: A 62 year old male, presented with a 2 month history of worsening diplopia, ataxia and headache. Past History-CM with obstructive hydrocephalus and VP shunt. He was treated with Amphotericin B (intrathecal and systemic) for 2 years followed by Fluconazole for 8 years. He had been off Fluconazole for the last 5 years. Physical exam—He was somnolent, but arousable. Eyes-limited upward movement with downbeating nystagmus, disconjugate gaze with mild right lateral ocular deviation. Lab. data-CT head—mild right encephalomalcia, enlargement of 3rd and 4th ventricles, catheter in the right lateral ventricle. CSF-(from the shunt and a lumber puncture)-including Gram stain-negative. Positive CSF Coccidioides IgG and serum IGG,IGM antibodies. Complement fixation (CF) titer 1:64. Catheter tip-Coagulase negative Staphylococcus. MRI of the head—ventriculomegaly, increased periventricular and meningeal enhancement. He was diagnosed with recurrent CM, shunt failure due to presumed Staphyloccal infection. He was started on Voriconazole and Vancomycin. The shunt was replaced. He improved with resolution of his neurological symptoms and signs. He was discharged with the plan to continue the Voriconazole indefinitely.
DISCUSSION: CM is a grave form of disseminated Coccidiodes infection. Of the nearly 100,000 cases per year, only 0.1 percent present as meningitis. This case has several interesting aspects, the first being the recurrence of the CM after several years. Recurrences usually occur shortly after discontinuing therapy, as despite adequate antifungal penetration the fungus is not easily cleared. In this case, the patient remained symptom free for 5 years after stopping therapy. Second, the temporal association of shunt blockage and recurrence of symptoms of CM made us postulate that the patient remained symptom free due to the drainage of CSF and clearance of the fungus. Little data is available as to the incidence or common etiologies of shunt failure, but many case reports have found bacterial shunt obstruction through colonization as well as fungal biofilm occlusion. Third, the diagnosis of CM recurrence was made based on the CSFand serum studies. As CSF cultures are positive in only one third of cases, positive CSF IgG or IgM and CF antibodies are very helpful in diagnosing CM in patients with a high pre-test probability and negative cultures. While there are definitive guidelines for the duration of treatment of CM, patients who experience a relapse should be continued lifelong therapy.
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