Hyperparathyroidism Presenting as Acute Pancreatitis: Case Report of Mortality

Background: Acute pancreatitis may be caused by a myriad of factors, hypercalcemia secondary to hyperparathyroidism, albeit is a rare cause of acute pancreatitis but not unheard of. If the underlying cause of acute pancreatitis is diagnosed, goal-directed management becomes possible, reducing morbidity and mortality. Though acute pancreatitis on its own presents significant mortality, hypercalcemia, especially detected late, augments this. Case Report: We report a case of acute pancreatitis secondary to hyperparathyroidism. The patient was undiagnosed at the time of admission and presented with non-specific gastrointestinal symptoms. After admission, he developed multi-organ dysfunction and was managed by intensive care. The patient died within hours of admission despite our best efforts. Diagnosis of acute pancreatitis secondary to hyperparathyroidism was suspected on the basis of hypercalcemia, confirmed by a posthumous result of a raised parathyroid hormone assay. Conclusion: When a patient is admitted in the emergency department with a suspicion of acute pancreatitis, serum calcium levels and its reporting should be expedited to as early as possible. Hypercalcemia in the setting of acute pancreatitis merits a multidisciplinary approach and expedited parathyroid hormone levels sent with a high suspicion of long standing untreated hyperparathyroidism. Hyperparathyroidism is a cause of silent hypercalcemia and can be lethal if not diagnosed in time

MECHANISMS OF DISEASE Acute Oxygen-Sensing Mechanisms

JOSEPH PRIESTLEY, ONE OF THE THREE SCIENTISTS CREDITED WITH THE discovery of oxygen, described the death of mice that were deprived of oxygen. However, he was also well aware of the toxicity of too much oxygen, stating, “For as a candle burns much faster in dephlogisticated [oxygen enriched] than in common air, so we might live out too fast, and the animal powers be too soon exhausted in this pure kind of air. A moralist, at least, may say, that the air which nature has provided for us is as good as we deserve.”1 In this review we examine the remarkable mechanisms by which different organs detect and respond to acute changes in oxygen tension. Specialized tissues that sense the local oxygen tension include glomus cells of the carotid body, neuroepithelial bodies in the lungs, chromaffin cells of the fetal adrenal medulla, and smooth-muscle cells of the resistance pulmonary arteries, fetoplacental arteries, systemic arteries, and the ductus arteriosus. Together, they constitute a specialized homeostatic oxygen-sensing system. Although all tissues are sensitive to severe hypoxia, these specialized tissues respond rapidly to moderate changes in oxygen tension within the physiologic range (roughly 40 to 100 mm Hg in an adult and 20 to 40 mm Hg in a fetus)Junta de Andalucí

Downsizing of acute inpatient beds associated with private finance initiative: Scotland's case study

OBJECTIVES: To evaluate whether the projected 24% reduction in acute bed numbers in Lothian hospitals, which formed part of the private finance initiative (PFI) plans for the replacement Royal Infirmary of Edinburgh, is being compensated for by improvements in efficiency and greater use of community facilities, and to ascertain whether there is an independent PFI effect by comparing clinical activity and performance in acute specialties in Lothian hospitals with other NHS hospitals in Scotland. DESIGN: Comparison of projected and actual trends in acute bed capacity and inpatient and day case admissions in the first five years (1995-6 to 2000-1) of Lothian Health Board's integrated healthcare plan. Population study of trends in bed rate, hospital activity, length of stay, and throughput in Lothian hospitals compared with the rest of Scotland from 1990-1 to 2000-1. MAIN OUTCOME MEASURES: Staffed bed rates, admission rates, mean lengths of stay, occupancy, and throughput in four adult acute specialty groups in 1990-1, 1995-6, and 2000-1. RESULTS: By 2000-1, rates for inpatient admission in all acute, medical, surgical, and intensive therapy specialties in Lothian hospitals were respectively 20%, 6%, 28%, and 38% below those in the rest of Scotland. Day case rates in all acute and acute surgical specialties were 13% and 33% lower. The proportion of delayed discharges in staffed acute and post-acute NHS beds in Lothian hospitals exceeded the Scottish average (15% and 12% respectively; P<0.001). CONCLUSION: The planning targets and increase in clinical activity in acute specialties in Lothian hospitals associated with PFI had not been achieved by 2000-1. The effect on clinical activity has been a steeper decline in the number of acute beds and rates of admission in Lothian hospitals compared with the rest of Scotland between 1995-6 and 2000-1

Does Foot Massage Relieve Acute Postoperative Pain? a Literature Review

Purpose: This study aimed to examine the current state of knowledge regarding foot massageto determine if foot massage has an effect on relieving acute postoperative pain.Method: The following questions were used to guide this review: How does pain occur?What is the pain management modalities used in relieving acute postoperative pain? Does footmassage relieve acute postoperative pain? A comprehensive systematic search of publishedliterature and journal articles from Science Direct, CINAHL, PubMed, ProQuest and fromrelevant textbooks was conducted. The universal case entry website, Google-scholar was usedas well. The following keywords were used: foot massage, pain management, andpostoperative pain. Eight studies on foot massage and more than thirty related articles werereviewed.Result: Postoperative pain is caused by tissue damage that induces release of chemicalmediators from the surgical wound. The four processes of pain are transduction, transmission,perception and modulation. Pain medication is the goal standard for acute postoperative painrelief. In addition, foot massage is a modality that can be used in relieving acute postoperativepain. Massage stimulates large nerve fibers and dermatome layers which contain tactile andpressure receptors. The receptors subsequently transmit the nerve impulse to the centralnervous system. The gate control system in the dorsal horn is activated through the inhibitoryinterneuron, thus closing the gate. Subsequently, the brain does not receive the pain message.Eight reviewed studies demonstrated that foot massage relieves acute postoperative pain.However, there were some methodological limitations of these studies.Conclusion: It is recommended to examine the effect of foot massage on acute postoperativepain with high homogenous samples using various duration of massage and range of time forpain measurement at different settings

Pancreatitis following Olanzapine Therapy: A Report of Three Cases

CONTEXT: Atypical antipsychotic agents (clozapine, olanzapine) have been linked to metabolic effects and acute pancreatitis. CASE REPORT: We reviewed the inpatient and outpatient records of three patients who developed acute pancreatitis while being treated with olanzapine. The mean age of the patients was 37.7 years (range 18–54 years, 2 female, 1 male). No alternative cause of acute pancreatitis was found in two of the three patients. In the remaining patient, olanzapine may have contributed to acute pancreatitis in the setting of hypertriglyceridemia. Olanzapine was discontinued in all instances. Over a mean follow-up of 14 months, one patient has had a relapsing course, but the remaining two patients have been symptom free without recurrence of acute pancreatitis. CONCLUSIONS: Our case series adds further support to the potential link between olanzapine use and acute pancreatitis. Close monitoring of metabolic parameters is suggested in patients treated with olanzapine. Alternative antipsychotic agents should be considered in patients at high risk for pancreatitis

Antioxidant status in acute stroke patients and patients at stroke risk

Background and Purpose: Antioxidant enzymes like copper/ zinc superoxide dismutase (SOD), catalase and gluthatione peroxidase (GSHPx) are part of intracellular protection mechanisms to overcome oxidative stress and are known to be activated in vascular diseases and acute stroke. We investigated the differences of antioxidant capacity in acute stroke and stroke risk patients to elucidate whether the differences are a result of chronic low availability in arteriosclerosis and stroke risk or due to changes during acute infarction. Methods: Antioxidant enzymes were examined in 11 patients within the first hours and days after acute ischemic stroke and compared to risk- and age-matched patients with a history of stroke in the past 12 months ( n = 17). Antioxidant profile was determined by measurement of glutathione (GSH), malondialdehyde (MDA), SOD, GSHPx and minerals known to be involved in antioxidant enzyme activation like selenium, iron, copper and zinc. Results: In comparison to stroke risk patients, patients with acute ischemic stroke had significant changes of the GSH system during the first hours and days after the event: GSH was significantly elevated in the first hours (p < 0.01) and GSHPx was elevated 1 day after the acute stroke (p < 0.05). Selenium, a cofactor of GSHPx, was decreased (p < 0.01). GSHPx levels were negatively correlated with National Institutes of Health Stroke Scale (NIHSS) scores on admission (r = - 0.84, p < 0.001) and NIHSS scores after 7 days ( r = - 0.63, p < 0.05). MDA levels showed a trend for elevation in the first 6 h after the acute stroke ( p = 0.07). No significant differences of SOD, iron, copper nor zinc levels could be identified. Conclusions: Differences of antioxidant capacity were found for the GSH system with elevation of GSH and GSHPx after acute stroke, but not for other markers. The findings support the hypothesis that changes of antioxidant capacity are part of acute adaptive mechanisms during acute stroke. Copyright (C) 2004 S. Karger AG, Basel

Prevalence and time course of post-stroke pain: A multicenter prospective hospital-based study

OBJECTIVE: Pain prevalence data for patients at various stages after stroke. DESIGN: Repeated cross-sectional, observational epidemiological study. SETTING: Hospital-based multicenter study. SUBJECTS: Four hundred forty-three prospectively enrolled stroke survivors. METHODS: All patients underwent bedside clinical examination. The different types of post-stroke pain (central post-stroke pain, musculoskeletal pains, shoulder pain, spasticity-related pain, and headache) were diagnosed with widely accepted criteria during the acute, subacute, and chronic stroke stages. Differences among the three stages were analyzed with χ(2)-tests. RESULTS: The mean overall prevalence of pain was 29.56% (14.06% in the acute, 42.73% in the subacute, and 31.90% in the chronic post-stroke stage). Time course differed significantly according to the various pain types (P < 0.001). The prevalence of musculoskeletal and shoulder pain was higher in the subacute and chronic than in the acute stages after stroke; the prevalence of spasticity-related pain peaked in the chronic stage. Conversely, headache manifested in the acute post-stroke stage. The prevalence of central post-stroke pain was higher in the subacute and chronic than in the acute post-stroke stage. Fewer than 25% of the patients with central post-stroke pain received drug treatment. CONCLUSIONS: Pain after stroke is more frequent in the subacute and chronic phase than in the acute phase, but it is still largely undertreated