Diagnosis and Treatment > Signs and Symptoms > Abdominal pain
You are looking at 1 - 10 of 49 items
Search for other papers by Tzy Harn Chua in
Google Scholar
PubMed
Search for other papers by Wann Jia Loh in
Google Scholar
PubMed
Summary
Severe hyponatremia and osmotic demyelination syndrome (ODS) are opposite ends of a spectrum of emergency disorders related to sodium concentrations. Management of severe hyponatremia is challenging because of the difficulty in balancing the risk of overcorrection leading to ODS as well as under-correction causing cerebral oedema, particularly in a patient with chronic hypocortisolism and hypothyroidism. We report a case of a patient with Noonan syndrome and untreated anterior hypopituitarism who presented with symptomatic hyponatremia and developed transient ODS.
Learning points:
-
Patients with severe anterior hypopituitarism with severe hyponatremia are susceptible to the rapid rise of sodium level with a small amount of fluid and hydrocortisone.
-
These patients with chronic anterior hypopituitarism are at high risk of developing ODS and therefore, care should be taken to avoid a rise of more than 4–6 mmol/L per day.
-
Early recognition and rescue desmopressin and i.v. dextrose 5% fluids to reduce serum sodium concentration may be helpful in treating acute ODS.
Search for other papers by Raku Son in
Google Scholar
PubMed
Search for other papers by Masahiko Nagahama in
Google Scholar
PubMed
Search for other papers by Fumiaki Tanemoto in
Google Scholar
PubMed
Search for other papers by Yugo Ito in
Google Scholar
PubMed
Search for other papers by Fumika Taki in
Google Scholar
PubMed
Search for other papers by Ryosuke Tsugitomi in
Google Scholar
PubMed
Search for other papers by Masaaki Nakayama in
Google Scholar
PubMed
Summary
The etiology of hyponatremia is assessed based on urine osmolality and sodium. We herein describe a 35-year-old Asian man with pulmonary tuberculosis and perforated duodenal ulcer who presented with hyponatremia with hourly fluctuating urine osmolality ranging from 100 to 600 mosmol/kg, which resembled urine osmolality observed in typical polydipsia and SIADH simultaneously. Further review revealed correlation of body temperature and urine osmolality. Since fever is a known non-osmotic stimulus of ADH secretion, we theorized that hyponatremia in this patient was due to transient ADH secretion due to fever. In our case, empiric exogenous glucocorticoid suppressed transient non-osmotic ADH secretion and urine osmolality showed highly variable concentrations. Transient ADH secretion-related hyponatremia may be underrecognized due to occasional empiric glucocorticoid administration in patients with critical illnesses. Repeatedly monitoring of urine chemistries and interpretation of urine chemistries with careful review of non-osmotic stimuli of ADH including fever is crucial in recognition of this etiology.
Learning points:
-
Hourly fluctuations in urine osmolality can be observed in patients with fever, which is a non-osmotic stimulant of ADH secretion.
-
Repeated monitoring of urine chemistries aids in the diagnosis of the etiology underlying hyponatremia, including fever, in patients with transient ADH secretion.
-
Glucocorticoid administration suppresses ADH secretion and improves hyponatremia even in the absence of adrenal insufficiency; the etiology of hyponatremia should be determined carefully in these patients.
Department of Endocrinology, University Hospital of Farhat Hached Sousse
Search for other papers by Taieb Ach in
Google Scholar
PubMed
Search for other papers by Perrine Wojewoda in
Google Scholar
PubMed
Search for other papers by Flora Toullet in
Google Scholar
PubMed
Search for other papers by Roxane Ducloux in
Google Scholar
PubMed
Search for other papers by Véronique Avérous in
Google Scholar
PubMed
Summary
Multiple endocrine metastases are a rare but possible complication of lung adenocarcinoma (LAC). Pituitary metastasis is a rare condition with poor clinical expression. Diabetes insipidus (DI) is its most common presenting symptom. Here we report an original case of a pituitary stalk (PS) metastasis from LAC presenting as central DI followed by adrenal insufficiency (AI) from bilateral adrenal metastasis, without known evidence of the primary malignancy. A 45-year-old woman whose first clinical manifestations were polyuria and polydipsia was admitted. She was completely asymptomatic with no cough, no weight loss or anorexia. Chest radiography was normal. Brain MRI showed a thick pituitary stalk (PS). DI was confirmed by water restriction test and treated with vasopressin with great clinical results. Explorations for systemic and infectious disease were negative. Few months later, an acute AI led to discovering bilateral adrenal mass on abdominal CT. A suspicious 2.3 cm apical lung nodule was found later. Histopathological adrenal biopsy revealed an LAC. The patient received systemic chemotherapy with hormonal replacement for endocrinological failures by both vasopressin and hydrocortisone. We present this rare case of metastatic PS thickness arising from LAC associated with bilateral adrenal metastasis. Screening of patients with DI and stalk thickness for lung and breast cancer must be considered. Multiple endocrine failures as a diagnostic motive of LAC is a rare but possible circumstance.
Learning points:
-
Adrenal metastasis is a common location in lung adenocarcinoma; however, metastatic involvement of the pituitary stalk remains a rare occurrence, especially as a leading presentation to diagnose lung cancer.
-
The posterior pituitary and the infundibulum are the preferential sites for metastases, as they receive direct arterial blood supply from hypophyseal arteries.
-
Patients diagnosed with diabetes insipidus due to pituitary stalk thickness should be considered as a metastasis, after exclusion of the classical systemic and infectious diseases.
-
The diagnosis of an endocrinological metastatic primary lung adenocarcinoma for patients without respiratory symptoms is often delayed due to a lack of correlation between endocrinological symptoms and lung cancer.
-
The main originality of our case is the concomitant diagnosis of both endocrinological failures, as it was initiated with a diabetes insipidus and followed by an acute adrenal insufficiency.
The University of Sydney, Faculty of Medicine and Health, Sydney, New South Wales, Australia
Search for other papers by Albert S Kim in
Google Scholar
PubMed
Search for other papers by Rashida Hakeem in
Google Scholar
PubMed
Search for other papers by Azaliya Abdullah in
Google Scholar
PubMed
Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth Hospital and Fiona Stanley Hospital Network, Perth, Western Australia, Australia
Search for other papers by Amanda J Hooper in
Google Scholar
PubMed
Department of Genetic Medicine, Westmead Hospital, Westmead, New South Wales, Australia
Search for other papers by Michel C Tchan in
Google Scholar
PubMed
Department of Maternal-Fetal Medicine, Westmead Institute for Maternal-Fetal Medicine, Westmead Hospital, Westmead, New South Wales, Australia
Search for other papers by Thushari I Alahakoon in
Google Scholar
PubMed
The University of Sydney, Faculty of Medicine and Health, Sydney, New South Wales, Australia
Department of Diabetes and Endocrinology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
Search for other papers by Christian M Girgis in
Google Scholar
PubMed
Summary
A 19-year-old female presented at 25-weeks gestation with pancreatitis. She was found to have significant hypertriglyceridaemia in context of an unconfirmed history of familial hypertriglyceridaemia. This was initially managed with fasting and insulin infusion and she was commenced on conventional interventions to lower triglycerides, including a fat-restricted diet, heparin, marine oil and gemfibrozil. Despite these measures, the triglyceride levels continued to increase as she progressed through the pregnancy, and it was postulated that she had an underlying lipoprotein lipase defect. Therefore, a multidisciplinary decision was made to commence therapeutic plasma exchange to prevent further episodes of pancreatitis. She underwent a total of 13 sessions of plasma exchange, and labour was induced at 37-weeks gestation in which a healthy female infant was delivered. There was a rapid and significant reduction in triglycerides in the 48 h post-delivery. Subsequent genetic testing of hypertriglyceridaemia genes revealed a missense mutation of the LPL gene. Fenofibrate and rosuvastatin was commenced to manage her hypertriglyceridaemia postpartum and the importance of preconception counselling for future pregnancies was discussed. Hormonal changes in pregnancy lead to an overall increase in plasma lipids to ensure adequate nutrient delivery to the fetus. These physiological changes become problematic, where a genetic abnormality in lipid metabolism exists and severe complications such as pancreatitis can arise. Available therapies for gestational hypertriglyceridaemia rely on augmentation of LPL activity. Where there is an underlying LPL defect, these therapies are ineffective and removal of triglyceride-rich lipoproteins via plasma exchange should be considered.
Learning points:
-
Hormonal changes in pregnancy, mediated by progesterone,oestrogen and human placental lactogen, lead to a two- to three-fold increase in serum triglyceride levels.
-
Pharmacological intervention for management of gestational hypertriglyceridaemia rely on the augmentation of lipoprotein lipase (LPL) activity to enhance catabolism of triglyceride-rich lipoproteins.
-
Genetic mutations affecting the LPL gene can lead to severe hypertriglyceridaemia.
-
Therapeutic plasma exchange (TPE) is an effective intervention for the management of severe gestational hypertriglyceridaemia and should be considered in cases where there is an underlying LPL defect.
-
Preconception counselling and discussion regarding contraception is of paramount importance in women with familial hypertriglyceridaemia.
Search for other papers by Skand Shekhar in
Google Scholar
PubMed
Search for other papers by Sriram Gubbi in
Google Scholar
PubMed
Computational Biomedicine Laboratory (CBML), Institute of Computer Science (ICS), Foundation for Research and Technology Hellas (FORTH), Heraklion, Greece
Search for other papers by Georgios Z Papadakis in
Google Scholar
PubMed
Search for other papers by Naris Nilubol in
Google Scholar
PubMed
Search for other papers by Fady Hannah-Shmouni in
Google Scholar
PubMed
Summary
Adrenococortical carcinoma (ACC) is a rare cancer, occurring at the rate of one case in two million person years. Cushing syndrome or a mixed picture of excess androgen and glucocorticoid production are the most common presentations of ACC. Other uncommon presentations include abdominal pain and adrenal incidentalomas. In the present report, a 71-year-old male presented with abdominal pain and was eventually diagnosed with ACC. He was found to have pulmonary thromboembolism following an investigation for hypoxemia, with the tumor thrombus extending upto the right atrium. This interesting case represents the unique presentation of a rare tumor, which if detected late or left untreated is associated with poor outcomes, highlighting the need for a low index of suspicion for ACC when similar presentations are encountered in clinical practice.
Learning points:
-
ACC is a rare but aggressive tumor.
-
ACC commonly presents with rapid onset of hypercortisolism, combined hyperandrogenism and hypercortisolism, or uncommonly with compressive symptoms.
-
Clinicians should have a low index of suspicion for ACC in patients presenting with rapid onset of symptoms related to hypercortisolism and/or hyperandrogenism.
-
Venous thromboembolism and extension of the tumor thrombus to the right side of the heart is a very rare but serious complication of ACC that clinicans should be wary of.
-
The increased risk of venous thromboembolism in ACC could be explained by direct tumor invasion, tumor thrombi or hypercoagulability secondary to hypercortisolism.
-
Early diagnosis and prompt treatment can improve the long-term survival of patients with ACC.
Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK
Search for other papers by A Chinoy in
Google Scholar
PubMed
Search for other papers by N B Wright in
Google Scholar
PubMed
Search for other papers by M Bone in
Google Scholar
PubMed
Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK
Search for other papers by R Padidela in
Google Scholar
PubMed
Summary
Hypokalaemia at presentation of diabetic ketoacidosis is uncommon as insulin deficiency and metabolic acidosis shifts potassium extracellularly. However, hypokalaemia is a recognised complication of the management of diabetic ketoacidosis as insulin administration and correction of metabolic acidosis shifts potassium intracellularly. We describe the case of a 9-year-old girl with newly diagnosed type 1 diabetes mellitus presenting in diabetic ketoacidosis, with severe hypokalaemia at presentation due to severe and prolonged emesis. After commencing management for her diabetic ketoacidosis, her serum sodium and osmolality increased rapidly. However, despite maximal potassium concentrations running through peripheral access, and multiple intravenous potassium ‘corrections’, her hypokalaemia persisted. Seventy two hours after presentation, she became drowsy and confused, with imaging demonstrating central pontine myelinolysis – a rare entity seldom seen in diabetic ketoacidosis management in children despite rapid shifts in serum sodium and osmolality. We review the literature associating central pontine myelinolysis with hypokalaemia and hypothesise as to how the hypokalaemia may have contributed to the development of central pontine myelinolysis. We also recommend an approach to the management of a child in diabetic ketoacidosis with hypokalaemia at presentation.
Learning points:
-
Hypokalaemia is a recognised complication of treatment of paediatric diabetic ketoacidosis that should be aggressively managed to prevent acute complications.
-
Central pontine myelinolysis is rare in children, and usually observed in the presence of rapid correction of hyponatraemia. However, there is observational evidence of an association between hypokalaemia and central pontine myelinolysis, potentially by priming the endothelial cell membrane to injury by lesser fluctuations in osmotic pressure.
-
Consider central pontine myelinolysis as a complication of the management of paediatric diabetic ketoacidosis in the presence of relevant symptoms with profound hypokalaemia and/or fluctuations in serum sodium levels.
-
We have suggested an approach to the management strategies of hypokalaemia in paediatric diabetic ketoacidosis which includes oral potassium supplements if tolerated, minimising the duration and the rate of insulin infusion and increasing the concentration of potassium intravenously (via central line if necessary).
Search for other papers by Chloe Broughton in
Google Scholar
PubMed
Search for other papers by Jane Mears in
Google Scholar
PubMed
Search for other papers by Adam Williams in
Google Scholar
PubMed
Search for other papers by Kathryn Lonnen in
Google Scholar
PubMed
Summary
Pituitary adenomas can be classified as functioning or non-functioning adenomas. Approximately 64% of clinically non-functioning pituitary adenomas are found to be gonadotroph adenomas on immunohistochemistry. There are reported cases of gonadotroph adenomas causing clinical symptoms, but this is unusual. We present the case of a 36-year-old female with abdominal pain. Multiple large ovarian cysts were identified on ultrasound requiring bilateral cystectomy. Despite this, the cysts recurred resulting in further abdominal pain, ovarian torsion and right oophorectomy and salpingectomy. On her 3rd admission with abdominal pain, she was found to have a rectus sheath mass which was resected and histologically confirmed to be fibromatosis. Endocrine investigations revealed elevated oestradiol, follicle-stimulating hormone (FSH) at the upper limit of the normal range and a suppressed luteinising hormone (LH). Prolactin was mildly elevated. A diagnosis of an FSH-secreting pituitary adenoma was considered and a pituitary MRI revealed a 1.5 cm macroadenoma. She underwent transphenoidal surgery which led to resolution of her symptoms and normalisation of her biochemistry. Subsequent pelvic ultrasound showed normal ovarian follicular development. Clinically functioning gonadotroph adenomas are rare, but should be considered in women presenting with menstrual irregularities, large or recurrent ovarian cysts, ovarian hyperstimulation syndrome and fibromatosis. Transphenoidal surgery is the first-line treatment with the aim of achieving complete remission.
Learning points:
-
Pituitary gonadotroph adenomas are usually clinically non-functioning, but in rare cases can cause clinical symptoms.
-
A diagnosis of a functioning gonadotroph adenoma should be considered in women presenting with un-explained ovarian hyperstimulation and/or fibromatosis.
-
In women with functioning gonadotroph adenomas, the main biochemical finding is elevated oestradiol levels. Serum FSH levels can be normal or mildly elevated. Serum LH levels are usually suppressed.
-
Transphenoidal surgery is the first-line treatment for patients with functioning gonadotroph adenomas, with the aim of achieving complete remission.
Search for other papers by Bidhya Timilsina in
Google Scholar
PubMed
Search for other papers by Niranjan Tachamo in
Google Scholar
PubMed
Search for other papers by Prem Raj Parajuli in
Google Scholar
PubMed
Search for other papers by Ilan Gabriely in
Google Scholar
PubMed
Summary
A 74-year-old woman presented with progressive lethargy, confusion, poor appetite and abdominal pain. She was found to have non-PTH-mediated severe hypercalcemia with renal failure and metabolic alkalosis. Extensive workup for hypercalcemia to rule out alternate etiology was unrevealing. Upon further questioning, she was taking excess calcium carbonate (Tums) for her worsening heartburn. She was diagnosed with milk-alkali syndrome (MAS). Her hypercalcemia and alkalosis recovered completely with aggressive hydration along with improvement in her renal function. High index of suspicion should be maintained and history of drug and supplements, especially calcium ingestion, should be routinely asked in patients presenting with hypercalcemia to timely diagnose MAS and prevent unnecessary tests and treatments.
Learning points:
-
Suspect milk-alkali syndrome in patients with hypercalcemia, metabolic alkalosis and renal failure, especially in context of ingestion of excess calcium-containing supplements.
-
Careful history of over-the-counter medications, supplements and diet is crucial to diagnose milk-alkali syndrome.
-
Milk-alkali syndrome may cause severe hypercalcemia in up to 25–30% of cases.
Search for other papers by Miriam Hinaa Ahmad in
Google Scholar
PubMed
Search for other papers by Ismat Shafiq in
Google Scholar
PubMed
Summary
We report a case of a 21-year-old African American female with history of pre-diabetes, and a diagnosis of a rare leukemia, blastic-plasmacytoid dendritic neoplasm (BPDCN), who developed diabetic ketoacidosis (DKA) after the third dose of PEG-asparaginase infusion. She was successfully treated with insulin. Asparaginase is a vital part of treatment protocols for acute lymphoblastic leukemia (ALL) in combination with other chemotherapeutic drugs. Asparaginase therapy has been reported to cause hyperglycemia especially when used in conjunction with glucocorticoids for the treatment of ALL in the pediatric population. Multiple mechanisms for hyperglycemia have been hypothesized which include decreased insulin secretion, impaired insulin receptor function and excess glucagon formation. Hyperglycemia is usually self-limiting but can deteriorate to diabetic ketoacidosis. DKA is a rare adverse effect with asparaginase therapy with an incidence rate of about 0.8%.
Learning points:
-
DKA is a rare finding following asparaginase therapy.
-
Hyperglycemia is most commonly seen with asparaginase treatment when used along with glucocorticoid.
-
Frequent blood glucose monitoring and prompt initiation of insulin treatment with hyperglycemia can prevent severe complications.
-
Patients and physician education on this complication can reduce morbidity due to DKA.
Eastern Health Clinical School, Monash University, Victoria, Australia
Search for other papers by Ming Li Yee in
Google Scholar
PubMed
Search for other papers by Rosemary Wong in
Google Scholar
PubMed
Medical Imaging, Eastern Health, Box Hill, Victoria, Australia
Search for other papers by Mineesh Datta in
Google Scholar
PubMed
Department of Medicine and Radiology, University of Melbourne, Victoria, Australia
Search for other papers by Timothy Nicholas Fazio in
Google Scholar
PubMed
Search for other papers by Mina Mohammad Ebrahim in
Google Scholar
PubMed
Search for other papers by Elissa Claire Mcnamara in
Google Scholar
PubMed
Search for other papers by Gerard De Jong in
Google Scholar
PubMed
Eastern Health Clinical School, Monash University, Victoria, Australia
Department of Medicine, Eastern Health, Box Hill, Victoria, Australia
Search for other papers by Christopher Gilfillan in
Google Scholar
PubMed
Summary
Mitochondrial diseases are rare, heterogeneous conditions affecting organs dependent on high aerobic metabolism. Presenting symptoms and signs vary depending on the mutation and mutant protein load. Diabetes mellitus is the most common endocrinopathy, and recognition of these patients is important due to its impact on management and screening of family members. In particular, glycemic management differs in these patients: the use of metformin is avoided because of the risk of lactic acidosis. We describe a patient who presented with gradual weight loss and an acute presentation of hyperglycemia complicated by the superior mesenteric artery syndrome. His maternal history of diabetes and deafness and a personal history of hearing impairment led to the diagnosis of a mitochondrial disorder.
Learning points:
-
The constellation of diabetes, multi-organ involvement and maternal inheritance should prompt consideration of a mitochondrial disorder.
-
Mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes (MELAS) and maternally inherited diabetes and deafness (MIDD) are the most common mitochondrial diabetes disorders caused by a mutation in m.3243A>G in 80% of cases.
-
Metformin should be avoided due to the risk of lactic acidosis.
-
There is more rapid progression to insulin therapy and higher prevalence of diabetic complications compared to type 2 diabetes.
-
Diagnosis of a mitochondrial disorder leads to family screening, education and surveillance for future complications.
-
Superior mesenteric artery syndrome, an uncommon but important cause of intestinal pseudo-obstruction in cases of significant weight loss, has been reported in MELAS patients.
