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12 results

  • 35 - Common Electrolyte Disorders (Sodium, Potassium, Calcium, Magnesium)

  • from Section 7 - Renal Emergencies
  • Edited by Kaushal Shah, Weill Cornell Medical Center, New York, Jarone Lee, Massachusetts General Hospital, Boston
  • Edited in association with Clark G. Owyang, Weill Cornell Medical Center, New York, Benjamin Christian Renne, Massachusetts General Hospital, Boston
  • Book:
    Practical Emergency Resuscitation and Critical Care
    Published online:
    02 November 2023
    Print publication:
    23 November 2023, pp 333-364

  • Summary

    Serum sodium (Na) concentration is mediated by free water intake, circulating levels of antidiuretic hormone (ADH) and renal filtration of sodium. Disorders of potassium, especially hyperkalemia, are the most feared electrolyte disorders due to their ability to cause life-threatening cardiac arrhythmia. Release of calcium stores into the circulation is regulated by extracellular calcium concentration, parathyroid hormone (PTH), vitamin D metabolites and calcitonin. Magnesium is one of the most abundant cations in the body and plays a large role in cardiac contractility as well as nerve conduction.

  • “This is not a doctors thing, it is witchcraft” - A case report of acute psychosis concomitant to primary hyperparathyroidism

  • L. Lopes, B. Moura, S. Pereira
  • Journal:
    European Psychiatry / Volume 64 / Issue S1 / April 2021
    Published online by Cambridge University Press:
    13 August 2021, p. S250
    • Article
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      • Open access
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  • Introduction

    Primary hyperparathyroidism (PHPT), usually caused by a parathyroid adenoma, is characterized by a pathologically high secretion of parathyroid hormone and consequent hypercalcemia. PHPT has a high prevalence among elderly patients and might be responsible for neuropsychiatric symptoms.

    Objectives

    We aim to report the rare manifestation of acute psychosis accompanying a PHPT diagnosis, and to discuss the neurobiological relationship between hyperparathyroidism, hypercalcaemia and neuropsychiatric symptoms.

    Methods

    We present a clinical case based on patient’s history and clinical data, along with a literature review on PHPT neuropsychiatric symptons.

    Results

    We present the case of a 68-year-old man diagnosed with PHPT in November 2019. He was brought up to psychiatric evaluation for the first time in May 2020 upon behavioral changes (aggressiveness and bizarre rituals). The patient described the sensation of burns scattered throughout the body since January 2020, felling anxious and frightened, sleeping poorly and progressive social isolation. He presented delusional ideas of mystical and paranoid content. No significant cognitive impairments were found. The patient’s psychosis was partially responsive to atypical antipsychotics. He’s waiting for surgery. Hypercalcaemia might manifest as mood disorders, cognitive changes and rarely as acute psychosis. Although there is not yet a clear mechanism to explain it, high calcium levels seem to cause neurotoxicity and neurotransmission dysfunction. Restoration of normal calcium levels tend to resolve neuropsychiatric symptoms, but in PHPT parathyroidectomy is usually recommended.

    Conclusions

    Neuropsychiatric symptoms are responsible for great disability, and demand an organic in-depth investigation. A multidisciplinary team approach must always be considered in the management of such conditions.

  • Hypercalcemia due to methadone-induced adrenal insufficiency in a case of oral cancer

  • Ankit Sharma, Mahajan Jitendra Subhash, Anuja Pandit, Swati Bhan, Sushma Bhatnagar
  • Journal:
    Palliative & Supportive Care / Volume 18 / Issue 6 / December 2020
    Published online by Cambridge University Press:
    29 October 2020, pp. 751-753

  • A 31-year-old patient of post-surgical recurrent buccal carcinoma (post-chemo and radiotherapy) on multimodal analgesia with methadone, paracetamol and gabapentin presented to pain clinic with occasional bleeding from tumor area and incidental hypercalcemia. The hypercalcemia was attributed to adrenal insufficiency due to methadone, with no other obvious reasons identified for hypercalcemia or adrenal insufficiency. The patient was managed with the change of opioid, regular aseptic wound dressings and management of hypercalcemia with hydration, calcitonin and steroid therapy. Hypercalcemia in a cancer patient can have multiple other causes like hypercalcemia of malignancy and primary or secondary parathyroid carcinoma. A strong clinical suspicion and appropriate battery of tests may be required to arrive at the diagnosis. Prompt management, including identification and management of the primary pathology along with aggressive hydration with hormonal therapy, may prove to be life-saving.

  • 61 - Adrenal crisis

  • from Section 10 - Endocrine emergencies
  • Edited by Kaushal Shah, Jarone Lee, Kamal Medlej, American University of Beirut, Scott D. Weingart
  • Book:
    Practical Emergency Resuscitation and Critical Care
    Published online:
    05 November 2013
    Print publication:
    24 October 2013, pp 403-407

  • Summary

    This chapter discusses the diagnosis, evaluation and management of common electrolyte disorders that include hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesemia and hypermagnesemia. The signs and symptoms of moderate hyponatremia are non-specific such as generalized weakness, lethargy, nausea, vomiting, and muscle cramps. Hyponatremia is most commonly caused by an excess of antidiuretic hormone (ADH) released in response to intravascular volume depletion, exacerbated by volume replacement with hypotonic fluids. Overly rapid correction of hypernatremia may lead to cerebral edema and seizure. As with hyponatremia, to ensure a safe and accurate replacement rate, serum sodium levels have to be checked frequently. Release of calcium stores in the circulation is regulated by extracellular calcium concentration, parathyroid hormone (PTH), vitamin D metabolites, and calcitonin. Mild hypomagnesemia is usually asymptomatic, but failure to correct low serum magnesium may contribute to refractory hypokalemia and hypocalcemia.

  • 59 - SCLERODERMA

  • from PART V: - SYSTEMIC DISORDERS THAT ALSO INVOLVE THE CEREBROVASCULAR SYSTEM
  • Edited by Louis R. Caplan, Julien Bogousslavsky
  • Book:
    Uncommon Causes of Stroke
    Published online:
    06 January 2010
    Print publication:
    09 October 2008, pp 429-432

  • Summary

    This chapter reviews the role of calcium and magnesium in causing and ameliorating brain ischemia, respectively. Three different effects of hypercalcemia are posited to contribute to the development and severity of brain ischemia: (i) hypercalcemia stimulates vascular smooth muscle causing vasoconstriction; (ii) increased calcium concentrations enhance platelet aggregation and activate the body's intrinsic coagulation system; and (iii) calcium entry into cells, a process enhanced by an elevated extracellular-to-intracellular calcium ion gradient, causes cytotoxic effects that promote cell death and brain infarction. The rationale for the use of calcium antagonists in the prevention or treatment of secondary brain ischemia was based on the assumption that these drugs reduce the frequency of vasospasm by counteracting the influx of calcium into vascular smooth muscle cells. There is some benefit from the use of the dihydropyridine CCA nimodipine for improving outcome after aneurysmal subarachnoid hemorrhage.