Article

Clinical physiology of acid-base and electrolyte disorders, 5th Edition

Authors:
To read the full-text of this research, you can request a copy directly from the authors.

No full-text available

Request Full-text Paper PDF

To read the full-text of this research,
you can request a copy directly from the authors.

... Clinical features of CDI may differ based on the site involved in ADH production/secretion: the hypothalamic osmoreceptors; the supraoptic or paraventricular nuclei; or the superior portion of the supra-opticohypophyseal tract (14). When the damage hits the tract below the median eminence or the posterior pituitary, it usually causes only transient polyuria because ADH produced in the hypothalamus can still be secreted into the systemic circulation via the portal capillaries in the median eminence (14). ...
... Clinical features of CDI may differ based on the site involved in ADH production/secretion: the hypothalamic osmoreceptors; the supraoptic or paraventricular nuclei; or the superior portion of the supra-opticohypophyseal tract (14). When the damage hits the tract below the median eminence or the posterior pituitary, it usually causes only transient polyuria because ADH produced in the hypothalamus can still be secreted into the systemic circulation via the portal capillaries in the median eminence (14). ...
... However, polyuria is the typical onset symptom of DI, arising suddenly in most cases of CDI (5). The polyuria severity mainly depends on plasma osmolality, circulating volume, and entity of vasopressin deficit (5,10,14). Notably, in patients affected by DI, dehydration and overt hypernatremia are less common when thirst perception is not impaired, and water is freely accessible (5,10,14). Conversely, in patients with altered mental status, impaired thirst mechanisms (e.g., hypothalamic disorders, "adipsic DI"), or restricted access to water, persistent polyuria may cause dehydration and hypernatremia, which may, in turn, (5,10,14). ...
Article
Full-text available
Immune checkpoint inhibitors have improved the survival in patients affected by an increasing number of malignancies, but they may also trigger various autoimmune side-effects, including endocrinopathies. Very rarely, immune checkpoint inhibitors have been reported to cause central diabetes insipidus. However, with their expanding use, the likelihood that oncologists will face this endocrine adverse event is expected to increase. By reviewing the limited literature on central diabetes insipidus induced by immune checkpoint inhibitors, some inconsistencies emerge in the diagnosis and the management of patients presenting with this toxicity, together with difficulties related to classifying its severity. Until now, specific guidelines on the management of central diabetes insipidus induced by immune checkpoint inhibitors are lacking. In clinical practice, endocrinological consultation may relieve medical oncologists from difficulties in treating this side-effect; oncologists, however, remain responsible for its early diagnose and the management of the causative drugs. To this aim, some practical suggestions are advised for the multidisciplinary management of cancer patients presenting with central diabetes insipidus induced by immune checkpoint inhibitors.
... Hypoaldosteronism is a clinical condition caused by a deficit in the action of the principal human mineralocorticoid, the adrenal hormone aldosterone (1). Hypoaldosteronism can be congenital or acquired, isolated or part of primary adrenal insufficiency (PAI). ...
... The direct result of insufficient mineralocorticoid action on these principal cells is an inadequate reduction in urinary potassium excretion. In fact, the latter is determined primarily by mineralocorticoid action, absent oliguric renal insufficiency, if sodium delivery to the distal nephron is sufficient (1). This potassium excretion deficit predisposes to the development of h y p e r k a l e m i a , t h e m o s t s a l i e n t c h a r a c t e r i s t i c o f hypoaldosteronism (5), albeit not a constant (1). ...
... In fact, the latter is determined primarily by mineralocorticoid action, absent oliguric renal insufficiency, if sodium delivery to the distal nephron is sufficient (1). This potassium excretion deficit predisposes to the development of h y p e r k a l e m i a , t h e m o s t s a l i e n t c h a r a c t e r i s t i c o f hypoaldosteronism (5), albeit not a constant (1). Thus, reduced potassium excretion is the defining characteristic of hypoaldosteronism, rather than hyperkalemia itself. ...
Article
Full-text available
Introduction Hypoaldosteronism can be congenital or acquired, isolated or part of primary adrenal insufficiency, and caused by an aldosterone deficit, resistance, or a combination of both. Reduced mineralocorticoid action can induce a decrease in urine K+ and H+ excretion and an increase in urine Na+ excretion, leading to hyperkalemia, and/or hyponatremia, often combined with metabolic acidosis. We aimed to characterize the clinical manifestations of hypoaldosteronism, and their associated factors. Methods Retrospective analysis of 112 episodes of hypoaldosteronism diagnosed in 86 adult patients from 2012-2019 by the Endocrinology and Nutrition Department of a tertiary hospital. The frequency of hyperkalemia, hypovolemic hyponatremia (HH) and metabolic acidosis (MA), and their associated factors were evaluated. Results Patients had a median age of 77 [65 – 84], 55.4% were male. 94.6% cases showed hyperkalemia, 54.5% HH, and 60.3% MA. The mean serum K+ of all cases was 5.4 ± 0.5 mmol/L, Na+: 132.1 ± 6.3 mmol/L, HCO3: 22.6 ± 3.3 mmol/L. Hypoaldosteronism was isolated in the majority of cases: only 6/112 (5%) had primary adrenal insufficiency. Hypovolemia was associated with hyponatremia and a more florid clinical presentation. HH was associated with a combined presence of aldosterone-lowering and mineralocorticoid resistance factors. MA was associated with the presence of mineralocorticoid resistance factors. Conclusions Hypoaldosteronism in adult endocrinological clinical practice is primarily isolated, and acquired. It predisposes not only to the development of hyperkalemia and MA, but also to that of HH. Hypoaldosteronism must be considered in the differential diagnosis of HH with urinary sodium wasting.
... Since above-ground CO 2 is 0.04% and the end-expiratory CO 2 may be~5%, direct or indirect sensing of arterial CO 2 closely controls minute ventilation in most animals, and thus hypercapnia is a key driver of hyperventilation. But apart from this important sensing consideration where NMRs possess relatively blunted hypercapnic responses (Clayson et al., 2020), high ambient CO 2 or high arterial pCO 2 as such do not preclude "normal" metabolism, as demonstrated by chronically hypercapnic patients with severe chronic lung disease (Rose and Post, 2001). The usual adaptation in mammals to hypercapnia is to increase circulating bicarbonate levels to restore a normal pH. ...
... When pH and pCO 2 are known, the bicarbonate level is determined accordingly. Subsequently, acid-base principles in mammals (Rose and Post, 2001;Kellum and Elbers, 2009), imply that this increase in bicarbonate requires an adaptive response from the kidneys or gut that leads to an increase in the strong-ion difference. As the strong ion difference is mainly determined by the difference between [Na + ] and [Cl − ], this response involves either enhanced absorption of sodium and/or enhanced excretion of chloride (Rose and Post, 2001;Kellum and Elbers, 2009), both leading to increased bicarbonate. ...
... Subsequently, acid-base principles in mammals (Rose and Post, 2001;Kellum and Elbers, 2009), imply that this increase in bicarbonate requires an adaptive response from the kidneys or gut that leads to an increase in the strong-ion difference. As the strong ion difference is mainly determined by the difference between [Na + ] and [Cl − ], this response involves either enhanced absorption of sodium and/or enhanced excretion of chloride (Rose and Post, 2001;Kellum and Elbers, 2009), both leading to increased bicarbonate. When the environmental CO 2 level is increased, the arterial pCO 2 must be at least equal to the environmental pCO 2 and when the observed pH then remains (initially) stable, bicarbonate must have increased (Park et al., 2017; Fig S1). ...
Article
Full-text available
Metabolic flexibility in mammals enables stressed tissues to generate additional ATP by converting large amounts of glucose into lactic acid; however, this process can cause transient local or systemic acidosis. Certain mammals are adapted to extreme environments and are capable of enhanced metabolic flexibility as a specialized adaptation to challenging habitat niches. For example, naked mole-rats (NMRs) are a fossorial and hypoxia-tolerant mammal whose metabolic responses to environmental stressors markedly differ from most other mammals. When exposed to hypoxia, NMRs exhibit robust hypometabolism but develop minimal acidosis. Furthermore, and despite a very long lifespan relative to other rodents, NMRs have a remarkably low cancer incidence. Most advanced cancers in mammals display increased production of lactic acid from glucose, irrespective of oxygen availability. This hallmark of cancer is known as the Warburg effect (WE). Most malignancies acquire this metabolic phenotype during their somatic evolution, as the WE benefits tumor growth in several ways. We propose that the peculiar metabolism of the NMR makes development of the WE inherently difficult, which might contribute to the extraordinarily low cancer rate in NMRs. Such an adaptation of NMRs to their subterranean environment may have been facilitated by modified biochemical responses with a stronger inhibition of the production of CO 2 and lactic acid by a decreased extracellular pH. Since this pH-inhibition could be deeply hard-wired in their metabolic make-up, it may be difficult for malignant cells in NMRs to acquire the WE-phenotype that facilitates cancer growth in other mammals. In the present commentary, we discuss this idea and propose experimental tests of our hypothesis.
... The FeNa and FeU are both useful tests used to discriminate these two entities. The primary use of FeNa which mainly reflects the function of distal nephron is that low levels of it (<1%) suggests prerenal failure whereas a high level (2%) favors intrinsic renal failure (1,13,21). However active transport of sodium chloride can be affected by diuretic usage leading to an alteration in FeNa, and this affects the utilization of FeNa in patients who were administered diuretics (9). ...
... Urea is a lipid-soluble molecule that can cross the membranes of the cell easily by passive diffusion (1,21). In the glomerulus urea is freely filtered, and then reabsorbed mainly in the proximal tubule, finally 50-60% of the filtered urea is excreted (1,21). ...
... Urea is a lipid-soluble molecule that can cross the membranes of the cell easily by passive diffusion (1,21). In the glomerulus urea is freely filtered, and then reabsorbed mainly in the proximal tubule, finally 50-60% of the filtered urea is excreted (1,21). Urea is also actively transported in the renal tubules. ...
Article
Full-text available
Objective: Fractional excretion of sodium (FeNa) and fractional excretion of urea (FeU) are used to differentiate prerenal and renal injuries in acute kidney injury (AKI). In this study, we aimed to compare the discriminative power of FeU with FeNa between prerenal and renal azotemia groups as well as among AKI stages according to pRIFLE criteria. Material and Methods: Laboratory and medical records of 55 pediatric AKI patients who had the measurements of random urine excretions of urea, creatinine and sodium as well as serum urea, creatinine and sodium levels in order to calculate FeU and FeNa values at the time of AKI diagnosis were evaluated retrospectively. Patients were divided into prerenal and renal injury groups according to the clinical findings and laboratory data. Sensitivities and specifities of FeNa and FeU in differentiating prerenal versus renal injury were determined. FeNa and FeU values were compared in patients with different RIFLE stages. Results: Among 55 pediatric AKI patients 31 were boys, 24 were girls. The mean age at the time of diagnosis was 71.1 ± 83.5 months (min-max: 1-216). When we grouped the patients as having FeU<35% and FeU≥35%, the difference between the numbers of the patients in prerenal and renal groups was significant (p=0.039). The sensitivity and specificity of FeU to determine prerenal vs renal injury were calculated as 50% and 77.1% respectively. When FeNa and FeU were used together (FeNa>1% and FeU>35%) in order to distinguish prerenal and renal injuries the specificity increased to 81% (p=0.020). Mean FeU was significantly different between AKI stages (p=0.022), and was higher in Injury and Failure stages when compared with the Risk stage. Conclusion: Fractional urea excretion is as important as FeNa in evaluating children with AKI. We recommend to obtain FeU in pediatric AKI in order to differentiate prerenal and renal etiology and to differentiate the severity of the injury according to the AKI stages in order to arrange the treatment. Keywords Acute kidney injury, Children, Fractional urea excretion, pRIFLE
... CDI results from a deficiency of vasopressin (antidiuretic hormone, ADH) due to a hypothalamic-pituitary disorder. Most CDI cases are idiopathic or result from primary or secondary cancers, or infiltrative diseases (i.e., Langerhans cell histiocytosis) (7). Less frequently, CDI may be caused by familial and congenital disorders, neurosurgery or trauma, hypoxic encephalopathy, post-supraventricular tachycardia, and anorexia nervosa (7,8). ...
... Most CDI cases are idiopathic or result from primary or secondary cancers, or infiltrative diseases (i.e., Langerhans cell histiocytosis) (7). Less frequently, CDI may be caused by familial and congenital disorders, neurosurgery or trauma, hypoxic encephalopathy, post-supraventricular tachycardia, and anorexia nervosa (7,8). Drugs may rarely trigger CDI, including lithium, amphotericin-b, cidofovir, demeclocycline, didanosine, foscarnet, ofloxacin, orlistat (5). ...
... Clinical features of CDI may differ based on whether disorders act at one or more of the sites involved in ADH secretion: the hypothalamic osmoreceptors; the supraoptic or paraventricular nuclei; or the superior portion of the supra-opticohypophyseal FIGURE 1 | At the magnetic resonance imaging, pituitary microinfarcts in an enlarged gland were shown; the hypophyseal stalk was normal, and the neurohypophyseal 'bright signal' in T1 sequences was undetectable. tract (7,8). When the damage hits the tract below the median eminence or the posterior pituitary, usually causes only transient polyuria, because ADH produced in the hypothalamus can still be secreted into the systemic circulation via the portal capillaries in the median eminence (7). ...
Article
Full-text available
Background Immune checkpoint inhibitors (ICIs), by unleashing the anticancer response of the immune system, can improve survival of patients affected by several malignancies, but may trigger a broad spectrum of adverse events, including autoimmune hypophysitis. ICI-related hypophysitis mainly manifests with anterior hypopituitarism, while the simultaneous involvement of both anterior and posterior pituitary (i.e., panhypophysitis) has rarely been described. Case Presentation In June 2015, a 64-year-old man affected by liver metastases of a uveal melanoma was referred to us due to polyuria and polydipsia. Two months prior, he had started ipilimumab therapy (3 mg/kg iv every 21 days). The treatment was well-tolerated (only mild asthenia and diarrhea were reported). A few days before the fourth cycle, the patient complained of intense headaches, profound fatigue, nocturia, polyuria (up to 10 L urine/daily), and polydipsia. Laboratory tests were consistent with adrenal insufficiency, hypothyroidism, and transient central diabetes insipidus. The pituitary MRI showed an enlarged gland with microinfarcts, while the hypophyseal stalk was normal, and the neurohypophyseal ‘bright signal’ in T1 sequences was not detected. The treatment included dexamethasone (then cortisone acetate at replacement dose), desmopressin, and levothyroxine. Within the next five days, the symptoms resolved, and blood pressure, electrolytes, glucose, and urinalysis were stable within the normal ranges; desmopressin was discontinued while cortisone acetate and levothyroxine were maintained. The fourth ipilimumab dose was entirely administered in the absence of further side effects. Conclusion As ICIs are increasingly used as anticancer agents, the damage to anterior and/or posterior pituitary can be progressively encountered by oncologists and endocrinologists in their clinical practice. Patients on ICIs and their caregivers should be informed about that risk and be empowered to alert the referring specialists early, at the onset of panhypopituitarism symptoms, including polyuria/polydipsia.
... Regarding the etiopathogenesis of hypernatremia, central diabetes insipidus (DIC), characterized by the partial or total absence of antidiuretic hormone (ADH) and causing a clinical picture consisting of polyuria and polydipsia, should be highlighted as an entity of its own. Most cases are idiopathic, followed by primary or secondary tumors affecting hypophysiothalamic structures [5,6]. ...
... Central diabetes insipidus can be a secondary manifestation of cancer and is often accompanied by elevated sodium levels [5]. We present an unusual case of hyponatremia as an initial manifestation of central diabetes insipidus as a paraneoplastic manifestation of lung adenocarcinoma. ...
Article
Full-text available
Altered natremia is a common electrolyte disorder in clinical practice and a paraneoplastic manifestation. The syndrome of inappropriate antidiuretic hormone secretion is the first diagnostic suspicion in a patient with cancer and hyponatremia, although entities such as adrenal insufficiency primary or secondary to metastatic involvement must be taken into account. Likewise, immunorelated endrocrinopathies such as hypophysitis have been reported after the introduction of checkpoint inhibitors. A 46-year-old man diagnosed with metastatic adenocarcinoma of the lung with severe hyponatremia (111 mmol/L) consulted due to altered level of consciousness. The initial cranial CT scan did not reveal pituitary brain metastatic involvement; however, an MRI could not be performed due to the patient’s clinical situation and subsequent exitus. The water restriction test confirmed the diagnostic suspicion of central diabetes insipidus. Medical treatment with desmopressin was started to avoid fluid depletion with improvement of natremia figures. It represents an exceptional case of central diabetes insipidus masked by severe hyponatremia in a patient with metastatic lung adenocarcinoma without initial evidence of pituitary metastatic involvement by CT imaging in treatment with nivolumab (anti-PD-1 agent). Secondary adrenal insufficiency due to pituitary metastatic involvement and endocrinologic toxicity immunorelated to the new checkpoint inhibitors should be considered as possible etiologic agents of central diabetes insipidus, even with hyponatremia.
... Disorders affecting the hypothalamus osmoreceptors, supraoptic or paraventricular nuclei, or the superior section of the supraoptic hypophyseal tract can all lead to a lack of ADH [6]. In approximately 30% to 50% of cases of central diabetes insipidus, hormone-secreting cells in the hypothalamus are destroyed. ...
... Drugs, such as lithium, which cause the aquaporin-2 water channel to malfunction [13]. Hypercalcemia over 11 mg/dL (2.75 mmol/L) or severe hypokalemia can interfere with ADH's ability to increase collecting tubule water permeability [6,14]. ...
Article
Full-text available
Vasopressin is a peptide hormone produced by the hypothalamus and stored in the posterior pituitary. It is secreted in response to hypotension and hyperosmolarity. Vasopressin and its analogs have been widely used in vasodilatory shocks such as septic shock and cardiogenic shock. The sudden withdrawal of vasopressin after its prolonged use can lead to polyuria and rising sodium levels, which is concerning for the diagnosis of diabetic insipidus (DI); likely central rather than nephrogenic in origin. We present a case of diabetic insipidus following the sudden discontinuation of a prolonged vasopressin infusion for septic shock, which responded to tapering doses of desmopressin.
... [13][14][15] Aldosterone-the final product of the RAAS-drives sodium reabsorption and is a key mediator in the pathophysiology of heart failure. 8,16,17 We hypothesized that higher prediuretic levels of renin, angiotensinogen, and aldosterone would be associated with lower diuretic response. ...
... Compared with angiotensin II concentration in the circulation, angiotensin II concentrations within the kidney are extremely high, and angiotensin II in the renal tissue appears to be locally produced and active. 16 Animal models of heart failure demonstrate renal angiotensinogen mRNA expression consistent with RAAS activation in heart failure; 38-40 the urine angiotensinogen level may likewise represent intrarenal RAAS activation, which could make it a useful biomarker in heart failure. 41,42 However, there remains limited evidence for the clinical relevance of this pathway, and our analyses did not provide additional support for these hypotheses. ...
Article
Full-text available
Rationale & Objective Heart failure treatment relies upon loop diuretics to induce natriuresis and decongestion, but therapy is often limited by diuretic resistance. We explored the association of renin-angiotensin-aldosterone system (RAAS) activation with diuretic response. Study Design Observational cohort. Setting & Population Euvolemic ambulatory adults with chronic heart failure were administered torsemide in a monitored environment. Predictors Plasma total renin, active renin, angiotensinogen and aldosterone. Urine total renin and angiotensinogen. Outcomes Sodium output per doubling of diuretic dose (Na-DE) and fractional excretion of sodium per doubling of diuretic dose (FENa-DE). Analytical Approach Robust linear regression models estimated associations of each RAAS intermediate with outcomes. Results Analysis included 56 participants, with median age 65 years; 50% female; 41% Black. Median home diuretic dose was 80 mg furosemide equivalents. In unadjusted and multivariable adjusted models, higher levels of RAAS measures were generally associated with lower diuretic efficiency (DE). Higher plasma total renin remained significantly associated with lower Na-DE (ß=-0.41 [-0.76, -0.059] per SD change) with adjustment; higher plasma total and active renin were significantly associated with lower FENa-DE (ß=-0.48 [-0.83, -0.14] and ß=-0.51 [-0.95, -0.08], respectively) in adjusted models. Stratification by RAAS inhibitor use did not substantially alter these associations. Limitations Small sample size; highly-selected participants; associations may not be causal. Conclusions Among multiple measures of RAAS activation, higher plasma total and active renin were consistently associated with lower diuretic response. These findings highlight potential drivers of diuretic resistance and underscore the need for high-quality trials of decongestive therapy enhanced by RAAS blockade.
... In a patient, like the one encountered in our case, with persistent hyperkalemia on heparin, in whom there is no apparent cause such as the use of potassium supplements or a potassium-sparing diuretic or renal failure, heparin-induced type 4 RTA must be considered [3][4][5]. Type 4 RTA may also stem from diseases that modify the kidney structure and function such as diabetic nephropathy, HIV/AIDS, Addison's disease, sickle cell disease, urinary tract obstruction, lupus, amyloidosis, removal or destruction of both adrenal glands, and kidney transplant rejection. The medications that may cause type 4 RTA include diuretics such as spironolactone or eplerenone, angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs), trimethoprim, pentamidine, heparin, and nonsteroidal anti-inflammatory drugs (NSAIDs) [2]. ...
... In COVID-19 patients, there exists a higher propensity for higher rates of thromboembolic disease and often prevention with heparin can serve as the best treatment. Heparin has a direct toxic impact on the adrenal zona glomerulosa cells, which may be facilitated by a drop in the number and affinity of adrenal angiotensin II receptors [4,6]. Even at lower doses, heparin given twice daily at 5000 units can cause a significant reduction in plasma aldosterone concentrations [7]. ...
Article
Type 4 renal tubular acidosis (RTA) is a type of metabolic acidosis characterized by hyperchloremia and hyperkalemia resulting from the reduction in and/or resistance to aldosterone. RTA can be caused by multiple different medications including angiotensin-converting enzyme (ACE) inhibitor/angiotensin receptor blocker (ARB), potassium-sparing diuretics, and heparin. In this case, we discuss renal tubular acidosis caused by heparin use for the prevention of thromboembolic disease in COVID-19 infections.
... As principais causas de alcalose metabólica são divididas em alcaloses hipoalbuminemicas que são ocasionadas devido a uma falha hepática, enteropatias ou nefropatias, com vasculite e perda proteica, e as alcaloses hipoclorêmicas, que são ocasionadas por distúrbios digestivos, como vômito prolongado (Morais, 2008). A alcalose também pode ocorrer devido a fatores fisiológicos, como o catabolismo, hormônios da neuro-hipófise, glucagon, progesterona, dieta rica em proteínas, sistema nervoso simpático, testosterona e tiroxina (Rose & Post, 2001). Ela também pode ocorrer após a acidose respiratória crônica, e ainda, por causas iatrogênicas, como administração excessiva de bicarbonato, terapia diurética e drenagem estomacal (Morais, 2008). ...
Article
Os problemas eletrolíticos são comuns na rotina clínica médica de pequenos animais, em que acomete sem distinção de espécie, idade e sexo. As doenças mais encontradas por ser causa base ou resultante de outra patogenia são acidose e alcalose metabólica, em que trazem junto uma bagagem de sinais clínicos inespecíficos, como diarreia, êmese, apatia, desidratação, insuficiência renal, anorexia e demais sinais clínicos que acompanham as doenças. Estas enfermidades são resultado de alterações do pH sanguíneo, causando a desregulação da homeostasia do organismo. O diagnóstico deve ser rápido, utilizando exame físico, laboratorial e contando com exame específico, como a gasometria. O tratamento das enfermidades deve corrigir a causa base, fluidoterapia e correção de sinais clínicos secundários.
... The symptoms are directly attributable to hyponatremia which primarily occur with acute and marked reductions in the plasma sodium concentration and reflect neurologic dysfunction induced by cerebral edema. 26 Anemia is very much prevalent in hemodialysis patients. In this study mean hemoglobin was 9.34gm/dl which is less than recommended for renal failure patients by DOQI Guidelines. ...
Article
Full-text available
Objective: To measure the frequency of depression and its risk factors in patients under going hemodialysis. Methodology: It is a cross-sectional prospective study conducted at Hemodialysis unit of Shalamar Hospital and Shaikh Zayed Hospital, Lahore from 1 st January 2006 to 30 th April 2006. All patients getting regular hemodialysis for more than three months were included. Beck's Depression Inventory-II (BDI-II; adapted in Urdu) was administered on all the patients who were able to read or understand it. Blood sample were drawn at the same time for routine hematological, biochemical parameters and viral markers (Anti HCV and HbsAg). Diagnosis was made as per Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM IV) for correlation of psychological variables with clinical, hematological and biochemical parameters. Results: Eighty nine patients were enrolled which included fifty two (58.4%) were male and seventy seven (86.5%) were married. Major causes of renal failure were diabetes, hypertension and chronic glomerulonephrotis. Duration of dialysis was from 03 to 49 months with mean of 19.64 ± 11.7 months. Severity of depression was categorized in to mild, moderate and severe on the basis of BDI score. Majority of the patients fifty (56.1%) were moderately to severely depressed and there was no gender difference in the prevalence of depression. Conclusions: Majority of patients undergoing hemodialysis were depressed. Major risk factors for depression were marital status, illiteracy, number of children, socioeconomic factors, gender, hypertension and hypoalbuminemia. Patients with anemia, hyponatremia and hyperkalemia had suicidal tendency. Patients with hepatitis C and disturbed liver function have strong correlation with psychological parameters.
... Pulmonary involvement in the form of pneumonia is widespread in people infected with COVID-19, as shown in our case and the literature [5]. SIADH is characterized by dilution hyponatremia (<135mmol / l), increased urinary sodium level (> 20mmol / l), high urine osmolality (> 100 mOsm / kg) compared to plasma osmolality (< 280 mOsm / kg), in euvolemic patients taking no diuretics, with normal cardiac, hepatic, renal, adrenal and thyroid functions [6,7]. SIADH can be induced by a variety of conditions, including atypical lung disease. ...
Article
Full-text available
Introduction Hyponatremia is one of the most common water–electrolyte imbalances in the human organism. This disorder is usually secondary to various diseases, including infections. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is among causes of hyponatremia in critical care. It can be induced by a variety of conditions, including atypical lung disease. Discussion The COVID-19 infection is associated with multiples metabolic disorders. However, hyponatremia associated with SIADH and Coronavirus disease 2019 (COVID-19) is not a usual clinical situation, but it was recently mentioned in a few case reports. Conclusion We discuss a unique case of an acute symptomatic hyponatremia and SIADH, attributed to COVID-19.
... The CDI is usually presented with hypernatremia and polyuria (ranging from 2 up to 10 L/day). The degree of polyuria reflects the level of antidiuretic hormone deficiency [3,10]. The diagnostic criteria of CDI include hypernatremia >145 mmol/L, urine output >200-250 mL/h, serum osmolality >300 mOsm/kg, and urine osmolality <300 mOsm/kg. ...
Article
Full-text available
b> Background: Disorders of sodium balance are common in critically ill neurologic patients. However, the coexisting of cerebral salt wasting syndrome (CSW) and central diabetes insipidus (CDI) in such patients is rare. Early recognition of such conditions is challenging, thus making the prognosis ominous. Case Presentation: A 50-year-old male patient presented with acute posterior cerebrovascular infarction complicated by several attacks of disturbed sodium homeostasis. The first attack manifested as hypernatremia (up to 161 mmol/L) and polyuria with high urine sodium (188 mmol/L) could only be explained by CSW on top of CDI. Especially the patient was not receiving any hyperosmolar or sodium-containing fluids. Serum sodium was corrected by desmopressin acetate. Later, the patient developed 2 attacks of hyponatremia (down to 119 mmol/L) diagnosed as CSW that was treated with fludrocortisone. Finally, he developed hypernatremia (up to 165 mmol/L) diagnosed as CDI and was treated with desmopressin acetate. Conclusion: Sodium hemostasis disorders require full consideration of serum electrolytes, intravascular volume state, and urine electrolytes in view of the clinical condition. Early diagnosis and administration of the proper treatment are the cornerstones of successful management.
... The other three major causes of polyuria are due to water diuresis including primary polydipsia, central diabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI). All present with large volumes of dilute urine where urine osmolality is usually lower than 300 mOsm/kg [1]. If the urine osmolality is less than 300 mOsm/kg it is likely that the aetiology of the polyuria is either DI or primary polydipsia. ...
... Em estudo envolvendo 312 pacientes normais (idade entre 21-69 anos e 213 homens) a média das FE de K+ foi 8%, variando de 4-16% 13 . Se há depleção importante de potássio, sua excreção urinária pode cair para níveis mínimos, como 5 a 10 mEq/dia 14,15 . Em casos de hipocalemia significativa, o achado de valores maiores que 13 mEq/dia de excreção urinária de potássio indica um componente renal na perda de potássio 15 . ...
Article
Full-text available
Polymyxins are antibiotics developed in the 1950s. Polymyxin-induced neurotoxicity has been often described in medical literature. The same cannot be said of nephrotoxicity or tubulopathy in particular. This report describes the case of a patient prescribed polymyxin B to treat a surgical wound infection, which led to significant increases in fractional excretion of calcium, magnesium, and potassium and subsequent persistent decreases in the levels of these ions, with serious consequences for the patient. Severe hypocalcemia, hypomagnesemia, and hypokalemia may occur during treatment with polymyxin. Calcium, magnesium and potassium serum levels must be monitored during treatment to prevent life-threatening conditions.
... However, compared with larger cations, such as Na + or K + , small H + ions have stronger affinities for small and negatively charged parts of molecules. Therefore, smaller fluctuations in H + concentrations are required for normal cellular functions [27]. ...
Article
Metabolic acidosis is one of the most common complications of chronic kidney disease (CKD). It is associated with the progression of CKD, and many other functional impairments. Until recently, only serum bicarbonate levels have been used to evaluate acid-base changes in patients with reduced kidney function. However, recent emerging evidence suggests that nephrologists should reevaluate the clinical approach for diagnosing metabolic acidosis in patients with CKD based on two perspectives; pH and anion gap. Biochemistry and physiology textbooks clearly indicate that blood pH is the most important acid-base parameter for cellular function. Therefore, it is important to determine if the prognostic impact of hypobicarbonatemia varies according to pH level. A recent cohort study of CKD patients showed that venous pH modified the association between a low bicarbonate level and the progression of CKD. Furthermore, acidosis with a high anion gap has recently been recognized as an important prognostic factor, because veverimer, a nonabsorbable hydrochloride-binding polymer, has been shown to improve kidney function and decrease the anion gap. Acidosis with high anion gap frequently develops in later stages of CKD. Therefore, the anion gap is a time-varying factor and renal function (estimated glomerular filtration rate) is a time-dependent confounder for the anion gap and renal outcomes. Recent analyses using marginal structural models showed that acidosis with a high anion gap was associated with a high risk of CKD. Based on these observations, reconsideration of the clinical approach to diagnosing and treating metabolic acidosis in CKD may be warranted.
... SIADH also called 'Schwartz-Bartter syndrome' is a disorder of impaired water excretion caused by the inability to suppress the secretion of antidiuretic hormone (ADH) [5]. It accounts for about 1/3 of all cas es of hyponatremia. ...
Article
Full-text available
Hyponatremia is the most common electrolyte abnormality. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is one of the main causes of Euvolemic hyponatremia and is often associated with medications or underlying neurological or pulmonary diseases. Linezolid is a potent antibiotic against resistant Gram-positive microorganisms that can be associated with hyponatremia very rarely. We present an elderly diabetic woman who developed severe hyponatremia during treatment with linezolid for cellulitis of her left feet. A thorough work-up during the hyponatremia, as well as after it resolved, firmly identified SIADH as its cause. Importantly, SIADH occurred after linezolid was started and resolved after it was stopped, and a work-up for another cause of SIADH was negative, suggesting that linezolid was the cause of SIADH in this patient. This is the fourth case of a linezolid-induced SIADH, diagnosed with a thorough work-up so to correctly differentiate between SIADH from other causes of hyponatremia.
... In proximal RTA, the T m is reduced (12-20 mEq/L compared to 24-26 mEq/L in normal dogs34 ), resulting in urinary loss of bicarbonate. However, once the plasma bicarbonate level equates to the new T m , a new steady state is achieved in which the amount of bicarbonate filtered by the glomerulus equals the resorptive capacity of the tubule.19 Consequently, as bicarbonate is supplemented during treatment, the plasma bicarbonate again rises above the T m , allowing bicarbonate loss in urine. ...
Article
Full-text available
Objective: To describe the clinical presentation and management of a critically ill dog with profound renal tubular acidosis (RTA) with proximal and distal renal tubular dysfunction. Case summary: A 3-year-old neutered female Border Terrier was presented with frequent regurgitation resulting from acute pancreatitis with severe ileus. Venous acid-base analysis and complete urinalysis confirmed the presence of normal anion gap metabolic acidosis with inappropriately alkaline urine (pH 8), consistent with distal RTA. Urinalysis, urine amino acids, and urinary fractional excretion of electrolytes revealed glycosuria (with normoglycemia), aminoaciduria, and increased fractional excretion of sodium, calcium, and phosphate consistent with generalized proximal renal tubulopathy or Fanconi syndrome. The dog responded well to supportive care and alkaline therapy and made a complete recovery. New or unique information provided: To the authors' knowledge, this is the first description of RTA with proximal and distal renal tubular dysfunction in the veterinary literature. Furthermore, the authors hypothesize that the transient RTA was a manifestation of acute kidney injury secondary to acute pancreatitis, the first report of this in the literature.
... Much of these derangements' clinical symptoms are primarily neurologic and parallel to the magnitude of neuronal injury. In addition, these conditions can occur with seizures or with increasingly progressive symptoms and signs of neurology, and therefore require emergency care (Rose and Post, 2001;Riggs, 2002). Abnormal glucose levels may cause seizures, whether they are too high or too low. ...
Article
Full-text available
Epileptic seizures lead to changes in the importance of the blood laboratory tests which represent changes in various systems of organs in the body. A present study assessed the association between the rs3812718 polymorphism in SCN1A gene and susceptibility with epilepsy. In total, 48 subjects (28 patients and 20 controls) were included in the study. Subjects’ age and sex were matched. The patients' demographic profiles, including the gender (female: 26 and male; 34), mean of ages (21±8.6), the controls gender (female: 6 and male; 19) and age mean (39±13.3). Single nucleotide polymorphisms (SNPs) was used to investigate the distribution of SCN1A rs3812718 genotypes (G > A) in patients with Epilepsy. Direct sequencing is use to identify the (G>A) polymorphisms of the SCN1A gene on chromosome 2q24. Genotypes and allelic frequencies for the SCN1A in both groups were compared. In addition, the results show two other SNPs for the first time in Iraqi patients rs2217199 T>C and rs3812719 G>T and the study determines some biochemical tests (potassium) were performed by Reflotron and (glucose, sodium, chloride and calcium) by a Spectrophotometer in the sera of subjects. In this population, the alleles frequency of rs2217199/ C, rs3812719/ T, rs3812718/A, the susceptibility of epileptic with gene polymorphisms was correlated (OR = 5.84, p = 0.0001; OR = 4.41, p = 0.001; OR = 5.33, p = 0.001; respectively). The haplotype (CTA) was also significantly related with Epileptic patients (OR = 7.08; p = 0.001). Also, the study showed an increase in glucose levels at p-value= 0.008, normal value in serum K, Cl, Ca and Na levels in Epileptic patient with seizure compare with control. The study in an Iraqi population suggests that SCN1A polymorphisms genetic risk factor for Epileptic patients. Simple blood testing, particularly for some encephalopathies, can be a crucial help for recognizing the etiology.
... HZN did not affect KFT measures such as creatinine and BUN in male and female animals when compared to controls, except for Uric acid, which revealed a considerably lower amount in male rats in the high dose satellite group when compared to controls. Electrolyte balance is a marker of osmotic regulation in blood, kidney, and heart function, digestion, and intermediate metabolism [47,48,49]. ...
Article
Full-text available
Background : Habb-e-Zeequn Nafas (HZN) is a traditional multi-ingredient Unani formulation that has been used to treat bronchial asthma. Datura metel L. is an ingredient in this formulationthat has a toxic alkaloid called tropane. Despite its favorable use, no investigations on its toxicity potential have been published. Methodology : The acute and sub-acute toxicity studies were carried out following OECD Guidelines 425 and 407, respectively. The acute toxicity study was carried out at the dose of 170, 550, and 2000 mg/kg bw/day. The dose levels used in the sub-acute toxicity research were 11, 55, and 110 mg/kg bw/day. Toxicity clinical symptoms, body weight, and feed consumption were all recorded. Results : In comparison to control animals, there were no significant variations in body weight increase, feed consumption, hematological, or clinical biochemistry in HZN-treated animals. There were no significant differences in gross pathological findings between the control and drug-treated animals. A few histological alterations were found in the control and HZN-treated animals. Conclusions : Except for a few histological abnormalities in the liver in the high-dose HZN group, as well as the vehicle and satellite control groups, no treatment-related toxicologically significant alterations were identified up to the 2000 mg/kg b.w. tested dose.
... Commonly prescribed cardiovascular medications impact our patients' susceptibility to heat-related illness [202][203][204]. Diuretics, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and sodium-glucose cotransporter-2 inhibitors increase the risk of hypovolemia and heatstroke [205][206][207]. Beta-blockers decrease blood flow to the skin and reduce cardiac output, also placing individuals at higher risk of heatstroke [208]. ...
Article
Full-text available
Climate change is a worsening global crisis that will continue negatively impacting population health and well-being unless adaptation and mitigation interventions are rapidly implemented. Climate change-related cardiovascular disease is mediated by air pollution, increased ambient temperatures, vector-borne disease and mental health disorders. Climate change-related cardiovascular disease can be modulated by climate change adaptation; however, this process could result in significant health inequity because persons and populations of lower socioeconomic status have fewer adaptation options. Clear scientific evidence for climate change and its impact on human health have not yet resulted in the national and international impetus and policies necessary to slow climate change. As respected members of society who regularly communicate scientific evidence to patients, clinicians are well-positioned to advocate on the importance of addressing climate change. This narrative review summarizes the links between climate change and cardiovascular health, proposes actionable items a cardiologist can execute both in their personal life and as an advocate of climate policies, and encourages communication of the health impacts of climate change when counseling patients. Our aim is to inspire the reader to invest more time in communicating the most crucial public health issue of the 21st century to their patients.
... FFA will then be transported to the hepatocytes, where FFA oxidation occurs, leading to acetyl-CoA production. When acetyl-CoA is produced in large amounts, a ketogenic pathway will be stimulated, leading to ketone bodies production and acidosis (2). Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist. ...
Article
Full-text available
Background: Metabolic acidosis is defined by reduced serum bicarbonate level; this reduction can be from the addition of acid, reduced acid excretion, or loss of alkali. Starvation acidosis is one of the differential diagnoses of high anion gap metabolic acidosis (HAGMA). Objective: We report a rare case presentation of HAGMA associated with Liraglutide and low carbohydrates diet. Case presentation: A 27-year-old female patient presented to the Emergency Department (ED) with a complaint of nausea and vomiting for two days. She was following a strict low carbohydrate diet for three months to reduce her weight as her body mass index (BMI) was 30 kg/m3. Her bedside investigations were significant for HAGMA. The patient was seen by the endocrine service and was admitted as a case of starvation ketoacidosis (SKA) vs. euglycemic diabetic ketoacidosis (DKA). The patient was treated with D10W 250 cc/hr with insulin infusion, her the anion gap was closed after 5 hours. She was discharged home as SKA secondary to diet with the possibility of drug superimposing the starvation state. She was given a follow-up clinic regularly to monitor her clinical status. Conclusion: This case highlights the possibility of a HAGMA as a rare complication of a low carbohydrate diet with the possibility of Liraglutide injection attribution in developing such critical complication. Further studies are needed to evaluate the safety of a low carbohydrate diet and the effect of Liraglutide injection on these patients following this diet.
... These electrolytes are typically required to assess the normal functioning capacity of different parts of the functioning unit of the kidney [48,49]. Moreover, balance in electrolyte is an indicator of osmotic regulation by blood, kidney and cardiac function, digestion and other intermediary metabolism [50,51]. Serum electrolytes especially Na, K, Ca and P levels were estimated in the present study and this was further supported by the studies of Unuofin et al. and Mei-Yin et al. [52,53]. ...
... Since the median age in our study population in the hyponatremia group was 65 years and according to the mentioned studies, we did not expect to detect low serum creatinine levels in this group. In SIADH, the serum level of potassium is expected to be normal (21), which was in agreement with our findings. The median serum level of potassium in both eunatremia and hyponatremia groups was in the normal range. ...
Article
Full-text available
Introduction: In patients with coronavirus disease 2019 (COVID-19), the prevalence of hyponatremia has been reported with varying outcomes. Objectives: The aim of this study was to evaluate the prevalence of hyponatremia in hospitalized patients with COVID-19. Patients and Methods: In this multicenter cross-sectional study, information about hospitalized patients with COVID-19 admitted between March 2020 and September 2020, including age, gender, and serum levels of sodium, creatinine, and potassium, as well as blood urea nitrogen (BUN), was analyzed, while P value level less than 0.05 was considered significant. Results: A total of 667 hospitalized patients with COVID-19 were enrolled in the study, of which 54.4% were male. The median age of patients was 63 years old. About 39.4% of patients had hyponatremia on admission day. More than 80% of patients had mild hyponatremia. The median age of the hyponatremia group was significantly higher than that of eunatremia group. Conclusion: Our data showed that hyponatremia is observed in hospitalized patients with COVID-19 and is often mild.
... Sin embargo, la síntesis de estas aumenta sobre todo dentro del glomérulo por vasoconstrictores como la angiotensina II, la noradrenalina, la vasopresina (ADH) (por receptores V 1 ) y la endotelina. La vasodilatación posterior al efecto de las prostaglandinas contrarresta en parte la vasoconstricción neurohumoral, minimizando así el grado de isquemia renal 19 . El efecto clínico resultante es que los AINE no selectivos no deterioran la perfusión renal en sujetos normales, pero pueden causar isquemia renal reversible e insuficiencia renal en diversas situaciones, en particular en las patologías hipovolémicas, en las que aumentan las secreciones de angiotensina II y noradrenalina, que es el efecto compensador del cuerpo que se traduce en una mayor vasoconstricción a nivel renal. ...
... However, the total base release was relatively low as compared to the average daily nonvolatile acid production in humans of ~70 mmol (Scialla, Asplin, & Dobre, 2017). In healthy patients, the elimination of this acid load is achieved by the urinary excretion of hydrogen ions, both as titratable acid and as ammonium (Rose & Post, 2001). ESKD leads to the retention of hydrogen ions. ...
Article
Full-text available
A system for sorbent-assisted peritoneal dialysis (SAPD) has been developed that continuously recirculates dialysate via a tidal mode using a single-lumen peritoneal catheter with the regeneration of spent dialysate by means of sorbents. SAPD treatment may improve plasma clearance by the maintenance of a high plasma-to-dialysate concentration gradient and by increasing the mass transfer area coefficient (MTAC) of solutes. The system is designed for daily 8-hr treatment (12 kg, nighttime system). A wearable system (2.3 kg, daytime system) may further enhance the clearance of phosphate and organic waste solutes during the day. Uremic pigs (n = 3) were treated with the day- (n = 3) and nighttime system (n = 15) for 4-8 hr per treatment. Plasma clearance (Cl), MTAC, and total mass transport (MT) of urea, creatinine, phosphate, and potassium were compared with a static dwell (n = 28). Cl, MTAC, and MT of urea, creatinine, phosphate, and potassium were low in the pig as compared to humans due to the pig's low peritoneal transport status and could be enhanced only to a limited extent by SAPD treatment compared with a static dwell (nighttime system: Cl urea: ×1.5 (p = .029), Cl creatinine: ×1.7 (p = .054), Cl phosphate: ×1.5 (p = .158), Cl potassium: ×1.6 (p = .011); daytime system: Cl creatinine: ×2.7 (p = .040), Cl phosphate: ×2.2 (p = .039)). Sorbent-assisted peritoneal dialysis treatment in a uremic pig model is safe and enhances small solute clearance as compared to a static dwell. Future studies in humans or animal species with higher peritoneal transport should elucidate whether our SAPD system enhances clearance to a clinically relevant extent as compared to conventional PD.
Chapter
Hypopituitarism results from various causes which can be either inherited or acquired. Its clinical presentation depends on the extent and severity of the pituitary hormone deficiency. Both the anterior and posterior pituitary can be affected with loss of one, multiple, or all hormonal axes. Deficits can also result from hypothalamic disease, which is the main regulator of pituitary function. This chapter reviews the etiology, clinical manifestations, diagnosis, and treatment of the deficiency of each of the pituitary hormones. It is important to diagnose and treat these hormonal deficiencies as in certain cases it can be lifesaving.
Article
Objective To describe the semiquantitative acid–base status of dogs with untreated naturally occurring typical hypoadrenocorticism and to compare this to the status determined by traditional acid–base analysis. Design Retrospective study. Setting University teaching hospital. Animals Thirty‐three dogs with newly diagnosed typical hypoadrenocorticism between 2000 and 2017. Interventions None. Measurements and main results Dogs were included if they had newly diagnosed hypoadrenocorticism, post‐ACTH stimulation serum cortisol concentration <2 μg/dL, and blood collected within 6 hours of presentation for acid–base, electrolyte, and serum biochemical assays. Dogs were excluded if the Na⁺:K⁺ ratio was ≥28 or the dog had received a mineralocorticoid‐containing corticosteroid medication within the preceding month. Traditional acid–base analysis identified normal acid–base status in 1 dog, simple respiratory acid–base abnormalities in 2 of 33 dogs, and simple metabolic acidosis in 14 of 33 dogs. A mixed disorder was most common, noted in 16 of 33 dogs. The semiquantitative approach identified metabolic abnormalities in all cases. All dogs had ≥1 acidifying process, and 29 of 33 had both acidifying and alkalinizing processes. Acidosis attributable to excess free water was present in all dogs, and an acidifying phosphate effect was present in 27 of 33. Hyperlactatemia contributed to the acidosis in 8 of 33 dogs, with a median (range) lactate concentration of 1.5 mmol/L (13.5 mg/dL) (0.3–4.2 mmol/L [2.7–37.8 mg/dL]). Conclusions Dogs with untreated Addison's disease have complex acid–base derangements. The semiquantitative approach to acid–base analysis provides greater insight into the underlying mechanisms of metabolic acid–base abnormalities in these dogs, particularly because lactic acidosis appears to be a minor influence in most cases.
Chapter
Electrolyte disorders are common in the ICU. Severe hyperkalemia is a life‐threatening disorder, requiring immediate therapy. This chapter provides information on the prevention, prognosis, diagnosis, management, and treatment of electrolyte disorders, namely hyperkalemia, hypokalemia, hyperphosphatemia, hypophosphatemia, hyponatremia, hypernatremia, hypercalcemia, and hypocalcemia. The prevalence of hyperkalemia in hospitalized patients has been reported to be between 1% and 10%. Physical examination is often unremarkable in patients with hyperkalemia but in severe cases can reveal ascending muscle weakness or an irregular heart rhythm. All changes will reverse with treatment of the hyperkalemia. Treatment of chronic hyperphosphatemia most often occurs in patients with renal dysfunction and revolves around dietary phosphate restriction (<900 mg/day) and phosphate binder therapy to decrease intestinal absorption.
Article
Full-text available
Introduction In patients with relapsed or refractory lymphoma, high-dose chemoimmunotherapy with subsequent autologous hematopoietic cell transplantation (HCT) is a standard of care. Bendamustine, an alkylating agent, is used in the BeEAM (bendamustine, etoposide, cytarabine, melphalan) protocol for conditioning therapy before autologous HCT in patients with relapsed or refractory lymphoma who are eligible for transplant. There is no consensus regarding an optimal salvage regimen and the approach varies according to toxicity. Case report We present a case of partial nephrogenic diabetes insipidus after receiving bendamustine, as part of the BeEAM protocol. Management and outcome: The patient was managed with parenteral fluid administration and intranasal desmopressin before the condition resolved on its own. Discussion We summarize published reports of bendamustine-induced diabetes insipidus.
Article
The Hyperosmolar Hyperglycaemia State (HHS) is an endocrine emergency with a mortality rate between 10 and 50%. The mainstay for the treatment of this condition is vigorous IV fluid replacement with close monitoring of blood glucose, serum osmolality, and electrolytes. However, after initial resuscitation, patients can develop hypernatremia and raised serum osmolality, which have deleterious consequences. While hypernatremia in HHS can be treated with infusions of 0.45% saline or 5% dextrose, alternate measures such as intravenous (IV) hypotonic fluid infusion [e.g. 0.18% sodium chloride (NaCl) containing 4% dextrose and 0.15% potassium chloride (KCl)], or free water administration through a nasogastric (NG) tube can be used. We report the case of a 70-year-old man, who was initially admitted to a medical high care ward (MHC) with HHS, and was transferred to the ICU 72 hours later with an altered level of consciousness and severe hypernatremia. His treatment consisted in an IV hypotonic 0.18% NaCl infusion containing 4% dextrose and 0.15% KCl. He also received free water through a NG tube at a rate that was calculated to correct natremia at an average rate of 0.55 meq L-1 hr-1 over 72 hours. A multipronged approach was instituted to manage this patient, including, in addition to natremia correction, blood glucose control with insulin, appropriate IV antibiotics to treat infected foot ulcers, adequate analgesic medications, low-molecular-weight- heparin (LMWH) for thromboprophylaxis, proton- pump inhibitors, and continuation of patient’s ongoing antidepressant drugs at the time of his Glasgow Coma Score improvement. This case report demonstrates the feasibility and success of IV hypotonic fluid (0.18% NaCl - 4% dextrose - 0.15% KCl), alongside NG free water for correcting sodium levels with lower fluid volumes than would have been otherwise required if corrected with 0.45% saline. This treatment seems to be a reasonable choice for correcting sodium levels and osmolality in HHS patients who present with hypernatremia after an initial resuscitation, insofar as it avoids fluid overload and provides dextrose as an energy substrate, in addition to potassium ions. However, while correcting natremia with hypotonic fluid, other aspects of management should not be ignored.
Chapter
Intravenous fluid (IV)This chapter highlights several considerations in the use of intravenous fluids in the geriatric patient, specifically sodium and water. It emphasizes that these key elements of routine intravenous fluid orders are also body nutrients, required in limits to avoid the adverse consequences of either excess or deficit. A review of basic sodium and water distribution, regulation, and excretion is provided. The sodium content of various salt-containing fluids and supplements are presented as well as general principles underlying sodium administration. The goal of intravenous fluid (IV) administration is to carefully achieve and maintain a euvolemic and isotonic environment within the body as well as to provide for a variety of nutritional and pharmacologic interventions. The selection of an appropriate IV solution is dependent upon the fluid volume and electrolyte status of the individual patient as well as any additional specific therapeutic goals.
Article
Objective: To describe renal tubular acidosis (RTA) and secondary acquired hyperaldosteronism in a cat as an adverse effect of topiramate therapy. Case summary: An 8-year-old neutered female cat on chronic oral topiramate therapy at a recommended dose (11.9 mg/kg q 8 h) for seizure control was presented with severe metabolic acidosis and hypokalemia. Plasma electrolyte and acid-base analysis identified a severe metabolic acidosis (pH 7.153, reference interval: 7.31-7.46), hypokalemia (2.08 mmol/L [2.08 mEq/L], reference interval: 3.5-4.8 mmol/L [3.5-4.8 mEq/L]), and ionized hypercalcemia (1.85 mmol/L [1.85 mEq/L], reference range: 1.1-1.4 mmol/L [1.1-1.4 mEq/L]). Urinalysis revealed a urine specific gravity of 1.021 and a pH of 7.0. Diagnostic workup suggested distal RTA as a cause of the cat's acid-base and electrolyte disturbances. Aldosterone concentration was moderately increased, suggestive of secondary hyperaldosteronism. The metabolic abnormalities resolved with supportive care and discontinuation of topiramate. New or unique information provided: Topiramate is suggested to have led to the development severe RTA in a cat.
Chapter
Serum calcium is tightly regulated within the normal range due to its importance in many physiological processes. The major regulatory hormones responsible for maintaining “eucalcemia” are parathyroid hormone (PTH) and vitamin D. PTH has direct and indirect actions on three key organs responsible for the regulation of calcium: the skeleton, kidney, and gastrointestinal tract. In the skeleton, PTH increases bone resorption and acts indirectly to effect the dissolution of calcium salts. In the kidney, PTH acts to increase calcium reabsorption and increase 1-alpha hydroxylase activity to enhance activation of vitamin D, which secondarily increases calcium absorption in the gastrointestinal tract. The concerted actions of these hormones and organs facilitate the maintenance of normal serum calcium. This chapter will review the normal regulation of serum calcium and phosphate, which is closely linked to the regulation of calcium.KeywordsCalciumPhosphorusMetabolismPTHVitamin D
Article
Purpose: To report on an unusual case of ketamine-precipitated syndrome of inappropriate antidiuretic hormone secretion (SIADH) in an individual managed by an outpatient pain specialty team. Clinical features: A 78-yr-old male presented to the emergency department with lethargy, malaise, nausea, and abdominal bloating three days following intravenous ketamine infusion for intractable postsurgical lumbar radicular pain with neuropathic features. The patient had a history of resected prostate cancer, hyperlipidemia, chronic kidney disease, and spinal stenosis and the cause of his symptoms was investigated. He was found to be hyponatremic and the treating team excluded reversible surgical and medical causes. A Naranjo score of 7 was calculated, suggesting that the correlation between ketamine and hyponatremia was "likely." Hence, a diagnosis of ketamine-precipitated SIADH was made. The patient was treated with fluid restriction and symptoms were controlled with antiemetics. He returned to baseline function with resolution of the hyponatremia within three days of discharge. Conclusion: This case is of clinical importance for providers using ketamine in the field of pain management as the effect of this medication reaction can be profound. Clinicians should develop an awareness that ketamine can potentiate adverse effects such as SIADH and they should monitor, detect, and manage as appropriate.
Chapter
Potassium is an essential cation critical in fluid and electrolyte balance, acid–base regulation, and neuromuscular functions. The normal serum potassium is kept within a narrow range of 3.5–5.2 meq/L while the intracellular concentration is approximately 140–150 meq/L. The total body potassium is about 45–55 mmol/kg; thus, a 70 kg male has an estimated ~136 g and 60 kg female has ~117 g of potassium. In total, 98% of the total body potassium is intracellular. Skeletal muscle contains ~80% of body potassium stores. The ratio of intracellular to extracellular potassium concentration (Ki/Ke) maintained by Na+/K+ ATPase determines the resting membrane potential. Disturbances of potassium homeostasis lead to hypo- and hyperkalemia, which if severe, can be life-threatening. Prompt diagnosis and management of these problems are important.
Chapter
Full-text available
ΝΕΦΡΟΛΙΘΙΑΣΗ ΣΤΗΝ ΠΑΙΔΙΚΗ ΗΛΙΚΙΑ
Article
We report a 4-monthboy infant withisolated congenital hypoaldosteronism due to a novel mutation in CYP11B2 gene who presented with, failure to thrive, profound hyponatremia, hyperkalemia and mild metabolic acidosis, which managed byintravenous saline, oral saline, resoniumandcaloriesformula. In infants with severe electrolyte disturbance,it is important to rule out CAH and consider other rare form of isolated hypoaldosteronism and pseudohypoaldosteronism, since prompt and appropriate treatment will correct the associated electrolytes abnormalities.
Article
Full-text available
Background: Presbycusis is a gradual hearing loss caused by the ageing process. This is a chronic condition that affects the elderly population, and sensorineural progressive bilateral symmetry occurs with predominantly high-frequency hearing loss. The ability to discriminate speech decreases; hence, most of the affected patients have conversation problems, especially in noisy environments.This situation is a serious problem among elderly individuals. Social isolation, depression, and paranoia can be related to presbycusis. Objective: The aim of this study was to investigate GPx and the GSH:GSSG ratio as risk factors for presbycusis. Methods: A case-control study was conducted to determine the role of GPx activity with the GSH:GSSG ratio as a presbycusis risk factor in 60 subjects aged 55 to 75 years old during the period of August 2012 - April 2014. All of the subjects passed an ENT examination, pure tone audiometry, and tympanometry. The activity of GPx was measured with the Paglia and Valentine method, and the GSH:GSSG ratio was measured by the calorimetric method. Results: The activity of GPx and the GSH:GSSG ratio were significantly different between the groups (p<0.05), and the odds ratio for high GPx with a low GSH:GSSG ratio was 135 (CI 95%: 5.17-20,028.88). Conclusion: High GPx activity with a low GSH:GSSG ratio is a risk factor for presbycusis.
Chapter
The regulation of K+ concentration of the extracellular fluid is critical for normal nerve and muscle function. The extracellular K+ concentration and the high permeability of the plasma membrane to K+ are the main determinants of the membrane potential. Potassium plays an important role in several cellular processes such as mitosis and glycogenesis and is necessary for the normal activity of several enzymes. For example, a decrease in the concentration of plasma K+ affects the renal capacity to concentrate urine; this effect is directly related to a loss of connecting and principal cells capacity to respond to AVP. The result is a marked polyuria, which is reversed when the extracellular and intracellular concentration of K+ is reestablished.
Article
Full-text available
Senescence is marked by several transition in the physique, all of which have a contradictory impact on the well-being and way of living of the geriatric. As a person grows older, nutrition becomes even more important. It has a notable influence on the life quality, including physical and mental health. Food intake decreases due to biological transition in the geriatric, consequently leading to nutritional deficiencies that in turn are the primary possibility for various persistent ailments and degenerating age-related well-being. Intervention can be used to address the ongoing state of dietary deficiency and malnutrition. In this article, an overview between dental health and nutritional condition in geriatric is discussed to aggrandize a healthy way of living in geriatric.
Unarousable child with short bowel A 4-year-old boy was admitted with progressive lethargy of a few hours’ duration and no other symptoms. His medical history was relevant for short bowel syndrome (SBS), following neonatal volvulus, with residual bowel length of 23 cm and intact ileocecal valve. He had similar self-limiting episodes in the past, after weaning parenteral nutrition, especially after eating large meals. The day before, he had consumed a large amount of apples. Arterial blood gas (ABG) analysis showed metabolic acidosis with normal lactacidaemia (pH 7.09, pCO 2 19 mm Hg, pO 2 101 mm Hg, HCO3 5.8 mmol/L, BE −24, anion gap 29.4, chloride 116 mmol/L, L-lactate level 4 mmol/L). On admission, the child could be awakened, but he was confused with slurred speech (Glasgow Coma Scale 14), with a body temperature of 37 C°, a heart rate of 125 beats/min and a respiratory rate of 38 breaths/min. The abdomen was distended, without guarding and with normal bowel sounds. Blood glucose levels were normal, as well as white blood cell count, liver and kidney function test and C reactive protein. An abdominal ultrasound ruled out an intussusception. An abdominal X-ray was performed too (see figure 1). Figure 1 Abdominal distension with gas and bloating. Questions Which is the most likely diagnosis? Encephalitis D-lactic acidosis Dehydration with third space fluid collection and acidosis Hereditary fructose intolerance. How is this diagnosis confirmed? D lactic dosage Breath test for bacterial overgrowth Urine organic acid dosage Search for reductive substances in the stools. How should this patient be managed? Intravenous fluids to facilitate D-lactic excretion Restrict carbohydrates in the diet Intravenous bicarbonates Antibiotic treatment to reduce bowel bacterial overgrowth. Answers can be found on page 2 .
ResearchGate has not been able to resolve any references for this publication.