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Ing TS, Ganta K, Bhave G, Lew SQ, Agaba EI, Argyropoulos C, Tzamaloukas AH. The Corrected Serum Sodium Concentration in Hyperglycemic Crises: Computation and Clinical Applications. Front Med (Lausanne) 2020; 7:477. [PMID: 32984372 PMCID: PMC7479837 DOI: 10.3389/fmed.2020.00477] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/20/2020] [Accepted: 07/15/2020] [Indexed: 12/15/2022] Open
Abstract
In hyperglycemia, hypertonicity results from solute (glucose) gain and loss of water in excess of sodium plus potassium through osmotic diuresis. Patients with stage 5 chronic kidney disease (CKD) and hyperglycemia have minimal or no osmotic diuresis; patients with preserved renal function and diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS) have often large osmotic diuresis. Hypertonicity from glucose gain is reversed with normalization of serum glucose ([Glu]); hypertonicity due to osmotic diuresis requires infusion of hypotonic solutions. Prediction of the serum sodium after [Glu] normalization (the corrected [Na]) estimates the part of hypertonicity caused by osmotic diuresis. Theoretical methods calculating the corrected [Na] and clinical reports allowing its calculation were reviewed. Corrected [Na] was computed separately in reports of DKA, HHS and hyperglycemia in CKD stage 5. The theoretical prediction of [Na] increase by 1.6 mmol/L per 5.6 mmol/L decrease in [Glu] in most clinical settings, except in extreme hyperglycemia or profound hypervolemia, was supported by studies of hyperglycemia in CKD stage 5 treated only with insulin. Mean corrected [Na] was 139.0 mmol/L in 772 hyperglycemic episodes in CKD stage 5 patients. In patients with preserved renal function, mean corrected [Na] was within the eunatremic range (141.1 mmol/L) in 7,812 DKA cases, and in the range of severe hypernatremia (160.8 mmol/L) in 755 cases of HHS. However, in DKA corrected [Na] was in the hypernatremic range in several reports and rose during treatment with adverse neurological consequences in other reports. The corrected [Na], computed as [Na] increase by 1.6 mmol/L per 5.6 mmol/L decrease in [Glu], provides a reasonable estimate of the degree of hypertonicity due to losses of hypotonic fluids through osmotic diuresis at presentation of DKH or HHS and should guide the tonicity of replacement solutions. However, the corrected [Na] may change during treatment because of ongoing fluid losses and should be monitored during treatment.
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Affiliation(s)
- Todd S Ing
- Department of Medicine, Stritch School of Medicine, Loyola University Chicago, Chicago, IL, United States
| | - Kavitha Ganta
- Medicine Service, Department of Medicine, Raymond G. Murphy Veterans Affairs Medical Center, University of New Mexico School of Medicine, Albuquerque, NM, United States
| | - Gautam Bhave
- Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States
| | - Susie Q Lew
- Department of Medicine, George Washington University School of Medicine, Washington, DC, United States
| | | | - Christos Argyropoulos
- Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM, United States
| | - Antonios H Tzamaloukas
- Research Service, Department of Medicine, Raymond G. Murphy Veterans Affairs Medical Center, University of New Mexico School of Medicine, Albuquerque, NM, United States
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Dialysis-associated hyperglycemia: manifestations and treatment. Int Urol Nephrol 2020; 52:505-517. [PMID: 31955362 DOI: 10.1007/s11255-019-02373-1] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/07/2019] [Accepted: 12/23/2019] [Indexed: 12/15/2022]
Abstract
PURPOSE Dialysis-associated hyperglycemia (DAH), is associated with a distinct fluid and electrolyte pathophysiology. The purpose of this report was to review the pathophysiology and provide treatment guidelines for DAH. METHODS Review of published reports on DAH. Synthesis of guidelines based on these reports. RESULTS The following fluid and solute abnormalities have been identified in DAH: (a) hypoglycemia: this is a frequent complication of insulin treatment and its prevention requires special attention. (b) Elevated serum tonicity. The degree of hypertonicity in DAH is lower than in similar levels of hyperglycemia in patients with preserved renal function. Typically, correction of hyperglycemia with insulin corrects the hypertonicity of DAH. (c) Extracellular volume abnormalities ranging from pulmonary edema associated with osmotic fluid shift from the intracellular into the extracellular compartment as a consequence of gain in extracellular solute (glucose) to hypovolemia from osmotic diuresis in patients with residual renal function or from fluid losses through extrarenal routes. Correction of DAH by insulin infusion reverses the osmotic fluid transfer between the intracellular and extracellular compartments and corrects the pulmonary edema, but can worsen the manifestations of hypovolemia, which require saline infusion. (d) A variety of acid-base disorders including ketoacidosis correctable with insulin infusion and no other interventions. (e) Hyperkalemia, which is frequent in DAH and is more severe when ketoacidosis is also present. Insulin infusion corrects the hyperkalemia. Extreme hyperkalemia at presentation or hypokalemia developing during insulin infusion require additional measures. CONCLUSIONS In DAH, insulin infusion is the primary management strategy and corrects the fluid and electrolyte abnormalities. Patients treated for DAH should be monitored for the development of hypoglycemia or fluid and electrolyte abnormalities that may require additional treatments.
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Gallo de Moraes A, Surani S. Effects of diabetic ketoacidosis in the respiratory system. World J Diabetes 2019; 10:16-22. [PMID: 30697367 PMCID: PMC6347653 DOI: 10.4239/wjd.v10.i1.16] [Citation(s) in RCA: 22] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/23/2018] [Revised: 11/08/2018] [Accepted: 12/13/2018] [Indexed: 02/05/2023] Open
Abstract
Diabetes affects approximately 30 million persons in the United States. Diabetes ketoacidosis is one of the most serious and acute complications of diabetes. At the time of presentation and during treatment of diabetic ketoacidosis (DKA), several metabolic and electrolyte derangements can ultimately result in respiratory compromise. Most commonly, hypokalemia, hypomagnesemia and hypophosphatemia can eventually lead to respiratory muscles failure. Furthermore, tachypnea, hyperpnea and more severely, Kussmaul breathing pattern can develop. Also, hydrostatic and non-hydrostatic pulmonary edema can occur secondary to volume shifts into the extracellular space and secondary to increased permeability of the pulmonary capillaries. The presence of respiratory failure in patients with DKA is associated with higher morbidity and mortality. Being familiar with the causes of respiratory compromise in DKA, and how to treat them, may represent better outcomes for patients with DKA.
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Affiliation(s)
- Alice Gallo de Moraes
- Department of Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN 55905, United States
| | - Salim Surani
- Division of Pulmonary, Critical Care and Sleep Medicine, Texas A and M University, Corpus Christy, TX 78412, United States
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Konstantinov NK, Rohrscheib M, Agaba EI, Dorin RI, Murata GH, Tzamaloukas AH. Respiratory failure in diabetic ketoacidosis. World J Diabetes 2015; 6:1009-1023. [PMID: 26240698 PMCID: PMC4515441 DOI: 10.4239/wjd.v6.i8.1009] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/26/2014] [Revised: 01/08/2015] [Accepted: 05/27/2015] [Indexed: 02/05/2023] Open
Abstract
Respiratory failure complicating the course of diabetic ketoacidosis (DKA) is a source of increased morbidity and mortality. Detection of respiratory failure in DKA requires focused clinical monitoring, careful interpretation of arterial blood gases, and investigation for conditions that can affect adversely the respiration. Conditions that compromise respiratory function caused by DKA can be detected at presentation but are usually more prevalent during treatment. These conditions include deficits of potassium, magnesium and phosphate and hydrostatic or non-hydrostatic pulmonary edema. Conditions not caused by DKA that can worsen respiratory function under the added stress of DKA include infections of the respiratory system, pre-existing respiratory or neuromuscular disease and miscellaneous other conditions. Prompt recognition and management of the conditions that can lead to respiratory failure in DKA may prevent respiratory failure and improve mortality from DKA.
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Tzamaloukas AH, Ing TS, Siamopoulos KC, Rohrscheib M, Elisaf MS, Raj DSC, Murata GH. Body fluid abnormalities in severe hyperglycemia in patients on chronic dialysis: review of published reports. J Diabetes Complications 2008; 22:29-37. [PMID: 18191075 DOI: 10.1016/j.jdiacomp.2007.06.012] [Citation(s) in RCA: 32] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/20/2006] [Revised: 05/29/2007] [Accepted: 06/19/2007] [Indexed: 02/08/2023]
Abstract
Reports of dialysis-associated hyperglycemia (DH) were compared to reports of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH) in patients with preserved renal function. Average serum values in DH (491 observations), DKA (1036 observations), and NKH (403 observations) were as follows, respectively: glucose, 772, 649, and 961 mg/dl; sodium, 127, 134, and 149, mmol/l; and tonicity, 298, 304, and 355 mOsm/kg. Assuming that euglycemic (serum glucose, 90 mg/dl) values were the same (sodium, 140 mmol/l; tonicity, 285 mOsm/kg) for all three states, the hyperglycemic rise in the average serum tonicity value per 100-mg/dl rise in serum glucose concentration was 1.9 mOsm/kg in DH, 3.5 mOsm/kg in DKA, and 8.1 mOsm/kg in NKH. Neurological manifestations in DH patients were caused by coexisting conditions (ketoacidosis, sepsis, and neurological disease) in most instances, and by severe hypertonicity (>320 mOsm/kg), with clearing after insulin administration, in a few instances. In 148 episodes of DH corrected with insulin only, the mean increase in serum sodium per 100-mg/dl decrease in serum glucose (Delta[Na]/Delta[Glu]) was -1.61 mmol/l. In agreement with theoretical predictions, Delta[Na]/Delta[Glu] was numerically smaller in patients with edema than in those with euvolemia. The average hyperglycemic increase in extracellular volume, calculated from changes in serum sodium concentration during correction of DH using insulin alone, was 0.013 l/l per 100-mg/dl increase in serum glucose concentration. A small number of DH patients presented with pulmonary edema rectified by insulin alone. DH causes modest hypertonicity, with few patients having neurological manifestations caused usually by other coexisting conditions. In contrast to DKA or NKH, which usually presents with hypovolemia, DH causes hypervolemia manifested occasionally by pulmonary edema. Insulin is adequate treatment for DH.
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7
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Fernandes Júnior CJ, Hidal JT, Barbas CS, Akamine N, Knobel E. Noncardiogenic pulmonary edema complicating diabetic ketoacidosis. Endocr Pract 2005; 2:379-81. [PMID: 15251497 DOI: 10.4158/ep.2.6.379] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
OBJECTIVE To alert physicians to the possibility of pulmonary edema as a complication of diabetic ketoacidosis. METHODS We report a case of adult respiratory distress syndrome after resuscitative efforts to compensate the first episode of diabetic ketoacidosis in a previously healthy young woman. RESULTS In a 26-year-old woman with a 3-day history of malaise, polyuria, nausea, and vomiting, severe hypoxia and rales developed, and intubation and mechanical ventilation became necessary. Hemodynamic evaluation and striking electron microscopic findings on open-lung biopsy confirmed the diagnosis of adult respiratory distress syndrome. Despite adequate ventilatory support and hemodynamic management, death ensued and was attributed to irresponsive and progressive acute respiratory failure due to increased pulmonary capillary permeability edema. CONCLUSION Clinicians should be aware of this possibly fatal pulmonary complication of diabetic ketoacidosis.
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McCloud LL, Parkerson JB, Freant L, Hoffman WH, Catravas JD. beta-hydroxybutyrate induces acute pulmonary endothelial dysfunction in rabbits. Exp Lung Res 2004; 30:193-206. [PMID: 15195553 DOI: 10.1080/01902140490276311] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
The authors examined the effects of high ketone body and glucose concentrations on endothelial cell (EC) function in perfused rabbit lungs. beta-Hydroxybutyrate (beta OHB), at 5 mM, decreased endothelial angiotensin-converting enzyme (eACE) activity, whereas 25 mM glucose (HG), 1 mM beta OHB, or 10 mM acetoacetate (AcAc) did not. Dry to wet weight ratios were also reduced in lungs perfused with 5 mM beta OHB, but not with AcAc. beta OHB, at 5 mM, caused massive hemorrhage and interstitial and alveolar neutrophil infiltration; AcAc only produced engorgement of septal capillaries. Thus, pulmonary EC dysfunction occurs in rabbit lungs acutely perfused with beta OHB, but not with AcAc or glucose.
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Affiliation(s)
- Laryssa L McCloud
- Vascular Biology Center, Medical College of Georgia, Augusta, GA 30912-2500, USA.
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9
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Hoffman WH, Locksmith JP, Burton EM, Hobbs E, Passmore GG, Pearson-Shaver AL, Deane DA, Beaudreau M, Bassali RW. Interstitial pulmonary edema in children and adolescents with diabetic ketoacidosis. J Diabetes Complications 1998; 12:314-20. [PMID: 9877465 DOI: 10.1016/s1056-8727(98)00012-9] [Citation(s) in RCA: 45] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/18/2023]
Abstract
The acute complications of diabetic ketoacidosis in children and adolescents are well recognized but not completely understood. Clinical studies have focused primarily on brain edema. We have investigated the prevalence and course of interstitial pulmonary edema in patients with severe diabetic ketoacidosis all of whom had uneventful clinical courses. High resolution computed tomography scans of the lungs were analyzed by determining the Hounsfield attenuation level and then converting to physical density values. All seven patients had evidence of interstitial pulmonary edema on the first scan, which was performed within 1 h of hydration and prior to receiving insulin; six of the seven patients had increased pulmonary density 6-8 h into treatment, and all had complete resolution of the interstitial changes at discharge. Our study suggests that subclinical interstitial pulmonary edema may be a frequent occurrence in children and adolescents with severe diabetic ketoacidosis and may very well be present prior to treatment. The study also supports the philosophy of cautious rehydration and the close monitoring of children and adolescents with diabetic ketoacidosis until a more complete understanding of this pathophysiologic event is achieved.
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Affiliation(s)
- W H Hoffman
- Department of Pediatrics, Medical College of Georgia, Augusta 30912, USA
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Affiliation(s)
- D S Holsclaw
- Department of Pediatrics, Hahnemann School of Medicine, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania 19102, USA
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11
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McEachern RC, Patel RG. Pneumopericardium associated with face-mask continuous positive airway pressure. Chest 1997; 112:1441-3. [PMID: 9367492 DOI: 10.1378/chest.112.5.1441] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023] Open
Abstract
This is an uncommon case of a patient who developed pneumopericardium while being treated with face-mask continuous positive airway pressure (CPAP) for hypoxic respiratory failure following a coronary artery bypass graft surgery. A pneumopericardium detected by chest radiograph resolved completely after discontinuation of face-mask CPAP. Possible mechanisms that may have been involved in this unusual complication are reviewed.
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Affiliation(s)
- R C McEachern
- Department of Medicine, University of Mississippi Medical Center, Jackson 39216-4505, USA
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12
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Affiliation(s)
- J Klekamp
- Department of Pediatrics and Anesthesiology, Vanderbilt Children's Hospital, Vanderbilt University Medical Center, Nashville, Tennessee, USA
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13
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Ladwig P, Coles R, Fischer E, Spurrett B. Thyrotoxicosis in pregnancy presenting as pancytopenia. Aust N Z J Obstet Gynaecol 1995; 35:457-60. [PMID: 8717580 DOI: 10.1111/j.1479-828x.1995.tb02168.x] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
Abstract
Delay in diagnosis of thyroid disease can result in morbidity and mortality. Thyroid disorders are not uncommon in the reproductive age group and therefore in pregnancy; recognition of both the common and the more unusual manifestations will optimize outcome.
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Affiliation(s)
- P Ladwig
- Nepean Hospital, Penrith, New South Wales
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14
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Abstract
This article reviews the pathogenesis of diabetic ketoacidosis (DKA) and provides a rational approach to the management of patients with DKA. The therapeutic discussion includes the use of low-dose insulin, no bicarbonate, or phosphate therapy on the majority of DKA patients, based on numerous prospective randomized studies. The article also discusses controversial subjects such as the use of hypotonic versus isotonic saline with and without colloids, hydration of subjects before insulin therapy, and admission of DKA patients to the general ward versus emergency ward versus intensive care unit. A concise, simple protocol is also presented as a suitable reference for management of patients with DKA.
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Affiliation(s)
- A E Kitabchi
- Division of Endocrinology and Metabolism, University of Tennessee, Memphis
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15
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16
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Affiliation(s)
- C R Reed
- Division of Pulmonary and Critical Care Medicine, Medical College of Virginia, Richmond
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17
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Abstract
Diabetes mellitus produces serious complications in several major organ systems. The pulmonary complications, although uncommon and not well recognized, may be life-threatening. We describe a 20-year-old patient with diabetic ketoacidosis in whom pulmonary zygomycosis developed. This condition was complicated by stenosis of the left upper lobe bronchus despite successful treatment of the zygomycosis. Bronchial obstruction has become a well-recognized complication of pulmonary zygomycosis. In addition to infections caused by Zygomycetes, mycobacteria, viruses, and bacteria, the pulmonary complications described in patients with diabetes include pulmonary edema, disordered breathing during sleep, and reductions in elastic recoil of the lungs, diffusing capacity of the lungs for carbon monoxide, and bronchomotor tone. Other reported complications are respiratory alkalosis, cardiorespiratory arrest, pneumothorax, pneumomediastinum, plugging of the airways with mucus, and aspiration pneumonia attributable to diabetic gastroparesis.
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Affiliation(s)
- L A Hansen
- Division of Thoracic Diseases, Mayo Clinic, Rochester, MN 55905
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18
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Laggner AN, Lenz K, Kleinberger G, Sommer G, Druml W, Schneeweiss B. Influence of fluid replacement on extravascular lung water (EVLW) in patients with diabetic ketoacidosis. Intensive Care Med 1988. [PMID: 3132489 DOI: 10.1007/b&00717987] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022]
Abstract
Fluid replacement is a major issue in the treatment of patients with diabetic ketoacidosis. During this therapy, development of pulmonary edema has been reported and attributed to an increase in pulmonary microvascular pressure and a decrease in colloid-osmotic pressure (COP). Because clinically apparent pulmonary edema is associated with an increase in extravascular lung water (EVLW) and impairment of pulmonary gas exchange, we studied the effect of fluid replacement on EVLW, COP, pulmonary hemodynamics and gas exchange parameters in 8 patients with diabetic ketoacidosis (blood glucose greater than 300 mg/dl, pH less than 7.1). EVLW was estimated by the thermal-dye technique. All variables were successively determined upon admission (A), after initial fluid replacement (IFR), when glucose had fallen below 180 mg/dl, after 8 h of intravenous glucose treatment (G), and after 24 h of total parenteral nutrition (TPN). Despite a total net fluid intake of 6.0 +/- 1.61, a significant decrease (p less than 0.001) in COP from 29.6 +/- 5.5 at A to 18.8 +/- 2.2 mmHg after TPE and a significant increase (p less than 0.001) in PCWP from 4 +/- 2 at A to 10 +/- 3 mmHg after TPE, EVLW remained almost unchanged. EVLW was 5.1 +/- 2.8 at A, 5.3 +/- 2.1 after IFR, 4.8 +/- 1.4 after G, and 5.3 +/- 1.7 ml/kg after TPN. However, PaO2 decreased from 137 +/- 17 at A to 87 +/- 10 mmHg after TPE (p less than 0.001), while Qs/Qt increased significantly (p less than 0.05). The alterations in gas exchange may be indicative of pulmonary dysfunction but as they were not associated with accumulation of EVLW, they may as well reflect the compensation of metabolic derangements in diabetic ketoacidosis.
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Affiliation(s)
- A N Laggner
- Department of Medicine, University of Vienna, Austria
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Laggner AN, Lenz K, Kleinberger G, Sommer G, Druml W, Schneeweiss B. Influence of fluid replacement on extravascular lung water (EVLW) in patients with diabetic ketoacidosis. Intensive Care Med 1988; 14:201-5. [PMID: 3132489 DOI: 10.1007/bf00717987] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
Fluid replacement is a major issue in the treatment of patients with diabetic ketoacidosis. During this therapy, development of pulmonary edema has been reported and attributed to an increase in pulmonary microvascular pressure and a decrease in colloid-osmotic pressure (COP). Because clinically apparent pulmonary edema is associated with an increase in extravascular lung water (EVLW) and impairment of pulmonary gas exchange, we studied the effect of fluid replacement on EVLW, COP, pulmonary hemodynamics and gas exchange parameters in 8 patients with diabetic ketoacidosis (blood glucose greater than 300 mg/dl, pH less than 7.1). EVLW was estimated by the thermal-dye technique. All variables were successively determined upon admission (A), after initial fluid replacement (IFR), when glucose had fallen below 180 mg/dl, after 8 h of intravenous glucose treatment (G), and after 24 h of total parenteral nutrition (TPN). Despite a total net fluid intake of 6.0 +/- 1.61, a significant decrease (p less than 0.001) in COP from 29.6 +/- 5.5 at A to 18.8 +/- 2.2 mmHg after TPE and a significant increase (p less than 0.001) in PCWP from 4 +/- 2 at A to 10 +/- 3 mmHg after TPE, EVLW remained almost unchanged. EVLW was 5.1 +/- 2.8 at A, 5.3 +/- 2.1 after IFR, 4.8 +/- 1.4 after G, and 5.3 +/- 1.7 ml/kg after TPN. However, PaO2 decreased from 137 +/- 17 at A to 87 +/- 10 mmHg after TPE (p less than 0.001), while Qs/Qt increased significantly (p less than 0.05). The alterations in gas exchange may be indicative of pulmonary dysfunction but as they were not associated with accumulation of EVLW, they may as well reflect the compensation of metabolic derangements in diabetic ketoacidosis.
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Affiliation(s)
- A N Laggner
- Department of Medicine, University of Vienna, Austria
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20
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Breidbart S, Singer L, St Louis Y, Saenger P. Adult respiratory distress syndrome in an adolescent with diabetic ketoacidosis. J Pediatr 1987; 111:736-8. [PMID: 3117997 DOI: 10.1016/s0022-3476(87)80256-1] [Citation(s) in RCA: 26] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Affiliation(s)
- S Breidbart
- Department of Pediatrics, Montefiore Medical Center/Albert Einstein College of Medicine, Bronx, NY 10467
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Abstract
The first objective in diabetic ketoacidosis is to restore the circulating volume and improve tissue perfusion. In any form of hypovolaemic shock the most efficient way of restoring circulating volume is to be use colloid solutions rather than crystalloids. At least three times the amount of crystalloid must be used to achieve the same effect. The historical reason for using isotonic saline in diabetic ketoacidosis is related not to its similarity to the fluid lost, but to its supposed efficiency in correcting the circulating volume. Excess crystalloid expands the interstitial space which results in pulmonary oedema, peripheral oedema and possibly cerebral oedema. Although currently difficult to define precisely in their more subtle forms, they all produce adverse pathophysiological effects. The fluid loss in diabetic ketoacidosis is equivalent to "half-normal" saline, a relatively hypotonic solution. As well as causing extensive oedema, resuscitation with isotonic saline can increase serum sodium and osmolarity while not providing free water to replace the intracellular losses.
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22
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Fouet P, Hilpert F, Wysocki M, Zarka D, Margent P. [Non-cardiogenic pulmonary edema associated with severe diabetic ketoacidosis]. ANNALES FRANCAISES D'ANESTHESIE ET DE REANIMATION 1987; 6:127-8. [PMID: 3109284 DOI: 10.1016/s0750-7658(87)80119-3] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
Non cardiogenic pulmonary oedema occurs rarely in patients with diabetic ketoacidosis, except in conjunction with an infection. A case is reported of non cardiogenic pulmonary oedema in a patient with severe diabetic ketoacidosis, which resolved within 72 h with oxygen supply only. There were no objective facts which could explain its pathogenesis, despite the important pulmonary asymmetry due to a unilateral diaphragmatic paralysis.
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25
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Leonard RC, Asplin C, McCormick CV, Hockaday TD. Acute respiratory distress in diabetic ketoacidosis: possible contribution of low colloid osmotic pressure. BMJ : BRITISH MEDICAL JOURNAL 1983; 286:760-2. [PMID: 6402236 PMCID: PMC1547034 DOI: 10.1136/bmj.286.6367.760] [Citation(s) in RCA: 29] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/20/2023]
Abstract
The "shock lung" syndrome may occur in diabetic ketoacidosis in association with disseminated intravascular coagulation; occasionally it occurs alone after treatment of the ketoacidosis. Two patients developed pulmonary opacities with clinical features of acute respiratory distress such as are seen in the shock lung syndrome; in both, however, the findings suggested a different mechanism from that occurring in the syndrome. Hypoalbuminaemia was prominent, and it is postulated that a low plasma osmotic pressure caused by high volume crystalloid infusions may have precipitated the acute respiratory complications. Plasma osmotic pressure may be an important variable in patients given large volumes of crystalloid infusions; further studies are required to elucidate mechanisms of pulmonary oedema in such patients.
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Abstract
Hemodynamic evaluation in two patients and analysis of pulmonary edema fluid in one patient with diabetic ketoacidosis and acute pulmonary edema were performed. Pulmonary arterial wedge pressures in both patients were low or normal (1 and 9 mm Hg). In one patient the colloid osmotic pressure of the pulmonary edema fluid was 68 percent of the value of the serum. The serum colloid osmotic pressure-pulmonary arterial wedge pressure gradient in the second patient was markedly reduced. Pulmonary edema complicating diabetic ketoacidosis may be the result of increased permeability of pulmonary capillary membranes and altered intravascular colloid-hydrostatic forces.
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28
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Greenbaum DM, Millen JE, Snyder JV, Grenoik A, Safar P. Continuous Positive Airway Pressure via Face Mask Is a Dangerous Step Backwards. Chest 1977. [DOI: 10.1378/chest.71.1.118-b] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/01/2022] Open
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Greenbaum DM, Millen JE, Eross B, Snyder JV, Grenvik A, Safar P. Continuous positive airway pressure without tracheal intubation in spontaneously breathing patients. Chest 1976; 69:615-20. [PMID: 773602 DOI: 10.1378/chest.69.5.615] [Citation(s) in RCA: 80] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022] Open
Abstract
Indications for the use of therapy with continuous positive airway pressure (CPAP) in spontaneously breathing patients are increasing in number. The value of this technique without tracheal intubation was investigated in 14 patients with acute respiratory distress. In most patients (eight patients, or 57 percent) the technique was successful, as evidenced by avoidance of the necessity for tracheal intubation and improvements in clinical appearance, arterial oxygen pressure, and chest x-ray films. Complications were observed in three patients, but these necessitated discontinuation of therapy in only one. The use of this technique allows avoidance of endotracheal intubation and mechanical ventilation, with their attendant risks.
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