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Jason Carson, Middle School Choir
Choir Director, Foster High School; Launched choir program at Pin Oak Middle School (2003);
Bachelor of Music degree, Baylor University and Master of Music in Choral Conducting,
Louisiana State University; Member of the Texas Music Educators Association, Texas Choral
Directors Association, American Choral Directors Association, Music Educators National
Conference, Organization of American Kodaly Educators, and the Pi Kappa Lambda Music
Amy Moore, Middle School Choir
Head Choral Director, Labay Middle School (14 years); Active adjudicator and clinician
throughout Texas; Bachelor of Music in Music Education, Baylor University (received
Outstanding Music Educator, Outstanding Choral Musician, Outstanding Senior Woman in the
School of Music and Who’s Who Among American College Students)
Joel Price, Middle School Choir Guest Conductor
Director of Choirs, Westwood Junior High, Richardson ISD; RISD Secondary Teacher of the Year
2004-2005;   Former Middle School/Junior High Vice President, Texas Choral Directors
Association; Finalist, H-E-B Excellence in Education award program, 2008; Bachelor of Music in
Music Education and Vocal Performance, Southern Methodist University;

Jed Ragsdale, High School Choir
Choir Director, Cy-Fair High School (15 years in CFISD); Bachelor or Music, Southwestern
University, Master’s in Education Administration, Lamar University; Frequent conductor and
clinician for All-Region Choirs; Has performed with Houston Symphony Chorus, Brazosport
Symphony Orchestra and Texas Master Chorale

Kimberly Tobola, High School Choir
Director of Choral Activities, Lanier Middle School (11 years); Conductor, Houston Girls Chorus;
Founding member, VOX; Bachelor of Music in Vocal Performance, Baylor University and Master
of Music in Vocal Performance, Cincinnati College-Conservatory of Music.

Giselle Wyers, High School Choir Guest Conductor
Donald E. Peterson Associate Professor of Choral Music at the University of Washington; Has
toured internationally with the University Chorus at University of Washington; Guest Conductor
for numerous high school groups across the U.S., including the Alaska All-State Women’s Honor
Choir and the Nebraska Wesleyan Honor Choir in the 2013-14 season; Choral compositions
published by Santa Barbara Music Press as “Giselle Wyers Choral Series”; Founder, San Lorenzo
Valley Community Chorus and Orchestra (California); D.M.A. in conducting, University of
Arizona, Master's degree, Westminster Choir College, Bachelor's degree, UC Santa Cruz
Cynthia Clayton
Associate Professor of Voice, Moores School of Music, University of Houston; Avid performer of
recitals, chamber music, and operas; Has held leading operatic roles with New York City Opera,
Houston Grand Opera, Dallas Opera, San Diego Opera, Utah Opera, Cleveland Opera, Opéra en
Plein Air (Belgium), and many others

Kelli Estes
Artistic Director & Co-Founder, Lone Star Lyric Festival; Original cast member Opera Company
of Brooklyn, Opera in the Heights, Allentown Concert Opera, Center City Opera Theater
(Philadelphia); B.A. California State University, Fresno; M.M., University of Houston
Melissa Givens
Area Coordinator, Vocal Studies and Assistant Professor in Music, Houston Baptist University;
Has performed as soloist with Vienna Volksoper Orchestra, the Budapest Concert Orchestra,
Austin Symphony Orchestra, Houston Symphony Orchestra, National Philharmonic and the
Duluth-Superior Symphony Orchestra; Core artist with Ars Lyrica Houston and the Bach Society
of Houston; Member of the National Association of Teachers of Singing, the American Guild of
Musical Artists, the Houston Tuesday Musical Club, and the honor societies Omicron Delta Kappa
and Pi Lambda Kappa; BA in Music, Davidson College, MM in Vocal Performance, Shepherd
School of Music, DMA in Music Performance, University of Houston

Brady Knapp
Associate Professor, Director of Choral Activities, University of St. Thomas; Frequent recitalist
and clinician; Has performed with numerous ensemble in the Southeast; Doctor of Musical Arts,
Master of Music in Vocal Performance, and Bachelor of Music in Performance.
Jason Lester
Instructor of Music and Choir Director, Wharton County Junior College; Active performer of
concert works, recitals and opera; Has performed with Glimmerglass Opera, Berkshire Opera,
Opera in the Heights, Woodlands Symphony Orchestra, Fort Bend Symphony Orchestra, Florida
State Opera, Opera Theater of Lucca, Italy, Tallahassee Bach Parley and has been heard on NPR’s
World of Opera; Doctor of Music, Florida State University, Master of Music, University of
Cincinnati College-Conservatory of Music, Bachelor of Music Education, Baylor University

Carole Nelson, Voice Department Head
Artistic Director, Houston Boychoir (on staff 23 years); Has toured internationally with Houston
Boychoir; Former Choir Director and Voice Teacher, High School for the Performing and Visual
Arts; Active clinician and adjudicator across the nation; Graduate, University of Houston, Moores
School of Music

Brian Shircliffe
Artist, Ars Lyrica; Has performed with Dayton Opera, Lake George Opera, Utah Festival Opera,
Opera in the Heights, Houston Grand Opera, and Opera Vista; Voice Teacher, San Jacinto College
and Lee College; Masters in Music, Moores School of Music.
Liz Wade
Freelance Artist; Has performed worldwide in concert and opera performances (Carmen,
Santuzza, and Der Komponist
0; Has studied with Katherine Ciesinski and Debria Brown; Has
worked with Frederika Von Stade, Carlile Floyd, and Robert Wilson
Holly Wilson Butler, High School Choir
Bachelor of Music, University of Houston and Performer’s Certificate, Conservatory of Music at
University of Missouri, Kansas City; Certificate of Performance, Russian School of Piano,
Freiburg, Germany; Has studied with Ruth Tomfohrde, Dr. Robert Weirich, Abby Simon, Dr.
Vitaly Margulis, and Sergei Babayan; Medalist in the San Antonio Music Club Competition, the
Ruth Burr Competition, the Missouri MTNA Competition and the UMKC Concerto Competition
Jasmine Hatem, Middle School Choir
Active soloist and chamber musician; has performed with Greenbriar Consortium, Houston Civic
Symphony, AURA, and Dominic Walsh Dance Company; Faculty, University of St. Thomas and
Bridges Academy at St. Luke’s Methodist Church; Master of Music in Piano performance, Moores
School of Music and Master of Music in chamber music and accompanying, Shepherd School of

Shawn Heller, High School Choir
Active freelance pianist; has performed in recitals in Asia, Steinway Hall, in universities
nationwide and in ensembles in Mexico, with Cincinnati Symphony Orchestra, and May Festival
Orchestra. He has studied with Horacio Guttierez, Ruth Tomfhorde, Abbey Simon and Dr.
William Black; Bachelor of Music degree in Piano Performance, University of Houston and
Master of Music program at the Cincinnati College-Conservatory of Music.
Catherine Schaefer, Middle School Choir
Accompanist, Music Theory and Aural Skills at University of Houston; Bachelor of Music and
Bachelor of Arts, Duquesne University, Pittsburgh and Master of Music, University of Houston

Source: http://www.afatexas.org/downloads/About/2014Faculty.Vocal.pdf

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Best Practice & Research Clinical Endocrinology & Metabolism 26 Suppl. 1 (2012) S16–S26 Contents lists available at ScienceDirect j o u rn a l ho m e pa g e : w w w . e l s e v i e r . c o m / l o c a t e / b e e m Considerations regarding the management ofhyponatraemia secondary to SIADH Alessandro Peri MD PhDa, *, Christian Combe MD PhDb,A a Department of Clinical Physiopathology, Endocrine Unit, Center for Research, Transfer and High Education on Chronic, Inﬂammatory,Degenerative and Neoplastic Disorders for the Development of Novel Therapies (DENOThe), University of Florence, 50139 Florence, Italyb Centre Hospitalier Universitaire de Bordeaux, Service de N´ephrologie Transplantation Dialyse, Bordeaux, France and Unit´e INSERM1026, Universit´e Bordeaux Segalen, Bordeaux, France Treatment of hyponatraemia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) should be guided by the symptomatology of the patient, which can be used as a surrogate for the duration of the hyponatraemia. However, in patients with acute symptomatic hyponatraemia (developing in <48 hours), the need to actively treat hyponatraemia is more imperative due to the potential risks associated with leaving hyponatraemia untreated (including the potential for development of serious neurological manifestations, such as seizures and brain stem herniation). In patients with hyponatraemia care needs to betaken not to exceed the recommended rates of correction, as thisincreases the risk of osmotic demyelination syndrome. This articlewill discuss the potential impact of prompt intervention in thetreatment of hyponatraemia, particularly secondary to SIADH, andthe need to weigh the beneﬁts of treatment against the potentialrisks associated with overly rapid correction.
2012 Elsevier Ltd. All rights reserved.
1. Introduction
Hyponatraemia – of which the syndrome of inappropriate secretion of antidiuretic hormone (SIADH),also known as the syndrome of inappropriate antidiuresis (SIAD), is one of the most common causes1 –is associated with increased morbidity and mortality.2 However, the optimum management of thiscondition continues to be the subject of debate amongst European physicians. When physicians aredeciding whether or not to treat hyponatraemia (serum sodium concentration ([Na+]) <136 mmol/L), * Corresponding author. Alessandro Peri MD PhD. Tel.: +39 55 4271366; Fax: +39 55 4271413. E-mail address:a.peri@dfc.uniﬁ.it.
A Tel.: +33 556 795537; Fax: +33 556 796032. E-mail address:
This supplement was commissioned by Otsuka Pharmaceutical Europe Ltd.
The European Hyponatraemia Network Academy meeting was organised and supported by Otsuka PharmaceuticalEurope Ltd.
Otsuka Pharmaceutical Europe Ltd. is the marketing authorisation holder for tolvaptan. information.
1521-690X/$ – see front matter 2012 Elsevier Ltd. All rights reserved.
A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 the risks associated with the hyponatraemia itself (e.g., development of cerebral oedema) are weighedagainst the potential risks of treatment. One of the primary considerations that physicians face whentreating hyponatraemia is the potential for development of osmotic demyelination syndrome, whichmay result from aggressive correction of serum [Na+].3 Therefore, physicians may be over-cautiousand delay treatment in these patients. Consequently, the impact of prompt intervention on patientoutcomes and length of hospital stay was the subject of a debate held during the inaugural meetingof the European Hyponatraemia Network. During this debate, arguments for and against the followingstatement were discussed: ‘A lack of prompt effective treatment of hyponatraemia increases morbidityand length of hospital stay’. Key points raised during this debate are presented here, along withsuggested approaches for the management of hyponatraemia secondary to SIADH.
1.1. Treatment options in patients with hyponatraemia secondary to SIADH Having identiﬁed a patient as having hyponatraemia secondary to SIADH via differential diagnosis,subsequent management of the condition should take into account the duration of the hyponatraemiaand the degree of symptomatology. In patients with acute hyponatraemia (developing in <48 hours)the primary goal of treatment should be the resolution of symptoms using hypertonic saline, withmodiﬁcation of treatment once symptoms have been resolved.4 Hypertonic saline solution also remainsthe preferred therapy in patients with chronic hyponatraemia (developing in >48 hours) with severesymptoms.
In moderate hyponatraemia, the recent approval of the vasopressin V receptor antagonist (also known as a vaptan), tolvaptan, has provided a new therapeutic option speciﬁcally targeted at thetreatment of hyponatraemia secondary to SIADH. Other conventional therapies for hyponatraemia(e.g., water restriction, demeclocycline, urea or lithium) have been used over the past decades;however, although effective in speciﬁc circumstances, they are suboptimal for many different reasons,including variable efﬁcacy, unpredictable compliance, slow responses, intolerable side effects andserious toxicities.5 In patients with mild or ‘asymptomatic’ chronic hyponatraemia, there is no immediate need for correction, although a therapeutic trial with ﬂuid restriction or a pharmacological agent may beconsidered to discern any potential improvements in the patient’s quality of life.5 1.2. Treatment choice for patients with hyponatraemia secondary to SIADH should promote free water Fluid restriction is often the standard of care in patients with asymptomatic hyponatraemia secondaryto SIADH. However, the likelihood of ﬂuid restriction successfully raising serum [Na+] in these patientscan be predicted based on the urine concentration. A high urine osmolality usually indicates a highconcentration of vasopressin within the serum; in these cases it is unlikely that ﬂuid restriction willcorrect the hyponatraemia, unless ﬂuid intake is restricted considerably.6 The response of patients toﬂuid restriction can be predicted using a quantiﬁcation of water and electrolyte balance – electrolytefree water clearance (CeH O):7 in which V is the 24 hour urine volume, U The clinical application of this equation is demonstrated in the following case study.
1.2.1. Case study: clinical application of the equation for free water clearanceA 72 year old man with metastatic lung cancer was admitted to hospital with hyponatraemia. At thetime of admission, he was not exhibiting any symptoms related to hypotonicity and was euvolaemic.
Following laboratory evaluation (Table 1), he was diagnosed with paraneoplastic SIADH.
As he was asymptomatic, the initial management prescribed was ﬂuid restriction to 1 L/day. However, the following day the patient’s serum [Na+] fell to 117 mmol/L. Prior investigation of electrolyte- A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 free water clearance would have revealed that this patient was retaining water. Electrolyte freewater clearance can be estimated using the patient’s urinary [K+], urinary [Na+] and serum [Na+],by calculating the urine/plasma (U/P) electrolyte ratio: is the urinary [Na+], U is the urinary [K+] and P Table 1
Diagnostic evaluation of a 72 year old man with hyponatraemia and metastatic lung cancer. This case study
shows the clinical application of the equation for free water clearance.
[K+] = Potassium concentration.
Case study provided by Professor T. Berl. Modiﬁed from Furst H et al. Am J Med Sci 2000; 319: 240–244.7
This simpliﬁed equation can be used to estimate free water loss in relation to the effective osmoles within the blood plasma. Approaches to raising serum [Na+] by ﬂuid restriction can be guided by thepatient’s U/P ratio (these can be seen in Table 2).7 Table 2
Approaches to raising serum tonicity with ﬂuid restriction. These approaches assume that urine sodium and
potassium losses are replaced, that a patient has an average body surface area of 1.73 m2 and eats a normal
diet, and calculate for the period during which the next 1 L of urine is excreted.
Reproduced from Furst H et al. Am J Med Sci 2000; 319: 240–2447 with permission.
As noted in Table 2, when the U/P ratio is greater than 1 almost no amount of water restriction will result in an increase in serum [Na+] because free water is being retained; a process that lowersserum [Na+].7 In such cases alternative approaches, involving an increase in solute intake or preferablya treatment that inhibits vasopressin action on the collecting duct and enhances free water excretion(a process that increases serum [Na+]) should be considered.
2. Debate: the need for prompt effective hyponatraemia management
During the European Hyponatraemia Network Academy Meeting, arguments for and against thefollowing statement were debated: ‘a lack of prompt effective treatment of hyponatraemia increasesmorbidity and length of hospital stay’. Key points from either side of this argument are discussedbelow.
A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 2.1. ‘A lack of prompt effective intervention in hyponatraemia increases morbidity and length of hospital stay’ The arguments against 2.1.1. Evidence supporting the link between hyponatraemia and worsening patient outcomes is not robustThere is an increasing accumulation of evidence to suggest that hyponatraemia in hospitalisedpatients is associated with increased morbidity,8–10 mortality,2,11 length of hospital stay9,11 and resourceutilisation.12 However, the majority of this evidence is in the form of retrospective investigations andpost-hoc analyses. There is therefore a lack of prospective data illustrating a reduction in patientmorbidity and length of hospital stay with the correction of hyponatraemia.
2.1.2. It is difﬁcult to ascertain to what extent worsening patient outcomes are caused as a direct result of the hyponatraemia rather than the underlying condition It is also important to consider that hyponatraemia is not a disease, but rather a consequence ofan underlying condition that limits the ability of the kidneys to excrete free water.3 In the majorityof cases, this results from the increased secretion of the hormone vasopressin.1,13 In the presence ofco-morbidities, it may be difﬁcult to ascertain the contribution of hyponatraemia to worsening patientoutcomes relative to the underlying condition.
2.1.3. Prompt treatment without taking into account the rate of onset of hyponatraemia could increase the risk of overcorrection and may lead to more harm than good The symptoms of hyponatraemia reﬂect the degree of hyponatraemia and the rate of serum [Na+]decline.3 Due to the danger of neurological complications, it is important to take into account the rateof onset when considering management options for hyponatraemia.
Following a fall in extracellular [Na+], there is a movement of water into the brain that results in cerebral oedema and increased intracranial pressure. When the onset of hyponatraemia is acute, thecranium restricts the swelling of the brain and complications, such as seizures, respiratory arrest andbrain stem herniation may occur. In this situation, rapid correction of hyponatraemia is necessarybecause the risk of brain stem herniation exceeds the risk of osmotic demyelination and treatmentwith hypertonic saline should be initiated.3,4 However, in cases of chronic hyponatraemia, rapid rises inserum [Na+] may increase the risk of overcorrection of serum [Na+]. When the onset of hyponatraemiais gradual, the cerebral oedema is ameliorated by a process of volume adaptation, involving theextrusion of intracellular potassium and organic osmolytes. This normalises brain volume, despitethe presence of persistent hyponatraemia.3,4,14 In light of the changes occurring within the brainin response to hyponatraemia, the importance of treating acute hyponatraemia rapidly and treatingchronic hyponatraemia slowly may be appreciated.
Overly rapid correction of hyponatraemia was demonstrated in a publication from Sterns and colleagues,14 who investigated the incidence of post-therapeutic complications in 56 patients treatedfor hyponatraemia (serum [Na+] <105 mmol/L). Patients with chronic hyponatraemia had a higherincidence of neurological sequelae than those classiﬁed with acute hyponatraemia (37% versus 0%,respectively, p < 0.01). The degree of serum [Na+] correction at 48 hours was found to be signiﬁcantlyassociated with the occurrence of neurological sequelae following treatment (p = 0.03).14 Given theseﬁndings, it is recommended that the rate of serum [Na+] correction is limited to <10–12 mmol/L in 24hours and to <18 mmol/L in 48 hours. However, it should be taken into consideration that patientswith severe malnutrition, alcoholism or advanced liver disease may be especially susceptible to osmoticdemyelination syndrome. Thus, given the risk of overshooting maximal recommended increases, it isbest to aim for correction by approximately 8 mmol/L per day.6,14 Despite the possibility of complications from treatment, chronic symptomatic hyponatraemia should not be ignored, as failing to address symptomatic hyponatraemia may result in adversepatient outcomes. In an investigation of 53 post-menopausal women with chronic symptomatichyponatraemia, deﬁned as a serum [Na+] <130 mmol/L (mean serum [Na+] 111 mmol/L) and withcentral nervous system manifestations,15 morbidity was lower and neurological outcomes were betterin patients that received active therapy with hypertonic saline compared with patients treated withﬂuid restriction (p < 0.01). The patients treated promptly with hypertonic saline (n = 17) recovered A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 without neurological sequelae or other complications. All patients treated only with ﬂuid restriction(n = 14) died or experienced permanent brain damage, despite having no associated medical conditionthat accounted for their morbidity.15 2.1.4. Although the use of vasopressin V receptor antagonists to correct hyponatraemia secondary to SIADH is an attractive option, there is a need for further assessment in prospective randomisedcontrolled trials Vasopressin V receptor antagonists, or vaptans, are novel drugs that may provide an alternative avenue of treatment for the prompt correction of hyponatraemia secondary to SIADH. Tolvaptan, a vasopressinV receptor antagonist, is the ﬁrst vaptan to be approved in Europe for the treatment of hyponatraemia secondary to SIADH. By binding to and blocking the V receptor, vasopressin-mediated activation of this receptor is prevented and free water clearance is increased.16–18 As a treatment approachfor hyponatraemia secondary to SIADH, a vaptan is attractive because it addresses the mechanismunderlying water retention (i.e., inappropriate secretion of vasopressin) without resulting in signiﬁcantelectrolyte losses.
Moreover, ﬂuid restriction, which may be difﬁcult for patients to maintain and slow to increase serum [Na+],6 is not necessary due to the state of aquaresis induced by vaptans.19 Overcorrection isunlikely if serum [Na+] is frequently measured and, to date, there have been no reported cases ofosmotic demyelination associated with its use.19 Vaptans, such as tolvaptan, represent promising treatment alternatives for the correction of hyponatraemia secondary to SIADH. However, a prospective, randomised trial comparing vaptans withthe standard of care would be useful to conﬁrm the relative effects of these promising agents on thelength of stay in hospital or the intensive care unit, rehospitalisation rates and patient compliance.
2.1.5. Illustrative case historyA 71 year old female presented 3 days after surgery for the removal of a pituitary adenoma(transsphenoidal endoscopic pituitary adenomectomy, presented to Professor G. Johannsson, Universityof G ¨oteborg); at admission she had a serum [Na+] of 146 mmol/L. The next day, the patient’sserum [Na+] fell to 130 mmol/L, and based on her hydration status, cortisol levels, thyroxine levelsand urine osmolality (Table 3), a diagnosis of SIADH induced by pituitary surgery was made. Thepatient was prescribed ﬂuid restriction on post-operative day 4 (ﬂuid restriction was initially 1 L/day).
Two days later the patient’s serum [Na+] had continued to decline so ﬂuid was further restrictedto 800 mL/day. Eventually, the patient’s serum [Na+] began to increase and ﬂuid restriction wasreturned to 1 L/day. The patient was ﬁnally discharged on post-operative day 13 with a serum [Na+]of 140 mmol/L.
Table 3
Laboratory result from illustrative case history.
BP = Blood pressure; F-T4 = Free thyroxine.
Case study provided by Professor G. Johannsson.
A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 2.2. ‘A lack of prompt effective intervention in hyponatraemia increases morbidity and length of hospital stay’ The arguments for 2.2.1. Hyponatraemia is frequently encountered in clinical practiceHyponatraemia is the most common electrolyte disorder encountered in clinical practice,3,20 withSIADH accounting for the majority of euvolaemic hyponatraemia cases.1 In a large database analysisof serum [Na+] measurements from 120,137 patients treated at a 1200-bed acute care hospital, andassociated outpatient services and community-care based polyclinics in Singapore, hyponatraemia(serum [Na+] <136 mmol/L) was present in 28.2% of patients admitted to acute hospital care, 21% ofpatients in ambulatory hospital care and 7.2% of hospital care.21 Consequently, any impact of treatmenton outcome measures such as morbidity and length of stay would only have to be small to have aconsiderable impact on patient outcomes.
2.2.2. Hyponatraemia is associated with increased patient mortalityIn a study conducted by Wald and colleagues, hyponatraemia (serum [Na+] <138 mmol/L) was presentin 38% of patients upon admission to a large academic medical centre in Boston during a 7-year period(53,236 patients admitted during this period were analysed).11 Furthermore, hyponatraemia developedin 38.2% of patients during admission (27,897 patients with normonatraemia upon admission and alength of stay >1 day were included in the analysis). An assessment of the relationship betweenin-patient mortality and admission serum [Na+] revealed that a serum [Na+] of 140 mmol/L wasassociated with the lowest risk of in-hospital mortality. Conversely, when serum [Na+] was evaluatedas a continuous variable, the adjusted risk of death was increased by 23% (odds ratio [OR], 1.23; 95%conﬁdence interval [CI], 1.19–1.27) for each 1 mmol/L decline below 138 mmol/L. Furthermore, thelength of hospital stay was increased in patients with hospital-acquired hyponatraemia relative tohospitalised patients without hyponatraemia (7.6 days vs. 4.9 days, respectively, adjusted difference2.7 days; 95% CI 2.5–2.9).11 The same study also reported an association between hospital-acquiredhyponatraemia, community-acquired hyponatraemia and the likelihood of discharge to a long- orshort-term care facility (see Fig. 1).11 Adjusted
Admission sodium concentration (mmol/L)
Fig. 1. Impact of community-acquired hyponatraemia on mortality, length of hospital stay and discharge to a short- or long-term
care facility. In this study, hyponatraemia was deﬁned as serum [Na+] <138 mmol/L. The reference range for normonatraemia
was deﬁned as 138–142 mmol/L. LTC = long-term care; STC = short-term care. Adapted with permission from Wald R et al. Arch
Intern Med
2010; 170: 294–302.11
2.2.3. Hyponatraemia is underdiagnosed and often incorrectly managed, leading to poor patient Despite the association between hyponatraemia and in-hospital mortality, this condition is oftenunderdiagnosed and inappropriately managed,22 due in part to a failure to order sufﬁcient diagnostictests.2,23,24 Ordering appropriate diagnostic tests could inﬂuence patient management and, in somecases, outcomes.23 Incorrect management and a failure to treat hyponatraemia appropriately may adversely affect patient outcomes. In a prospective review of laboratory and chart data from 104 patients with a A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 serum [Na+] <125 mmol/L, identiﬁed at a large teaching hospital in England, 33% of cases were deemedto have ‘signiﬁcant management errors’ (including blind infusion of hypertonic saline in non-criticalsituations and ﬂuid restriction in patients with diuretic-induced hyponatraemia). This inappropriatemanagement was associated with a signiﬁcant increase in excess mortality relative to those patientsthat were managed appropriately (41% vs. 20%, respectively, OR 2.8, 95% CI 1.02–7.55; p = 0.002).23 2.2.4. Acute hyponatraemia can be lethal if not recognised and treated appropriatelyThe imperative to correct hyponatraemia is determined largely by the patient’s symptomatology andthe duration of the hyponatraemia.6 In a study of the symptomatology of severe hyponatraemia(serum [Na+] <125 mmol/L) in a small cohort of patients (n = 14) from San Francisco, the occurrenceof stupor or coma, seizures and mortality were all increased in patients with acute hyponatraemiacompared to those with chronic hyponatraemia of greater than 3 days duration (see Table 4).25 Whilemortality in patients with hyponatraemia may stem from underlying co-morbidities, 36% of the deathsoccurring in patients with acute hyponatraemia in this study were directly attributed to the presenceof a low serum [Na+].25 Due to the potential for complications, acute hyponatraemia is a medicalemergency and should be treated urgently with hypertonic saline.6,26 Table 4
Acute versus chronic hyponatraemia.
Consults at 1 hospital in 1 year; serum [Na+] <128 mmol/L.
Data from Arieff AI et al. Medicine (Baltimore) 1976; 55: 121–129.25
Reproduced with permission from Sterns RH et al. Semin Nephrol 2009; 29: 282–299.26
2.2.5. Chronic hyponatraemia is not asymptomatic but associated with increased patient morbidityRecent studies suggest that mild or chronic hyponatraemia is associated with increased patientmorbidity. An investigation by Renneboog and colleagues reported deﬁcits in gait and attention inpatients with apparently ‘asymptomatic’ chronic hyponatraemia (mean serum [Na+] 126±5 mmol/L),which was improved following the correction of serum [Na+].8 In a further study of 223 patientswith chronic thiazide-induced hyponatraemia (mean serum [Na+] 116 mmol/L), symptoms reportedincluded malaise/lethargy, dizzy spells, vomiting, falls, headaches and seizures.10 Recently, evidence has also been accumulating to suggest that chronic ‘asymptomatic’ hyponatraemia may also have long-term consequences pertaining to bone metabolism, with several studies reportingan association between hyponatraemia and fracture occurrence27 or osteoporosis.28 Investigations intothe mechanism of hyponatraemia-induced bone loss, and the beneﬁts of serum sodium correction onmorbidity and reduction in hospital stay in patients with chronic hyponatraemia, are still ongoing. Itshould be noted that a recent study published after the ﬁrst meeting of the European HyponatraemiaNetwork has demonstrated that sustained low extracellular [Na+] directly stimulates osteoclastogenesisand resorptive activity in vitro.29 2.2.6. Correction of hyponatraemia in patients with SIADH using a vaptan is associated with a reduction The safety and efﬁcacy of the vasopressin V receptor antagonist, tolvaptan, was assessed in the Study of Ascending Levels of Tolvaptan in Hyponatraemia 1 and 2 (SALT-1 and SALT-2), identical prospective,multicentre, randomised, double-blind, placebo-controlled trials comparing treatment with tolvaptan A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 to placebo in raising serum [Na+] in patients with euvolaemic and hypervolaemic hyponatraemia. Thepooled analysis of the SALT-1 and SALT-2 studies included patients with hypotonic hyponatraemiadiagnosed with cirrhosis, heart failure or SIADH and other (i.e., patients that did not meet the diagnosticcriteria for cirrhosis or heart failure).30 In these, tolvaptan was reported to raise serum [Na+] within8 hours of treatment.30 A post-hoc analysis of the SALT-1 and SALT-2 trials conﬁrmed the efﬁcacyand tolerability of tolvaptan in patients with SIADH. Tolvaptan treatment signiﬁcantly improvedserum [Na+] in patients with SIADH over the ﬁrst 4 days of treatment (p < 0.0001), and throughoutthe 30-day study period compared to patients who received placebo.19 This was associated witha signiﬁcantly shorter length of stay in hospital for tolvaptan compared to placebo (4.70 vs. 8.40,respectively, p = 0.045).
2.2.7. Correction of hyponatraemia in patients with SIADH using a vaptan increases patient-reported In addition to assessing changes in serum [Na+], the SALT-1 and SALT-2 trials also investigated changesin self-assessed health status following tolvaptan treatment. In the post-hoc analysis of patients withSIADH, treatment with tolvaptan was reported to increase scores on the 12 Item Short Form (SF-12)General Health Survey.19 A signiﬁcantly greater change in Physical Component Summary (PCS) scorefrom baseline was also noted in patients with SIADH treated with tolvaptan compared to those whoreceived placebo (3.64 vs. −0.16, respectively, p = 0.019). These ﬁndings suggest that patients whoreceived treatment with tolvaptan perceived an improvement in physical functioning.19 Interestingly, a tendency towards an improvement in Mental Component Summary (MCS) score from baseline was also reported (5.47 change from baseline with tolvaptan vs. −0.45 change from baselinewith placebo, p = 0.051). This increase in MCS score was of comparable magnitude to that observedin the full analysis of the SALT trials and approached, but failed to reach, statistical signiﬁcance. Theauthors attributed this to the reduced patient numbers available within the SIADH subgroup analysisreducing the power of the analysis to detect differences between the treatment groups.19 Questions remain about the optimum degree of correction of hyponatraemia in speciﬁc patient populations; however, there is a growing body of evidence to suggest that prompt effective treatmentof hyponatraemia decreases morbidity and length of hospital stay.
2.2.8. Illustrative case historyA 64 year old female was admitted to hospital with a serum [Na+] of 114 mmol/L and fast atrialﬁbrillation, but was discharged after a slow [Na+] increase and a change in medication (bisoprolol inplace of propafenone). The patient was referred to a consultant endocrinologist (Professor C. Thompson,Beaumont Hospital) with poor cognition, myoclonus, a change in personality and serum [Na+] of 125–130 mmol/L. Further investigations were performed (outlined in Table 5). Thyroid function was normal,as was cortisol response to ACTH stimulation test, a CT of the brain, thorax, abdomen and brain MRI.
Table 5
Laboratory results from illustrative case history.
ACTH = Adrenocorticotropic hormone; CT = Computed tomography; T4 = Thyroxine;TSH = Thyroid stimulating hormone; MRI = Magnetic resonance imaging.
Case study provided by Professor C. Thompson.
A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 The patient was provisionally diagnosed with SIADH and initially treated with ﬂuid restriction (restricted to 1 L/day). However, as can often be the case in patients with hyponatraemia, shefound it difﬁcult to comply with ﬂuid restriction, even with hospital supervision. Consequently, thepatient’s serum [Na+] remained between 125 and 130 mmol/L during which time she experiencedepisodic absences and myoclonic jerking. Demeclocycline was subsequently prescribed to decreaseher serum [Na+], however, it had no treatment effect.
Eventually, 17 days after hospitalisation, the patient received tolvaptan which immediately resulted in a controlled increase in serum [Na+] to 140 mmol/L. This corresponded with relief of the patient’ssymptoms and she was discharged four days later (before Christmas). However, after Christmas thepatient’s neurological symptoms returned. A subsequent test for potassium channel antibodies and arepeat MRI revealed hippocampal abnormalities leading to a diagnosis of limbic encephalitis.
Although SIADH associated with limbic encephalitis is rare, this is not the ﬁrst reported case in the literature.31–33 In this instance, resolution of the hyponatraemia provided diagnostic clarity, as thepersistence of symptoms indicated an underlying cerebral pathology. The use of tolvaptan provided aprompt resolution of hyponatraemia, which resulted in clinical improvement (the low-grade seizuresexperienced by the patient occurred less frequently). Prior to treatment, the patient had spent 17 daysin hospital but was discharged 4 days after treatment with tolvaptan was initiated. It is possiblethat the prompt resolution of hyponatraemia could translate to a reduction in the ﬁnancial impact ofhyponatraemia secondary to SIADH following treatment with tolvaptan.
3. Summary
Hyponatraemia may be considered across a spectrum of diseases. While it is necessary to treathyponatraemia, the speed at which treatment is initiated should depend on the presentation of thepatient. Treatment of patients with hyponatraemia with hypertonic saline has been known to causeosmotic demyelination syndrome with overly rapid correction. Other conventional treatments, suchas ﬂuid restriction, have been shown not to be very satisfactory. Novel drugs, such as the vasopressinV receptor antagonist, tolvaptan, may provide an alternative avenue of treatment for the prompt correction of hyponatraemia in patients with hyponatraemia secondary to SIADH. There is a need forfurther randomised controlled trials assessing the relative beneﬁts of newer pharmacological agents,such as tolvaptan, compared with the standard of care.
Practice points
Failure to promptly correct acute, symptomatic hyponatraemia can result in adverse patient The speed of correction of the hyponatraemia should reﬂect its speed of onset – overly rapid correction of chronic hyponatraemia can lead to osmotic demyelination syndrome.
Research agenda
Ongoing randomised, controlled trials comparing treatment with tolvaptan to standard of care in patients with hyponatraemia secondary to SIADH, will add to the evidence already availablefrom existing subgroup analyses.
Reductions in length of hospital stay in patients treated for hyponatraemia need to be The link between hyponatraemia and osteoporosis needs to be investigated further in order to determine the value of treating mild, asymptomatic hyponatraemia.
A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 4. Acknowledgements
This supplement was commissioned by Otsuka Pharmaceutical Europe Ltd. and summarises theproceedings of a meeting organised and supported by Otsuka Pharmaceutical Europe Ltd. The authorshave not received any honorarium in relation to this supplement. Otsuka Pharmaceutical Europe Ltd.
has had the opportunity to comment on the medical content and accuracy of the article and editorialsupport has been provided by Otsuka Pharmaceutical Europe Ltd.; however, ﬁnal editorial contentresides with the authors and Best Practice & Research: Clinical Endocrinology & Metabolism.
5. Conﬂict of interest
Prof. Peri has worked as an advisor for Otsuka Pharmaceutical Europe Ltd. and Otsuka PharmaceuticalItaly S.r.l. and has no other conﬂict of interest related to this publication. Prof. Combe reports to havereceived lecture fees from Otsuka Pharmaceutical and has no other conﬂict of interest related to thispublication.
1. Baylis PH. The syndrome of inappropriate antidiuretic hormone secretion. Int J Biochem Cell Biol 2003; 35: 1495–1499.
2. Hoorn EJ, Lindemans J & Zietse R. Development of severe hyponatraemia in hospitalized patients: treatment-related risk factors and inadequate management. Nephrol Dial Transplant 2006; 21: 70–76.
3. Adrogu ´e HJ & Madias NE. Hyponatremia. N Engl J Med 2000; 342: 1581–1589.
4. Schrier RW & Berl T. The patient with hyponatremia or hypernatremia. In: Schrier W (ed). Manual of Nephrology, pp 22–37.
Philadelphia, Pennsylvania: Lippincott, Williams & Wilkins; 2009.
5. Verbalis JG. Managing hyponatremia in patients with syndrome of inappropriate antidiuretic hormone secretion. Endocrinol Nutr 2010; 57(Suppl. 2): 30–40.
6. Verbalis JG, Goldsmith SR, Greenberg A et al. Hyponatremia treatment guidelines 2007: expert panel recommendations.
Am J Med 2007; 120(11 Suppl. 1): S1–S21.
7. Furst H, Hallows KR, Post J et al. The urine/plasma electrolyte ratio: a predictive guide to water restriction. Am J Med Sci 2000; 319: 240–244.
8. Renneboog B, Musch W, Vandemergel X et al. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deﬁcits. Am J Med 2006; 119: 71.e1–71.e8.
9. Gill G, Huda B, Boyd A et al. Characteristics and mortality of severe hyponatraemia – a hospital-based study. Clin Endocrinol (Oxf) 2006; 65: 246–249.
10. Chow KM, Kwan BC & Szeto CC. Clinical studies of thiazide-induced hyponatremia. J Natl Med Assoc 2004; 96: 1305–1308.
11. Wald R, Jaber BL, Price LL et al. Impact of hospital-associated hyponatremia on selected outcomes. Arch Intern Med 2010; 170: 294–302.
12. Boscoe A, Paramore C & Verbalis JG. Cost of illness of hyponatremia in the United States. Cost Eff Resour Alloc 2006; 4: 10.
13. Ellison DH & Berl T. Clinical practice. The syndrome of inappropriate antidiuresis. N Engl J Med 2007; 356: 2064–2072.
14. Sterns RH, Cappuccio JD, Silver SM & Cohen EP. Neurologic sequelae after treatment of severe hyponatremia: a multicenter
perspective. J Am Soc Nephrol 1994; 4: 1522–1530.
15. Ayus JC & Arieff AI. Chronic hyponatremic encephalopathy in postmenopausal women: association of therapies with morbidity and mortality. JAMA 1999; 281: 2299–2304.
16. Yamamura Y, Nakamura S, Itoh S et al. OPC-41061, a highly potent human vasopressin V2-receptor antagonist: pharmacological proﬁle and aquaretic effect by single and multiple oral dosing in rats. J Pharmacol Exp Ther 1998; 287:
17. Greenberg A & Verbalis JG. Vasopressin receptor antagonists. Kidney Int 2006; 69: 2124–2130.
18. Hirano T, Yamamura Y, Nakamura S et al. Effects of the V(2)-receptor antagonist OPC-41061 and the loop diuretic furosemide alone and in combination in rats. J Pharmacol Exp Ther 2000; 292: 288–294.
19. Verbalis JG, Adler S, Schrier RW et al. Efﬁcacy and safety of oral tolvaptan therapy in patients with the syndrome of inappropriate antidiuretic hormone secretion. Eur J Endocrinol 2011; 164: 725–732.
20. Upadhyay A, Jaber BL & Madias NE. Epidemiology of hyponatremia. Semin Nephrol 2009; 29: 227–238.
21. Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta 2003; 337: 169–172.
22. Miller M, Morley JE & Rubenstein LZ. Hyponatremia in a nursing home population. J Am Geriatr Soc 1995; 43: 1410–1413.
23. Huda MS, Boyd A, Skagen K et al. Investigation and management of severe hyponatraemia in a hospital setting. Postgrad
Med J 2006; 82: 216–219.
24. Hoorn EJ, van der Lubbe N & Zietse R. SIADH and hyponatraemia: why does it matter? NDT Plus 2009; 2(Suppl. 3): iii5–
25. Arieff AI, Llach F & Massry SG. Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. Medicine (Baltimore) 1976; 55: 121–129.
26. Sterns RH, Nigwekar SU & Hix JK. The treatment of hyponatremia. Semin Nephrol 2009; 29: 282–299.
27. Kinsella S, Moran S, Sullivan MO et al. Hyponatremia independent of osteoporosis is associated with fracture occurrence.
Clin J Am Soc Nephrol 2010; 5: 275–280.
A. Peri, C. Combe / Best Practice & Research Clinical Endocrinology & Metabolism 26 (2012) S16S26 28. Verbalis JG, Barsony J, Sugimura Y et al. Hyponatremia-induced osteoporosis. J Bone Miner Res 2010; 25: 554–563.
29. Barsony J, Sugimura Y & Verbalis JG. Osteoclast response to low extracellular sodium and the mechanism of hyponatremia-
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31. Kuriki A, Ishihara K, Satoh H et al. Syndrome of inappropriate secretion of anti-diuretic hormone associated with limbic encephalitis due to herpes simplex virus infection – a case report. Rinsho Shinkeigaku 2008; 48: 184–190.
32. Sakuma K, Kano Y, Fukuhara M & Shiohara T. Syndrome of inappropriate secretion of antidiuretic hormone associated with limbic encephalitis in a patient with drug-induced hypersensitivity syndrome. Clin Exp Dermatol 2008; 33: 287–290.
33. Touz ´e E, Auliac JB, Carras P et al. Limbic encephalitis and SIADH revealing small-cell anaplastic lung cancer: MRI and immunologic ﬁndings. Rev Neurol (Paris) 1998; 154: 539–541.

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Thursday, April 3, 2014

Lent Day 26: God's tender heart

Z is a dear friend of +25 years. She's also one of the best moms and grandmas I've ever met. Every second week, between long one-week work shifts, she  and her husband fly to another state. Not for fun. Not for relaxation. Not for sunshine.

Their daughter and her husband are doctors. So they go to watch their daughter's 3- and 7-year old kids. I'm staggered by the practical love that this couple demonstrates. They could send emails and letters. They could just talk on the phone. Instead, Z and S meet their children and grandkids face to face.

Isn't that just like God's love for us?

Our Father in heaven sent us letters (scriptures) and his emissaries (the prophets). And then, when the time was right, He came and lived among us.

I am astonished by Jesus. He became Immanuel, God with us. More than a political deliverer, he freed us from our broken humanity. He took our burdens and shame. He extended God's forgiveness, wholeness, and abundant life.

Do we care for others in the same way?

"See what [an incredible] quality of love the Father has given (shown, bestowed on) us,
that we should [be permitted to] be named
and called and counted the children of God!
 And so we are!" 1 John 3:1 Amplified

What makes your heart sing when you think about God as Father? About Jesus as our Redeemer? About the Spirit who makes His home in us and guides us in all truth?

Read more:
*Those who mock the poor insult their Maker; those who are glad at calamity will not go unpunished. Proverbs 17:5 NEV

*Jesus says, "When you give a banquet, invite the poor, the crippled, the lame, and the blind. And you will be blessed, because they cannot repay you." Luke 14:13-14 NEV

*Do not repay anyone evil for evil. Be careful to do what is right in the eyes of everyone. If it is possible, as far as it depends on you, live at peace with everyone. Do not take revenge, my dear friends, but leave room for God's wrath, for it is written: "It is mine to avenge; I will repay," says the Lord.

On the contrary: "If your enemy is hungry, feed him; if he is thirsty, give him something to drink. In doing this, you will heap burning coals on his head." Do not be overcome by evil, but overcome evil with good. Romans 12:17-21   NIV

*[We are] looking to Jesus, the founder and perfecter of our faith, who for the joy that was set before him endured the cross, despising the shame, and is seated at the right hand of the throne of God. Hebrews 12:2 ESV

Moravian Prayer: God of all, we thank you that you have included all people into your embrace. Forgive us when we leave people out and inspire us to reach out to include everybody. Amen.

CS Lewis: The Great Divorceon choosing the absence of God in hell over the presence of God

"There are only two kinds of people in the end: those who say to God, ‘Thy will be done’ and those to whom God says, in the end, ‘Thy will be done.’ All that are in Hell choose it. Without that self-choice, there could be no Hell. No soul that seriously and constantly desires joy will ever miss it. Those who seek, find. To those who knock, it is opened.”. . .

“Hell is a state of mind—ye never said a truer word. And every state of mind, left to itself, every shutting up of the creature within the dungeon of its own mind is, in the end, Hell. But Heaven is not a state of mind. Heaven is reality itself. All that is fully real is Heavenly.”. . .

“Hell is smaller than one pebble of your earthly world: but it is smaller than one atom of this world, the Real World. Look at yon butterfly. If it swallowed all Hell, Hell would not be big enough to do it any harm or to have any taste. . . .

“A damned soul is nearly nothing: it is shrunk, shut up in itself. Good beats upon the damned incessantly as sound waves beat on the ears of the deaf, but they cannot receive it. Their fists are clenched, their teeth are clenched, their eyes fast shut. First they will not, in the end they cannot, open their hands for gifts, or their mouths for food, or their eyes to see.”

“Then no one can ever reach them?”

“Only the Greatest of all can make Himself small enough to enter Hell. For the higher a thing is, the lower it can descend—a man can sympathise with a horse but a horse cannot sympathise with a rat. Only One has descended into Hell.”

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Tuesday, October 7, 2014

Two Teas till Tuesday

A find: where to enjoy Indian food
We discover a good Indian restaurant with our friends from India. So Sunday, our post-church lunch is excellent. The debate is where to eat that is not too warm. Ah, a breeze is blowing through the patio. Snag a seat, enjoy a banana leaf plate, and eat with your (newly washed) fingers. Totally yummy. So what if your thumb gets stained yellow by the curries.

Monday, October 7

After class, we run some errands. The bank reminds us that we need our original passports and visas for banking transactions. So our bank business must wait until tomorrow. One more stop before we head home: the water bill has to be paid each month in person,  downtown. (Apparently our bank doesn't do money transfers to pay online. Oh well.)

We're home in time to take a short nap. W's not 100% well yet and I'm tired from a short night. Crash.

The strange juxtaposition that is Bandung: palm trees,
Dutch heritage (a windmill on a bakery), planes overhead,
and the chaos of unregulated buildings
Dr. W crosses the street at 5, from her house to ours. She exclaims over the new arrangement. We've moved furniture, making the rooms more livable with the same stuff we inherited. We haven't added art or made it our own yet.

We share a late tea of homemade apple pancakes, cut papaya and lime, and a few local baked goods. The pancakes are fresh and hot. We've begun a neighborly tradition of taking food home. We always have goodies after visiting Dr. W's house so she happily takes some pancakes for tomorrow's breakfast with her. We talk about how God loves us and how grateful we are for his care.

In the evening, I try to review some of our language studies. A few things are starting to stick in my brain. Acquisition is slow but W insists that we'll reach a critical mass when lots of words will sort themselves out. We're glad to be learning grammar as well as vocabulary. Having a TV helps SO much. We've begun to piece together patterns of how the language is used.

Tuesday, October 8

Watch your feet. A typical
sidewalk ... when there is one.
Today's class focus is review - just the two of us and a tutor, without Augustine and Sumathi. They've flown off for a week, conducting business in India. I miss my friends already. During the half-hour class break, W heads to the bank with our passports. He comes back with the mission accomplished.

We are welcomed home by the usual savory smells of Bu A's cooking. Today she's cut up a fresh mango and baked a casserole of rice, broccoli, cauliflower, and sausage. It's another winner - she has a flair for seasoning! Both W and I have seconds. One of us has thirds. I ask her if she will cook this - (and the gourami fish and the wilted green veges) when we have company. They'll love it!

She and her husband Pak E are living in the house while we're gone next week. He and another fellow will open the ceilings to clean out the insect damage. Theoretically that will clear out most of the mess we live in. I don't really want to be here while that's done! Ibu A will clear out what falls down. I'm hoping to come back to a clean house, but she warns me that the men might not finish the whole place before we get back.

W heads out for a haircut while I wrap my blanket over my head and nap for an hour. It was another short night last night. I woke a few minutes after falling asleep and then couldn't get back to resting until almost midnight. The morning arrived too soon: on Tuesdays and Thursdays, we're up at 5:30am.

Dr. H is a wonderful hostess.
At 4, we get lost on our way to tea at Dr H's place. She's the medical doctor we met on the way to church Sunday. Luckily, we have a phone number. We turn around and go the opposite way. There she is! waiting on the street for us. Her husband cannot speak English and we're not yet fluent in bahasa Indonesia. Soon, we tell ourselves. Soon.

Dr. H speaks excellent English, among other languages. Before she retired, she studied or worked in public health in Thailand, Nepal, Bangladesh, and around Indonesia. Her house is lovely. She's collected ethic art throughout SE Asia. The territorial views from the upper floor - on three sides of the house - are stunning. The rooms wrap around a plant-filled, two-storey atrium that makes us feel like we've stowed away in a secluded greenbelt. The wind rustles the palm fronds reaching for the sky beside us as we sip tea and eat.

Oh my - she has prepared a lot for her high school reunion which ended before we arrived, and also for us. We sample the banana-leaf wrapped rice and Dutch Croquettes. Both delicious. (Regrets because we ate so much of Ibu A's good home-cooking? Ah ... nope. Never.)

Before: the windowsill looks a little worn but not bad
After: simply lift the sill off for evidence: happy termites indeed
The sun has set by the time we get home. House repairs are ongoing. W packs for Seattle and Springfield and is asleep by 8pm. Meanwhile, I write, read, and send out a New Normal photo to subscribers.

Email us at rosemee@hotmail.com, subject line: New Normal, if you'd enjoy a photo every week or two = something that is normal here but not seen in Seattle. There's no obligation and it's one click to unsubscribe if you change your mind.

Read more:
*If you do what is right, will you not be accepted? But if you do not do what is right, sin is crouching at your door; it desires to have you, but you must rule over it. Genesis 4:7 NIV

*Be glad, people of Zion, rejoice in the Lord your God, for he has given you the autumn rains because he is faithful. He sends you abundant showers, both autumn and spring rains, as before. The threshing floors will be filled with grain; the vats will overflow with new wine and oil. Joel 2:23-24 NIV

*Keep alert, stand firm in your faith, be courageous, be strong. 1 Corinthians 16:13 ESV*See what great love the Father has lavished on us, that we should be called children of God! And that is what we are! The reason the world does not know us is that it did not know him. Dear friends, now we are children of God, and what we will be has not yet been made known.

But we know that when Christ appears, we shall be like him, for we shall see him as he is. All who have this hope in him purify themselves, just as he is pure. 1 John 3:1-3 NIV

Moravian Prayer: Great conqueror of sin and death, thank you for the strength and courage that your Spirit provides. Keep us firm in our faith and grounded in truth. Lead us not into temptation but deliver us from the destruction of sin. In the name of Jesus. Amen.

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