Project OUTCOMEs from 2018-2021 documented by Dr Manasa, MD medicine Resident from 2018
– DISTRIBUTIUON OF HYPONATREMIA CASES IN
IN DIFFERENT AGE GROUPS
DISTRIBUTION OF HYPONATREMIA CASES BASED ON SERUM SODIUM LEVEL
FIGURE 9 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON SERUM SODIUM LEVEl
FIGURE 10 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON SERUM SODIUM LEVEL
Out of the 60 hyponatremia patients studied, only 2 patients have severe
Hyponatremia, majority of patients have mild asympomatic hyponatremia.
Most of the cases of mild hyponatremia are secondary to chronic kidney
Disease.
TABLE 4 – ETIOLOGY OF HYPONATREMIA
FIGURE 11 – ETIOLOGY OF HYPONATREMIA
TABLE 5 – MIXED CAUSES OF HYPONATREMIA
FIGURE 12 – FREQUENCY DISTRIBUTION OF MIXED CAUSES OF HYPONATREMIA
Most common cause of hyponatremia in present study is
Hypervolumic hyponatremia secondary to chronic kidney
Disease. Second most common cause being SIADH followed by
Hypovolemia which is secondary to vomitings,loose stools and
Dehydration.
Hypothyroidism alone rarely causes hyponatremia. Hypothyroidism
Need to be severe (myxedema coma) to cause hyponatremia.
Most of the mixed Causes of hyponatremia are associated
with hypothyroidism. In most of the mixed causes of hyponatremia
which one actually lead to hyponatremia remains Unclear.
TABLE 6 – PRIMARY DISEASES ASSOCIATED WITH HYPONATREMIA
FIGURE 13 – PERCENTAGE DISTRIBUTION OF PRIMARY DISEASES ASSOCIATED WITH HYPONATREMIA
Primary cause of hyponatremia in most of the cases chronic kidney
Disease followed by SIADH .Dehydration Secondary to vomitings, loose
stools and sepsis also contributed to large number of hyponatremia
cases. Surgical causes like Renal colic, appendicitis, intestional
obstruction and pyloric stenosis are the causes of vomiting which lead to
hyponatremia in the study group
TABLE 7 – MISCELLANEOUS PRIMARY DISEASES ASSOCIATED WITH HYPONATREMIA
TABLE 8 – DISTRIBUTION OF CASES BASED ON TONICITY OF HYPONATREMIA
Most of the cases of hyponatremia are hypotonic which includes
Hypovolemic, euvolemic and hypervolemic causes of hyponatremia.
Isotonic hyponatremia is considered as pseudohyponatremia. Hypertonic
Causes of hyponatremia are secondary to hyperglycemia.
FIGURE 14 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON TONICITY
FIGURE 15 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON TONICITY
TABLE 9 – DISTRIBUTION OF HYPONATREMIA CASES BASED ON VOLUME STATUS
FIGURE 16– PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON VOLUME STATUS
FIGURE 17 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON VOLUME STATUS
Hypovolumic and hypervolumic hyponatremia cases are much higher
Compared to euvolemic cases
TABLE 10– DISTRIBUTION OF HYPONATREMIA CASES BASED ON CHRONICITY
FIGURE 18 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON CHRONICITY
FIGURE 19 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON CHRONICITY
Out of the 60 hyponatremia patients studied, 40 are chronic hyponatremia
Patients and 20 are acute hyponatremia cases.
TABLE 11 – TREATMENT OF HYPONATREMIA
FIGURE 20 – TREATMENT OF HYPONATREMIA
Fluids like 0.9% NaCl were given to patients with hypovolumic
Hyponatremia who have signs of dehydration. 3% NaCl was given to
Patients with severe hypovolemic hyponatremia who have neurological
Symptoms. Diuretics were given to patients with hypervolumic
Hyponatremia. Fluid restriction and vaptans were used in SIADH.
Insulin and thyroxine supplementation were used in hyperglycaemia and
Hypothyroidism respectively.
TABLE 12 – DISTRIBUTION OF HYPONATREMIA CASES BASED ON OUTCOME
FIGURE 21 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON OUTCOME
DISCUSSION
The present study included patients with serum sodium less than
130meq/l. there were 42 males and 18 females with ratio of 2.3 : 1 .
In general, more number of males were admitted in KIMS, Narketpally
When compared to females . so no conclusion was made on this
Difference in incidence.
In present study, hyponatremia was seen more commomly in patients
above 45 years of age than in younger patients. youngest patient with
hyponatremia in our study is of 25 years age. Eldest patient is of 87 years
age. Incidence of hyponatremia is higher in elderly patients similar
trend was also observed by Hochman (9) and Vurgese (10) in their study
The hydration status in the present study was noted based on clinical
Examination like capillary refilling time, jugular venous pulse, blood
Pressure, pressure or absence of pedal edema and IVC (inferior vena
Cava diameter) .Hydration status was divided into euvolumic,
Hypovolemic and hypervolemic states. In the present study 26 patients
Were hypovolemic, 22 patients were hypervolemic and 9 patients were
Euvolumic representing 43%, 37% and 15% respectively.
TABLE : 13
In the present study hypervolumic cases are more compared to Hochman
Study. Most of them are secondary to chronic kidney disease as in our
Hospital locality (Nalgonda district) renal failure is commonly which was
Thought to be due to fluorosis. Hypovolemia cases slightly higher than
Both the studies. Most of the hypovolemic cases are due to vomitings,
Loose stools and dehydration. Study also includes surgical causes of
Vomiting which leads to hyponatremia.
Euvolumic cases are less compared to Hochman and Anderson studies
In the present study may due to underdiagnosis of adrenal insufficiency
In our hospital setting and also relatively more cases of ESRD (end stage
Renal disease) which contribute to hypervolumic hyponatremia.
The mean age was 58.4 years. The commonest age group affected was
40 to 79 years. The commonest cause of hyponatremia was chronic
Kidney disease and vomitings,loose stools and dehydration. Next
Common cause was SIADH which was secondary to pneumonia,
Pulmonary tuberculosis and sub arachnoid hemorrhage.
In study done by vurgese, the incidence of hyponatremia was 3.6%
With the defnation of hyponatremia as serum sodium levels less than
Or equal to 130meq/l. the study population consisted of 66 patients with
56%
males and 44 % females. The mean age was 57.07 years. The
Commonest age group affected was 45 to 64 years (72.8 %) and the least
Affected group was 12 to 25 years.
TABLE 14
Hyponatremia cases in the present study were also distributed based on
serum sodium level. Most of the cases of hyponatremia are with the
serum sodium level between the range of 120 to 129 meq/l (39 patients
out of 60 ). most of the cases with mild hyponatremia are hypervolemic
secondary to chronic kidney disease.
In the present study, In patients with euvolumic hyponatremia, 9 patients
satisfied the criteria to diagnose SIADH. They had low serum osmolality,
high urine osmolality and high urine sodium. However, in brain injury
cases like cerebral sinus venous thrombosis (CSVT) if patient presents
with hyponatremia probable diagnosis of hyponatremia can be kept as
SIADH or cerebral salt wasting syndrome. Clear cut differentiation
Between SIADH and cerebral salt wasting syndrome will be very difficult
In the first 24 hours as important differentiating feature between SIADH
And cerebral salt wasting syndrome is urine output.
Hypovolemic cases of hyponatremia are secondary to acute
Gastroenteritis mostly due to Ecoli, salmonella and staph aureus.
Surgical causes of vomiting like intestional obstruction, pyloric stenosis,
Appendicitis and renal colic also contributed to hypovolemic causes of
Hyponatremia. Thiazide diuretics usuage in patients with hypertention
And chronic renal disease also contributed to hypovolemic
hyponatremia.
Hyponatremia secondary to anti psychotic drugs presented with
increased thirst, patient drank 6 to 7 litres of water for 2 days and
passed only 1 to 2 litres of urine each day for 2 days.
Thyroid function tests and adrenal function
Thyroid function tests and random serum cortisol test was done in all
this patients. There are 2 cases of hypothyroidism, in both the patients
cause of hypothyroidism is mixed. In one patient cause of hyponatremia
is both hypothyroidism and thiazide diuretics volume status in this
patient is hypovolemic. In another case cause of cause of hyponatremia
is both hypothyroidism and vomitings secondary to acute illness like
dengue.
Patients with hypovolemic hyponatremia are 26 patients (43 %) among
60 Patients of hyponatremia. Cause of hypovolemic hyponatremia is
Mostly dehydration. Other cause of hypovolemic hyponatremia is
Cerebral salt wasting syndrome. In present study there are 4 cases of
Hypovolemic hyponatremia are cerebral salt wasting syndrome.
Majority of cases in present study are of hypervolumic hyponatremia
Chronic kidney disease is the major cause of hypervolumic
Hyponatremia. Other causes are dilated cardiomyopathy, chronic liver
Disease and mixed causes like CCF + CLD +CKD. Patients with mild
hyponatremia are almost always asymptomatic. Severe hyponatremia is
usually associated with central nervous system symptoms and can be
life-threatening. Diagnostic evaluation of patients with hyponatremia is
directed toward identifying the extracellular fluid volume status, the
neurological symptoms and signs, the severity and duration of
hyponatremia, the rate at which hyponatremia developed. The first step
to determine the probable cause of hyponatremia is the differentiation of
the hypervasopressinemic and non-hypervasopressinemic
hyponatremias with measurement of plasma osmolality, glucose, lipids
and proteins. For further differential diagnosis of hyponatremia, the
determination of urine osmolality, the clinical assessment of
extracellular fluid volume status and the measurement of urine sodium
concentration provide important information. The most important
representative of euvolemic hyponatremias is SIADH. The diagnosis of
SIADH is based on the exclusion of other hyponatremic conditions; low
plasma osmolality (<275 mosmol/kg) and inappropriate urine
concentration (urine osmolality >100 mosmol/kg) are of pathognomic
value. Acute (<48 hrs) severe hyponatremia (<120 mmol/l) necessitates
emergency care with rapid restoration of normal osmotic milieu
(1 mmol/l/hr increase rate of serum sodium). Patients with chronic
symptomatic hyponatremia have a high risk of osmotic demyelination
syndrome in brain if rapid correction of the plasma sodium occurs
(maximal rate of correction of serum sodium should be 0.5 mmol/l/hr or
less). The conventional treatments for chronic asymptomatic
hyponatremia (except hypovolemic patients) include water restriction
and/or the use of demeclocycline or lithium or furosemide and salt
supplementation. Vasopressin receptor antagonists have opened a new
forthcoming therapeutic era. V2 receptor antagonists, such as
lixivaptan, tolvaptan, satavaptan and the V2+V1A receptor antagonist
conivaptan promote the electrolyte-sparing excretion of free water and
lead to increased serum sodium
TREATMENT AND MONITORING
Monitoring of sodium was done on a 6 hourly to12 hourly basis in most
Of the patients with symptomatic and severe hyponatremia.
Fluid correction depended on the type, cause and presence of
symptoms.
The mean rate of correction was adequate and comparable with most of
The international studies. Normal saline alone, 3% saline, fluid
restriction, + duration, dialysis, steroids alone and in combination were
used to treat symptomatic and severe hyponatremia.
Excessive antidiuretic hormone and continued fluid intake are the
pathogenetic causes of these hyponatremias. Whereas hypovolemic
hyponatremia is best corrected by isotonic saline, conventional
proposals for euvolemic and hypervolemic hyponatremia consist of the
following: fluid restriction, lithium carbonate, demeclocycline, urea and
loop diuretic. None of these nonspecific treatments is entirely
satisfactory. Recently a new class of pharmacological agents -orally
available vasopressin antagonists, collectively called vaptans- have
been described. A number of clinical trials using vaptans have been
performed already. They showed vaptans to be effective, specific and
safe in the treatment of euvolemic and hypervolemic hyponatremia.
vaptans generally had favorable effects on fluid balance
also. To date two vaptans, ie, conivaptan and tolvaptan, have been
marketed in the United States for the treatment of euvolemic and
hypervolemic hyponatremia, whereas tolvaptan has been marketed in
Europe with the limitation of euvolemic hyponatremia. Although these
drugs have a good safety profile, caution should be used, and treatment
should be initiated in a hospital setting in order to closely monitor
patients and avoid overly rapid correction or overcorrection. Vaptans
can be considered a new effective tool for the treatment of euvolemic
and hypervolemic hyponatremia. Nevertheless, more comparative
research of vaptans vs other therapies on clinical grounds is needed to
more accurately assess the value of these drugs in the treatment of
hyponatremia. Acute hyponatremia causes serious brain swelling that
can lead to permanent disability or death. A 4-6 mEq/l increase in serum
sodium is sufficient to reverse impending herniation. Brain swelling is
minimal in chronic hyponatremia, and to avoid osmotic demyelination,
correction should not exceed 8 mEq/l/day. In high-risk patients,
correction should not exceed 4-6 mEq/l/day. Inadvertent overcorrection
of hyponatremia is common and preventable by controlling unwanted
urinary water losses with desmopressin. Even mild chronic
hyponatremia is associated with increased mortality, attention deficit,
gait instability, osteoporosis, and fractures, but it is not known if the
correction of mild hyponatremia improves outcomes.
Controlled trials are needed to identify affordable treatments for
hyponatremia that reduce the need for hospitalization, decrease hospital
length of stay, and decrease morbidity. Such trials could also help
answer the question of whether hyponatremia causes excess mortality
or whether it is simply a marker for severe, lethal, underlying disease
CONCLUSIONS
Asymptomatic hyponatremia is more common than symptomatic
Hyponatremia
Renal failure,dehydration and SIADH formed the largest subgroup in the study
Drugs, especially thiazide diuretics are common cause of
Hyponatremia
Incidence of hyponatremia is higher in patients aged above
45years
Symptoms of hyponatremia increased with severity of
Hyponatremia
Neurological symptoms like headache, seizures and altered
Sensorium are commonly seen in severe hyponatremia patients
To distinguish between SIADH and cerebral salt wasting syndrome
In patients of hyponatremia with head injury is difficult
REFERENCES
Rafat, C., Flamant, M., Gaudry, S. et al. Hyponatremia in the intensive care unit: How to avoid a Zugzwang situation?. Ann. Intensive Care 5, 39 (2015).
Sahay M, Sahay R. Hyponatremia: A practical approach. Indian J Endocrinol Metab. 2014;18(6):760-771.
Rondon H, Badireddy M. Hyponatremia. [Updated 2020 Sep 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan
Zieg J. Pathophysiology of Hyponatremia in Children. Front Pediatr. 2017;5:213. Published 2017 Oct 16.
Lee JJ, Kilonzo K, Nistico A, Yeates K. Management of hyponatremia. CMAJ. 2014;186(8):E281-E286.
Schrier RW, Bansal S. Diagnosis and management of hyponatremia in acute illness. Curr Opin Crit Care. 2008;14(6):627-634.
Weismann D, Schneider A, Höybye C. Clinical aspects of symptomatic hyponatremia. Endocr Connect. 2016;5(5):R35-R43.
Dineen R, Thompson CJ, Sherlock M. Hyponatraemia - presentations and management. Clin Med (Lond). 2017;17(3):263-269.
Hochman I, Cabili S, Peer G. Hyponatremia in internal medicine ward patients: cause, treatment and prognosis. Isr J Med Sci 1989; 25: 73 – 6.
Vurgese TA,Radakrishnan ,Mapkar .Frequency and etiology of hyponatremia in adult hospitalised patients in medical wards of a general hospital in Kuwait.kuwait medical journal 2006:38(3):211-213
Gross P. Treatment of hyponatremia. Intern Med. 2008;47(10):885-91. doi: 10.2169/internalmedicine.47.0918. Epub 2008 May 15. PMID: 18480571. Peri A.
Clinical review: the use of vaptans in clinical endocrinology. J Clin Endocrinol Metab. 2013 Apr;98(4):1321-32.
Laczi F. A hyponatraemiás állapotok etiológiája, diagnosztikája és terápiája
Burst V. Etiology and Epidemiology of Hyponatremia. Front Horm Res. 2019;52:24-35. doi: 10.1159/000493234. Epub 2019 Jan 15.
Lu X, Wang X. Hyponatremia induced by antiepileptic drugs in patients with epilepsy. Expert Opin Drug Saf. 2017 Jan;16(1):77-87. doi: 10.1080/14740338.2017.1248399. Epub 2016 Oct 27.
Adrogué HJ, Madias NE. The challenge of hyponatremia. J Am Soc Nephrol. 2012 Jul;23(7):1140-8.
Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol. 2009 May;29(3):282-99.
George JC, Zafar W, Bucaloiu ID, Chang AR. Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia. Clin J Am Soc Nephrol. 2018 Jul 6;13(7):984-992.
John S, Thuluvath PJ. Hyponatremia in cirrhosis: pathophysiology and management. World J Gastroenterol. 2015 Mar 21;21(11):3197-205.
Liamis G, Barkas F, Megapanou E, Christopoulou E, Makri A, Makaritsis K, Ntaios G, Elisaf M, Milionis H. Hyponatremia in Acute Stroke Patients: Pathophysiology, Clinical Significance, and Management Options. Eur Neurol. 2019;82(1-3):32-40.
Gross P, Pusl T. Hyponatriämie [Causes, diagnosis and differential diagnosis of hyponatremia]. Dtsch Med Wochenschr. 2016 Oct;141(21):1543-1548. German.
Chen Z, Jia Q, Liu C. Association of Hyponatremia and Risk of Short- and Long-Term Mortality in Patients with Stroke: A Systematic Review and Meta-Analysis. J Stroke Cerebrovasc Dis. 2019 Jun;28(6):1674-1683.
Dineen R, Thompson CJ, Sherlock M. Hyponatraemia - presentations and management. Clin Med (Lond). 2017 Jun;17(3):263-269.
Tee K, Dang J. The suspect - SIADH. Aust Fam Physician. 2017 Sep;46(9):677-68
Lunøe M, Overgaard-Steensen C. [Prevention of hospital-acquired hyponatremia]. Ugeskr Laeger. 2014 Sep 1;176(36):V03140182.
Braun MM, Barstow CH, Pyzocha NJ. Diagnosis and management of sodium disorders: hyponatremia and hypernatremia. Am Fam Physician. 2015 Mar 1;91(5):299-307. PMID: 25822386.
Feld LG, Neuspiel DR, Foster BA, Leu MG, Garber MD, Austin K, Basu RK, Conway EE Jr, Fehr JJ, Hawkins C, Kaplan RL, Rowe EV, Waseem M, Moritz ML; SUBCOMMITTEE ON FLUID AND ELECTROLYTE THERAPY. Clinical Practice Guideline: Maintenance Intravenous Fluids in Children. Pediatrics. 2018 Dec;142(6):e20183083.
Jones DP. Syndrome of Inappropriate Secretion of Antidiuretic Hormone and Hyponatremia. Pediatr Rev. 2018 Jan;39(1):27-35.
Tanındı A, Töre HF. Hiponatremi tedavisinde Vaptan kullanımı [Use of "Vaptans" in treatment of hyponatremia]. Turk Kardiyol Dern Ars. 2015 Apr;43(3):292-301. Turkish.
Rondon-Berrios H. Urea for Chronic Hyponatremia. Blood Purif. 2020;49(1-2):212-218. Epub 2019 Dec 18.
Jang CM, Jung YK. [Hyponatremia in Liver Cirrhosis]. Korean J Gastroenterol. 2018 Aug 25;72(2):74-78. Korean.
Ackermann D. Therapie von Aszites, Hyponatriämie und hepatorenalem Syndrom bei der Leberzirrhose [Treatment of ascites, hyponatremia and hepatorenal syndrome in liver cirrhosis]. Ther Umsch. 2009 Nov;66(11):747-51. German.
Thomas DR, Cote TR, Lawhorne L, Levenson SA, Rubenstein LZ, Smith DA, Stefanacci RG, Tangalos EG, Morley JE; Dehydration Council. Understanding clinical dehydration and its treatment. J Am Med Dir Assoc. 2008 Jun;9(5):292-301.
Grant P, Ayuk J, Bouloux PM, Cohen M, Cranston I, Murray RD, Rees A, Thatcher N, Grossman A. The diagnosis and management of inpatient hyponatraemia and SIADH. Eur J Clin Invest. 2015 Aug;45(8):888-94.
Verbalis JG, Grossman A, Höybye C, Runkle I. Review and analysis of differing regulatory indications and expert panel guidelines for the treatment of hyponatremia. Curr Med Res Opin. 2014 Jul;30(7):1201-7.
Kitchlu A, Rosner MH. Hyponatremia in patients with cancer. Curr Opin Nephrol Hypertens. 2019 Sep;28(5):433-440.
Pfennig CL, Slovis CM. Sodium disorders in the emergency department: a review of hyponatremia and hypernatremia. Emerg Med Pract. 2012 Oct;14(10):1-26. Epub 2012 Sep 20.
Lee A, Jo YH, Kim K, Ahn S, Oh YK, Lee H, Shin J, Chin HJ, Na KY, Lee JB, Baek SH, Kim S. Efficacy and safety of rapid intermittent correction compared with slow continuous correction with hypertonic saline in patients with moderately severe or severe symptomatic hyponatremia: study protocol for a randomized controlled trial (SALSA trial). Trials. 2017 Mar 29;18(1):147.
Patterson JH. The impact of hyponatremia. Pharmacotherapy. 2011 May;31(5 Suppl):5S-8S.
McNab S. Intravenous maintenance fluid therapy in children. J Paediatr Child Health. 2016 Feb;52(2):137-40.
Aylwin S, Burst V, Peri A, Runkle I, Thatcher N. 'Dos and don'ts' in the management of hyponatremia. Curr Med Res Opin. 2015;31(9):1755-61.
Ball SG, Iqbal Z. Diagnosis and treatment of hyponatraemia. Best Pract Res Clin Endocrinol Metab. 2016 Mar;30(2):161-73.
PROFORMA
S.no sex Ipno. DOA
Age DOD
Weight
Primary diagnosis
H/o present illness
If others please specify
Diet habits:
Fluid intake
Decreased intake
CURRENT MEDICATIONS
CLINICAL FINDINGS
Pulse rate
Blood pressure
Volume status at the time of admission; hypo/hyper/euvolumic
Oedema y/n
Dehydration y/n
Ascitis /paedal edema
Others
BIOCHEMICAL PARAMETERS(AT THE TIME OF ADMISSION)
Serum sodium level
Urine spot sodium
Serum osmolarity
Serum urea
Grbs
Random serum cortisol done/not done
Tft: done/not done
Tsh : free t4
TREATMENT GIVEN
Infusion plan
Diuretics y/n
Fluid restriction y/n
Specific drugs if given
Other treatment
OUTCOME
Asymptomatic/symptomatically better/same status
Discharged/discharged at request/lama/reffered to higher centre
hyponatremia cause:
possible secondary cause
CONSENT FORM
Thesis title ; Etiology, management and outcome in patients with hyponatremia in ICU KIMS, Narketpally
I/We, relative of patient have read and understood the information provided in the “ patient information sheet “ and have been informed and explained the purpose and nature of the study in the language I understand.
Iam aware of the fact that I may not derive any benefit from the study and that I reserve the right to opt out of the study at any point of time
I willingly agree to participate in this study.
Patient’s sign / thumb impression witness’s sign
Name; Name;
Date; Date;
Resident’s sign;
Resident’s name;
Date
