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  IN THIS Article
 ::  Introduction
 ::  Material and methods
 ::  Results
 ::  Discussion
 ::  References

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Year : 1982  |  Volume : 28  |  Issue : 2  |  Page : 92-7

Syndrome of inappropriate ADH secretion; prevalence in respiratory disorders.







How to cite this article:
Kudva B T, Kamat S R, Bhandarkar S D. Syndrome of inappropriate ADH secretion; prevalence in respiratory disorders. J Postgrad Med 1982;28:92


How to cite this URL:
Kudva B T, Kamat S R, Bhandarkar S D. Syndrome of inappropriate ADH secretion; prevalence in respiratory disorders. J Postgrad Med [serial online] 1982 [cited 2019 Nov 18];28:92. Available from: http://www.jpgmonline.com/text.asp?1982/28/2/92/5575




  ::   Introduction Top

Syndrome of inappropriate antidiuretic hormone secretion (SIADHS) is a known cause of hyponatremia. When the hyponatremia is severe it can be symptomatic. It is important in treating acutely ill patients with hyponatremia to be aware of the above two facts. This is so because different types of hyponatremia need different managements. In particular, hyponatremia due to SIADHS requires to be managed without administration of salt. Therefore, the diagnosis of SIADHS as a cause of hyponatremia in a given case is important.
SIADHS has been reported to occur in various acute on chronic and chronic medical disorders. The purpose of this study was to find out the frequency of SIADHS in patients with respiratory disorders.

  ::   Material and methods Top

Fifty-one patients with various types of respiratory disorders admitted into the ward of the Department of Chest Medicine were screened for the existence of SIADHS. The diagnosis of SIADHS was made when the following were present.
1. Plasma sodium less than 130 mEq/1.
2. Plasma osmolality less than 275 mOsm/kg.
3. Urine that was hypertonic to plasma.
4. Urinary sodium more than 20 mEq/1.
5. Abnormal water load test.
6. Plasma creatinine, serum albumin and BUN normal or low.
Patients who were on drugs known to cause SIADHS, and those who were in congestive cardiac failure, renal failure, adrenal failure, dehydration or oedematous states were excluded. The detailed history and physical examination of each patient were recorded. The following tests were done-haemogram; fasting and post-lunch blood sugar; liver function tests; blood urea nitrogen; creatinine clearance; plasma and urine sodium, potassium, chloride and osmolality; and water load test. Osmolality was determined with a Fiske Osmometer. The other estimations were done by standard biochemical methods. The water load test was done by administering 20 ml of water per kg of body weight to the fasting patient and measuring urinary output for the next 5 hours. A urinary output less than 8017o of water intake was considered abnormal. Body water excess was calculated as follows.
EBW = 0.6 x CBW x (1- APO)
NPO
where
EBW = Excess body water,
CBW = Current body water,
APO = Actual plasma osmolality,
NPO = Normal plasma osmolality (taken as 285 mOsm/kg).
The diagnosis of the respiratory disorder was established by the conventional tests including X-ray chest, sputum examination, bronchoscopy, lung function tests, blood gas analysis, pleural tapping and biopsy, and lung scan.
The patients received treatment appropriate to their respiratory disorder. Only one patient with hyponatremia (plasma sodium 115 mEq/1) and drowsiness was treated with hypertonic saline infusion. The biochemical tests were repeated- in 46 out of 51 patients after treatment of their respiratory disorder.

  ::   Results Top

[Table - 1] shows the frequency of SIADHS in different groups of patients. It also shows the number of patients in whom SIADHS resolved after treatment.
Twenty four patients had evidence of SIADHS on admission. [Table - 2] shows the differences between the patients who had SIADHS and those who did not have it. As the table shows, the plasma sodium and osmolality were significantly lower in patients with SIADHS than in those without it. The urinary sodium and urinary osmolality were significantly higher in patients with SIADHS. U/P sodium and U/P osmolality ratios were significantly higher in patients with SIADHS. The water excretion was grossly defective in patients with SIADHS, who also showed a body water excess to the tune of 3.54 litres. Not shown in the table are the values for BUN, plasma creatinine and creatinine clearance which showed no significant difference between the two groups.
As the table shows, the tests could be repeated in 19 out of 24 patients who had SIADHS on admission. The parameters of SIADHS reverted to normal in 18 of the 19 patients. One patient in whom they did not revert to normal had inoperable bronchogenic carcinoma. The five patients with SIADHS in whom the test was not repeated after treatment comprised four who took discharge against medical advice and one who was put on vincristine for Ewing's sarcoma with pleural involvement.
As an illustration, we narrate here a case of bronchopneumonia who developed symptomatic hyponatremia due to SIADHS. This was a 42 year old man with E. coli bronchopneumonia. He was admitted with fever and cough with profuse purulent expectoration for 8 days, during which he had become progressively drowsy. On examination, he was emaciated, drowsy and had a pulse rate of 120 per minute, respiratory rate of 30 per minute and blood pressure of 130/90 mm Hg. X-ray of the chest showed normal sized heart, areas of consolidation of varying sizes all over both the lungs and multiple cavities in the right lung. The sputum grew E. coli which were sensitive to gentamicin. Routine plasma biochemistry (sugar, bilirubin, proteins, alkaline phosphatase) was normal. Haemoglobin was 11 gm%; total WBC count was 14,500/cmm, with 90% polymorphs and 10% lymphocytes. The other laboratory findings were as shown in[Table 4].
As the patient was drowsy and had a plasma sodium of 115 mEq/1, he was treated with hypertonic saline intravenously. However, his plasma sodium failed to rise and his drowsiness did not improve during the next 3 days. He was also treated with gentamicin after sputum culture report became available on the third day. He rapidly became afebrile, but his drowsiness took 8 days to disappear. The plasma sodium started rising 4 days after starting gentamicin and returned to normal after 8 days. This case demonstrates that symptomatic hyponatremia due to SIADHS does not respond to salt administration but can resolve with resolution of the underlying cause.

  ::   Discussion Top

Hyponatremia in respiratory disorders seems to have been first described by Winkler and Crankshaw in 1938.[28] Several others in the subsequent years recorded the occurrence of hyponatremia in various respiratory disorders including pulmonary tuberculosis.[2],[5],[8],[14],[15],[16],[18],[21],[22],[24],[25],[26],[27] In 1957, Schwartz et al[20] demonstrated the presence of a substance with bioassayable ADH activity in tumour tissue in bronchogenic carcimia. In 1967, Bartter and Schwartz[3] conceived of the syndrome of inappropriate ADH secretion and laid the following criteria:
(1) Hypo-natremia with corresponding hypo-osmolality of the serum and extra cellular fluid. (2) Continued renal excretion of sodium. 3) Absence of clinical evidence of fluid volume depletion (i.e. normal skin turgor and blood pressure). (4) Osmolality of the urine greater than appropriate for the concomitant toxicity of the plasma i.e. urine less than maximally dilute. (5) Normal renal function. 6) normal adrenal function. These criteria were stated in different terms by Streeten et al.[23] Since then, SIADHS has been described in a variety of conditions including respiratory disorders such as pulmonary tuberculosis, pneumonias, and bronchogenic carcinoma.[1], [2], [4], [9], [11], [12], [13], [17], [19], [23] We have used the criteria as defined by Streeten et al[23] but have additionally used abnormal water load test as a criterion.
No data is available in the literature on the frequency of the occurrence of SIADHS in different respiratory disorders. As the present study shows, SIADHS may occur in as many as 50, per cent of patients with chronic and acute on chronic respiratory diseases. The number of patients in each sub-group was too small to permit determination of frequency in each individual sub-group.
When hyponatremia is detected in a patient, every attempt should be made to rule out SIADHS as its cause. As described earlier, this can be done by using relatively simple tests. The basic management of SIADHS comprises restriction of water intake, in addition to the treatment of the primary disorder. That the administration of salt does not always help in this condition has been well documented in the literature.[9], [23] This is probably because the administered salt is rapidly excreted in the urine as a result of the suppressed plasma aldosterone levels because of expanded plasma volume.[7] The other forms of treatment tried in this condition are demethychlorteracycline,[23] lithium,[23] phenytoin,[23] urea,[10] and intravenous furosemide followed by appropriate sodium and potassium replacements
In general, the prognosis of SIADHS is that of the underlying disorder. But if severe, SIADHS adds to the morbidity of the primary disorder. Finally, since SIADHS may antedate the appearance of a malignancy,[8], [23] recognition of the syndrome may lead to the earlier diagnosis of the malignancy at a time when surgical care is possible.

  ::   References Top

1.Amatruda, T. T. Jr., Mulrow, P. J., Gallaghar, J. C. and Sawyer, W. H.: Carcinoma of the lung with inappropriate antidiuresis. Demonstration of the antidiuretic hormone like activity in tumour extract. New Engl. J. Med., 269: 544-549, 1963.  Back to cited text no. 1    
2.Anderson, G.: Paramalignant syndromes. In, "Recent Advances in Medicine". No. 16, Editors: D. N. Baron, N. Comston and A.. M. Dawson, Churchill Livingstone, Edinburgh and London, 1973, pp. 1-30.   Back to cited text no. 2    
3.Bartter, F. C. and Schwartz, W. B.: The syndrome of inappropriate secretion of antidiuretic hormone. Amer. J. Med., 42: 790-806, 1967.  Back to cited text no. 3    
4.Bower, B. F., Mason, D. M. and Forsham, P. H.: Bronchogenic carcinoma with inappropriate antidiuretic activity in plasma and tumour. New Engl. J. Med., 271: 934-938, 1964.  Back to cited text no. 4    
5.Catell, W. R.: Hypo- and hypernatremic syndromes. In, "Sixth Symposium on Advanced Medicine". Proceedings of a Conference held in the Royal College of Physicians in London from 23rd to 27th February 1970. Editor: J. D. H. Slator, Pitman Medical Publishing Company, London, 1970, pp. 191-202.  Back to cited text no. 5    
6.Chung, D. K. and Hubbard, W. W.: Hyponatremia in untreated active pulmonary tuberculosis. Amer. Rev. Resp. Dis., 99: 595-597, 1969.  Back to cited text no. 6    
7.Cooke, C. R., Turin, M. D. and Walker, W. G.: The syndrome of inappropriate antidiuretic hormone secretion. Pathophysiologic mechanisms in solute and volume regulation. Medicine, 58: 240-251, 1979.  Back to cited text no. 7    
8.Coombes, R. C., Ellison, M.. I. and Neville, A. M.: Biochemical markers in bronchogenic carcinoma. Brit. J. Dis. Chest, 72: 283-287, 1978.  Back to cited text no. 8    
9.Costrini, N. V. and Thomsson, W. M.: Fluid and electrolyte disturbances. In, "Manual of Medical Therapeutics Washington Manual". 22nd Edition, Little Brown and Company, Boston and Igaku Shoin Ltd., Tokyo, 1977, pp. 27-46.  Back to cited text no. 9    
10.Decaux, G., Brimioulle, S., Genette, F. and Mockell, J.: Treatment of the syndrome of inappropriate antidiuretic hormone secretion by urea. Amer. J. Med., 69: 99-106, 1980.  Back to cited text no. 10    
11.George, J. M., Capen, C. C. and Phillips, A. S.: Biosynthesis of vasopressin in vitro and ultrastructure of bronchogenic carcinoma: Patients with syndrome of inappropriate secretion of antidiuretic hormone. J. Clin. Invest., 51: 141-148, 1972.  Back to cited text no. 11    
12.Gilby, E. D., Bondy, P. K. and Forsling, M.: Impaired water excretion in oat cell carcinoma of the lung. Brit. J. Cancer, 34: 323-328, 1976.  Back to cited text no. 12    
13.Ivy. H. K.: Renal sodium and bronchogenic carcinoma: Associated autonomic neuropathy. Arch. Intern. Med., 108: 4755, 1961.  Back to cited text no. 13    
14.Kleeman, C. R. and Vorherr, H.: Hypoosmolar Syndromes. In, "Duncan's Diseases of Metabolism, Genetic Metabolism and Endocrinology." Editors: P. K. Bondy and L. E. Rosenberg, 7th Edition, W. B. Saunders and Company, Philadelphia and London, 1974, pp. 1500-1512.  Back to cited text no. 14    
15.Kolmer, H. S., Elli, D., Smith, T., Collini, P. and Greisheimar, E. M.: Acid base balance in tuberculosis. Amer. Rev. Tuberc., 57: 400-408, 1948.  Back to cited text no. 15    
16.Petty, B. G. and Smith, C. R.: Syndrome of inappropriate secretion with anaerobic thoracic emphyema. Amer. Rev. Resp. Dis., 115: 695-688, 1977.  Back to cited text no. 16    
17.Rees, J. R., Rosalki, S. B. and Maclean, A.. D. W.: Hyponatremia and impaired renal tubular function with carcinoma bronchus. Lancet, 2: 1005-1009, 1960.  Back to cited text no. 17    
18.Rosenow, E. C. III, Segar, W. E. and Zehr, J. E.: Inappropriate antidiuretic hormone secretion in pneumonia. Mayo Clin. Proc., 47: 169-174, 1972.  Back to cited text no. 18    
19.Ross, E. J.: Hyponatremic syndromes associated with carcinoma of the bronchus. Quart. J. Med., 32: 297-320, 1963.  Back to cited text no. 19    
20.Schwartz, W. B., Bennet, W., Curelop, S. A. and Bartter, F. C.: A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Amer. J. Med., 23: 529-542, 1957.  Back to cited text no. 20    
21.Shalhoub, R. J. and Antoniou, L. D.: The mechanism of hyponatremia in pulmonary tuberculosis. Ann. Intern, Med., 70: 943-962, 1969.  Back to cited text no. 21    
22.Sims, E. A. H., Welt, G., Orloff, J. and Needham, J. W.: Asymptomatic hyponatremia in pulmonary tuberculosis. J. Clin. Inves., 29: 1545-1557, 1950.  Back to cited text no. 22    
23.Streeten, D. H. P., Moses, A. M. and Miller, M.: Disorders of neurohypophysis. In, "Harrison's Principles of Internal Medicine". 8th Edition, Editors: Thorn, G. W., Adams, R. D., Braunwald. E., Uselbacher, K. J. and Petersdorf, R. G., McGraw Hill, Kogakusha Ltd., A Blackiston Publication, Tokyo, Auckland, Dusseldorf, Johannesburg, London, Mexico, and New Delhi, 1977, pp. 449-450.  Back to cited text no. 23    
24.Taclob, L. T. and Needle, M. A.: Hyponatremic syndromes. Med. Clin. North Amer., 57: 1423-1433, 1973.  Back to cited text no. 24    
25.Thorn, G. W., Howard, R. P. and Dyman. H.: Electrolyte changes in pulmonary tuberculosis with special reference to adrenal cortical function. Bull. Johns. Hopk. Hosp., 67: 345-364, 1940.  Back to cited text no. 25    
26.Weiss, H. and Katz, S.: Hyponatremia resulting from apparantly inappropriate secretion of antidiuretic hormone in patients with pulmonary tuberculosis. Amer. Rev. Resp. Dis., 92: 609-616, 1965.   Back to cited text no. 26    
27.Westwater, J. O., Stiven, D. and Garry, R. C.: A note on the serum sodium level in patients suffering from tuberculosis. Clin. Sci., 4: 73-77, 1939.  Back to cited text no. 27    
28.Winkler, A. W. and Crankshaw, O. F.: Chloride depletion in conditions other than Addision's disease. J. Clin. Invest., 17: 1-6, 1938.  Back to cited text no. 28    

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